Protein Kinase C
Protein Kinases
Cyclic AMP
Cyclic AMP-Dependent Protein Kinases
Calcium-Calmodulin-Dependent Protein Kinases
Protein-Serine-Threonine Kinases
Mitogen-Activated Protein Kinases
Phosphorylation
MAP Kinase Signaling System
p38 Mitogen-Activated Protein Kinases
Phosphatidylinositol 3-Kinases
Enzyme Activation
Mitogen-Activated Protein Kinase 1
Protein Kinase C-alpha
Mitogen-Activated Protein Kinase Kinases
Protein Kinase C-delta
Mitogen-Activated Protein Kinase 3
Signal Transduction
JNK Mitogen-Activated Protein Kinases
AMP-Activated Protein Kinases
Isoenzymes
Protein Kinase C-epsilon
Protein Kinase C beta
src-Family Kinases
Tetradecanoylphorbol Acetate
Cyclic GMP-Dependent Protein Kinases
Protein-Tyrosine Kinases
Enzyme Inhibitors
Molecular Sequence Data
CDC2 Protein Kinase
Casein Kinase II
Amino Acid Sequence
Cells, Cultured
Calcium-Calmodulin-Dependent Protein Kinase Type 2
MAP Kinase Kinase Kinases
eIF-2 Kinase
p21-Activated Kinases
Calcium
MAP Kinase Kinase 1
Extracellular Signal-Regulated MAP Kinases
Ribosomal Protein S6 Kinases
Protein Binding
Serine
Proto-Oncogene Proteins c-akt
Transfection
Casein Kinases
Blotting, Western
Proto-Oncogene Proteins
MAP Kinase Kinase 4
Phorbol 12,13-Dibutyrate
Cyclin-Dependent Kinases
Substrate Specificity
Mutation
Isoquinolines
Staurosporine
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Phorbol Esters
Base Sequence
Intracellular Signaling Peptides and Proteins
Creatine Kinase
RNA, Messenger
DNA-Activated Protein Kinase
Indoles
Glycogen Synthase Kinase 3
Cyclic AMP-Dependent Protein Kinase Type II
Binding Sites
Pyruvate Kinase
Phosphotransferases (Alcohol Group Acceptor)
3-Phosphoinositide-Dependent Protein Kinases
Apoptosis
Receptor Protein-Tyrosine Kinases
Tumor Cells, Cultured
Dose-Response Relationship, Drug
Tyrosine
rho-Associated Kinases
Adenosine Triphosphate
Gene Expression Regulation, Enzymologic
Recombinant Fusion Proteins
Threonine
Phosphoprotein Phosphatases
Protein Structure, Tertiary
Androstadienes
Mitogen-Activated Protein Kinase 8
Rats, Sprague-Dawley
Sequence Homology, Amino Acid
I-kappa B Kinase
Gene Expression Regulation
Carbazoles
Adenosine Monophosphate
Thymidine Kinase
Immunoblotting
Pyridines
Alkaloids
Cell Division
Ribosomal Protein S6 Kinases, 90-kDa
3T3 Cells
MAP Kinase Kinase Kinase 1
1-Phosphatidylinositol 4-Kinase
CDC2-CDC28 Kinases
Carrier Proteins
Diacylglycerol Kinase
Aurora Kinases
Cytosol
DNA-Binding Proteins
MAP Kinase Kinase 2
Precipitin Tests
Imidazoles
Models, Biological
Transcription, Genetic
Cell Membrane
Cell Cycle Proteins
Cloning, Molecular
Cattle
Myosin-Light-Chain Kinase
8-Bromo Cyclic Adenosine Monophosphate
HeLa Cells
Down-Regulation
Calcium-Calmodulin-Dependent Protein Kinase Kinase
Colforsin
Death-Associated Protein Kinases
Benzophenanthridines
Cyclic GMP
Cyclic GMP-Dependent Protein Kinase Type I
Cell Nucleus
A Kinase Anchor Proteins
MAP Kinase Kinase 6
Transcription Factors
Focal Adhesion Kinase 1
MAP Kinase Kinase 3
Peptide Mapping
Calmodulin
Membrane Proteins
Multienzyme Complexes
Proteins
Rabbits
TOR Serine-Threonine Kinases
Electrophoresis, Polyacrylamide Gel
Cell Cycle
Mitogen-Activated Protein Kinase 14
Focal Adhesion Protein-Tyrosine Kinases
Mitogen-Activated Protein Kinase 9
Mutagenesis, Site-Directed
Protein Transport
Adaptor Proteins, Signal Transducing
Calcium-Calmodulin-Dependent Protein Kinase Type 1
Aminoimidazole Carboxamide
Type C Phospholipases
Fibroblasts
Calcium-Calmodulin-Dependent Protein Kinase Type 4
Cyclic AMP-Dependent Protein Kinase RIalpha Subunit
NF-kappa B
Cell Survival
RNA, Small Interfering
Bucladesine
Cyclic AMP Response Element-Binding Protein
Janus Kinase 2
Phosphothreonine
Mitogen-Activated Protein Kinase 7
DNA Primers
Insulin
Epidermal Growth Factor
Protein Phosphatase 1
Nuclear Proteins
Phosphorylase Kinase
Myocardium
1-Methyl-3-isobutylxanthine
Gene Expression
Mice, Knockout
Catalytic Domain
Okadaic Acid
Casein Kinase I
Phosphotyrosine
Peptides
Glucose
Second Messenger Systems
Up-Regulation
Nitriles
Saccharomyces cerevisiae
Cyclin-Dependent Kinase 5
Cyclin-Dependent Kinase 2
MAP Kinase Kinase 7
AMP-activated protein kinase phosphorylation of endothelial NO synthase. (1/2280)
The AMP-activated protein kinase (AMPK) in rat skeletal and cardiac muscle is activated by vigorous exercise and ischaemic stress. Under these conditions AMPK phosphorylates and inhibits acetyl-coenzyme A carboxylase causing increased oxidation of fatty acids. Here we show that AMPK co-immunoprecipitates with cardiac endothelial NO synthase (eNOS) and phosphorylates Ser-1177 in the presence of Ca2+-calmodulin (CaM) to activate eNOS both in vitro and during ischaemia in rat hearts. In the absence of Ca2+-calmodulin, AMPK also phosphorylates eNOS at Thr-495 in the CaM-binding sequence, resulting in inhibition of eNOS activity but Thr-495 phosphorylation is unchanged during ischaemia. Phosphorylation of eNOS by the AMPK in endothelial cells and myocytes provides a further regulatory link between metabolic stress and cardiovascular function. (+info)AMP-activated protein kinase: an ultrasensitive system for monitoring cellular energy charge. (2/2280)
The AMP-activated protein kinase cascade is activated by elevation of AMP and depression of ATP when cellular energy charge is compromised, leading to inhibition of anabolic pathways and activation of catabolic pathways. Here we show that the system responds in intact cells in an ultrasensitive manner over a critical range of nucleotide concentrations, in that only a 6-fold increase in activating nucleotide is required in order for the maximal activity of the kinase to progress from 10% to 90%, equivalent to a co-operative system with a Hill coefficient (h) of 2.5. Modelling suggests that this sensitivity arises from two features of the system: (i) AMP acts at multiple steps in the cascade (multistep sensitivity); and (ii) the upstream kinase is initially saturated with the downstream kinase (zero-order ultrasensitivity). (+info)AMP-activated kinase reciprocally regulates triacylglycerol synthesis and fatty acid oxidation in liver and muscle: evidence that sn-glycerol-3-phosphate acyltransferase is a novel target. (3/2280)
AMP-activated kinase (AMPK) is activated in response to metabolic stresses that deplete cellular ATP, and in both liver and skeletal muscle, activated AMPK stimulates fatty acid oxidation. To determine whether AMPK might reciprocally regulate glycerolipid synthesis, we studied liver and skeletal-muscle lipid metabolism in the presence of 5-amino-4-imidazolecarboxamide (AICA) riboside, a cell-permeable compound whose phosphorylated metabolite activates AMPK. Adding AICA riboside to cultured rat hepatocytes for 3 h decreased [14C]oleate and [3H]glycerol incorporation into triacylglycerol (TAG) by 50% and 38% respectively, and decreased oleate labelling of diacylglycerol by 60%. In isolated mouse soleus, a highly oxidative muscle, incubation with AICA riboside for 90 min decreased [14C]oleate incorporation into TAG by 37% and increased 14CO2 production by 48%. When insulin was present, [14C]oleate oxidation was 49% lower and [14C]oleate incorporation into TAG was 62% higher than under basal conditions. AICA riboside blocked insulin's antioxidative and lipogenic effects, increasing fatty acid oxidation by 78% and decreasing labelled TAG 43%. Similar results on fatty acid oxidation and acylglycerol synthesis were observed in C2C12 myoblasts, and in differentiated C2C12 myotubes, AICA riboside also inhibited the hydrolysis of intracellular TAG. These data suggest that AICA riboside might inhibit sn-glycerol-3-phosphate acyltransferase (GPAT), which catalyses the committed step in the pathway of glycerolipid biosynthesis. Incubating rat hepatocytes with AICA riboside for both 15 and 30 min decreased mitochondrial GPAT activity 22-34% without affecting microsomal GPAT, diacylglycerol acyltransferase or acyl-CoA synthetase activities. Finally, purified recombinant AMPKalpha1 and AMPKalpha2 inhibited hepatic mitochondrial GPAT in a time-and ATP-dependent manner. These data show that AMPK reciprocally regulates acyl-CoA channelling towards beta-oxidation and away from glycerolipid biosynthesis, and provide strong evidence that AMPK phosphorylates and inhibits mitochondrial GPAT. (+info)Apoptosis induced by growth factor withdrawal in fibroblasts overproducing fructose 2,6-bisphosphate. (4/2280)
Fructose 2,6-bisphosphate is a potent endogenous stimulator of glycolysis. A high aerobic glycolytic rate often correlates with increased cell proliferation. To investigate this relationship, we have produced clonal cell lines of Rat-1 fibroblasts that stably express transgenes coding for 6-phosphofructo-2-kinase, which catalyzes the synthesis of fructose 2,6-bisphosphate, or for fructose 2,6-bisphosphatase, which catalyzes its degradation. While serum deprivation in culture reduced the growth rate of control cells, it caused apoptosis in cells overproducing fructose 2,6-bisphosphate. Apoptosis was inhibited by 5-amino-4-imidazolecarboxamide riboside, suggesting that 5'-AMP-activated protein kinase interferes with this phenomenon. (+info)Evidence for the involvement of the Glc7-Reg1 phosphatase and the Snf1-Snf4 kinase in the regulation of INO1 transcription in Saccharomyces cerevisiae. (5/2280)
Binding of the TATA-binding protein (TBP) to the promoter is a pivotal step in RNA polymerase II transcription. To identify factors that regulate TBP, we selected for suppressors of a TBP mutant that exhibits promoter-specific defects in activated transcription in vivo and severely reduced affinity for TATA boxes in vitro. Dominant mutations in SNF4 and recessive mutations in REG1, OPI1, and RTF2 were isolated that specifically suppress the inositol auxotrophy of the TBP mutant strains. OPI1 encodes a repressor of INO1 transcription. REG1 and SNF4 encode regulators of the Glc7 phosphatase and Snf1 kinase, respectively, and have well-studied roles in glucose repression. In two-hybrid assays, one SNF4 mutation enhances the interaction between Snf4 and Snf1. Suppression of the TBP mutant by our reg1 and SNF4 mutations appears unrelated to glucose repression, since these mutations do not alleviate repression of SUC2, and glucose levels have little effect on INO1 transcription. Moreover, mutations in TUP1, SSN6, and GLC7, but not HXK2 and MIG1, can cause suppression. Our data suggest that association of TBP with the TATA box may be regulated, directly or indirectly, by a substrate of Snf1. Analysis of INO1 transcription in various mutant strains suggests that this substrate is distinct from Opi1. (+info)Phosphorylation control of cardiac acetyl-CoA carboxylase by cAMP-dependent protein kinase and 5'-AMP activated protein kinase. (6/2280)
Acetyl-CoA carboxylase (ACC) is regarded in liver and adipose tissue to be the rate-limiting enzyme for fatty acid biosynthesis; however, in heart tissue it functions as a regulator of fatty acid oxidation. Because the control of fatty acid oxidation is important to the functioning myocardium, the regulation of ACC is a key issue. Two cardiac isoforms of ACC exist, with molecular masses of 265 kDa and 280 kDa (ACC265 and ACC280). In this study, these proteins were purified from rat heart and used in subsequent phosphorylation and immunoprecipitation experiments. Our results demonstrate that 5' AMP-activated protein kinase (AMPK) is able to phosphorylate both ACC265 and ACC280, resulting in an almost complete loss of ACC activity. Although cAMP-dependent protein kinase phosphorylated only ACC280, a dramatic loss of ACC activity was still observed, suggesting that ACC280 contributes most, if not all, of the total heart ACC activity. ACC280 and ACC265 copurified under all experimental conditions, and purification of heart ACC also resulted in the specific copurification of the alpha2 isoform of the catalytic subunit of AMPK. Although both catalytic subunits of AMPK were expressed in crude heart homogenates, our results suggest that alpha2, and not alpha1, is the dominant isoform of AMPK catalytic subunit regulating ACC in the heart. Immunoprecipitation studies demonstrated that specific antibodies for both ACC265 and ACC280 were able to coimmunoprecipitate the alternate isoform along with the alpha2 isoform of AMPK. Taken together, the immunoprecipitation and the purification studies suggest that the two isoforms of ACC in the heart exist in a heterodimeric structure, and that this structure is tightly associated with the alpha2 subunit of AMPK. (+info)Effect of AMPK activation on muscle glucose metabolism in conscious rats. (7/2280)
The effect of AMP-activated protein kinase (AMPK) activation on skeletal muscle glucose metabolism was examined in awake rats by infusing them with 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR; 40 mg/kg bolus and 7.5 mg. kg-1. min-1 constant infusion) along with a variable infusion of glucose (49.1 +/- 2.4 micromol. kg-1. min-1) to maintain euglycemia. Activation of AMPK by AICAR caused 2-deoxy-D-[1,2-3H]glucose (2-DG) uptake to increase more than twofold in the soleus and the lateral and medial gastrocnemius compared with saline infusion and occurred without phosphatidylinositol 3-kinase activation. Glucose uptake was also assessed in vitro by use of the epitrochlearis muscle incubated either with AICAR (0.5 mM) or insulin (20 mU/ml) or both in the presence or absence of wortmannin (1.0 microM). AICAR and insulin increased muscle 2-DG uptake rates by approximately 2- and 2.7-fold, respectively, compared with basal rates. Combining AICAR and insulin led to a fully additive effect on muscle glucose transport activity. Wortmannin inhibited insulin-stimulated glucose uptake. However, neither wortmannin nor 8-(p-sulfophenyl)-theophylline (10 microM), an adenosine receptor antagonist, inhibited the AICAR-induced activation of glucose uptake. Electrical stimulation led to an about threefold increase in glucose uptake over basal rates, whereas no additive effect was found when AICAR and contractions were combined. In conclusion, the activation of AMPK by AICAR increases skeletal muscle glucose transport activity both in vivo and in vitro. This cellular pathway may play an important role in exercise-induced increase in glucose transport activity. (+info)AMP-activated protein kinase, a metabolic master switch: possible roles in type 2 diabetes. (8/2280)
Adenosine 5'-monophosphate-activated protein kinase (AMPK) now appears to be a metabolic master switch, phosphorylating key target proteins that control flux through metabolic pathways of hepatic ketogenesis, cholesterol synthesis, lipogenesis, and triglyceride synthesis, adipocyte lipolysis, and skeletal muscle fatty acid oxidation. Recent evidence also implicates AMPK as being responsible for mediating the stimulation of glucose uptake induced by muscle contraction. In addition, the secretion of insulin by insulin secreting (INS-1) cells in culture is modulated by AMPK activation. The net effect of AMPK activation is stimulation of hepatic fatty acid oxidation and ketogenesis, inhibition of cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibition of adipocyte lipolysis and lipogenesis, stimulation of skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulation of insulin secretion by pancreatic beta-cells. In skeletal muscle, AMPK is activated by contraction. Type 2 diabetes mellitus is likely to be a disease of numerous etiologies. However, defects or disuse (due to a sedentary lifestyle) of the AMPK signaling system would be predicted to result in many of the metabolic perturbations observed in Type 2 diabetes mellitus. Increased recruitment of the AMPK signaling system, either by exercise or pharmaceutical activators, may be effective in correcting insulin resistance in patients with forms of impaired glucose tolerance and Type 2 diabetes resulting from defects in the insulin signaling cascade. (+info)Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
Medical Term: Cardiomegaly
Definition: An abnormal enlargement of the heart.
Symptoms: Difficulty breathing, shortness of breath, fatigue, swelling of legs and feet, chest pain, and palpitations.
Causes: Hypertension, cardiac valve disease, myocardial infarction (heart attack), congenital heart defects, and other conditions that affect the heart muscle or cardiovascular system.
Diagnosis: Physical examination, electrocardiogram (ECG), chest x-ray, echocardiography, and other diagnostic tests as necessary.
Treatment: Medications such as diuretics, vasodilators, and beta blockers, lifestyle changes such as exercise and diet modifications, surgery or other interventions in severe cases.
Note: Cardiomegaly is a serious medical condition that requires prompt diagnosis and treatment to prevent complications such as heart failure and death. If you suspect you or someone else may have cardiomegaly, seek medical attention immediately.
Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.
There are several different types of neuroblastoma, including:
1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.
Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:
* Abdominal pain
* Fever
* Loss of appetite
* Weight loss
* Fatigue
* Bone pain
* Swelling in the abdomen or neck
* Constipation
* Increased heart rate
Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
There are several types of lung neoplasms, including:
1. Adenocarcinoma: This is the most common type of lung cancer, accounting for approximately 40% of all lung cancers. It is a malignant tumor that originates in the glands of the respiratory tract and can be found in any part of the lung.
2. Squamous cell carcinoma: This type of lung cancer accounts for approximately 25% of all lung cancers and is more common in men than women. It is a malignant tumor that originates in the squamous cells lining the airways of the lungs.
3. Small cell lung cancer (SCLC): This is a highly aggressive form of lung cancer that accounts for approximately 15% of all lung cancers. It is often found in the central parts of the lungs and can spread quickly to other parts of the body.
4. Large cell carcinoma: This is a rare type of lung cancer that accounts for only about 5% of all lung cancers. It is a malignant tumor that originates in the large cells of the respiratory tract and can be found in any part of the lung.
5. Bronchioalveolar carcinoma (BAC): This is a rare type of lung cancer that originates in the cells lining the airways and alveoli of the lungs. It is more common in women than men and tends to affect older individuals.
6. Lymphangioleiomyomatosis (LAM): This is a rare, progressive, and often fatal lung disease that primarily affects women of childbearing age. It is characterized by the growth of smooth muscle-like cells in the lungs and can lead to cysts, lung collapse, and respiratory failure.
7. Hamartoma: This is a benign tumor that originates in the tissue of the lungs and is usually found in children. It is characterized by an overgrowth of normal lung tissue and can be treated with surgery.
8. Secondary lung cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
9. Metastatic cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
10. Mesothelioma: This is a rare and aggressive form of cancer that originates in the lining of the lungs or abdomen. It is caused by asbestos exposure and can be treated with surgery, chemotherapy, and radiation therapy.
Lung diseases can also be classified based on their cause, such as:
1. Infectious diseases: These are caused by bacteria, viruses, or other microorganisms and can include pneumonia, tuberculosis, and bronchitis.
2. Autoimmune diseases: These are caused by an overactive immune system and can include conditions such as sarcoidosis and idiopathic pulmonary fibrosis.
3. Genetic diseases: These are caused by inherited mutations in genes that affect the lungs and can include cystic fibrosis and primary ciliary dyskinesia.
4. Environmental diseases: These are caused by exposure to harmful substances such as tobacco smoke, air pollution, and asbestos.
5. Radiological diseases: These are caused by exposure to ionizing radiation and can include conditions such as radiographic breast cancer and lung cancer.
6. Vascular diseases: These are caused by problems with the blood vessels in the lungs and can include conditions such as pulmonary embolism and pulmonary hypertension.
7. Tumors: These can be benign or malignant and can include conditions such as lung metastases and lung cancer.
8. Trauma: This can include injuries to the chest or lungs caused by accidents or other forms of trauma.
9. Congenital diseases: These are present at birth and can include conditions such as bronchopulmonary foregut malformations and congenital cystic adenomatoid malformation.
Each type of lung disease has its own set of symptoms, diagnosis, and treatment options. It is important to seek medical attention if you experience any persistent or severe respiratory symptoms, as early diagnosis and treatment can improve outcomes and quality of life.
Symptoms of pheochromocytoma can include:
* Rapid heartbeat
* High blood pressure
* Sweating
* Weight loss
* Fatigue
* Headaches
* Nausea and vomiting
If left untreated, pheochromocytoma can lead to complications such as heart failure, stroke, and even death. Therefore, it is important that individuals who experience any of the above symptoms seek medical attention as soon as possible.
Treatment options for pheochromocytoma may include surgery to remove the tumor, medication to manage symptoms, and in some cases, radiation therapy. In rare cases, the tumor may recur after treatment, so regular monitoring is necessary to ensure that any new symptoms are detected early on.
Overall, while pheochromocytoma is a rare and potentially life-threatening condition, prompt medical attention and appropriate treatment can help manage symptoms and prevent complications.
There are several types of colonic neoplasms, including:
1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.
Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.
Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.
1. Tumor size and location: Larger tumors that have spread to nearby tissues or organs are generally considered more invasive than smaller tumors that are confined to the original site.
2. Cellular growth patterns: The way in which cancer cells grow and divide can also contribute to the overall invasiveness of a neoplasm. For example, cells that grow in a disorganized or chaotic manner may be more likely to invade surrounding tissues.
3. Mitotic index: The mitotic index is a measure of how quickly the cancer cells are dividing. A higher mitotic index is generally associated with more aggressive and invasive cancers.
4. Necrosis: Necrosis, or the death of cells, can be an indication of the level of invasiveness of a neoplasm. The presence of significant necrosis in a tumor is often a sign that the cancer has invaded surrounding tissues and organs.
5. Lymphovascular invasion: Cancer cells that have invaded lymphatic vessels or blood vessels are considered more invasive than those that have not.
6. Perineural invasion: Cancer cells that have invaded nerve fibers are also considered more invasive.
7. Histological grade: The histological grade of a neoplasm is a measure of how abnormal the cancer cells look under a microscope. Higher-grade cancers are generally considered more aggressive and invasive than lower-grade cancers.
8. Immunohistochemical markers: Certain immunohistochemical markers, such as Ki-67, can be used to evaluate the proliferative activity of cancer cells. Higher levels of these markers are generally associated with more aggressive and invasive cancers.
Overall, the degree of neoplasm invasiveness is an important factor in determining the likelihood of the cancer spreading to other parts of the body (metastasizing) and in determining the appropriate treatment strategy for the patient.
There are several types of gliomas, including:
1. Astrocytoma: This is the most common type of glioma, accounting for about 50% of all cases. It arises from the star-shaped cells called astrocytes that provide support and nutrients to the brain's nerve cells.
2. Oligodendroglioma: This type of glioma originates from the oligodendrocytes, which are responsible for producing the fatty substance called myelin that insulates the nerve fibers.
3. Glioblastoma (GBM): This is the most aggressive and malignant type of glioma, accounting for about 70% of all cases. It is fast-growing and often spreads to other parts of the brain.
4. Brain stem glioma: This type of glioma arises in the brain stem, which is responsible for controlling many of the body's vital functions such as breathing, heart rate, and blood pressure.
The symptoms of glioma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory, or speech.
Gliomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and tissue biopsy to confirm the presence of cancer cells. Treatment options for glioma depend on the type and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment to remove as much of the tumor as possible, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells.
The prognosis for glioma patients varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the prognosis is better for patients with slow-growing, low-grade tumors, while those with fast-growing, high-grade tumors have a poorer prognosis. Overall, the 5-year survival rate for glioma patients is around 30-40%.
1. Activation of oncogenes: Some viruses contain genes that code for proteins that can activate existing oncogenes in the host cell, leading to uncontrolled cell growth.
2. Inactivation of tumor suppressor genes: Other viruses may contain genes that inhibit the expression of tumor suppressor genes, allowing cells to grow and divide uncontrollably.
3. Insertional mutagenesis: Some viruses can insert their own DNA into the host cell's genome, leading to disruptions in normal cellular function and potentially causing cancer.
4. Epigenetic changes: Viral infection can also cause epigenetic changes, such as DNA methylation or histone modification, that can lead to the silencing of tumor suppressor genes and the activation of oncogenes.
Viral cell transformation is a key factor in the development of many types of cancer, including cervical cancer caused by human papillomavirus (HPV), and liver cancer caused by hepatitis B virus (HBV). In addition, some viruses are specifically known to cause cancer, such as Kaposi's sarcoma-associated herpesvirus (KSHV) and Merkel cell polyomavirus (MCV).
Early detection and treatment of viral infections can help prevent the development of cancer. Vaccines are also available for some viruses that are known to cause cancer, such as HPV and hepatitis B. Additionally, antiviral therapy can be used to treat existing infections and may help reduce the risk of cancer development.
There are several types of melanoma, including:
1. Superficial spreading melanoma: This is the most common type of melanoma, accounting for about 70% of cases. It usually appears as a flat or slightly raised discolored patch on the skin.
2. Nodular melanoma: This type of melanoma is more aggressive and accounts for about 15% of cases. It typically appears as a raised bump on the skin, often with a darker color.
3. Acral lentiginous melanoma: This type of melanoma affects the palms of the hands, soles of the feet, or nail beds and accounts for about 5% of cases.
4. Lentigo maligna melanoma: This type of melanoma usually affects the face and is more common in older adults.
The risk factors for developing melanoma include:
1. Ultraviolet (UV) radiation exposure from the sun or tanning beds
2. Fair skin, light hair, and light eyes
3. A history of sunburns
4. Weakened immune system
5. Family history of melanoma
The symptoms of melanoma can vary depending on the type and location of the cancer. Common symptoms include:
1. Changes in the size, shape, or color of a mole
2. A new mole or growth on the skin
3. A spot or sore that bleeds or crusts over
4. Itching or pain on the skin
5. Redness or swelling around a mole
If melanoma is suspected, a biopsy will be performed to confirm the diagnosis. Treatment options for melanoma depend on the stage and location of the cancer and may include surgery, chemotherapy, radiation therapy, or a combination of these. Early detection and treatment are key to successful outcomes in melanoma cases.
In conclusion, melanoma is a type of skin cancer that can be deadly if not detected early. It is important to practice sun safety, perform regular self-exams, and seek medical attention if any suspicious changes are noticed on the skin. By being aware of the risk factors, symptoms, and treatment options for melanoma, individuals can take steps to protect themselves from this potentially deadly disease.
Malignant prostatic neoplasms are cancerous tumors that can be aggressive and spread to other parts of the body (metastasize). The most common type of malignant prostatic neoplasm is adenocarcinoma of the prostate, which accounts for approximately 95% of all prostate cancers. Other types of malignant prostatic neoplasms include sarcomas and small cell carcinomas.
Prostatic neoplasms can be diagnosed through a variety of tests such as digital rectal examination (DRE), prostate-specific antigen (PSA) test, imaging studies (ultrasound, CT scan or MRI), and biopsy. Treatment options for prostatic neoplasms depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health. Treatment options can include active surveillance, surgery (robotic-assisted laparoscopic prostatectomy or open prostatectomy), radiation therapy (external beam radiation therapy or brachytherapy), and hormone therapy.
In summary, Prostatic Neoplasms are tumors that occur in the prostate gland, which can be benign or malignant. The most common types of malignant prostatic neoplasms are adenocarcinoma of the prostate, and other types include sarcomas and small cell carcinomas. Diagnosis is done through a variety of tests, and treatment options depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health.
MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.
The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.
The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.
The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.
Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.
In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.
There are several types of hypertrophy, including:
1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).
Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.
In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.
Some common types of adrenal gland neoplasms include:
1. Adrenocortical carcinoma: A rare and aggressive malignancy that arises in the outer layer of the adrenal cortex.
2. Adrenocortical adenoma: A benign tumor that arises in the outer layer of the adrenal cortex.
3. Pheochromocytoma: A rare tumor that arises in the inner part of the adrenal medulla and produces excessive amounts of hormones such as epinephrine and norepinephrine.
4. Paraganglioma: A rare tumor that arises in the sympathetic nervous system, often near the adrenal glands.
Symptoms of adrenal gland neoplasms can include:
* Weight gain or weight loss
* High blood pressure
* Fatigue
* Abdominal pain
* Headache
* Nausea and vomiting
* Palpitations
Diagnosis of adrenal gland neoplasms typically involves imaging tests such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and positron emission tomography (PET) scans, as well as hormone level assessments. Treatment options vary depending on the type and size of the tumor, and may include surgery, chemotherapy, and hormone therapy.
There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
There are several factors that can contribute to the development of insulin resistance, including:
1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.
There are several ways to diagnose insulin resistance, including:
1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.
There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:
1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.
Medications that may be used to treat insulin resistance include:
1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.
It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.
Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.
There are several types of myocardial ischemia, including:
1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.
Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.
Glioblastomas are highly malignant tumors that can grow rapidly and infiltrate surrounding brain tissue, making them difficult to remove surgically. They often recur after treatment and are usually fatal within a few years of diagnosis.
The symptoms of glioblastoma can vary depending on the location and size of the tumor but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory or cognitive function.
Glioblastomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and a biopsy to confirm the presence of cancerous cells. Treatment typically involves surgery to remove as much of the tumor as possible, followed by radiation therapy and chemotherapy to slow the growth of any remaining cancerous cells.
Prognosis for glioblastoma is generally poor, with a five-year survival rate of around 5% for newly diagnosed patients. However, the prognosis can vary depending on factors such as the location and size of the tumor, the patient's age and overall health, and the effectiveness of treatment.
There are several risk factors for developing HCC, including:
* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity
HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:
* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss
If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:
* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope
Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:
* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer
Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.
Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:
1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)
The symptoms of adenocarcinoma depend on the location of the cancer and can include:
1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
7. Fatigue
8. Coughing up blood (in the case of lung adenocarcinoma)
The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.
Treatment options for adenocarcinoma depend on the location of the cancer and can include:
1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.
The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.
The BCR-ABL gene is a fusion gene that is present in the majority of cases of CML. It is created by the translocation of two genes, called BCR and ABL, which leads to the production of a constitutively active tyrosine kinase protein that promotes the growth and proliferation of abnormal white blood cells.
There are three main phases of CML, each with distinct clinical and laboratory features:
1. Chronic phase: This is the earliest phase of CML, where patients may be asymptomatic or have mild symptoms such as fatigue, night sweats, and splenomegaly (enlargement of the spleen). The peripheral blood count typically shows a high number of blasts in the blood, but the bone marrow is still functional.
2. Accelerated phase: In this phase, the disease progresses to a higher number of blasts in the blood and bone marrow, with evidence of more aggressive disease. Patients may experience symptoms such as fever, weight loss, and pain in the joints or abdomen.
3. Blast phase: This is the most advanced phase of CML, where there is a high number of blasts in the blood and bone marrow, with significant loss of function of the bone marrow. Patients are often symptomatic and may have evidence of spread of the disease to other organs, such as the liver or spleen.
Treatment for CML typically involves targeted therapy with drugs that inhibit the activity of the BCR-ABL protein, such as imatinib (Gleevec), dasatinib (Sprycel), or nilotinib (Tasigna). These drugs can slow or stop the progression of the disease, and may also produce a complete cytogenetic response, which is defined as the absence of all Ph+ metaphases in the bone marrow. However, these drugs are not curative and may have significant side effects. Allogenic hematopoietic stem cell transplantation (HSCT) is also a potential treatment option for CML, but it carries significant risks and is usually reserved for patients who are in the blast phase of the disease or have failed other treatments.
In summary, the clinical course of CML can be divided into three phases based on the number of blasts in the blood and bone marrow, and treatment options vary depending on the phase of the disease. It is important for patients with CML to receive regular monitoring and follow-up care to assess their response to treatment and detect any signs of disease progression.
Examples of experimental liver neoplasms include:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.
The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.
There are several types of skin neoplasms, including:
1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.
While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.
Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.
There are several different types of pathologic neovascularization, including:
* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.
The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.
In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.
PALL is a rare form of leukemia, accounting for only about 5-10% of all cases of acute leukemia. It is most commonly seen in adults between the ages of 40 and 60, although it can occur at any age.
The symptoms of PALL are similar to those of other types of leukemia and may include fatigue, fever, night sweats, weight loss, and an enlarged spleen. The diagnosis of PALL is typically made through a combination of physical examination, medical history, and laboratory tests, including a bone marrow biopsy.
Treatment for PALL usually involves chemotherapy, which can be effective in achieving a complete remission in many cases. In some instances, bone marrow transplantation may also be considered as a form of treatment. The prognosis for PALL is generally poor, with a five-year survival rate of about 20-30%. However, with prompt and appropriate treatment, many people with PALL can achieve long-term remission and a good quality of life.
Erythroleukemia typically affects adults in their 50s and 60s, although it can occur at any age. Symptoms may include fever, night sweats, weight loss, and fatigue. The cancer cells can spread to other parts of the body, including the spleen, liver, and lymph nodes.
Erythroleukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore normal blood cell production. In some cases, a bone marrow transplant may be necessary. The prognosis for erythroleukemia is generally poor, with a five-year survival rate of about 20%.
Erythroleukemia is classified as an acute leukemia, meaning it progresses rapidly and can lead to life-threatening complications if left untreated. It is important for patients to receive prompt and appropriate treatment to improve their chances of survival and quality of life.
Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
There are several subtypes of astrocytoma, including:
1. Low-grade astrocytoma: These tumors grow slowly and are less aggressive. They can be treated with surgery, radiation therapy, or chemotherapy.
2. High-grade astrocytoma: These tumors grow more quickly and are more aggressive. They are often resistant to treatment and may recur after initial treatment.
3. Anaplastic astrocytoma: These are the most aggressive type of astrocytoma, growing rapidly and spreading to other parts of the brain.
4. Glioblastoma (GBM): This is the most common and deadliest type of primary brain cancer, accounting for 55% of all astrocytomas. It is highly aggressive and resistant to treatment, often recurring after initial surgery, radiation, and chemotherapy.
The symptoms of astrocytoma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality or behavior.
Astrocytomas are diagnosed through a combination of imaging tests such as MRI or CT scans, and tissue biopsy. Treatment options vary depending on the type and location of the tumor, but may include surgery, radiation therapy, chemotherapy, or a combination of these.
The prognosis for astrocytoma varies based on the subtype and location of the tumor, as well as the patient's age and overall health. In general, low-grade astrocytomas have a better prognosis than high-grade tumors. However, even with treatment, the survival rate for astrocytoma is generally lower compared to other types of cancer.
There are several different types of leukemia, including:
1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.
Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
Pancreatic adenocarcinoma is the most common type of malignant pancreatic neoplasm and accounts for approximately 85% of all pancreatic cancers. It originates in the glandular tissue of the pancreas and has a poor prognosis, with a five-year survival rate of less than 10%.
Pancreatic neuroendocrine tumors (PNETs) are less common but more treatable than pancreatic adenocarcinoma. These tumors originate in the hormone-producing cells of the pancreas and can produce excess hormones that cause a variety of symptoms, such as diabetes or high blood sugar. PNETs are classified into two main types: functional and non-functional. Functional PNETs produce excess hormones and are more aggressive than non-functional tumors.
Other rare types of pancreatic neoplasms include acinar cell carcinoma, ampullary cancer, and oncocytic pancreatic neuroendocrine tumors. These tumors are less common than pancreatic adenocarcinoma and PNETs but can be equally aggressive and difficult to treat.
The symptoms of pancreatic neoplasms vary depending on the type and location of the tumor, but they often include abdominal pain, weight loss, jaundice, and fatigue. Diagnosis is typically made through a combination of imaging tests such as CT scans, endoscopic ultrasound, and biopsy. Treatment options for pancreatic neoplasms depend on the type and stage of the tumor but may include surgery, chemotherapy, radiation therapy, or a combination of these.
Prognosis for patients with pancreatic neoplasms is generally poor, especially for those with advanced stages of disease. However, early detection and treatment can improve survival rates. Research into the causes and mechanisms of pancreatic neoplasms is ongoing, with a focus on developing new and more effective treatments for these devastating diseases.
SCC typically appears as a firm, flat, or raised bump on the skin, and may be pink, red, or scaly. The cancer cells are usually well-differentiated, meaning they resemble normal squamous cells, but they can grow rapidly and invade surrounding tissues if left untreated.
SCC is more common in fair-skinned individuals and those who spend a lot of time in the sun, as UV radiation can damage the skin cells and increase the risk of cancer. The cancer can also spread to other parts of the body, such as lymph nodes or organs, and can be life-threatening if not treated promptly and effectively.
Treatment for SCC usually involves surgery to remove the cancerous tissue, and may also include radiation therapy or chemotherapy to kill any remaining cancer cells. Early detection and treatment are important to improve outcomes for patients with SCC.
The term "basophilic" refers to the staining properties of these abnormal cells, which have a distinctive appearance under a microscope. The disease is often referred to as "acute" because it progresses rapidly and can be fatal within weeks or months if left untreated.
There are two main subtypes of basophilic leukemia: acute and chronic. Acute basophilic leukemia is the more aggressive and common form of the disease, accounting for approximately 75% of all cases. It typically affects adults in their 40s and 50s and is characterized by a high white blood cell count, anemia, and splenomegaly (enlargement of the spleen).
Chronic basophilic leukemia, on the other hand, is a rarer form of the disease that progresses more slowly and typically affects adults in their 60s and 70s. It is characterized by a lower white blood cell count, splenomegaly, and an increased risk of developing myelodysplastic syndrome (a precancerous condition).
The exact cause of basophilic leukemia is not known, but it is believed to be linked to genetic mutations and exposure to certain chemicals or radiation. Treatment typically involves chemotherapy and/or bone marrow transplantation, and the prognosis varies depending on the subtype and overall health of the patient.
Types of experimental neoplasms include:
* Xenografts: tumors that are transplanted into animals from another species, often humans.
* Transgenic tumors: tumors that are created by introducing cancer-causing genes into an animal's genome.
* Chemically-induced tumors: tumors that are caused by exposure to certain chemicals or drugs.
The use of experimental neoplasms in research has led to significant advances in our understanding of cancer biology and the development of new treatments for the disease. However, the use of animals in cancer research is a controversial topic and alternatives to animal models are being developed and implemented.
Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.
There are several types of liver neoplasms, including:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.
The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.
Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.
Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.
There are several subtypes of carcinoma, including:
1. Adenocarcinoma: This type of carcinoma originates in glandular cells, which produce fluids or mucus. Examples include breast cancer, prostate cancer, and colon cancer.
2. Squamous cell carcinoma: This type of carcinoma originates in squamous cells, which are found on the surface layers of skin and mucous membranes. Examples include head and neck cancers, cervical cancer, and anal cancer.
3. Basal cell carcinoma: This type of carcinoma originates in the deepest layer of skin, called the basal layer. It is the most common type of skin cancer and tends to grow slowly.
4. Neuroendocrine carcinoma: This type of carcinoma originates in cells that produce hormones and neurotransmitters. Examples include lung cancer, pancreatic cancer, and thyroid cancer.
5. Small cell carcinoma: This type of carcinoma is a highly aggressive form of lung cancer that spreads quickly to other parts of the body.
The signs and symptoms of carcinoma depend on the location and stage of the cancer. Some common symptoms include:
* A lump or mass
* Pain
* Skin changes, such as a new mole or a change in the color or texture of the skin
* Changes in bowel or bladder habits
* Abnormal bleeding
The diagnosis of carcinoma typically involves a combination of imaging tests, such as X-rays, CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a small sample of tissue for examination under a microscope. Treatment options for carcinoma depend on the location and stage of the cancer and may include surgery, radiation therapy, chemotherapy, or a combination of these.
In conclusion, carcinoma is a type of cancer that originates in epithelial cells and can occur in various parts of the body. Early detection and treatment are important for improving outcomes.
References:
1. American Cancer Society. (2022). Carcinoma. Retrieved from
2. Mayo Clinic. (2022). Carcinoma. Retrieved from
3. MedlinePlus. (2022). Carcinoma. Retrieved from
Hyperalgesia is often seen in people with chronic pain conditions, such as fibromyalgia, and it can also be a side effect of certain medications or medical procedures. Treatment options for hyperalgesia depend on the underlying cause of the condition, but may include pain management techniques, physical therapy, and medication adjustments.
In clinical settings, hyperalgesia is often assessed using a pinprick test or other pain tolerance tests to determine the patient's sensitivity to different types of stimuli. The goal of treatment is to reduce the patient's pain and improve their quality of life.
Starvation is a condition where an individual's body does not receive enough nutrients to maintain proper bodily functions and growth. It can be caused by a lack of access to food, poverty, poor nutrition, or other factors that prevent the intake of sufficient calories and essential nutrients. Starvation can lead to severe health consequences, including weight loss, weakness, fatigue, and even death.
Types of Starvation:
There are several types of starvation, each with different causes and effects. These include:
1. Acute starvation: This occurs when an individual suddenly stops eating or has a limited access to food for a short period of time.
2. Chronic starvation: This occurs when an individual consistently does not consume enough calories and nutrients over a longer period of time, leading to gradual weight loss and other health problems.
3. Malnutrition starvation: This occurs when an individual's diet is deficient in essential nutrients, leading to malnutrition and other health problems.
4. Marasmus: This is a severe form of starvation that occurs in children, characterized by extreme weight loss, weakness, and wasting of muscles and organs.
5. Kwashiorkor: This is a form of malnutrition caused by a diet lacking in protein, leading to edema, diarrhea, and other health problems.
Effects of Starvation on the Body:
Starvation can have severe effects on the body, including:
1. Weight loss: Starvation causes weight loss, which can lead to a decrease in muscle mass and a loss of essential nutrients.
2. Fatigue: Starvation can cause fatigue, weakness, and a lack of energy, making it difficult to perform daily activities.
3. Weakened immune system: Starvation can weaken the immune system, making an individual more susceptible to illnesses and infections.
4. Nutrient deficiencies: Starvation can lead to a deficiency of essential nutrients, including vitamins and minerals, which can cause a range of health problems.
5. Increased risk of disease: Starvation can increase the risk of diseases such as tuberculosis, pellagra, and other infections.
6. Mental health issues: Starvation can lead to mental health issues such as depression, anxiety, and irritability.
7. Reproductive problems: Starvation can cause reproductive problems, including infertility and miscarriage.
8. Hair loss: Starvation can cause hair loss, which can be a sign of malnutrition.
9. Skin problems: Starvation can cause skin problems, such as dryness, irritation, and infections.
10. Increased risk of death: Starvation can lead to increased risk of death, especially in children and the elderly.
It is important to note that these effects can be reversed with proper nutrition and care. If you or someone you know is experiencing starvation, it is essential to seek medical attention immediately.
Neoplastic metastasis can occur in any type of cancer but are more common in solid tumors such as carcinomas (breast, lung, colon). It is important for cancer diagnosis and prognosis because metastasis indicates that the cancer has spread beyond its original site and may be more difficult to treat.
Metastases can appear at any distant location but commonly found sites include the liver, lungs, bones, brain, and lymph nodes. The presence of metastases indicates a higher stage of cancer which is associated with lower survival rates compared to localized cancer.
Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.
There are several different types of brain neoplasms, including:
1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.
These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.
Some common types of pituitary neoplasms include:
1. Adenomas: These are benign tumors that grow slowly and often do not cause any symptoms in the early stages.
2. Craniopharyngiomas: These are rare, slow-growing tumors that can be benign or malignant. They can affect the pituitary gland, the hypothalamus, and other areas of the brain.
3. Pituitary carcinomas: These are malignant tumors that grow quickly and can spread to other parts of the body.
4. Pituitary metastases: These are tumors that have spread to the pituitary gland from another part of the body, such as breast cancer or lung cancer.
Symptoms of pituitary neoplasms can vary depending on the size and location of the tumor, but they may include:
* Headaches
* Vision changes, such as blurred vision or loss of peripheral vision
* Hormonal imbalances, which can lead to a variety of symptoms including fatigue, weight gain or loss, and irregular menstrual cycles
* Cognitive changes, such as memory loss or difficulty with concentration
* Pressure on the brain, which can cause nausea, vomiting, and weakness or numbness in the limbs
Diagnosis of pituitary neoplasms typically involves a combination of imaging tests, such as MRI or CT scans, and hormone testing to determine the level of hormones in the blood. Treatment options can vary depending on the type and size of the tumor, but they may include:
* Watchful waiting: Small, benign tumors may not require immediate treatment and can be monitored with regular imaging tests.
* Medications: Hormone replacement therapy or medications to control hormone levels may be used to manage symptoms.
* Surgery: Tumors can be removed through a transsphenoidal surgery, which involves removing the tumor through the nasal cavity and sphenoid sinus.
* Radiation therapy: May be used to treat residual tumor tissue after surgery or in cases where the tumor cannot be completely removed with surgery.
Overall, pituitary neoplasms are rare and can have a significant impact on the body if left untreated. If you suspect you may have a pituitary neoplasm, it is important to seek medical attention for proper diagnosis and treatment.
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
There are different types of hyperplasia, depending on the location and cause of the condition. Some examples include:
1. Benign hyperplasia: This type of hyperplasia is non-cancerous and does not spread to other parts of the body. It can occur in various tissues and organs, such as the uterus (fibroids), breast tissue (fibrocystic changes), or prostate gland (benign prostatic hyperplasia).
2. Malignant hyperplasia: This type of hyperplasia is cancerous and can invade nearby tissues and organs, leading to serious health problems. Examples include skin cancer, breast cancer, and colon cancer.
3. Hyperplastic polyps: These are abnormal growths that occur in the gastrointestinal tract and can be precancerous.
4. Adenomatous hyperplasia: This type of hyperplasia is characterized by an increase in the number of glandular cells in a specific organ, such as the colon or breast. It can be a precursor to cancer.
The symptoms of hyperplasia depend on the location and severity of the condition. In general, they may include:
* Enlargement or swelling of the affected tissue or organ
* Pain or discomfort in the affected area
* Abnormal bleeding or discharge
* Changes in bowel or bladder habits
* Unexplained weight loss or gain
Hyperplasia is diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and biopsy. Treatment options depend on the underlying cause and severity of the condition, and may include medication, surgery, or other interventions.
The hallmark symptoms of AT are:
1. Ataxia: difficulty with coordination, balance, and gait.
2. Telangiectasias: small, red blood vessels visible on the skin, particularly on the face, neck, and arms.
3. Ocular telangiectasias: small, red blood vessels visible in the eyes.
4. Cognitive decline: difficulty with memory, learning, and concentration.
5. Seizures: episodes of abnormal electrical activity in the brain.
6. Increased risk of cancer: particularly lymphoma, myeloid leukemia, and breast cancer.
The exact cause of AT is not yet fully understood, but it is thought to be due to mutations in the ATM gene, which is involved in DNA damage response and repair. There is currently no cure for AT, but various treatments are available to manage its symptoms and prevent complications. These may include:
1. Physical therapy: to improve coordination and balance.
2. Occupational therapy: to assist with daily activities and fine motor skills.
3. Speech therapy: to improve communication and swallowing difficulties.
4. Medications: to control seizures, tremors, and other symptoms.
5. Cancer screening: regular monitoring for the development of cancer.
AT is a rare disorder, and it is estimated that only about 1 in 40,000 to 1 in 100,000 individuals are affected worldwide. It is important for healthcare providers to be aware of AT and its symptoms, as early diagnosis and intervention can improve outcomes for patients with this condition.
There are several types of osteosarcomas, including:
1. High-grade osteosarcoma: This is the most common type of osteosarcoma and tends to grow quickly.
2. Low-grade osteosarcoma: This type of osteosarcoma grows more slowly than high-grade osteosarcoma.
3. Chondrosarcoma: This is a type of osteosarcoma that arises in the cartilage cells of the bone.
4. Ewing's family of tumors: These are rare types of osteosarcoma that can occur in any bone of the body.
The exact cause of osteosarcoma is not known, but certain risk factors may increase the likelihood of developing the disease. These include:
1. Previous radiation exposure
2. Paget's disease of bone
3. Li-Fraumeni syndrome (a genetic disorder that increases the risk of certain types of cancer)
4. Familial retinoblastoma (a rare inherited condition)
5. Exposure to certain chemicals, such as herbicides and industrial chemicals.
Symptoms of osteosarcoma may include:
1. Pain in the affected bone, which may be worse at night or with activity
2. Swelling and redness around the affected area
3. Limited mobility or stiffness in the affected limb
4. A visible lump or mass on the affected bone
5. Fractures or breaks in the affected bone
If osteosarcoma is suspected, a doctor may perform several tests to confirm the diagnosis and determine the extent of the disease. These may include:
1. Imaging studies, such as X-rays, CT scans, or MRI scans
2. Biopsy, in which a sample of tissue is removed from the affected bone and examined under a microscope for cancer cells
3. Blood tests to check for elevated levels of certain enzymes that are produced by osteosarcoma cells
4. Bone scans to look for areas of increased activity or metabolism in the bones.
Types of Experimental Diabetes Mellitus include:
1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.
Experimental Diabetes Mellitus has several applications in research, including:
1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.
In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.
There are several possible causes of hyperglycemia, including:
1. Diabetes: This is a chronic condition where the body either does not produce enough insulin or cannot use insulin effectively.
2. Insulin resistance: This occurs when the body's cells become less responsive to insulin, leading to high blood sugar levels.
3. Pancreatitis: This is inflammation of the pancreas, which can lead to high blood sugar levels.
4. Cushing's syndrome: This is a rare hormonal disorder that can cause high blood sugar levels.
5. Medications: Certain medications, such as steroids and some types of antidepressants, can raise blood sugar levels.
6. Stress: Stress can cause the release of hormones such as cortisol and adrenaline, which can raise blood sugar levels.
7. Infections: Certain infections, such as pneumonia or urinary tract infections, can cause high blood sugar levels.
8. Trauma: Traumatic injuries can cause high blood sugar levels due to the release of stress hormones.
9. Surgery: Some types of surgery, such as heart bypass surgery, can cause high blood sugar levels.
10. Pregnancy: High blood sugar levels can occur during pregnancy, especially in women who have a history of gestational diabetes.
Hyperglycemia can cause a range of symptoms, including:
1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Headaches
5. Cuts or bruises that are slow to heal
6. Tingling or numbness in the hands and feet
7. Dry, itchy skin
8. Flu-like symptoms, such as weakness, dizziness, and stomach pain
9. Recurring skin, gum, or bladder infections
10. Sexual dysfunction in men and women
If left untreated, hyperglycemia can lead to serious complications, including:
1. Diabetic ketoacidosis (DKA): A life-threatening condition that occurs when the body produces high levels of ketones, which are acidic substances that can cause confusion, nausea, and vomiting.
2. Hypoglycemia: Low blood sugar levels that can cause dizziness, confusion, and even loss of consciousness.
3. Nerve damage: High blood sugar levels over an extended period can damage the nerves, leading to numbness, tingling, and pain in the hands and feet.
4. Kidney damage: The kidneys may become overworked and damaged if they are unable to filter out the excess glucose in the blood.
5. Eye damage: High blood sugar levels can cause damage to the blood vessels in the eyes, leading to vision loss and blindness.
6. Cardiovascular disease: Hyperglycemia can increase the risk of cardiovascular disease, including heart attacks, strokes, and peripheral artery disease.
7. Cognitive impairment: Hyperglycemia has been linked to cognitive impairment and an increased risk of dementia.
It is essential to manage hyperglycemia by making lifestyle changes, such as following a healthy diet, regular exercise, and taking medication if prescribed by a healthcare professional. Monitoring blood sugar levels regularly can help identify the signs of hyperglycemia and prevent long-term complications.
There are two main types of myotonic dystrophy:
1. Type 1 (also known as DM1): This is the most common form of the disorder and affects about 90% of all cases. It is caused by a mutation in the DMPK gene on chromosome 19.
2. Type 2 (also known as DM2): This form of the disorder is less common and affects about 10% of all cases. It is caused by a mutation in the CNBP gene on chromosome 3.
Symptoms of myotonic dystrophy typically appear in adults between the ages of 20 and 40, but can sometimes be present at birth. They may include:
* Muscle stiffness and rigidity
* Weakness of the face, neck, and limbs
* Difficulty swallowing (dysphagia)
* Difficulty speaking or slurred speech (dysarthria)
* Eye problems, such as cataracts or muscle imbalance in the eyelids
* Cramps and muscle spasms
* Fatigue and weakness
* Slowed muscle relaxation after contraction (myotonia)
Myotonic dystrophy is diagnosed through a combination of physical examination, medical history, and genetic testing. There is currently no cure for the disorder, but various treatments can help manage symptoms and slow its progression. These may include:
* Physical therapy to improve muscle strength and function
* Medications to relax muscles and reduce spasms
* Speech therapy to improve communication and swallowing difficulties
* Occupational therapy to assist with daily activities and independence
* Orthotics and assistive devices to help with mobility and other challenges
It is important for individuals with myotonic dystrophy to work closely with their healthcare providers to manage their symptoms and maintain a good quality of life. With appropriate treatment and support, many people with the disorder are able to lead active and fulfilling lives.
There are several types of lymphoma, including:
1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.
The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:
* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching
Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.
Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.
Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.
There are many different types of fibrosis, including:
* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.
Fibrosis can be diagnosed through a variety of methods, including:
* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.
There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:
* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.
It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.
AMP-activated protein kinase
Protein kinase, AMP-activated, alpha 1
Life extension
PRKAG1
Theo Wallimann
Diet and cancer
Antipyretic
Carotid body
PRKAG3
PRKAG2
PRKAB2
Acadesine
MTORC1
Food-entrainable oscillator
List of drugs banned by the World Anti-Doping Agency
Randle cycle
Metformin
Aspirin
Glycogenesis
Stress granule
ACACB
Arie Lev Gruzman
HMG-CoA reductase
CBS domain
Ribosomal RNA
Protein kinase A
Adrenaline
Hypoxia in fish
Histone deacetylase 5
Pinealocyte
Olfactory receptor neuron
Histone H2B
INPP5D
PDE4B
NFATC4
Cystic fibrosis transmembrane conductance regulator
Dephospho-(reductase kinase) kinase
Glycogen phosphorylase
CAB39
Ubiquitin
CCL8
Obesogen
Glycolysis
Adenosine monophosphate
Ribonucleotide
RAPGEF2
Autosomal dominant polycystic kidney disease
SESN1
Sperm chemotaxis
CREB1
Mushroom bodies
NUAK2
G beta-gamma complex
RPS6KA1
FYN
PDE4D
Alpha cell
No data available that match "amp activated protein kinases"
AMPK34
- At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism. (nih.gov)
- 5′-AMP-activated protein kinase (AMPK) is important for metabolic sensing. (diabetesjournals.org)
- 5′-AMP-activated protein kinase (AMPK) is a cellular energy sensor that responds to alterations in the AMP-to-ATP ratio. (diabetesjournals.org)
- The adenosine monophosphate (AMP)-activated protein kinase (AMPK) has a crucial role in maintaining cellular energy homeostasis. (rupress.org)
- This study shows that human and mouse T lymphocytes express AMPKα1 and that this is rapidly activated in response to triggering of the T cell antigen receptor (TCR). (rupress.org)
- However, TCR and Ca 2+ stimulation of AMPK required the activity of Ca 2+ -calmodulin-dependent protein kinase kinases (CaMKKs), whereas AMPK activation induced by increased AMP/ATP ratios did not. (rupress.org)
- The rapid activation of AMPK in response to Ca 2+ signaling in T lymphocytes thus reveals that TCR triggering is linked to an evolutionally conserved serine kinase that regulates energy metabolism. (rupress.org)
- AMP-activated protein kinase (AMPK) is a central enzyme of cellular energy balance and metabolism that has been shown to confer cardio- protection and antioxidant defense which thereby contributes to vascular health . (bvsalud.org)
- Collectively, these observations indicate that AKG extends Drosophila lifespan by activating AMPK signaling and inhibiting the mTOR pathway. (nih.gov)
- Analysis of possible processes involved in these alterations indicated that AMP-activated protein kinase (AMPK), a cell energy sensor that intervenes in angiogenic signaling and interacts with IGF-I, was also abnormally activated in APP/PS2 brains. (nih.gov)
- Although these effects were also independently elicited by IGF-I, when both IGF-I and AMPK pathways were simultaneously activated on brain endothelial cells, VEGF production and endothelial cell proliferation ceased while cells remained metabolically activated (glucose use, peroxide production, and mitochondrial activity were elevated) and became more resistant to oxidative stress. (nih.gov)
- This technology relates to the identification and use of a group of compounds that activate the AMP-activated protein kinase (AMPK) and also effectively reduce lysosomal cholesterol accumulation in patients with Niemann-Pick disease Type C (NPC). (nih.gov)
- A computer modeling was used to identify the group of compounds that bind and activate AMPK. (nih.gov)
- In addition, the allosteric modulation of AMPK function by these compounds is more tolerable as a treatment because beta-cyclodextrin directly activates the AMPK alpha-subunit which can cause significant cytotoxicity. (nih.gov)
- To better understand the role of AMPK mutations in HCM/WPW and other inherited cardiomyophathies, all 7 subunit genes were screened for mutations in a panel of probands: 3 with HCM/WPW, 4 with DCM/WPW, 38 with HCM alone (in whom contractile protein mutations had not been found) and 13 with DCM alone. (ox.ac.uk)
- AMP-activated protein kinase (AMPK) is responsible for sensing of the cell's energetic status and it phosphorylates numerous substrates involved in anabolic and catabolic processes as well as interacting with signaling cascades. (ox.ac.uk)
- As part of a study to examine the role of AMPK in the heart, we tested whether specific domains of the thick filament component cardiac myosin binding protein-C (cMyBP-C) were good in vitro AMPK substrates. (ox.ac.uk)
- In vitro phosphorylation with activated kinase showed that the purified fusion protein was a good AMPK substrate, phosphorylated at a similar rate to the control SAMS peptide and with phosphate incorporation specifically in serine residues. (ox.ac.uk)
- Recent studies have implicated an enzyme called AMP-activated protein kinase (AMPK). (nih.gov)
- We have shown that when we activate the [AMPK] gene in the intestine or the nervous system, we see the aging process is slowed beyond the organ system in which the gene is activated," Walker says. (nih.gov)
- The PRKAG2 gene provides instructions for making one part (the gamma-2 subunit) of a larger enzyme called AMP-activated protein kinase (AMPK). (medlineplus.gov)
- 17. Salicylate activates AMPK and synergizes with metformin to reduce the survival of prostate and lung cancer cells ex vivo through inhibition of de novo lipogenesis. (nih.gov)
- 18. AMPed up to treat prostate cancer: novel AMPK activators emerge for cancer therapy. (nih.gov)
- 20. AMPK: A metabolic checkpoint that regulates the growth of EGFR activated glioblastomas. (nih.gov)
- We herein demonstrated that AMP-activated protein kinase (AMPK) and adenylate kinase (ADK) cooperated to maintain cellular ATP levels regardless of glucose levels. (elifesciences.org)
- The present study demonstrates that cellular ATP homeostasis ensures proteostasis and revealed that suppressing the high volatility of cellular ATP levels prevented cytotoxic protein aggregation, implying that AMPK and ADK are important factors that prevent proteinopathies, such as neurodegenerative diseases. (elifesciences.org)
- In addition, GA inhibited the de novo lipogenesis of cancer cells through inducing activation of AMP-activated protein kinase (AMPK) signaling and downregulated the expression of key enzymes (e.g. acetyl-CoA carboxylase [ACC], fatty acid synthase [FASN]) involved in lipogenesis. (oncotarget.com)
- The genes control the protein AMP-activated protein kinase (AMPK), an enzyme that is switched on when you exercise. (mcmaster.ca)
- Less receptor binding in turn leads to chronic activation of AMP-activated protein kinase (AMPK), a key regulator of energy homeostasis and fat metabolism. (nih.gov)
- They theorized that when AMPK is chronically activated, it becomes less sensitive to imbalances in energy demand and nutrient supply. (nih.gov)
- Testing that theory, the researchers chemically inhibited the chronically activated AMPK in the patient-derived RPE model and found fewer deposits of apolipoprotein E, and less abnormal secretion of vascular endothelial growth factor. (nih.gov)
- [ 4 ] STK11 functions as a tumor suppressor gene and is involved in the activation of AMP-activated protein kinase (AMPK), which modulates cell glucose and lipid metabolism. (medscape.com)
- AMP-activated protein kinase (AMPK) is a sensor of cellular energy status that plays a central role in skeletal muscle metabolism. (wellnessresources.com)
- 5. FGF21 does not require adipocyte AMP-activated protein kinase (AMPK) or the phosphorylation of acetyl-CoA carboxylase (ACC) to mediate improvements in whole-body glucose homeostasis. (nih.gov)
Adenosine5
- AMP-activated protein kinase regulates chemical pathways involving the cell's main energy source, a molecule called adenosine triphosphate (ATP). (medlineplus.gov)
- My central area of research concerns the pharmacology and biochemistry of G protein-coupled receptors (in particular, cannabinoid, adenosine and glutamate) in the CNS and peripheral tissues. (nottingham.ac.uk)
- Adenosine triphosphate (ATP) at millimolar levels has recently been implicated in the solubilization of cellular proteins. (elifesciences.org)
- Adenosine monophosphate (AMP) -- One of the four nucleotides in an RNA molecule. (nih.gov)
- Harms improves insulin resistance and hepatic lipid accumulation by modulation of liver adenosine monophosphate-activated protein kinase activity and lipogenic gene expression in high-fat diet-fed obese mice. (nih.gov)
Phosphorylation6
- Salicylate binds at the same site as the synthetic activator A-769662 to cause allosteric activation and inhibition of dephosphorylation of the activating phosphorylation site, threonine-172. (nih.gov)
- Determination of AMP-activated protein kinase phosphorylation sites in recombinant protein expressed using the pET28a vector: a cautionary tale. (ox.ac.uk)
- Dr Miratul Muqit, MRC Protein Phosphorylation and Ubiquitylation Unit, Dundee. (cam.ac.uk)
- To study whether estrogen has a nonclassical effect on basal forebrain cholinergic system, we measured the intensity of cAMP response element-binding protein (CREB) phosphorylation (pCREB) in cholinergic neurons after administration of 17beta-estradiol to ovariectomized (OVX) mice. (nih.gov)
- Oxidative phosphorylation on the other hand in general favors an anti-inflammatory phenotype such as that of alternatively activated M2 macrophages and regulatory T cells (T reg ). (nature.com)
- 2-Deoxy-d-glucose increases GFAT1 phosphorylation resulting in endoplasmic reticulum-related apoptosis via disruption of protein N-glycosylation in pancreatic cancer cells. (harvard.edu)
Subunit2
- The mutation responsible for this condition changes a single protein building block (amino acid) in the gamma-2 subunit of AMP-activated protein kinase. (medlineplus.gov)
- These mutations change single amino acids in the gamma-2 subunit of AMP-activated protein kinase. (medlineplus.gov)
Mtor2
LKB13
- Here we show that inactivation of the frequently mutated tumour suppressor gene LKB1 (encoding liver kinase B1) has evolving effects throughout the progression of lung cancer, which leads to the differential epigenetic re-programming of early-stage primary tumours compared with late-stage metastases. (nih.gov)
- Using an in vivo model of metastatic progression, we further show that loss of LKB1 activates the early endoderm transcription factor SOX17 in metastases and a metastatic-like sub-population of cancer cells within primary tumours. (nih.gov)
- Serine/threonine kinase 11 ( STK11 ), also known as liver kinase B1 ( LKB1 ), is a gene found on chromosome 19p13. (medscape.com)
Mutation1
- L-ORD is caused by a mutation in the gene that encodes the protein CTRP5. (nih.gov)
Pathway3
- The brain on drugs Drugs elevate CREB activity in the nucleus accumbens by activating cyclic AMP pathway, causing protein kinase A to translocate to the nucleus and phosphorylate CREB. (the-scientist.com)
- 17. Arctigenin suppresses transforming growth factor-β1-induced expression of monocyte chemoattractant protein-1 and the subsequent epithelial-mesenchymal transition through reactive oxygen species-dependent ERK/NF-κB signaling pathway in renal tubular epithelial cells. (nih.gov)
- 9. Metformin decreases high-fat diet-induced renal injury by regulating the expression of adipokines and the renal AMP-activated protein kinase/acetyl-CoA carboxylase pathway in mice. (nih.gov)
Intracellular3
- Elevation of intracellular cyclic AMP levels leads to diverse cellular responses dependent on the cell type. (nottingham.ac.uk)
- Intracellular signaling protein kinases that play a signaling role in the regulation of cellular energy metabolism. (nih.gov)
- cAMP acts as an intracellular signaling molecule by activating cyclic-AMP-dependent protein kinase. (nih.gov)
Epithelial cells2
Metabolism1
- AMP-activated protein kinases modify enzymes involved in LIPID METABOLISM , which in turn provide substrates needed to convert AMP into ATP . (nih.gov)
Enzyme1
- Prominent examples include reprogramming a classically activated M1 macrophage towards a more anti-inflammatory M2 macrophage using dimethyl fumarate (DMF, a drug currently approved for the treatment of multiple sclerosis), metformin (which is used to treat Type 2 diabetes) 2 or TEPP-46 which promotes the tetramerization of the key glycolytic enzyme Pyruvate kinase M2 (PKM2). (nature.com)
Mitochondrial2
- Mitochondria produce several small polypeptides that may influence mitochondrial function and may impact on insulin sensitivity, such as humanin (HN) and the mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c) that are mitochondrial derived proteins (MDP). (frontiersin.org)
- Perilipin 5, a lipid droplet protein adapted to mitochondrial energy utilization. (nih.gov)
Autophagy2
- A potential mechanism has been proposed indicating that beta-cyclodextrin activated AMP-activated protein kinase, leading to restoration of autophagy in cells from NPC patients. (nih.gov)
- 3. Endoplasmic reticulum stress induces epithelial-mesenchymal transition through autophagy via activation of c-Src kinase. (nih.gov)
Adenylate1
- This led to the discovery of marked stability of [ATP] cyto (at millimolar concentration) in wildtype yeast and wild fluctuations in [ATP] cyto in yeasts mutant in AMP kinase and adenylate kinase. (elifesciences.org)
Regulation2
- The AMP-Activated Protein Kinase Plays a Role in Antioxidant Defense and Regulation of Vascular Inflammation. (bvsalud.org)
- Other studies have found that altered AMP-activated protein kinase activity is related to changes in the regulation of certain ion channels in the heart. (medlineplus.gov)
Pathways1
- 4. Targeting the 5'-AMP-activated protein kinase and related metabolic pathways for the treatment of prostate cancer. (nih.gov)
Metabolic2
Receptor4
- OConnell and Baver [39] showed the fact that NMDA receptor-based legislation of CB-839 small molecule kinase inhibitor Kv2.1 activity occurs in the lack of Kv2.1 clustering. (ampkpathway.com)
- G protein-coupled receptor list: recommendations for new pairings with cognate ligands. (nottingham.ac.uk)
- Cell Receptor, or discriminator point -- A chemical group or molecule, such as a protein, on a cell's surface or in the cell interior with an affinity for a specific chemical group, molecule, or virus. (nih.gov)
- These actions were produced by a D 1 receptor-mediated increase of cAMP but were independent of protein kinase A. A portion of the actions of DA can be attributed to effects in the apical dendrites. (jneurosci.org)
Lipid2
Plays a Role1
- s results suggest that ATP plays a role in stopping proteins from sticking together, explaining why cells may store excess ATP, since it could aid survival. (elifesciences.org)
Synthesis2
Stress3
- AKG-reared flies were resistant to heat stress and demonstrated higher expression of heat shock protein genes ( Hsp22 and Hsp70 ) than control flies. (nih.gov)
- AMP-activated protein kinase is activated during times of cellular stress (such as low oxygen levels or muscle exercise), when ATP is broken down rapidly to produce energy. (medlineplus.gov)
- 2. Activation of AMP-activated protein kinase inhibits albumin-induced endoplasmic reticulum stress and apoptosis through inhibition of reactive oxygen species. (nih.gov)
Extracellular1
- Extracellular and organization of tissue-specific proteins and polysaccharides. (nih.gov)
Activation1
- 16. Activation of AMP-activated Protein Kinase by Metformin Induces Protein Acetylation in Prostate and Ovarian Cancer Cells. (nih.gov)
Presenilin2
Cellular3
- Condensates separation from the surrounding CYTOPLASM or nucleoplasm or by the concentration of proteins and nucleic acids into droplets as they aggregate on static cellular structures such as CELL MEMBRANES. (nih.gov)
- Research suggests that these mutations alter the activity of AMP-activated protein kinase in the heart, disrupting the enzyme's ability to respond to changes in cellular energy demands. (medlineplus.gov)
- The paper is remarkable for suggesting an important link between cellular energetics and protein folding homeostasis, which may be broadly applicable to cells of diverse phyla. (elifesciences.org)
Vitro1
- 9. [Effects of induction of tubular epithelial-myofibroblast transition by monocyte chemoattractant protein-1 and mechanism thereof: an in vitro experiment]. (nih.gov)
Molecules2
- Activating certain molecules in key tissues slowed aging in fruit flies. (nih.gov)
- Proteins are molecules that perform diverse roles, keeping cells alive. (elifesciences.org)
Accumulation1
- The latter fluctuations included deep dips in [ATP] cyto , which correlated with enhanced accumulation of model abnormal human disease-associated proteins (α-Synuclein, huntingtin etc). (elifesciences.org)
Activity5
- Studies suggest that AMP-activated protein kinase may play a role in controlling the activity of other genes, although many of these genes have not been identified. (medlineplus.gov)
- Studies indicate that changes in AMP-activated protein kinase activity allow a complex sugar called glycogen to build up abnormally within cardiac muscle cells. (medlineplus.gov)
- G proteins -- A protein with GTPase activity that binds GTP, which activates the protein. (nih.gov)
- The intrinsic GTPase activity eventually converts the GTP to GDP that activates the protein. (nih.gov)
- AMP-activated protein kinase phosphorylates glutamine : fructose-6-phosphate amidotransferase 1 at Ser243 to modulate its enzymatic activity. (harvard.edu)
Mutations1
- Familial hypertrophic cardiomyopathy (HCM) has been defined as a disease of the cardiac sarcomere, although sarcomeric protein mutations are not found in one third of cases. (ox.ac.uk)
Role2
- The high levels of Kv2.1 protein in multiple cell types suggest a structural role and these high levels would also mandate the non-conducting state, for without this, neurons would be electrically silenced. (ampkpathway.com)
- AMP-activated protein kinase is likely involved in the development of the heart before birth, although its role in this process is unknown. (medlineplus.gov)
Mutant2
- L-ORD patient RPE cell (borders are white) showing mutant protein CTRP5 (red) trapped inside the cell and partially in autophagosomes (green). (nih.gov)
- The researchers also found that the patient-derived RPE secreted far less of the mutant and the non-mutant CTRP5 protein compared with the models made from the unaffected siblings. (nih.gov)
Currents1
- To check whether Kv2.1 clusters acted as reservoirs of nonconducting stations which were activated upon discharge, we following measured whole cell currents before and after inducing Kv2.1 declustering via either actin depolymerization to dissolve the hypothesized diffusion-limiting fence, or alkaline phosphatase within the patch clamp pipet to dephosphorylate the clustered route [37]. (ampkpathway.com)
Aggregate1
- provide a possible cause for why proteins aggregate in these diseases, which may be worth further study. (elifesciences.org)
Stimulates1
- The patient-derived RPE shared key characteristics of the disorder in humans, including deposits of apolipoprotein E near the tissue, and abnormal secretions of vascular endothelial growth factor, a protein that stimulates blood vessel growth. (nih.gov)
Cell3
- Furthermore, our group would afterwards discover that the nonconducting CB-839 small molecule kinase inhibitor condition was governed by surface area route density rather than location in the cell surface area [40]. (ampkpathway.com)
- Single-cell imaging of ATP-reduced yeast mutants revealed that ATP levels in these mutants underwent stochastic and transient depletion, which promoted the cytotoxic aggregation of endogenous proteins and pathogenic proteins, such as huntingtin and α-synuclein. (elifesciences.org)
- A6: Cyclin B/Cdk1, a cell cycle-dependent kinase, is capable of phosphorylating SIRT1 at T530 and S540. (nih.gov)
Nucleus1
- However, the most characteristic feature of nonmammalian RBCs is the presence of a nucleus which allows them to transcribe and translate proteins and therefore intervene in additional functions different from delivery of oxygen to tissues ( Figure 1 ) [ 3 ]. (intechopen.com)
Peptide1
- Crystal Structure of an Activated Akt/Protein Kinase B Ternary Complex with Gsk-3 Peptide and AMP-Pnp. (expasy.org)