Receptor, Adenosine A2A
Receptor, Adenosine A1
Adenosine A2 Receptor Antagonists
Purinergic P1 Receptor Antagonists
Adenosine A1 Receptor Antagonists
Interleukin 1 Receptor Antagonist Protein
Receptor, Adenosine A3
Receptor, Adenosine A2B
Neurokinin-1 Receptor Antagonists
Receptors, Adenosine A2
Receptors, Purinergic P1
Adenosine A2 Receptor Agonists
Dose-Response Relationship, Drug
Histamine H2 Antagonists
Serotonin 5-HT3 Receptor Antagonists
Excitatory Amino Acid Antagonists
Adenosine A3 Receptor Antagonists
Angiotensin Receptor Antagonists
Serotonin 5-HT2 Receptor Antagonists
Purinergic P2 Receptor Antagonists
Histamine H1 Antagonists
GABA-A Receptor Antagonists
Receptor, Endothelin A
Serotonin 5-HT1 Receptor Antagonists
Adrenergic alpha-1 Receptor Antagonists
Adrenergic alpha-2 Receptor Antagonists
Serotonin Receptor Agonists
Histamine H3 Antagonists
Purinergic P2X Receptor Antagonists
GABA-B Receptor Antagonists
Receptor, Endothelin B
Receptors, Dopamine D2
Receptor, Cannabinoid, CB1
Serotonin 5-HT4 Receptor Antagonists
Disease Models, Animal
Cannabinoid Receptor Antagonists
Adrenergic beta-2 Receptor Antagonists
Receptors, Purinergic P2
Receptors, Histamine H3
Mineralocorticoid Receptor Antagonists
Receptor, Bradykinin B2
Receptors, Dopamine D1
Receptors, Calcitonin Gene-Related Peptide
Receptors, Opioid, mu
Receptors, Corticotropin-Releasing Hormone
Receptor, Angiotensin, Type 1
Calcium Channel Blockers
Rats, Inbred Strains
Receptors, Opioid, kappa
Analysis of Variance
Receptor, Serotonin, 5-HT2A
Receptors, Histamine H2
Purinergic P2Y Receptor Antagonists
Brief, repeated, oxygen-glucose deprivation episodes protect neurotransmission from a longer ischemic episode in the in vitro hippocampus: role of adenosine receptors. (1/50)1. Ischemic preconditioning in the brain consists of reducing the sensitivity of neuronal tissue to further, more severe, ischemic insults. We recorded field epsps (fepsps) extracellularly from hippocampal slices to develop a model of in vitro ischemic preconditioning and to evaluate the role of A1, A2A and A3 adenosine receptors in this phenomenon. 2. The application of an ischemic insult, obtained by glucose and oxygen deprivation for 7 min, produced an irreversible depression of synaptic transmission. Ischemic preconditioning was induced by four ischemic insults (2 min each) separated by 13 min of normoxic conditions. After 30 min, an ischemic insult of 7 min was applied. This protocol substantially protected the tissue from the irreversible depression of synaptic activity. 3. The selective adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 100 nm), completely prevented the protective effect of preconditioning. The selective adenosine A2A receptor antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phe nol (ZM 241385, 100 nm) did not modify the magnitude of fepsp recovery compared to control slices. The selective A3 adenosine receptor antagonists, 3-propyl-6-ethyl-5[ethyl(thio)carbonyl]-2-phenyl-4-propyl-3-pyridinecarboxylate (MRS 1523, 100 nm) significantly improved the recovery of fepsps after 7 min of ischemia. 4. Our results show that in vitro ischemic preconditioning allows CA1 hippocampal neurons to become resistant to prolonged exposure to ischemia. Adenosine, by stimulating A1 receptors, plays a crucial role in eliciting the cell mechanisms underlying preconditioning; A2A receptors are not involved in this phenomenon, whereas A3 receptor activation is harmful to ischemic preconditioning. (+info)
Pharmacological preconditioning with resveratrol: role of CREB-dependent Bcl-2 signaling via adenosine A3 receptor activation. (2/50)Recent studies demonstrated that resveratrol, a grape-derived polyphenolic phytoalexin, provides pharmacological preconditioning (PC) of the heart through a NO-dependent mechanism. Because adenosine receptors play a role in PC, we examined whether they play any role in resveratrol PC. Rats were randomly assigned to groups perfused for 15 min with 1) Krebs-Henseleit bicarbonate buffer (KHB) only; 2) KHB containing 10 microM resveratrol; 3) 10 microM resveratrol + 1 microM 8-cyclopentyl-1,3-dimethylxanthine (CPT; adenosine A(1) receptor blocker); 4) 10 microM resveratrol + 1 microM 8-(3-chlorostyryl)caffeine (CSC; adenosine A(2a) receptor blocker); 5) 10 microM resveratrol + 1 microM 3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(+/-)-dihydropyridine-3,5- dicarboxylate (MRS-1191; adenosine A(3) receptor blocker); or 6) 10 microM resveratrol + 3 microM 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride [LY-294002, phosphatidylinositol (PI)3-kinase inhibitor], and groups perfused with adenosine receptor blockers alone. Hearts were then subjected to 30-min ischemia followed by 2-h reperfusion. The results demonstrated significant cardioprotection with resveratrol evidenced by improved ventricular recovery and reduced infarct size and cardiomyocyte apoptosis. CPT and MRS 1191, but not CSC, abrogated the cardioprotective abilities of resveratrol, suggesting a role of adenosine A(1) and A(3) receptors in resveratrol PC. Resveratrol induced expression of Bcl-2 and caused its phosphorylation along with phosphorylation of cAMP response element-binding protein (CREB), Akt, and Bad. CPT blocked phosphorylation of Akt and Bad without affecting CREB, whereas MRS 1191 blocked phosphorylation of all compounds, including CREB. LY-294002 partially blocked the cardioprotective abilities of resveratrol. The results indicate that resveratrol preconditions the heart through activation of adenosine A(1) and A(3) receptors, the former transmitting a survival signal through PI3-kinase-Akt-Bcl-2 signaling pathway and the latter protecting the heart through a CREB-dependent Bcl-2 pathway in addition to an Akt-Bcl-2 pathway. (+info)
Activation of A3 adenosine receptors attenuates lung injury after in vivo reperfusion. (3/50)BACKGROUND: A3 adenosine receptor (AR) activation worsens or protects against renal and cardiac ischemia-reperfusion (IR) injury, respectively. The aims of the current study were to examine in an in vivo model the effect of A3AR activation on IR lung injury and investigate the mechanism by which it exerts its effect. METHODS: The arterial branch of the left lower lung lobe in intact-chest, spontaneously breathing cats was occluded for 2 h and reperfused for 3 h (IR group). Animals were treated with the selective A3 receptor agonist IB-MECA (300 microg/kg intravenously) given 15 min before ischemia or with IB-MECA as described, with pretreatment 15 min earlier with the selective A3AR antagonist MRS-1191, the nonsulfonylurea adenosine triphosphate-sensitive potassium channel-blocking agent U-37883A, or the nitric oxide synthase inhibitor N-nitro-l-arginine benzyl ester. RESULTS: IB-MECA markedly (P < 0.01) reduced the percentage of injured alveoli (IR, 48 +/- 4%; IB-MECA, 18 +/- 2%), wet:dry weight ratio (IR, 8.2 +/- 0.4; IB-MECA, 4 +/- 2), and myeloperoxidase activity (IR, 0.52 +/- 0.06 U/g; IB-MECA, 0.17 +/- 0.04 U/g). This protective effect was completely blocked by pretreatment with the selective A3AR antagonist MRS-1191 and the adenosine triphosphate-sensitive potassium channel blocking agent U-37883A but not the nitric oxide synthase inhibitor N-nitro-l-arginine benzyl ester. CONCLUSIONS: In the feline lung, the A3AR agonist IB-MECA confers a powerful protection against IR lung injury. This effect is mediated by a nitric oxide synthase-independent pathway and involves opening of adenosine triphosphate-sensitive potassium channels. Therefore, selective activation of A3AR may be an effective means of protecting the reperfused lung. (+info)
A3 adenosine receptor activation inhibits cell proliferation via phosphatidylinositol 3-kinase/Akt-dependent inhibition of the extracellular signal-regulated kinase 1/2 phosphorylation in A375 human melanoma cells. (4/50)Adenosine exerts its effects through four subtypes of G-protein-coupled receptors: A(1), A(2A), A(2B), and A(3). Stimulation of the human A(3) receptor has been suggested to influence cell death and proliferation. The phosphatidylinositide-3-OH kinase (PI3K)/Akt and the Raf/mitogen-activated protein kinase (MAPK/ERK) kinase (MEK)/mitogen-activated protein kinase (MAPK) pathways have central roles in the regulation of cell survival and proliferation. Due to their importance, the cross-talk between these two pathways has been investigated. Here, we show that the A(3) adenosine receptor agonist Cl-IB-MECA stimulates PI3K-dependent phosphorylation of Akt leading to the reduction of basal levels of ERK1/2 phosphorylation, which in turn inhibits cell proliferation. The response to Cl-IB-MECA was not blocked by A(1), A(2A), or A(2B) receptor antagonists, although it was abolished by A(3) receptor antagonists. Furthermore, the response to Cl-IB-MECA was generated at the cell surface, since the inhibition of A(3) receptor expression, by using small interfering RNA, abolished agonist effects. Using A375 cells, we show that A(3) adenosine receptor stimulation results in PI3K-dependent phosphorylation of Akt, leading to the reduction of basal levels of ERK1/2 phosphorylation, which in turn inhibits cell proliferation. (+info)
Resveratrol-mediated activation of cAMP response element-binding protein through adenosine A3 receptor by Akt-dependent and -independent pathways. (5/50)A recent study documented a role of adenosine A(3)-Akt-cAMP response element-binding protein (CREB) survival signaling in resveratrol preconditioning of the heart. In this study, we demonstrate that resveratrol-mediated CREB activation can also occur through an Akt-independent pathway. Isolated rat hearts were perfused for 15 min with Krebs-Henseleit bicarbonate (KHB) buffer containing resveratrol in the absence or presence of adenosine A(3) receptor blocker MRS-1191 [3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(+/-)-dihydropyridine-3,5 -dicar-boxylate], phosphatidylinositol 3 (PI3)-kinase inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride], mitogen-activated extracellular signal-regulated protein kinase inhibitor PD098059 [2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one], or a combination of LY294002 and PD098059. All hearts were subsequently subjected to 30-min ischemia followed by 2-h reperfusion. Cardioprotection was examined by determining infarct size, cardiomyocyte apoptosis, and ventricular recovery. Resveratrol phosphorylated both Akt and CREB that was blocked by MRS-1191, which also abolished cardioprotective abilities of resveratrol. LY294002 completely inhibited Akt phosphorylation but partially blocked the phosphorylation of CREB. Inhibition of PI3-kinase also partially blocked resveratrol's ability to precondition the heart. PD098059 partially blocked the phosphorylation of CREB and resveratrol-mediated cardioprotection. Preperfusing the hearts with LY294002 and PD098059 together completely abolished the phosphorylation of CREB, simultaneously inhibiting resveratrol-mediated cardioprotection. The results indicate that resveratrol preconditions the hearts through adenosine A(3) receptor signaling that triggers the phosphorylation of CREB through both Akt-dependent and -independent pathways, leading to cardioprotection. (+info)
Phosphatidylinositol 3-kinase and ERK1/2 are not involved in adenosine A1, A2A or A3 receptor-mediated preconditioning in rat ventricle strips. (6/50)Mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase 1 and 2 (ERK1/2) and phosphatidylinositol 3-kinase (PI3-kinase)/protein kinase B (PKB; also known as Akt) are important antiapoptotic signalling pathways which have recently been implicated in cardioprotection. However, at present the involvement of ERK1/2 and PI3-kinase/PKB in adenosine receptor-mediated cardioprotection is poorly understood. In this study we used isolated rat right ventricular strips, contracted by electrical-field stimulation, in order to investigate the role of ERK1/2 and PI3-kinase/PKB in adenosine receptor-induced cardioprotection. Ventricle strips were pretreated for 2 min with the agonists adenosine (non-selective), CPA (A1 selective), CGS 21680 (A2A selective) and Cl-IB-MECA (A3 selective) before 30 min hypoxia followed by 30 min reoxygenation. Each agonist significantly improved posthypoxic percentage contraction recovery compared to control strips. Similarly hypoxic preconditioning (10 min hypoxia followed by 20 min reoxygenation) significantly improved posthypoxic percentage contraction recovery compared to non-preconditioned strips. The selective adenosine receptor antagonists DPCPX (A1), ZM 241385 (A2A) and MRS 1220 (A3) attenuated cardioprotection induced by CPA, CGS 21680 and Cl-IB-MECA, respectively. Pre-incubation (30 min) of ventricle strips with the MEK1 inhibitor PD 98059 (50 microM) or the PI3-kinase inhibitor wortmannin (100 nM) significantly reduced posthypoxic percentage contraction recovery induced by hypoxic preconditioning. In contrast, PD 98059 and wortmannin had no significant effect on cardioprotection induced by CPA, Cl-IB-MECA or CGS 21680. Overall these data indicate that although selective A1, A2A and A3 adenosine receptor agonists induce preconditioning in rat right ventricular strips the effects are independent of ERK1/2- and PI3-kinase-dependent pathways. In contrast ERK1/2 and PI3-kinase-dependent pathways do appear to be involved in early hypoxic preconditioning. (+info)
"Reversine" and its 2-substituted adenine derivatives as potent and selective A3 adenosine receptor antagonists. (7/50)The dedifferentiation agent "reversine" [2-(4-morpholinoanilino)-N(6)-cyclohexyladenine 2] was found to be a moderately potent antagonist for the human A(3) adenosine receptor (AR) with a K(i) value of 0.66 microM. This result prompted an exploration of the structure-activity relationship of related derivatives, synthesized via sequential substitution of 6-chloro-2-fluoropurine with selected nucleophiles. Optimization of substituents at these two positions identified 2-(phenylamino)-N(6)-cyclohexyladenine (12), 2-(phenylamino)-N(6)-cycloheptyladenine (19), and 2-phenylamino-N(6)-endo-norbornyladenine (21) as potent A(3) AR ligands with K(i) values of 51, 42, and 37 nM, respectively, with 30-200-fold selectivity in comparison to A(1) and A(2A) ARs. The most selective A(3) AR antagonist (>200-fold) was 2-(phenyloxy)-N(6)-cyclohexyladenine (22). 9-Methylation of 12, but not 19, was well-tolerated in A(3) AR binding. Extension of the 2-phenylamino group to 2-benzyl- and 2-(2-phenylethylamino) reduced affinity. In the series of 2-(phenylamino), 2-(phenyloxy), and 2-(phenylthio) substitutions, the order of affinity at the A(3) AR was oxy > or = amino > thio. Selected derivatives, including reversine (K(B) value of 466 nM via Schild analysis), competitively antagonized the functional effects of a selective A(3) AR agonist, i.e., inhibition of forskolin-stimulated cAMP production in stably transfected Chinese hamster ovary (CHO) cells. These results are in agreement with other studies suggesting the presence of a lipophilic pocket in the AR binding site that is filled by moderately sized cycloalkyl rings at the N(6) position of both adenine and adenosine derivatives. Thus, the compound series reported herein comprise an important new series of selective A(3) AR antagonists. We were unable to reproduce the dedifferentiation effect of reversine, previously reported, or to demonstrate any connection between A(3) AR antagonist effects and dedifferentiation. (+info)
The cross-species A3 adenosine-receptor antagonist MRS 1292 inhibits adenosine-triggered human nonpigmented ciliary epithelial cell fluid release and reduces mouse intraocular pressure. (8/50)PURPOSE: Antagonists to A3 adenosine receptors (ARs) lower mouse intraocular pressure (IOP), but extension to humans is limited by species variability. We tested whether the specific A3AR antagonist MRS 1292, designed to cross species, mimicks the effects of other A3AR antagonists on cultured human nonpigmented ciliary epithelial (NPE) cells and mouse IOP. METHODS: NPE cell volume was monitored by electronic cell sorting. Mouse IOP was measured with the Servo-Null Micropipette System. RESULTS: Adenosine triggered A3AR-mediated shrinkage of human NPE cells. Shrinkage was blocked by MRS 1292 (IC50 = 42 +/- 11 nM, p < 0.01) and by another A3AR antagonist effective in this system, MRS 1191. Topical application of the A3AR agonist IB-MECA increased mouse IOP. MRS 1292 reduced IOP by 4.0 +/- 0.8 mmHg at 25-microM droplet concentration (n = 10, p < 0.005). CONCLUSIONS: MRS 1292 inhibits A3AR-mediated shrinkage of human NPE cells and reduces mouse IOP, consistent with its putative action as a cross-species A3 antagonist. (+info)
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.
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.
There are several different types of pain, including:
1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.
The medical field uses a range of methods to assess and manage pain, including:
1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.
It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.
Vomiting can be caused by a variety of factors, such as:
1. Infection: Viral or bacterial infections can inflame the stomach and intestines, leading to vomiting.
2. Food poisoning: Consuming contaminated or spoiled food can cause vomiting.
3. Motion sickness: Traveling by car, boat, plane, or other modes of transportation can cause motion sickness, which leads to vomiting.
4. Alcohol or drug overconsumption: Drinking too much alcohol or taking certain medications can irritate the stomach and cause vomiting.
5. Pregnancy: Hormonal changes during pregnancy can cause nausea and vomiting, especially during the first trimester.
6. Other conditions: Vomiting can also be a symptom of other medical conditions such as appendicitis, pancreatitis, and migraines.
When someone is vomiting, they may experience:
1. Nausea: A feeling of queasiness or sickness in the stomach.
2. Abdominal pain: Crampy or sharp pain in the abdomen.
3. Diarrhea: Loose, watery stools.
4. Dehydration: Loss of fluids and electrolytes.
5. Headache: A throbbing headache can occur due to dehydration.
6. Fatigue: Weakness and exhaustion.
Treatment for vomiting depends on the underlying cause, but may include:
1. Fluid replacement: Drinking fluids to replenish lost electrolytes and prevent dehydration.
2. Medications: Anti-inflammatory drugs or antibiotics may be prescribed to treat infections or other conditions causing vomiting.
3. Rest: Resting the body and avoiding strenuous activities.
4. Dietary changes: Avoiding certain foods or substances that trigger vomiting.
5. Hospitalization: In severe cases of vomiting, hospitalization may be necessary to monitor and treat underlying conditions.
It is important to seek medical attention if the following symptoms occur with vomiting:
1. Severe abdominal pain.
2. Fever above 101.5°F (38.6°C).
3. Blood in vomit or stools.
4. Signs of dehydration, such as excessive thirst, dark urine, or dizziness.
5. Vomiting that lasts for more than 2 days.
6. Frequent vomiting with no relief.
It is important to note that catalepsy is not the same as catatonia, which is a more specific condition characterized by a wide range of symptoms, including immobility, mutism, negativism, and emotional dysregulation. However, catalepsy and catatonia do share some similarities, and the terms are often used interchangeably in clinical practice.
The exact cause of catalepsy is not fully understood, but it is thought to be related to dysfunction in certain areas of the brain, such as the neocortex and basal ganglia. In some cases, catalepsy may be a side effect of medication or drug intoxication.
Treatment for catalepsy typically focuses on addressing the underlying cause, such as managing seizures or withdrawing from drugs. In some cases, medications such as benzodiazepines or antipsychotics may be used to help manage symptoms. Other approaches, such as physical therapy and behavioral interventions, may also be helpful in improving mobility and function.
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:
3. Heart disease
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 edema, including:
1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.
Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.
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.
* Muscle and bone pain
* Nausea and vomiting
* Seizures (in severe cases)
The specific symptoms of substance withdrawal syndrome can vary depending on the substance being withdrawn from, but some common symptoms include:
* Alcohol: tremors, anxiety, insomnia, nausea and vomiting, headaches, and seizures
* Opioids: withdrawal symptoms can include anxiety, muscle aches, sweating, nausea and vomiting, diarrhea, and depression
* Benzodiazepines: withdrawal symptoms can include anxiety, insomnia, tremors, and seizures
The diagnosis of substance withdrawal syndrome is typically made based on the patient's history of substance use and the presence of withdrawal symptoms. A healthcare provider may also order laboratory tests to rule out other conditions that may be causing the symptoms. Treatment for substance withdrawal syndrome usually involves supportive care, such as rest, hydration, and pain management, as well as medication to manage withdrawal symptoms. In some cases, medical professionals may also recommend a gradual tapering of the substance over a period of time to minimize withdrawal symptoms.
It is important for individuals who are experiencing withdrawal symptoms to seek medical attention as soon as possible, as untreated withdrawal can lead to serious complications, such as seizures and dehydration. With appropriate treatment, most individuals with substance withdrawal syndrome can recover fully and successfully overcome their addiction.
In some cases, hyperemia can be a sign of a more serious underlying condition that requires medical attention. For example, if hyperemia is caused by an inflammatory or infectious process, it may lead to tissue damage or organ dysfunction if left untreated.
Hyperemia can occur in various parts of the body, including the skin, muscles, organs, and other tissues. It is often diagnosed through physical examination and imaging tests such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI). Treatment for hyperemia depends on its underlying cause, and may include antibiotics, anti-inflammatory medications, or surgery.
In the context of dermatology, hyperemia is often used to describe a condition called erythema, which is characterized by redness and swelling of the skin due to increased blood flow. Erythema can be caused by various factors, such as sun exposure, allergic reactions, or skin infections. Treatment for erythema may include topical medications, oral medications, or other therapies depending on its underlying cause.
There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:
1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.
Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Lack of exercise
* High sodium intake
* Low potassium intake
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
In medical terminology, nausea is sometimes used interchangeably with the term "dyspepsia," which refers to a general feeling of discomfort or unease in the stomach, often accompanied by symptoms such as bloating, belching, or heartburn. However, while nausea and dyspepsia can be related, they are not always the same thing, and it's important to understand the specific underlying cause of any gastrointestinal symptoms in order to provide appropriate treatment.
Some common causes of nausea include:
* Gastrointestinal disorders such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and gastritis
* Motion sickness or seasickness
* Medication side effects, including chemotherapy drugs, antibiotics, and painkillers
* Pregnancy and morning sickness
* Food poisoning or other infections
* Migraines and other headaches
* Anxiety and stress
Treatment for nausea will depend on the underlying cause, but may include medications such as antihistamines, anticholinergics, or anti-nausea drugs, as well as non-pharmacological interventions such as ginger, acupressure, or relaxation techniques. In severe cases, hospitalization may be necessary to manage symptoms and prevent dehydration or other complications.
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.
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.
The term "decerebrate" comes from the Latin word "cerebrum," which means brain. In this context, the term refers to a state where the brain is significantly damaged or absent, leading to a loss of consciousness and other cognitive functions.
Some common symptoms of the decerebrate state include:
* Loss of consciousness
* Flaccid paralysis (loss of muscle tone)
* Dilated pupils
* Lack of responsiveness to stimuli
* Poor or absent reflexes
* Inability to speak or communicate
The decerebrate state can be caused by a variety of factors, including:
* Severe head injury
* Stroke or cerebral vasculature disorders
* Brain tumors or cysts
* Infections such as meningitis or encephalitis
* Traumatic brain injury
Treatment for the decerebrate state is typically focused on addressing the underlying cause of the condition. This may involve medications to control seizures, antibiotics for infections, or surgery to relieve pressure on the brain. In some cases, the decerebrate state may be a permanent condition, and individuals may require long-term care and support.
There are several causes of hypotension, including:
1. Dehydration: Loss of fluids and electrolytes can cause a drop in blood pressure.
2. Blood loss: Losing too much blood can lead to hypotension.
3. Medications: Certain medications, such as diuretics and beta-blockers, can lower blood pressure.
4. Heart conditions: Heart failure, cardiac tamponade, and arrhythmias can all cause hypotension.
5. Endocrine disorders: Hypothyroidism (underactive thyroid) and adrenal insufficiency can cause low blood pressure.
6. Vasodilation: A condition where the blood vessels are dilated, leading to low blood pressure.
7. Sepsis: Severe infection can cause hypotension.
Symptoms of hypotension can include:
1. Dizziness and lightheadedness
2. Fainting or passing out
3. Weakness and fatigue
4. Confusion and disorientation
5. Pale, cool, or clammy skin
6. Fast or weak pulse
7. Shortness of breath
8. Nausea and vomiting
If you suspect that you or someone else is experiencing hypotension, it is important to seek medical attention immediately. Treatment will depend on the underlying cause of the condition, but may include fluids, electrolytes, and medication to raise blood pressure. In severe cases, hospitalization may be necessary.
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.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
Hyperkinesis can manifest in different ways, including:
1. Excessive movement or restlessness: This can include fidgeting, pacing, or other forms of constant motion.
2. Involuntary movements: These can include tremors, tics, or other sudden, uncontrolled movements.
3. Overactive behavior: This can include rapid speaking, excessive talking, or other behaviors that are not typical for the individual.
4. Difficulty sitting still or remaining quiet: This can be due to an inability to focus or a sense of inner restlessness or agitation.
5. Increased energy levels: This can result in excessive physical activity, such as running, jumping, or other forms of high-energy behavior.
Hyperkinesis can have a significant impact on daily life, making it difficult to focus, complete tasks, and maintain relationships. It is important to seek medical attention if symptoms persist or worsen over time, as hyperkinesis can be a sign of an underlying neurological or psychiatric condition that requires treatment.
Pruritus can be acute or chronic, depending on its duration and severity. Acute pruritus is usually caused by a specific trigger, such as an allergic reaction or insect bite, and resolves once the underlying cause is treated or subsides. Chronic pruritus, on the other hand, can persist for months or even years and may be more challenging to diagnose and treat.
Some common causes of pruritus include:
1. Skin disorders such as atopic dermatitis, psoriasis, eczema, and contact dermatitis.
2. Allergic reactions to medications, insect bites, or food.
3. Certain systemic diseases such as kidney disease, liver disease, and thyroid disorders.
4. Pregnancy-related itching (obstetric pruritus).
5. Cancer and its treatment, particularly chemotherapy-induced itching.
6. Nerve disorders such as peripheral neuropathy and multiple sclerosis.
7. Infections such as fungal, bacterial, or viral infections.
8. Parasitic infestations such as scabies and lice.
Managing pruritus can be challenging, as it often leads to a vicious cycle of scratching and skin damage, which can exacerbate the itching sensation. Treatment options for pruritus depend on the underlying cause, but may include topical corticosteroids, oral antihistamines, immunomodulatory drugs, and other medications. In severe cases, hospitalization may be necessary to address the underlying condition and provide symptomatic relief.
In conclusion, pruritus is a common symptom with many possible causes, ranging from skin disorders to systemic diseases and infections. Diagnosis and management of pruritus require a comprehensive approach, involving both physical examination and laboratory tests to identify the underlying cause, as well as appropriate treatment options to provide relief and prevent complications.
Example Sentence: The patient was diagnosed with pulmonary hypertension and began treatment with medication to lower her blood pressure and improve her symptoms.
Word class: Noun phrase / medical condition
The term ischemia refers to the reduction of blood flow, and it is often used interchangeably with the term stroke. However, not all strokes are caused by ischemia, as some can be caused by other factors such as bleeding in the brain. Ischemic stroke accounts for about 87% of all strokes.
There are different types of brain ischemia, including:
1. Cerebral ischemia: This refers to the reduction of blood flow to the cerebrum, which is the largest part of the brain and responsible for higher cognitive functions such as thought, emotion, and voluntary movement.
2. Cerebellar ischemia: This refers to the reduction of blood flow to the cerebellum, which is responsible for coordinating and regulating movement, balance, and posture.
3. Brainstem ischemia: This refers to the reduction of blood flow to the brainstem, which is responsible for controlling many of the body's automatic functions such as breathing, heart rate, and blood pressure.
4. Territorial ischemia: This refers to the reduction of blood flow to a specific area of the brain, often caused by a blockage in a blood vessel.
5. Global ischemia: This refers to the reduction of blood flow to the entire brain, which can be caused by a cardiac arrest or other systemic conditions.
The symptoms of brain ischemia can vary depending on the location and severity of the condition, but may include:
1. Weakness or paralysis of the face, arm, or leg on one side of the body
2. Difficulty speaking or understanding speech
3. Sudden vision loss or double vision
4. Dizziness or loss of balance
5. Confusion or difficulty with memory
7. Slurred speech or inability to speak
8. Numbness or tingling sensations in the face, arm, or leg
9. Vision changes, such as blurred vision or loss of peripheral vision
10. Difficulty with coordination and balance.
It is important to seek medical attention immediately if you experience any of these symptoms, as brain ischemia can cause permanent damage or death if left untreated.
Morphine dependence can occur after taking the drug for a short or long period, and it is often seen in individuals who use morphine for chronic pain management. The risk of developing morphine dependence increases with higher doses and longer durations of use.
Signs and symptoms of morphine dependence may include:
1. Increased tolerance to the drug, requiring higher doses to achieve the same effect.
2. Withdrawal symptoms when stopping or reducing the drug, such as anxiety, restlessness, muscle and bone pain, sweating, and insomnia.
3. Compulsive drug-seeking behavior, such as doctor shopping or stealing medication to maintain a supply of morphine.
4. Neglect of responsibilities and activities due to the pursuit of morphine use.
5. Continued use despite negative consequences, such as relationship problems, financial issues, or legal troubles.
6. Feeling a strong need or craving for morphine, which can be difficult to control.
7. Experiencing withdrawal symptoms when stopping or reducing the drug, such as nausea, vomiting, diarrhea, and tremors.
8. Developing tolerance to other opioids, which can lead to a cycle of increasing doses and dependence on multiple drugs.
9. Feeling irritable, anxious, or depressed when unable to obtain morphine.
10. Engaging in risky behaviors, such as sharing needles or using unregulated sources of the drug, which can increase the risk of overdose or infection.
Morphine dependence is a serious condition that can have significant negative consequences on an individual's physical and mental health, relationships, and overall quality of life. Treatment options for morphine dependence include medication-assisted therapy, counseling, and support groups to help individuals manage withdrawal symptoms and cravings, as well as address any underlying psychological or social issues that may be contributing to the addiction.
The different types of Neurotoxicity Syndromes include:
1. Organophosphate-induced neurotoxicity: This syndrome is caused by exposure to organophosphate pesticides, which can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
2. Heavy metal neurotoxicity: Exposure to heavy metals, such as lead, mercury, and arsenic, can damage the nervous system and cause symptoms such as tremors, muscle weakness, and cognitive impairment.
3. Pesticide-induced neurotoxicity: This syndrome is caused by exposure to pesticides, which can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
4. Solvent-induced neurotoxicity: Exposure to solvents, such as toluene and benzene, can damage the nervous system and cause symptoms such as memory loss, difficulty with concentration, and mood changes.
5. Medication-induced neurotoxicity: Certain medications, such as antidepressants and antipsychotics, can damage the nervous system and cause symptoms such as tremors, muscle rigidity, and cognitive impairment.
6. Environmental neurotoxicity: Exposure to environmental toxins, such as air pollution and pesticides, can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
7. Neurodegenerative disease-induced neurotoxicity: Neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, can cause neurotoxicity and lead to symptoms such as cognitive decline, memory loss, and motor dysfunction.
8. Traumatic brain injury-induced neurotoxicity: Traumatic brain injury can cause neurotoxicity and lead to symptoms such as cognitive impairment, memory loss, and mood changes.
9. Stroke-induced neurotoxicity: A stroke can cause neurotoxicity and lead to symptoms such as weakness or paralysis on one side of the body, difficulty with speech and language, and memory loss.
10. Neurodevelopmental disorder-induced neurotoxicity: Neurodevelopmental disorders, such as autism spectrum disorder, can cause neurotoxicity and lead to symptoms such as cognitive impairment, social withdrawal, and repetitive behaviors.
It is important to note that these are just a few examples of the many different types of neurotoxicity that can occur, and that each type may have its own unique set of causes, symptoms, and treatments. If you suspect that you or someone you know may be experiencing neurotoxicity, it is important to seek medical attention as soon as possible in order to receive an accurate diagnosis and appropriate treatment.
There are several types of ischemia, including:
1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.
Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.
Asthma can cause recurring episodes of wheezing, coughing, chest tightness, and shortness of breath. These symptoms occur when the muscles surrounding the airways contract, causing the airways to narrow and swell. This can be triggered by exposure to environmental allergens or irritants such as pollen, dust mites, pet dander, or respiratory infections.
There is no cure for asthma, but it can be managed with medication and lifestyle changes. Treatment typically includes inhaled corticosteroids to reduce inflammation, bronchodilators to open up the airways, and rescue medications to relieve symptoms during an asthma attack.
Asthma is a common condition that affects people of all ages, but it is most commonly diagnosed in children. According to the American Lung Association, more than 25 million Americans have asthma, and it is the third leading cause of hospitalization for children under the age of 18.
While there is no cure for asthma, early diagnosis and proper treatment can help manage symptoms and improve quality of life for those affected by the condition.
The inner ear, brain, and sensory nerves are all involved in the development of motion sickness. The inner ear contains the vestibular system, which is responsible for maintaining balance and equilibrium. The brain processes visual, proprioceptive (position and movement), and vestibular information to determine the body's position and movement. When these signals are not in harmony, the brain can become confused and motion sickness can occur.
There are several factors that can contribute to the development of motion sickness, including:
1. Conflicting sensory input: This can occur when the visual, proprioceptive, and vestibular systems provide conflicting information about the body's position and movement. For example, if the body is moving but the eyes do not see any movement, this can confuse the brain and lead to motion sickness.
2. Movement of the body: Motion sickness can occur when the body is in motion, such as on a boat or airplane, or during a car ride. This can be particularly problematic for people who are prone to motion sickness.
3. Reading or looking at screens: Reading or looking at screens can exacerbate motion sickness, as it can provide conflicting visual and vestibular information.
4. Other medical conditions: Certain medical conditions, such as inner ear problems or migraines, can increase the risk of developing motion sickness.
5. Medications: Some medications, such as antidepressants and antihistamines, can increase the risk of developing motion sickness.
There are several ways to prevent and treat motion sickness, including:
1. Avoiding heavy meals before traveling: Eating a light meal before traveling can help reduce the risk of motion sickness.
2. Choosing a seat with less motion: In vehicles, choosing a seat with less motion can help reduce the risk of motion sickness.
3. Keeping the eyes on the horizon: Looking at the horizon can help reduce the conflict between visual and vestibular information.
4. Taking medication: There are several over-the-counter and prescription medications available to prevent and treat motion sickness, such as dramamine and scopolamine patches.
5. Using wristbands: Sea bands or wristbands that apply pressure to a specific point on the wrist have been shown to be effective in preventing motion sickness.
6. Avoiding alcohol and caffeine: Consuming these substances can exacerbate motion sickness, so it is best to avoid them before and during travel.
7. Staying hydrated: Drinking plenty of water and other fluids can help reduce the symptoms of motion sickness.
8. Getting fresh air: Fresh air can help reduce the symptoms of motion sickness, so it is best to sit near an open window or take breaks outside.
* Heart block: A condition where the electrical signals that control the heart's rhythm are blocked or delayed, leading to a slow heart rate.
* Sinus node dysfunction: A condition where the sinus node, which is responsible for setting the heart's rhythm, is not functioning properly, leading to a slow heart rate.
* Medications: Certain medications, such as beta blockers, can slow down the heart rate.
* Heart failure: In severe cases of heart failure, the heart may become so weak that it cannot pump blood effectively, leading to a slow heart rate.
* Electrolyte imbalance: An imbalance of electrolytes, such as potassium or magnesium, can affect the heart's ability to function properly and cause a slow heart rate.
* Other medical conditions: Certain medical conditions, such as hypothyroidism (an underactive thyroid) or anemia, can cause bradycardia.
Bradycardia can cause symptoms such as:
* Dizziness or lightheadedness
* Shortness of breath
* Chest pain or discomfort
In some cases, bradycardia may not cause any noticeable symptoms at all.
If you suspect you have bradycardia, it is important to consult with a healthcare professional for proper diagnosis and treatment. They may perform tests such as an electrocardiogram (ECG) or stress test to determine the cause of your slow heart rate and develop an appropriate treatment plan. Treatment options for bradycardia may include:
* Medications: Such as atropine or digoxin, to increase the heart rate.
* Pacemakers: A small device that is implanted in the chest to help regulate the heart's rhythm and increase the heart rate.
* Cardiac resynchronization therapy (CRT): A procedure that involves implanting a device that helps both ventricles of the heart beat together, improving the heart's pumping function.
It is important to note that bradycardia can be a symptom of an underlying condition, so it is important to address the underlying cause in order to effectively treat the bradycardia.
There are different types of myocardial infarctions, including:
1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.
Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.
Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.
Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.
Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.
Neuralgia is often difficult to diagnose and treat, as the underlying cause can be challenging to identify. However, various medications and therapies can help manage the pain and other symptoms associated with this condition. These may include pain relievers, anticonvulsants, antidepressants, and muscle relaxants, as well as alternative therapies such as acupuncture or physical therapy.
Some common forms of neuralgia include:
1. Trigeminal neuralgia: This is a condition that affects the trigeminal nerve, which carries sensation from the face to the brain. It is characterized by sudden, intense pain in the face, typically on one side.
2. Postherpetic neuralgia (PHN): This is a condition that occurs after a shingles infection, and is characterized by persistent pain in the affected area.
3. Occipital neuralgia: This is a condition that affects the nerves in the back of the head and neck, and can cause pain in the back of the head, neck, and face.
4. Geniculate neuralgia: This is a rare condition that affects the nerves in the jaw and ear, and can cause pain in the jaw, face, and ear.
Overall, neuralgia is a complex and debilitating condition that can significantly impact an individual's quality of life. It is important for individuals experiencing symptoms of neuralgia to seek medical attention to determine the underlying cause and develop an appropriate treatment plan.
Hypothermia can be mild, moderate, or severe. Mild hypothermia is characterized by shivering and a body temperature of 95 to 97 degrees Fahrenheit (32 to 36.1 degrees Celsius). Moderate hypothermia has a body temperature of 82 to 94 degrees Fahrenheit (28 to 34 degrees Celsius), and the person may appear lethargic, drowsy, or confused. Severe hypothermia is characterized by a body temperature below 82 degrees Fahrenheit (28 degrees Celsius) and can lead to coma and even death if not treated promptly.
Treatment for hypothermia typically involves warming the person up slowly, using blankets or heating pads, and providing warm fluids to drink. In severe cases, medical professionals may use a specialized warm water bath or apply warm packs to specific areas of the body.
Preventing hypothermia is important, especially in cold weather conditions. This can be done by dressing appropriately for the weather, staying dry and avoiding wet clothing, eating regularly to maintain energy levels, and seeking shelter if you become stranded or lost. It's also essential to recognize the signs of hypothermia early on so that treatment can begin promptly.
1. Cocaine dependence: This is a condition in which an individual becomes psychologically and physiologically dependent on cocaine, and experiences withdrawal symptoms when they stop using the drug.
2. Cocaine intoxication: This is a state of altered consciousness that can occur when an individual takes too much cocaine, and can cause symptoms such as agitation, confusion, and hallucinations.
3. Cocaine-induced psychosis: This is a condition in which an individual experiences a break from reality, characterized by delusions, hallucinations, and disorganized thinking.
4. Cocaine-associated cardiovascular problems: Cocaine use can increase heart rate and blood pressure, and can cause damage to the heart and blood vessels.
5. Cocaine-associated respiratory problems: Cocaine use can constrict the airways and make breathing more difficult, which can lead to respiratory failure.
6. Cocaine-associated neurological problems: Cocaine use can cause nerve damage and seizures, particularly in individuals who use the drug frequently or in large quantities.
7. Cocaine withdrawal syndrome: This is a set of symptoms that can occur when an individual stops using cocaine, including depression, anxiety, and fatigue.
8. Cocaine-related anxiety disorders: Cocaine use can exacerbate anxiety disorders such as generalized anxiety disorder, panic disorder, and social anxiety disorder.
9. Cocaine-related mood disorders: Cocaine use can also exacerbate mood disorders such as depression and bipolar disorder.
10. Cocaine-related cognitive impairment: Chronic cocaine use can impair cognitive function, particularly in areas such as attention, memory, and decision-making.
It is important to note that the effects of cocaine can vary depending on the individual, the dose and frequency of use, and other factors such as the method of administration and any underlying medical conditions. If you or someone you know is struggling with cocaine addiction, it is important to seek professional help as soon as possible.
A type of hypertension that is caused by a problem with the kidneys. It can be acute or chronic and may be associated with other conditions such as glomerulonephritis, pyelonephritis, or polycystic kidney disease. Symptoms include proteinuria, hematuria, and elevated blood pressure. Treatment options include diuretics, ACE inhibitors, and angiotensin II receptor blockers.
Note: Renal hypertension is also known as renal artery hypertension.
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.
Synonyms: Bronchial Constriction, Airway Spasm, Reversible Airway Obstruction.
Antonyms: Bronchodilation, Relaxation of Bronchial Muscles.
1. The patient experienced bronchial spasms during the asthma attack and was treated with an inhaler.
2. The bronchial spasm caused by the allergic reaction was relieved by administering epinephrine.
3. The doctor prescribed corticosteroids to reduce inflammation and prevent future bronchial spasms.
Adenosine A3 receptor
Adenosine A2A receptor
Adenosine A2B receptor
Caffeine-induced anxiety disorder
Adenosine diphosphate receptor inhibitor
Multiple electrode aggregometry
Hydrogen potassium ATPase
History of catecholamine research
Prostaglandin EP3 receptor
Nicotinic acetylcholine receptor
Mechanism of anoxic depolarization in the brain
Cannabinoid receptor type 2
Discovery and development of proton pump inhibitors
Beta-2 adrenergic receptor
Index of oncology articles
AMP-activated protein kinase
Truncated Methanocarba Adenosine Derivatives as A3 Adenosine Receptor Antagonists | Technology Transfer
Research Materials & Licensing - NIDDK
Jacobson - 2021 | National Institute of Biomedical Imaging and Bioengineering
Papers: 14 Mar 2020 - 20 Mar 2020 Archives - International Association for the Study of Pain (IASP)
A1 and A3 Adenosine receptors mediate hypothermia via distinct mechanisms | NIH Research Festival
People - The University of Nottingham
Pesquisa | Portal Regional da BVS
Kenneth A. Jacobson, Ph.D. | Principal Investigators | NIH Intramural Research Program
Biologics Offer Great Results in Treating Psoriasis, but at a Cost
Adenosine A2A receptor blockade prevents synaptotoxicity and memory dysfunction caused by beta-amyloid peptides via p38 mitogen...
Oxidosqualene-lanosterol cyclase inhibitor
The role of adenosine receptors and endogenous adenosine in citalopram-induced cardiovascular toxicity Oransay K, Hocaoglu N,...
National Institute on Drug Abuse Intramural Research Program
Cook, Donald and Kenneth Jacobson 2022 - Office of NIH History and Stetten Museum
NEW (2011) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; 8/9/2010
BREAKING! COVID-19 News: Scientists From Brazil Discover That The SARS-CoV-2 Spike Protein Alters Microglial Purinergic...
Interaction of A3 adenosine receptor ligands with the human multidrug transporter ABCG2 - PubMed
Targeting immunometabolism as an anti-inflammatory strategy | Cell Research
Marina Annetta Lynch : School of Biochemistry and Immunology - Trinity College Dublin
Dr Bronwen Evans - People - Cardiff University
NDF-RT Code NDF-RT Name
Adenosine Reduces Glutamate Release in Rat Spinal Synaptosomes | Anesthesiology | American Society of Anesthesiologists
Persistent Pulmonary Hypertension of the Newborn (PPHN): Practice Essentials, Overview, Etiology
Amylin Receptors - Structural basis for the potent and selective PI3 Kinase Inhibitor
Toxicological Phenomena - Dose-Response Relationship, Drug | CU Experts | CU Boulder
Agonists and antagonists4
- Among the ligand tools available are selective agonists and antagonists, including radioligands, but most high-affinity non-nucleoside antagonists are limited in selectivity to primate species. (nih.gov)
- 17. Current Status in the Design and Development of Agonists and Antagonists of Adenosine A3 Receptor as Potential Therapeutic Agents. (nih.gov)
- Our overall goals are to design, chemically synthesize, and characterize pharmacologically new agonists and antagonists for the four subtypes of adenosine receptors (ARs) and eight subtypes of P2Y receptors and to explore their potential for treating human disease conditions. (nih.gov)
- Recent accomplishments include the design and synthesis of the highly potent and selective A3 adenosine receptor agonists and antagonists, using a combination of library screening and optimization of known adenosine receptor ligands. (nih.gov)
- 2. The A3 adenosine receptor agonist, namodenoson, ameliorates non‑alcoholic steatohepatitis in mice. (nih.gov)
- 6. An adenosine A3 receptor agonist inhibits DSS-induced colitis in mice through modulation of the NF-κB signaling pathway. (nih.gov)
- 11. CF102 an A3 adenosine receptor agonist mediates anti-tumor and anti-inflammatory effects in the liver. (nih.gov)
- 13. A3 Adenosine Receptor Agonist Inhibited Survival of Breast Cancer Stem Cells via GLI-1 and ERK1/2 Pathway. (nih.gov)
- A3AR agonist, but not A1AR agonists induced hypothermia was prevented by pretreatment with histamine H1 antagonists (i.p. (nih.gov)
- I am interested in how activation of one of these classes of receptor leads to modification of the response to other receptor classes (cross-talk), as well as how different ligands can provoke different signalling profiles at the same receptor (agonist bias). (nottingham.ac.uk)
- The determination of the X-ray crystallographic structures of the P2Y1 receptor and an agonist bound A2A adenosine receptor by our lab in collaboration with Ray Stevens of Scripps Research Institute is providing a new path to designing drugs that act at these receptors. (nih.gov)
- We recently found an A1 adenosine receptor agonist that has antiseizure effects in mice without some of the side effects associated with such agonists in the past. (nih.gov)
- Glutamate release evoked by the TRPV-1 receptor agonist, capsaicin, was measured. (asahq.org)
Subtypes of P2Y receptors1
- Organic synthesis and characterization of novel heterocyclic derivatives as antagonists of several subtypes of P2Y receptors. (nih.gov)
Examined the role of adenosine1
- The current experiments examined the role of adenosine agonists at the A1AR and A3AR in eliciting these effects. (nih.gov)
- 18. Pharmacological and therapeutic effects of A3 adenosine receptor agonists. (nih.gov)
- Introduction: Pharmacological activation of adenosine receptors in mice and rats causes torpor, which is characterized by reduced body temperature (hypothermia) and reduced physical activity. (nih.gov)
- We are interested in correlating structure of receptors and small molecular drugs with pharmacological properties. (nih.gov)
- Substances developed as potent and selective agents acting through adenosine and P2 receptors have proven useful as pharmacological probes and have potential for treating diseases of the central nervous system, immune system, and cardiovascular system. (nih.gov)
- The pharmacological probes designed in our section have been used to demonstrate the connection between purine receptors and apoptosis (programmed cell death). (nih.gov)
- Our experiments showed that D3tail can indeed rescue the activity of D3nf, and that the pharmacological profile of this split D3nf/D3tail receptor is identical to that of the wild type D3 receptor. (shengsci.com)
- Our current focus is on receptors for purines, encompassing both adenosine receptors and P2 receptors, which are activated by ATP, UTP and other extracellular nucleotides. (nih.gov)
- Recently, the involvement of extracellular loops of GPCRs have been implicated in the receptor binding of small molecules. (nih.gov)
- Jacobson: Yes, the purinergic system is a collection of receptors and enzymes that process or modulate signals related to extracellular purines-those being adenosine and various nucleotides. (nih.gov)
- Adenosine tri-phosphate (ATP) belongs to the purinergic signaling system, which includes P2X, P2Y, and P1 receptors, as well as other proteins participating in ATP secretion and extracellular ATP degradation, and molecules that recognize purines as a ligand. (thailandmedical.news)
- experimental strategies claim that IL-12 downregulation was because of extracellular calcium influxes that resulted from receptor ligation. (edrc2013.org)
- 2)Structure of the atrial natriuretic peptide receptor extracellular domain in the unbound and hormone-bound states by single-particle electron microscopy. (edu.in)
- We are currently designing adenosine receptor agonists for use in treating chronic neuropathic pain, an unmet medical need, and P2Y receptor antagonists for inflammation. (nih.gov)
- Treatment of chronic neuropathic pain: purine receptor modulation. (iasp-pain.org)
- We recently published in collaboration with Daniela Salvemini of St. Louis University the protective effect of A3 agonists in animal models of neuropathic pain. (nih.gov)
- We have discovered highly specific A3 agonists that reduce neuropathic pain in the mouse and rat and prevent its development. (nih.gov)
- 4,5 The primary aim of the current study was to determine whether adenosine-mediated inhibition of spinal glutamate release was increased in an animal model of neuropathic pain, potentially providing an explanation for this selective effect of intrathecal adenosine in hypersensitive states. (asahq.org)
- 6-9 Peripheral noxious stimulation increases the release of glutamate from the rat dorsal spinal cord in vivo , 10 whereas pharmacologic and electrophysiologic studies indicate that glutamate receptor antagonists produce antinociceptive effects in rodents and humans. (asahq.org)
- We collaborate on the X-ray crystallographic structures of various purine (adenosine and P2Y) receptors with Ray Stevens of the University of Southern California. (nih.gov)
- In particular, the use of A 1 and A 2 selective ligands has been limited by the ubiquity of expression of the receptors throughout the body and the resultant side effects. (nih.gov)
- Detailed information about the three-dimensional structure of this receptor family aids in the design and chemical synthesis of novel ligands. (nih.gov)
- The opioid system of mu, delta and kappa receptors (MOR, DOR, KOR) and their peptide ligands (β-endorphin, enkephalin, dynorphin) have complex and partially opposing effects on amygdala function. (iasp-pain.org)
- Cannabinoid receptors and their ligands: beyond CB₁ and CB₂. (nottingham.ac.uk)
- G protein-coupled receptor list: recommendations for new pairings with cognate ligands. (nottingham.ac.uk)
- Novel ligands (small molecules) for these receptors are developed using classical synthetic approaches and also by semirational methods based on molecular modeling and template design. (nih.gov)
- 26)New ligands for melanocortin receptors. (edu.in)
- Compounds that selectively bind to and block the activation of ADENOSINE A3 RECEPTORS . (nih.gov)
- 16. Activation of adenosine A3 receptor inhibits inflammatory cytokine production in colonic mucosa of patients with ulcerative colitis by down-regulating the nuclear factor-kappa B signaling. (nih.gov)
- We have used convergent modeling, mutagenesis and structure activity approaches to gather information about the three-dimensional structure of the receptors and its relationship to binding and activation functions. (nih.gov)
- Another potential method of using the protective effects of AR activation has been achieved through receptor engineering. (nih.gov)
- We recently showed that ATP is the primary chemoattractor to tissue damage in vivo and elicits opposite effects on the motility of activated microglia in vitro through activation of adenosine A2A receptors. (nih.gov)
-  Activation of A 1 receptors depresses heart by negative inotropic, chronotropic, and dromotropic effects. (ijp-online.com)
- Activation of A 2 receptors cause a reduction in mean arterial pressure by causing a relaxation in vascular smooth muscle cells. (ijp-online.com)
-  It was observed that the negative inotropic and chronotropic effects induced by citalopram can be explained by the inhibition of re-uptake of adenosine or the activation of adenosine A 1 receptors. (ijp-online.com)
- Current evidence demonstrates that SARS-CoV-2 Spike protein can reach different brain regions, irrespective of viral brain replication resulting in activation of pattern recognition receptors (PRRs) and neuroinflammation. (thailandmedical.news)
- A1 adenosine receptor activation reduces hypersensitivity in animal models of chronic pain, but intrathecal adenosine does not produce analgesia to acute noxious stimuli. (asahq.org)
- These observations confirm previous neurophysiologic studies that presynaptic adenosine A1 receptor activation inhibits glutamate release from primary afferents. (asahq.org)
- Covalent attachment via an isopeptide bond to its substrates requires prior activation by the E1 complex SAE1-SAE2 and linkage to the E2 enzyme UBE2I, and can be promoted by an E3 ligase such as PIAS1-4, RANBP2 or CBX4. (nih.gov)
- 21)Protection conferred by Corticotropin-releasing hormone in rat primary cortical neurons against chemical ischemia involves opioid receptor activation. (edu.in)
- Selective A3 adenosine receptor antagonists derived from nucleosides containing a bicyclo[3.1.0]hexane ring system. (nih.gov)
- Two selective A3 adenosine receptor agonists developed in our laboratory are currently in clinical trials for hepatocellular carcinoma, glaucoma, psoriasis, and rheumatoid arthritis. (nih.gov)
- We have synthesized the first P2Y1 receptor-selective antagonists through functionalization of adenine nucleotides. (nih.gov)
- 7. A₃ adenosine receptor allosteric modulator induces an anti-inflammatory effect: in vivo studies and molecular mechanism of action. (nih.gov)
- The adenosine receptors are known to be anti-inflammatory. (nih.gov)
- We don't want it to get out of hand-we only want it to go so far, and that's when the anti-inflammatory adenosine receptors kick in to tone down the inflammation. (nih.gov)
- The use of KCF-18, a peptide originating from cytokine receptors, as a therapeutic approach for anti-inflammatory purposes through binding to proinflammatory cytokines. (suaway.com)
- Blockade of capsaicin-evoked glutamate release by adenosine was reversed similarly in synaptosomes from normal and spinal nerve-ligated animals by an A1 adenosine receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) but not by an A2 adenosine receptor antagonist DMPX (3'7-dimethyl-1-proparaglyxanthine). (asahq.org)
- This technology relates to highly specific antagonists and partial agonists of A 3 adenosine receptors, which are negatively coupled to adenylate cyclase and have been broadly implicated in inflammation, cardiovascular disease, endocrine conditions and cancer. (nih.gov)
- ADENOSINE and synthetic adenosine receptor agonists produce antinociception in a broad range of pain models in animals, including hypersensitivity from nerve injury and inflammation. (asahq.org)
- The use of peptides derived from cytokine receptors as a therapeutic strategy for anti-inflammation has been. (suaway.com)
- 9. The A3 adenosine receptor (A3AR): therapeutic target and predictive biological marker in rheumatoid arthritis. (nih.gov)
- Receptors are computer-modeled by homology to GPCRs of known structure, and the models for ligand recognition are tested and refined using site-directed mutagenesis of the receptor proteins. (nih.gov)
- Analyzing the process dynamics in 3D cultures of primary microglia indicated that only A2A , but not A1 or A3 receptors, mediate process retraction in LPS-activated microglia. (nih.gov)
- We included P2X7 receptors in our study for the reason you mentioned, and also P2Y14 receptors that respond to certain pro-inflammatory nucleosides and nucleotides, and A3 adenosine receptors that respond to adenosine. (nih.gov)
- Adenosine is an endogenous nucleoside that shows its well-known cardiovascular effects by A 1 , A 2a , and A 2b receptors. (ijp-online.com)
- Some studies have shown that adenosine A 1 receptor stimulation and/or endogenous adenosine may have a role in amitriptyline-a tricyclic antidepressant (TCA)-induced cardiovascular toxicity such as hypotension, QRS, and QT prolongation. (ijp-online.com)
- Therefore, aim of this study is to clarify the role of adenosine receptors and/or endogenous adenosine in the mechanism of the cardiovascular toxic effects induced by citalopram overdose in rats. (ijp-online.com)
- Cyclic AC-253, also known as cAC-253, is a new and potent amylin receptor antagonist that has been shown to alleviate cognitive impairments in Alzheimer's disease. (suaway.com)
- We have explored the structure-activity relationship of a previously reported A 3 AR antagonist DPTN 9 ( N -[4-(3,5-dimethylphenyl)-5-(4-pyridyl)-1,3-thiazol-2-yl]nicotinamide) for radiolabeling, including 3-halo derivatives (3-iodo, MRS7907), and characterized 9 as a high -affinity radioligand [ 3 H]MRS7799. (nih.gov)
- 20. Effects of synthetic A3 adenosine receptor agonists on cell proliferation and viability are receptor independent at micromolar concentrations. (nih.gov)
- 13)Androgen-induced human breast cancer cell proliferation is mediated by discrete mechanisms in estrogen receptor-alpha-positive and -negative breast cancer cells. (edu.in)
- 15)Cross-Linking of a DOPA-Containing Peptide Ligand into its G Protein-Coupled Receptor. (edu.in)
- We surmised that these receptors could be utilized to tone down the excessive immune response leading to the cytokine storm and acute lung injury accompanying severe COVID-19 diseases. (nih.gov)
- Following 399 pubmed articles published in the last 90 days are fetched with the text keyword [peptide AND hormone AND receptor] along with other URL parameters discussed above in the table. (edu.in)
- 8)Vasoactive intestinal peptide acts via multiple signal pathways to regulate hippocampal NMDA receptors and synaptic transmission. (edu.in)
- 14)Characterization of peptide 20-30 of follicle stimulating hormone receptor as an antagonist of receptor activity: significance of charged residues. (edu.in)
- Description: A sandwich ELISA kit for detection of Opioid Receptor Kappa 1 from Mouse in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (antibody-tech.com)
- Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human OPRK1 / Kappa Opioid Receptor (C-Terminus). (antibody-tech.com)
- Description: Rabbit Polyclonal Opioid Receptor κ Antibody. (antibody-tech.com)
- Description: A sandwich ELISA for quantitative measurement of Mouse Sigma non opioid intracellular receptor 1 in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (antibody-tech.com)
- A3 adenosine receptor agonists at low concentrations and P2Y6 receptor agonists have antiapoptotic effects. (nih.gov)
- Adenosine concentrations, mean arterial pressure (MAP), heart rate (HR), QRS duration and QT interval were evaluated. (ijp-online.com)
- In the second protocol, citalopram infusion did not cause a significant change in plasma adenosine concentrations, but a significant increase observed in EHNA/NBTI groups. (ijp-online.com)
- Here, the authors test whether increased inhibition by adenosine of glutamate release from afferents after injury accounts for this difference. (asahq.org)
- Capsaicin-evoked glutamate release, as well as its inhibition by adenosine, did not differ between synaptosomes prepared from tissue ipsilateral and contralateral to spinal nerve ligation. (asahq.org)
- The NIDDK, Laboratory of Bioorganic Chemistry is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize A3 adenosine receptor antagonists. (nih.gov)
- Organic synthesis and characterization of new nucleoside analogues as agonists of the adenosine receptors, aimed at expanding the structure activity relationship. (nih.gov)
- PMID- 214398 TI - Characterization of an adenosine triphosphatase of the avian myeloblastosis virus and the virus-infected myeloblast. (nih.gov)
- PMID- 214392 TI - Regulation of lipogenesis by adenosine 3', 5'-cyclic monophosphate in chicken liver in vitro. (nih.gov)
- PMID- 214393 TI - Regulation of growth & metabolism of ovariectomised rat uterus by adenosine 3', 5'-cyclic monophosphate. (nih.gov)
- Adenosine monophosphate has an equivalent in the molecule known as AICAR. (suaway.com)
- Subsequent immunohistochemistry experiments confirmed high expression of the P2X7 receptor in microglial cells in CA3/DG hippocampal regions after spike infusion. (thailandmedical.news)
- Methods: Adenosine agonists were administered intraperitoneally (i.p.) or intracerebroventricularly (i.c.v.) and core body temperature and physical activity were monitored by telemetry in freely active wild type, Adora1-/-, and Adora3-/- mice. (nih.gov)
- Finally, bone tissue marrowCderived macrophages from FcR chainCdeficient mice, which neglect to flux calcium mineral after receptor ligation, didn't inhibit IL-12(p40) mRNA induction. (edrc2013.org)
- 27)Effect of lapatinib on the development of estrogen receptor-negative mammary tumors in mice. (edu.in)
- Development and optimization of fluorescent assays for receptor binding in whole cells. (nih.gov)
- Regulates E3 ubiquitin-protein ligase activity of RNF19A (By similarity). (nih.gov)
- We study the structure and pharmacology of receptors and discover drugs that act as agonists or antagonists of G protein-coupled receptors (GPCRs). (nih.gov)
- I am a medicinal chemist with interests in the structure and pharmacology of receptors and in developing drugs that act as agonists or antagonists of G protein-coupled receptors (GPCRs). (nih.gov)
- Jacobson: The purinergic receptors and their enzymes play an important role in the immune system, both the innate and the adaptive immune systems. (nih.gov)
- It has been shown that the erythropoietin variation known as ARA-290 may reduce the activity of inflammatory pathways by using paracrine signalling and the innate repair receptors. (suaway.com)
- The A 3 adenosine receptor (A 3 AR) is a target for pain, ischemia, and inflammatory disease therapy. (nih.gov)
- A 3 receptors are particularly highly expressed in inflammatory cells, making it a potentially desirable target for inflammatory diseases. (nih.gov)
- Two agonists of the A3 adenosine receptor (both discovered in our lab) have progressed to advanced clinical trials for the treatment of autoimmune inflammatory diseases, liver diseases and cancer. (nih.gov)
- 19)Hippocampal dynorphin immunoreactivity increases in response to gonadal steroids and is positioned for direct modulation by ovarian steroid receptors. (edu.in)
- Second, publicity of macrophages towards the calcium mineral ionophores, a23187 or ionomycin, mimicked receptor ligation and inhibited IL-12(p40) mRNA induction by LPS. (edrc2013.org)
- These outcomes indicate which the calcium mineral influxes that take place due to receptor ligation are in charge of inhibiting the induction of IL-12 by LPS. (edrc2013.org)
- Therefore, the ligation of phagocytic receptors on macrophages can result in a dramatic reduction in IL-12 induction. (edrc2013.org)
- 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)
- 4. Targeting the A3 adenosine receptor to treat hepatocellular carcinoma: anti-cancer and hepatoprotective effects. (nih.gov)
- 1)Type I Gonadotropin-Releasing Hormone Receptor (GnRH-R) Mediates the Antiproliferative Effects of GnRH-II on Prostate Cancer Cells. (edu.in)
- 16)New topics in vasopressin receptors and approach to novel drugs:effects of vasopressin receptor on regulations of hormone secretion and metabolisms of glucose, fat, and protein. (edu.in)
- Receptor docking predicted its orthosteric site binding by engaging residues that were previously found to be essential for AR binding. (nih.gov)
- AN - traumatic kidney injury: index KIDNEY/ inj HN - 2011 MH - Adenosine A1 Receptor Agonists UI - D058907 MN - D27.505.519.625.7126.96.36.199 MN - D27.505.696.577.7188.8.131.52 MS - Compounds that bind to and stimulate ADENOSINE A1 RECEPTORS. (nih.gov)
- On the other hand, high levels of A 3 receptor expression are limited to the CNS, testes, and the immune system. (nih.gov)