Cannabinoid Receptor Modulators
Receptor, Cannabinoid, CB1
Receptor, Cannabinoid, CB2
Cannabinoid Receptor Agonists
Selective Estrogen Receptor Modulators
Cannabinoid Receptor Antagonists
Estrogen Receptor Modulators
Dose-Response Relationship, Drug
Estrogen Receptor alpha
Calcium Channel Blockers
Estrogen Receptor beta
Drug Evaluation, Preclinical
Drug Inverse Agonism
TRPV Cation Channels
Disease Models, Animal
Androgen Receptor Antagonists
Gene Expression Regulation
Bone Density Conservation Agents
Antineoplastic Agents, Hormonal
Reverse Transcriptase Polymerase Chain Reaction
Contraceptive Agents, Male
Excitatory Postsynaptic Potentials
GTP-Binding Protein alpha Subunits, Gi-Go
Receptors, Opioid, mu
Tumor Cells, Cultured
Substance Withdrawal Syndrome
Chromatography, High Pressure Liquid
Estrogen Replacement Therapy
Inhibitory Postsynaptic Potentials
Bone and Bones
Biosynthesis and inactivation of the endocannabinoid 2-arachidonoylglycerol in circulating and tumoral macrophages. (1/954)The stimulus-induced biosynthesis of the endocannabinoid 2-arachidonoylglycerol (2-AG) in intact mouse J774 macrophages and the inactivation of 2-AG by the same cells or by rat circulating macrophages was studied. By using gas chromatography-mass spectrometry, we found that ionomycin (5 microM) and lipopolysaccharide (LPS, 200 microg x mL-1) cause a 24-fold and 2.5-fold stimulation of 2-AG levels in J774 cells, respectively, thus providing unprecedented evidence that this cannabimimetic metabolite can be synthesized by macrophages. In J774 cells, LPS also induced a 7.8-fold increase of the levels of the other endocannabinoid, anandamide, and, in rat circulating macrophages, an almost twofold increase of 2-AG levels. Extracellular [3H]2-AG was cleared from the medium of intact J774 macrophages (t1/2 = 19-28 min) and esterified to phospholipids, diacylglycerols and triglycerides or hydrolyzed to [3H]arachidonic acid and glycerol. These catabolic processes were attenuated differentially by various enzyme inhibitors. Rat circulating macrophages were shown to contain enzymatic activities for the hydrolysis of 2-AG, including: (a) fatty acid amide hydrolase (FAAH), the enzyme responsible for anandamide breakdown and previously shown to catalyse also 2-AG hydrolysis, and (b) a 2-AG hydrolase activity different from FAAH and down-regulated by LPS. High levels of FAAH mRNA were found in circulating macrophages but not platelets, which, however, contain a 2-AG hydrolase. Both platelets and macrophages were shown to express the mRNA for the CB1 cannabinoid receptor. A macrophage 2-AG hydrolase with apparent Km = 110 microM and Vmax = 7.9 nmol x min-1 x (mg protein)-1 was partially characterized in J774 cells and found to exhibit an optimal pH of 6-7 and little or no sensitivity to typical FAAH inhibitors. These findings demonstrate for the first time that macrophages participate in the homeostasis of the hypotensive and immunomodulatory endocannabinoid 2-AG through metabolic mechanisms that are subject to regulation. (+info)
The endothelial component of cannabinoid-induced relaxation in rabbit mesenteric artery depends on gap junctional communication. (2/954)1. We have shown that the endocannabinoid anandamide and its stable analogue methanandamide relax rings of rabbit superior mesenteric artery through endothelium-dependent and -independent mechanisms that are unaffected by blockade of NO synthase and cyclooxygenase. 2. The endothelium-dependent component of the responses was attenuated by the gap junction inhibitor 18alpha-glycyrrhetinic acid (18alpha-GA; 50 microM), and a synthetic connexin-mimetic peptide homologous to the extracellular Gap 27 sequence of connexin 43 (43Gap 27, SRPTEKTIFII; 300 microM). By contrast, the corresponding connexin 40 peptide (40Gap 27, SRPTEKNVFIV) was inactive. 3. The cannabinoid CB1 receptor antagonist SR141716A (10 microM) also attenuated endothelium-dependent relaxations but this inhibition was not observed with the CB1 receptor antagonist LY320135 (10 microM). Furthermore, SR141716A mimicked the effects of 43Gap 27 peptide in blocking Lucifer Yellow dye transfer between coupled COS-7 cells (a monkey fibroblast cell line), whereas LY320135 was without effect, thus suggesting that the action of SR141716A was directly attributable to effects on gap junctions. 4. The endothelium-dependent component of cannabinoid-induced relaxation was also attenuated by AM404 (10 microM), an inhibitor of the high-affinity anandamide transporter, which was without effect on dye transfer. 5. Taken together, the findings suggest that cannabinoids derived from arachidonic acid gain access to the endothelial cytosol via a transporter mechanism and subsequently stimulate relaxation by promoting diffusion of an to adjacent smooth muscle cells via gap junctions. 6. Relaxations of endothelium-denuded preparations to anandamide and methanandamide were unaffected by 43Gap 27 peptide, 18alpha-GA, SR141716A, AM404 and indomethacin and their genesis remains to be established. (+info)
Comparison of novel cannabinoid partial agonists and SR141716A in the guinea-pig small intestine. (3/954)The controversial nature of the CB(1) receptor antagonist, SR141716A, in the guinea-pig small intestine was investigated by comparing it with four analogues of Delta(8)-tetrahydrocannabinol (Delta(8)-THC): O-1184, O-1238, O-584 and O-1315. These compounds (10 - 1000 nM) inhibited the electrically-evoked contractions with a rank order of potency of O-1238>O-1184>O-584>O-1315. Log concentration-response curves for O-1238, O-1184 and O-1315 were significantly shifted to the right by SR141716A and the maxima were significantly less than that of the CB(1) agonist, WIN55212-2, an indication of partial agonism. Partial saturation of the triple bond in O-1184 to a cis double bond (O-1238) increased its potency as an agonist (pEC(50) from 6.42 to 7.63) and as an antagonist of WIN55212-2, (pK(B), from 8.36 to 9.49). Substitution of the terminal azide group by an ethyl group (O-584) or removal of the phenolic hydroxyl group (O-1315) had no significant effect on the agonist or antagonist potency. None of these analogues increased the twitch response in a manner resembling that of SR141716A. O-1184 (10 and 100 nM) shifted the log concentration-response curve of WIN55212-2 for inhibition of the twitch responses to the right with pK(B) values of 8.29 and 8.38, respectively. We conclude that these Delta(8)-THC analogues behave as partial agonists rather than silent antagonists at CB(1) binding sites in this tissue. There was no evidence of antagonism of endocannabinoids thus supporting the hypothesis that, in this tissue, SR141716A is an inverse agonist of constitutively active CB(1) receptors. (+info)
Reversal of dopamine D(2) receptor responses by an anandamide transport inhibitor. (4/954)We characterized the pharmacological properties of the anandamide transport inhibitor N-(4-hydroxyphenyl)-arachidonamide (AM404) in rats and investigated the effects of this drug on behavioral responses associated with activation of dopamine D(2) family receptors. Rat brain slices accumulated [(3)H]anandamide via a high-affinity transport mechanism that was blocked by AM404. When administered alone in vivo, AM404 caused a mild and slow-developing hypokinesia that was significant 60 min after intracerebroventricular injection of the drug and was reversed by the CB1 cannabinoid receptor antagonist SR141716A. AM404 produced no significant catalepsy or analgesia, two typical effects of direct-acting cannabinoid agonists. However, AM404 prevented the stereotypic yawning produced by systemic administration of a low dose of apomorphine, an effect that was dose-dependent and blocked by SR141716A. Furthermore, AM404 reduced the stimulation of motor behaviors elicited by the selective D(2) family receptor agonist quinpirole. Finally, AM404 reduced hyperactivity in juvenile spontaneously hypertensive rats, a putative model of attention deficit hyperactivity disorder. The results support a primary role of the endocannabinoid system in the regulation of psychomotor activity and point to anandamide transport as a potential target for neuropsychiatric medicines. (+info)
Endocannabinoid 2-arachidonyl glycerol is a full agonist through human type 2 cannabinoid receptor: antagonism by anandamide. (5/954)The endocannabinoids anandamide and 2-arachidonyl glycerol (2-AG) bind to G protein-coupled central and peripheral cannabinoid receptors CB1 and CB2, respectively. Due to the relatively high expression of the CB2 isotype on peripheral immune cells, it has been hypothesized that this receptor mediates the immunosuppressive effects of cannabinoids. Unfortunately, there was a dearth of pharmacological studies with the endocannabinoids and human CB2 (hCB2). These studies compare and contrast the potency and efficacy of anandamide, 2-AG, and the synthetic cannabinoid HU210 at hCB2. Using [(35)S]guanosine-5'-O-(3-thio)triphosphate (GTPgammaS) and radioligand bindings in insect Sf9-hCB2 membranes, we showed that both endocannabinoids bound hCB2 with similar affinity and that the cannabinoids acted as full agonists in stimulating [(35)S]GTPgammaS exchange, although 2-AG was 3-fold more potent than anandamide (EC(50) = 38.9 +/- 3.1 and 121 +/- 29 nM, respectively). In a mammalian expression system (Chinese hamster ovary-hCB2 cells), HU210 and 2-AG maximally inhibited forskolin-stimulated cAMP synthesis (IC(50) = 1.61 +/- 0.42 nM and 1.30 +/- 0.37 microM, respectively) although anandamide was ineffective. In Chinese hamster ovary-hCB2 membranes, HU210 and 2-AG were also full agonists in stimulating [(35)S]GTPgammaS binding (EC(50) = 1.96 +/- 0.35 and 122 +/- 17 nM, respectively), but anandamide was a weak partial agonist (EC(50) = 261 +/- 91 nM; 34 +/- 4% of maximum). Due to its low intrinsic activity, coincubation with anandamide effectively attenuated the functional activity of 2-AG at hCB2. Collectively, the data showed that both endocannabinoids bound hCB2 with similar affinity, but only 2-AG functioned as a full agonist. Moreover, the agonistic activity of 2-AG was attenuated by anandamide. (+info)
Are anandamide and cannabinoid receptors involved in ethanol tolerance? A review of the evidence. (6/954)There have been significant developments towards the elucidation of molecular and cellular changes in neuronal second messenger pathways involved in the development of tolerance to and dependence on ethanol (EtOH). The long-term exposure to EtOH has been shown to affect several aspects of neuronal signal transduction as well as ligand-gated ion channels and receptor systems, including the receptors that are coupled to the superfamily of GTP binding regulatory proteins (G-proteins). The recent identification of a G-protein coupled receptor that was activated by delta-9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, led to the discovery of endogenous agonists. One such agonist found to exist in mammalian brain was characterized to be an arachidonic acid (AA) metabolite and was named anandamide (AnNH). AnNH has been shown to bind specifically to the cannabinoid receptor (CB(1)) and mimic many of the pharmacological and behavioural effects of THC including tolerance development. The role of endocannabinoids and the CB(1) receptor signal transduction system in tolerance development to drugs of abuse has not been explored until recently. The findings presented in this review provide evidence for the first time that some of the pharmacological actions of EtOH including tolerance development may be mediated through participation of the endocannabinoid-CB(1) receptor signal transduction system. Recent studies have shown that chronic EtOH exposure produces downregulation of CB(1) receptors and an inhibition of CB(1) receptor agonist-stimulated GTPgammaS binding in mouse brain synaptic plasma membranes (SPM). The observed receptor downregulation results from the persistent stimulation of the receptors by the endogenous CB(1) receptor agonist AnNH, the synthesis of which is increased by chronic EtOH exposure. Further, the CB(1) receptor antagonist SR-141716A has been shown to block voluntary EtOH intake in rats and mice. Based on these studies, a hypothesis is presented to explain the possible involvement of the endocannabinoid system in the pharmacological and behavioural effects of EtOH. (+info)
Down-regulation of anandamide hydrolase in mouse uterus by sex hormones. (7/954)Endocannabinoids are an emerging class of lipid mediators, which mimic several effects of cannabinoids. Anandamide (arachidonoylethanolamide) is a major endocannabinoid, which has been shown to impair pregnancy and embryo development. The activity of anandamide is controlled by cellular uptake through a specific transporter and intracellular degradation by the enzyme anandamide hydrolase (fatty acid amide hydrolase, FAAH). We characterized FAAH in mouse uterus by radiochromatographic and immunochemical techniques, showing that the enzyme is confined to the epithelium and its activity decreases appreciably during pregnancy or pseudopregnancy because of lower gene expression at the translational level. Ovariectomy prevented the decrease in FAAH, and both progesterone and estrogen further reduced its basal levels, suggesting hormonal control of the enzyme. Anandamide was shown to induce programmed cell death in mouse blastocysts, through a pathway independent of type-1 cannabinoid receptor. Blastocysts, however, have a specific anandamide transporter and FAAH, which scavenge this lipid. Taken together, these results provide evidence of an interplay between endocannabinoids and sex hormones in pregnancy. These findings may also be relevant for human fertility, as epithelial cells from healthy human uterus showed FAAH activity and expression, which in adenocarcinoma cells was increased fivefold. (+info)
Age dependent accumulation of N-acyl-ethanolamine phospholipids in ischemic rat brain. A (31)P NMR and enzyme activity study. (8/954)N-acyl-ethanolamine phospholipids (NAPE) can be formed as a stress response during neuronal injury, and they are precursors for N-acyl-ethanolamines (NAE), some of which are endocannabinoids. The levels of NAPE accumulated during post-decapitative ischemia (6 h at 37 degrees C) were studied in rat brains of various age (1, 6, 12, 19, 30, and approximately 70 days) by the use of (31)P NMR spectroscopy of lipid extracts. This ability to accumulate NAPE was compared with the activity of N-acyltransferase and of NAPE-hydrolyzing phospholipase D (NAPE-PLD) in brain microsomes. These two enzymes are involved in the formation and degradation of NAPE, respectively. The results showed that 1) the ability to accumulate NAPE during post-decapitative ischemia is especially high in the youngest rats and is markedly reduced in older brains [in 1-day-old rat brains NAPE accumulated to 1.5% of total phospholipids, while in 30-day-old rat brains NAPE accumulation could not be detected (detection limit 0.09%)] and 2) this age pattern of accumulation can be explained by a combination of the decreased activity of N-acyltransferase and the increased activity of NAPE-PLD during development. These results point out that it would be advantageous to investigate a potential cytoprotective role of NAPE in the brains of very young rats. (+info)
Leiomyomas are the most common type of gynecologic tumor and affect up to 80% of women at some point in their lifetime. They are more common in women who have a family history of leiomyomas or who are obese.
There are several different types of leiomyomas, including:
1. Submucosal leiomyomas: These tumors grow into the uterine cavity and can cause bleeding and other symptoms.
2. Intramural leiomyomas: These tumors grow within the muscle of the uterus and can cause pelvic pain and heavy menstrual bleeding.
3. Pedunculated leiomyomas: These tumors are attached to the uterine wall by a stalk-like structure and can be felt during a pelvic exam.
4. Broad ligament leiomyomas: These tumors grow on the broad ligament, which is a band of tissue that connects the uterus to the pelvis.
Leiomyomas are typically diagnosed through a combination of pelvic examination, ultrasound, and hysteroscopy (a procedure in which a small camera is inserted into the uterus to examine the inside of the organ). Treatment options for leiomyomas depend on the size and location of the tumors, as well as the severity of symptoms. Treatment may include watchful waiting, medications to regulate hormones or shrink the tumors, or surgery to remove the tumors.
In some cases, leiomyomas can be associated with other conditions such as endometriosis or adenomyosis, and it is important for women with these tumors to receive ongoing care from a healthcare provider to monitor for any changes in their condition.
1. Endometrial carcinoma (cancer that starts in the lining of the uterus)
2. Uterine papillary serous carcinoma (cancer that starts in the muscle layer of the uterus)
3. Leiomyosarcoma (cancer that starts in the smooth muscle of the uterus)
4. Adenocarcinoma (cancer that starts in the glands of the endometrium)
5. Clear cell carcinoma (cancer that starts in the cells that resemble the lining of the uterus)
6. Sarcoma (cancer that starts in the connective tissue of the uterus)
7. Mixed tumors (cancers that have features of more than one type of uterine cancer)
These types of cancers can affect women of all ages and are more common in postmenopausal women. Risk factors for developing uterine neoplasms include obesity, tamoxifen use, and a history of endometrial hyperplasia (thickening of the lining of the uterus).
Symptoms of uterine neoplasms can include:
1. Abnormal vaginal bleeding (heavy or prolonged menstrual bleeding, spotting, or postmenopausal bleeding)
2. Postmenopausal bleeding
3. Pelvic pain or discomfort
4. Vaginal discharge
5. Weakness and fatigue
6. Weight loss
7. Pain during sex
8. Increased urination or frequency of urination
9. Abnormal Pap test results (abnormal cells found on the cervix)
If you have any of these symptoms, it is essential to consult your healthcare provider for proper evaluation and treatment. A diagnosis of uterine neoplasms can be made through several methods, including:
1. Endometrial biopsy (a small sample of tissue is removed from the lining of the uterus)
2. Dilation and curettage (D&C; a surgical procedure to remove tissue from the inside of the uterus)
3. Hysteroscopy (a thin, lighted tube with a camera is inserted through the cervix to view the inside of the uterus)
4. Imaging tests (such as ultrasound or MRI)
Treatment for uterine neoplasms depends on the type and stage of cancer. Common treatments include:
1. Hysterectomy (removal of the uterus)
2. Radiation therapy (uses high-energy rays to kill cancer cells)
3. Chemotherapy (uses drugs to kill cancer cells)
4. Targeted therapy (uses drugs to target specific cancer cells)
5. Clinical trials (research studies to test new treatments)
It is essential for women to be aware of their bodies and any changes that occur, particularly after menopause. Regular pelvic exams and screenings can help detect uterine neoplasms at an early stage, when they are more treatable. If you experience any symptoms or have concerns about your health, talk to your healthcare provider. They can help determine the cause of your symptoms and recommend appropriate treatment.
During menopause, the levels of estrogen in the body decrease significantly, which can lead to a loss of bone density and an increased risk of developing osteoporosis. Other risk factors for postmenopausal osteoporosis include:
* Family history of osteoporosis
* Early menopause (before age 45)
* Poor diet or inadequate calcium and vitamin D intake
* Sedentary lifestyle or lack of exercise
* Certain medications, such as glucocorticoids and anticonvulsants
* Other medical conditions, such as rheumatoid arthritis and liver or kidney disease.
Postmenopausal osteoporosis can be diagnosed through a variety of tests, including bone mineral density (BMD) measurements, which can determine the density of bones and detect any loss of bone mass. Treatment options for postmenopausal osteoporosis typically involve a combination of medications and lifestyle changes, such as:
* Bisphosphonates, which help to slow down bone loss and reduce the risk of fractures
* Hormone replacement therapy (HRT), which can help to replace the estrogen that is lost during menopause and improve bone density
* Selective estrogen receptor modulators (SERMs), which mimic the effects of estrogen on bone density but have fewer risks than HRT
* RANK ligand inhibitors, which can help to slow down bone loss and reduce the risk of fractures
* Parathyroid hormone (PTH) analogues, which can help to increase bone density and improve bone quality.
It is important for women to discuss their individual risks and benefits with their healthcare provider when determining the best course of treatment for postmenopausal osteoporosis. Additionally, lifestyle changes such as regular exercise, a balanced diet, and avoiding substances that can harm bone health (such as smoking and excessive alcohol consumption) can also help to manage the condition.
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.
The DSM-5 defines marijuana abuse as:
1. Taking marijuana in larger amounts or for a longer period than intended.
2. Desire or unsuccessful efforts to cut down or control use.
3. Spending a lot of time obtaining, using, or recovering from the effects of use.
4. Craving or strong desire to use marijuana.
5. Interference with work, school, or home responsibilities due to use.
6. Continuing to use despite social or personal problems caused by use.
7. Giving up important activities in order to use.
8. Using marijuana in hazardous situations, such as while driving or operating machinery.
9. Continued use despite physical or psychological problems caused or worsened by use.
10. Developing tolerance (needing to use more to achieve the desired effect).
11. Experiencing withdrawal symptoms when stopping or reducing use.
Marijuana abuse can lead to a range of negative consequences, including:
* Addiction: Marijuana can be addictive, and long-term use can lead to dependence and withdrawal symptoms when trying to stop.
* Mental Health Problems: Marijuana use has been linked to an increased risk of depression, anxiety, psychosis, and other mental health issues.
* Respiratory Problems: Smoking marijuana can irritate the lungs and increase the risk of respiratory problems, such as bronchitis and lung infections.
* Cognitive Impairment: Marijuana use can impair memory, attention, and decision-making skills.
* Impaired Coordination and Judgment: Marijuana use can impair coordination and judgment, which can increase the risk of accidents and injuries.
If you or someone you know is struggling with marijuana abuse, it is important to seek professional help as soon as possible. Treatment options may include counseling, medication, and support groups. With the right treatment and support, it is possible to overcome marijuana abuse and achieve a healthier, happier life.
There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
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.
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 types of osteoporosis, including:
1. Postmenopausal osteoporosis: This type of osteoporosis is caused by hormonal changes that occur during menopause. It is the most common form of osteoporosis and affects women more than men.
2. Senile osteoporosis: This type of osteoporosis is caused by aging and is the most common form of osteoporosis in older adults.
3. Juvenile osteoporosis: This type of osteoporosis affects children and young adults and can be caused by a variety of genetic disorders or other medical conditions.
4. secondary osteoporosis: This type of osteoporosis is caused by other medical conditions, such as rheumatoid arthritis, Crohn's disease, or ulcerative colitis.
The symptoms of osteoporosis can be subtle and may not appear until a fracture has occurred. They can include:
1. Back pain or loss of height
2. A stooped posture
3. Fractures, especially in the spine, hips, or wrists
4. Loss of bone density, as determined by a bone density test
The diagnosis of osteoporosis is typically made through a combination of physical examination, medical history, and imaging tests, such as X-rays or bone density tests. Treatment for osteoporosis can include medications, such as bisphosphonates, hormone therapy, or rANK ligand inhibitors, as well as lifestyle changes, such as regular exercise and a balanced diet.
Preventing osteoporosis is important, as it can help to reduce the risk of fractures and other complications. To prevent osteoporosis, individuals can:
1. Get enough calcium and vitamin D throughout their lives
2. Exercise regularly, especially weight-bearing activities such as walking or running
3. Avoid smoking and excessive alcohol consumption
4. Maintain a healthy body weight
5. Consider taking medications to prevent osteoporosis, such as bisphosphonates, if recommended by a healthcare provider.
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.
* 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.
Gliosis is made up of glial cells, which are non-neuronal cells that provide support and protection to neurons. When neural tissue is damaged, glial cells proliferate and form a scar-like tissue to fill in the gap and repair the damage. This scar tissue can be made up of astrocytes, oligodendrocytes, or microglia, depending on the type of injury and the location of the damage.
Gliosis can have both beneficial and harmful effects on the brain. On one hand, it can help to prevent further damage by providing a physical barrier against invading substances and protecting the surrounding neural tissue. It can also promote healing by bringing in immune cells and growth factors that aid in the repair process.
On the other hand, gliosis can also have negative effects on brain function. The scar tissue can disrupt normal communication between neurons, leading to impaired cognitive and motor function. In addition, if the scar tissue is too extensive or severe, it can compress or displaces surrounding neural tissue, leading to long-term neurological deficits or even death.
There are several ways to diagnose gliosis, including magnetic resonance imaging (MRI), positron emission tomography (PET), and histopathology. Treatment options for gliosis depend on the underlying cause of the condition and can include medications, surgery, or a combination of both.
In summary, gliosis is a type of scar tissue that forms in the brain and spinal cord as a result of damage to neural tissue. It can have both beneficial and harmful effects on brain function, and diagnosis and treatment options vary depending on the underlying cause of the condition.
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.
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.
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- Specific topics of interest vary among Institutes, Centers, and Offices, but overall the research portfolio includes studies investigating the whole or parts of the Cannabis sativa plant, cannabis extracts or enriched extracts, cannabinoid compounds extracted and derived from cannabis extracts, non-cannabinoid constituents of cannabis, synthetic cannabinoids, and the components of the endocannabinoid system (the signaling pathways in the body activated by cannabinoids). (nih.gov)
- as well as the physiological systems affected by cannabis (e.g., endocannabinoid system) and modulators thereof (e.g., fatty acid amide hydrolase [FAAH] inhibitors). (nih.gov)
- The laboratory aims to exploit and maximize the therapeutic potential of the endocannabinoid system central and peripheral receptors with unique small molecule-based approaches. (nih.gov)
- 3 ?Endocannabinoid Modulators The endocannabinoid system is a group of cannabinoid receptors located in the brain and throughout the nervous system. (velveta.cz)
- Effects of mixed cannabinoid CB 1 /CB 2 agonists, CB 2 -selective agonists, and modulators of the endocannabinoid system (i.e. inhibitors of transport or degradation) are compared. (thecannabisadvisory.com)
- Here, you can learn about medicinal cannabis in general, including scientific information about cannabinoids and the body's endocannabinoid system. (wecare-medicalcannabis.com)
- The endocannabinoid system (ECS) is a complex network of cell receptors , endocannabinoids, and enzymes that work together to regulate a variety of physiological processes in the body. (thehappycampers.com)
- The endocannabinoid system (ECS) is a complex network of receptors, endocannabinoids (cannabinoids produced naturally by the body), and enzymes that work together to maintain balance in various physiological processes, including mood, appetite, pain, and inflammation. (thehappycampers.com)
- When it comes to cannabis, we're talking about more than 100 cool cannabinoids that know how to party with the ECS (Endocannabinoid System) in all sorts of funky ways. (thehappycampers.com)
- CBD is a modulator of the endocannabinoid system that controls the work of the other systems of our body. (verdeskin.co)
- These receptors make up the body's endocannabinoid system. (verdeskin.co)
- They are structurally distinct from CANNABINOIDS and were originally discovered as a group of endogenous CANNABINOID RECEPTOR AGONISTS . (nih.gov)
- Disclosed are the coordinates for the crystal structure, and methods for determining agonists, partial agonists, antagonists, partial antagonists and selective androgen receptors modulators (SARMs) of the androgen receptor. (clubset.com)
- Gurgle HE, White K, McAdam-Marx C. SGLT2 inhibitors or GLP-1 receptor agonists as second-line therapy in type 2 diabetes: patient selection and perspectives. (uams.edu)
- Cannabinoid agonists stimulate G protein-coupled receptors (GPCRs) by binding to an "orthosteric" site on the receptor, which initiates a series of micro-conformational changes in the receptor structure, that ultimately leads to G-activation. (lipocanna.com)
- THC stimulates cannabinoid receptors in the brain to release endocannabinoids, natural pain-relieving molecules. (livescience.com)
- Therapeutic Cannabinoid Research - This subset of the Cannabinoid Research category (above) reports all NIH projects examining the therapeutic properties of all classes of cannabinoids (endocannabinoids, phytocannabinoids, and synthetic). (nih.gov)
- There is evidence that the metabolic effects of endocannabinoids are mediated by CB1 receptors in peripheral tissues. (nih.gov)
- Vertebrates also produce their own cannabinoid-like substances called endocannabinoids, including anandamide and 2-arachidonoylglyceral. (medicalmarijuana411.com)
- It works by speaking with receptors, blocking reuptake of the body endocannabinoids. (irelandoffline.com)
- It's got three main players: endocannabinoids, receptors, and enzymes. (thehappycampers.com)
- Endocannabinoids are like these natural superheroes that your body makes, and they're all about getting cozy with those ECS receptors. (thehappycampers.com)
- Hohmann's compounds, called positive allosteric modulators, or PAMs, bind to a recently discovered site on a cannabinoid brain receptor called CB1, but they do not bind to the typical THC receptor or the opioid receptor. (livescience.com)
- Here, we find that, unlike the phytocannabinoid Δ 9 -tetrahydrocannabinol, the indole-moiety containing SCs, AM2201 and JWH-018, act as positive allosteric modulators (PAMs) at the 5-HT 1A receptor (5-HT 1A R). This suggests that some biological effects of SCs might involve allosteric interactions with 5-HT 1A Rs. (nih.gov)
- Here, we find that, unlike the phytocannabinoid Δ9-tetrahydrocannabinol, the indole-moiety containing SCs, AM2201 and JWH-018, act as positive allosteric modulators (PAMs) at the 5-HT1A receptor (5-HT1AR). (nih.gov)
- Synthesis, Biological Evaluation, and Molecular Modeling Studies of 3,4-Diarylpyrazoline Series of Compounds as Potent, Nonbrain Penetrant Antagonists of Cannabinoid-1 (CB(1)R) Receptor with Reduced Lipophilicity. (nih.gov)
- Cannabinoid antagonists block activation of G proteins by binding to an "allosteric" site on the receptor that is involved in the G protein activation process, thereby precluding the ability of the orthosteric agonist-mediated conformational stimulus to execute activation. (lipocanna.com)
- The plant also contains more than 500 other chemicals, including more than 100 compounds that are chemically related to THC, called cannabinoids . (nih.gov)
- Researchers in recent years have attempted to create drug compounds that can target pain receptors in the brain but not affect opioid receptors, the source for opioid addiction. (livescience.com)
- Unlike marijuana or prescription opioids , the PAM compounds "do not hit every receptor everywhere," she added. (livescience.com)
- Compounds that interact with and modulate the activity of CANNABINOID RECEPTORS . (nih.gov)
- The present invention provides compounds of formula IThe formula I compounds inhibit the tyrosine kinase activity of growth factor receptors such as VEGFR-2, FGFR-1, thereby making them useful as anti-cancer agents. (clubset.com)
- The formula I compounds are also useful for the treatment of other diseases associated with signal transduction pathways operating through growth factor receptors. (clubset.com)
- While prior attempts at generating CB1 receptor blockers have had serious neuropsychiatric side effects, inventors at NIH have discovered compounds that block CB1 receptors with reduced brain penetrance. (nih.gov)
- 2. Characterization of new estrogen receptor destabilizing compounds: effects on estrogen-sensitive and tamoxifen-resistant breast cancer. (nih.gov)
- 16. Potential of endogenous estrogen receptor beta to influence the selective ER modulator ERbeta complex. (nih.gov)
- Rimegepant (BMS-927711) is a highly potent, oral calcitonin gene-related peptide ( CGRP ) receptor antagonist with a K i of 0.027 nM and an IC 50 of 0.14 nM for hCGRP receptor  . (medchemexpress.com)
- Olcegepant (BIBN-4096) is a potent and selective non-peptide antagonist of the calcitonin gene-related peptide 1 (CGRP1) receptor with IC 50 of 0.03 nM and K i of 14.4 pM for human CGRP   . (medchemexpress.com)
- Rat CGRP-(8-37) (VTHRLAGLLSRSGGVVKDNFVPTNVGSEAF) is a highly selective CGRP receptor antagonist. (medchemexpress.com)
- CGRP antagonist 2 is a CGRP receptor antagonist. (medchemexpress.com)
- Adrenomedullin (AM) (22-52), human, an NH2 terminal truncated adrenomedullin analogue, is an adrenomedullin receptor antagonist, and also antagonizes the calcitonin generelated peptide ( CGRP ) receptor in the hindlimb vascular bed of the cat   . (medchemexpress.com)
- Adrenomedullin (AM) (22-52), human (22-52-Adrenomedullin human) TFA, an NH 2 terminal truncated adrenomedullin analogue, is an adrenomedullin receptor antagonist. (medchemexpress.com)
- International essential tremor in mainstream and movement, no studies appear to change in cannabinoid cb1 receptor antagonist, vogel z. (amanovaraonlus.it)
- Cannabidiol Research - This subset of the Cannabinoid Research category (above) reports all NIH projects examining basic, preclinical, and therapeutic properties of cannabidiol (CBD). (nih.gov)
- Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. (nih.gov)
- Evidence that pre-cannabidiol is a powerful plant antibiotic was obtained and more recent investigations have demonstrated, to various degrees, antibacterial activity for the nonpsychotropic cannabinoids cannabichromene (CBC), cannabigerol (CBG), cannabidiol (CBD) and tetrahydrocannabidiol (THC). (medicalmarijuana411.com)
- Cannabidiol CBD and furthermore its sister compound tetrahydrocannabinol are both cannabinoids in cannabis. (irelandoffline.com)
- 4 The two most researched and most used cannabinoids are Δ 9 -tetrahydrocannabinol (THC) and cannabidiol (CBD). (wecare-medicalcannabis.com)
- CBD (or cannabidiol) is the second most studied cannabinoid. (wecare-medicalcannabis.com)
- Design, Synthesis and Biological Evaluation of Novel Non-Brain Penetrant Hybrid Cannabinoid CB 1 R inverse agonist/inducible nitric oxide synthase (iNOS) inhibitors for the treatment of liver fibrosis. (nih.gov)
- This differentiates these cannabinoids from cyclooxygenase-2 inhibitors that suppress the synthesis of eicosanoids that promote the induction of the inflammatory process. (medicalmarijuana411.com)
- Today's findings reveal a better understanding of the body's cannabinoid system and how to modulate it," said Margaret Haney, a drug-abuse expert at Columbia University in New York who was not associated with either research project. (livescience.com)
- She trained as a postdoctoral fellow with Dr. Kenner Rice at NIDA studying the medicinal chemistry of opioid receptors and sigma receptors in substance use disorders towards developing non-addicting pharmacotherapies. (nih.gov)
- CBD is also a receptor modulator, supporting it can improve or forestall the transmission of signs between cell receptors. (irelandoffline.com)
- CBD's activation of serotonin receptors allows your body to make use of already existing serotonin molecules more efficiently. (onlinesrs.co)
- RCS-8 (also known as 1-(2-cyclohexylethyl)-3-(2-methoxyphenylacetyl)indole , SR-18 , and BTM-8 ) is a synthetic cannabinoid that has been found as an ingredient of "herbal" synthetic cannabis blends. (thcscience.wiki)
- The nonmedical (i.e., recreational) misuse of synthetic cannabinoids (SCs) is a worldwide public health problem. (nih.gov)
- 1. Evaluation of a polymeric topical formulation of Endoxifen in an estrogen receptor positive breast cancer murine model. (nih.gov)
- 3. Comparison of the selective estrogen receptor modulator arzoxifene (LY353381) with tamoxifen on tumor growth and biomarker expression in an MCF-7 human breast cancer xenograft model. (nih.gov)
- 4. Regulation of aryl hydrocarbon receptor function by selective estrogen receptor modulators. (nih.gov)
- 5. Effectiveness of Selective Estrogen Receptor Modulators in Breast Cancer Therapy: An Update. (nih.gov)
- 8. The use of selective estrogen receptor modulators and selective estrogen receptor down-regulators in breast cancer. (nih.gov)
- 10. MiRNA-27a sensitizes breast cancer cells to treatment with Selective Estrogen Receptor Modulators. (nih.gov)
- 11. Acquired resistance to selective estrogen receptor modulators (SERMs) in clinical practice (tamoxifen & raloxifene) by selection pressure in breast cancer cell populations. (nih.gov)
- 13. Effects of SERM (selective estrogen receptor modulator) treatment on growth and proliferation in the rat uterus. (nih.gov)
- Recently, the orphan G protein-coupled receptor 55 (GPR55) was proposed to be an atypical cannabinoid receptor. (medicalmarijuana411.com)
- CGRP receptor is a heterodimer formed by calcitonin-receptor-like receptor (CRLR), a type II (family B) G-protein-coupled receptor, and receptor-activity-modifying protein 1 (RAMP1), a single-membrane-pass protein. (medchemexpress.com)
- 7 Beyond its activity at the CB 1 and CB 2 receptors, THC may also interact with other receptors, including TRPA 1 (Transient Receptor Potential Cation Channel Subfamily A 11 Member 1), TRPV 2 (Transient Receptor Potential Cation Channel Subfamily V Member 2), GPR 55 (G Protein Coupled Receptor 55), 5-HT 3A (5-Hydroxytryptamine Receptor Type 3 Subunit A), and other receptors. (wecare-medicalcannabis.com)
- 7 CBD interacts with a range of receptors to elicit these properties, including TRPV 1 (Transient Receptor Potential Cation Channel Subfamily V Member 1), GPR 55 (G Protein Coupled Receptor 55), 5-HT 1A (5-Hydroxytryptamine Receptor Type 1 Subunit A), 5-HT 2A (5-Hydroxytryptamine Receptor Type 2 Subunit A), adenosine receptors A 1 & A 2 , TNFα (Tumor Necrosis Factor Alpha), and other receptors. (wecare-medicalcannabis.com)
- Both end cannabinoids in our own bodies are additionally 2-arachidonoylglycerol and anandamide. (irelandoffline.com)
- Cannabinoids, drugs that share the same target as Δ 9 -tetrahydrocannabinol (Δ 9 -THC), the psychoactive ingredient in cannabis, have the potential to address this unmet need. (thecannabisadvisory.com)
- THC (or Δ 9 -tetrahydrocannabinol) is the primary psychoactive cannabinoid. (wecare-medicalcannabis.com)
- First up, we've got delta-9-tetrahydrocannabinol (THC), the rockstar of cannabinoids. (thehappycampers.com)
- Cannabinoid Research - This category reports the total NIH investment in all cannabinoid research including basic research, animal and human preclinical studies, and clinical research. (nih.gov)
- Here, we review studies evaluating cannabinoids for neuropathic pain management in the clinical and preclinical literature. (thecannabisadvisory.com)
- Clinical studies largely affirm that neuropathic pain patients derive benefits from cannabinoid treatment. (thecannabisadvisory.com)
- Despite the ongoing political debate regarding the legality of medical marijuana, clinical investigations of the therapeutic use of cannabinoids are now more prevalent than at any time in history. (medicalmarijuana411.com)
- 5 These other cannabinoids, including cannabidiravin (CBDV), cannabigerol (CBG) or cannabichromene (CBC), have shown pharmacological activity at a pre-clinical level. (wecare-medicalcannabis.com)
- 5 Much of our knowledge about these cannabinoids is derived from in vitro and in vivo studies and a limited number of well-conducted, rigorous clinical studies. (wecare-medicalcannabis.com)
- In 1995, researchers (Mechoulam et.al) discovered that the two receptors (now deemed the CB1 and CB2 receptors) were found not only in rats, but within thousands of other species (including humans). (lipocanna.com)
- solventfree CO2 extraction process All of FABs products are superclean and are loaded with beneficial cannabinoids and healthboosting terpenes. (velveta.cz)
- Another group of researchers, led by Jason Clapper, a scientist at Abide Therapeutics in San Diego, took a different approach and developed a compound that indirectly increased the amount of natural cannabinoids in the brains of rats, which relieved the animals' chronic pain symptoms . (livescience.com)
- Use of a compound for treating a respiratory disease in a mammal wherein the compound is a cannabinoid receptor modulator is disclosed. (clubset.com)
- 6. Tamoxifen Isomers and Metabolites Exhibit Distinct Affinity and Activity at Cannabinoid Receptors: Potential Scaffold for Drug Development. (nih.gov)
- Cannabis brings up to 1% delta-8 THC and as much as 20% CBD Delta-8 is an analog of delta-9 THC, indicating it has a similar molecular structure and affinity with your cannabinoid receptors (causes a blissful high). (onlinesrs.co)
- Furthermore, CBD enhanced the transcription of oxidative stress modulators with potent anti-inflammatory activity that are controlled by Nfe2l2/Nrf2 (Mt1, Mt2a, Slc30a1, Hmox1). (nih.gov)
- Cholesterol as a modulator of cannabinoid CB 2 Yeliseev, A. (nih.gov)
- Finally, limitations of cannabinoid pharmacotherapies are discussed together with directions for future research. (thecannabisadvisory.com)
- In 2015, NIH developed three reporting categories to describe and account for the research efforts underway to examine the chemical, physiological, and therapeutic properties of cannabinoids and the physiological systems they affect. (nih.gov)
- Effects of genetic disruption of cannabinoid receptors or enzymes controlling endocannabinoid degradation on neuropathic nociception are described. (thecannabisadvisory.com)
- The ECS was discovered in 1992, by Raphael Mechoulam (Hebrew University of Jerusalem), who observed that the ECS facilitates homeostasis through an elaborate, interactive, signaling scheme , involving cannabinoids, receptors and their regulatory enzymes. (lipocanna.com)
- Desde la segunda quincena de marzo de 2020, se observó un 64,2 % de disminución en la aplicación de vacunas. (bvsalud.org)
- The complexity of medical cannabis stems from the millions of combinations of doses and cannabinoid/terpene profiles. (thcscience.wiki)
- Fatty acid derivatives that have specificity for CANNABINOID RECEPTORS . (nih.gov)
- We found that both 5-HT 1A R effects were potentiated by AM2201, suggesting that PAM activity at 5-HT 1A R may represent a novel noncannabinoid receptor mechanism underlying the complex profile of effects for certain SCs. (nih.gov)
- By demonstrating that these "knock out" rats could did not get "high", they proved that "binding to CB1 receptors" is the mechanism by which THC works. (lipocanna.com)
- After a research fellowship with Dr. George Kunos at NIAAA, she led a Medicinal Chemistry Core Program at NIAAA to develop translational approaches targeting the peripheral CB1 receptors. (nih.gov)
- CB1 receptors are all up in your brain and central nervous system, while CB2 receptors are like the popular kids, hanging out in your immune system and peripheral tissues. (thehappycampers.com)
- When the cannabis plant is mature, it produces an oil containing chemicals called cannabinoids. (wecare-medicalcannabis.com)
- Just like these plant-derived medicines, the term 'cannabis-based medicines' refers to any medicine that is based on cannabinoids extracted from the cannabis plant. (wecare-medicalcannabis.com)
- Cannabinoids are a group of chemicals produced by the cannabis plant. (wecare-medicalcannabis.com)
- The cannabis plant contains over 100 cannabinoids. (wecare-medicalcannabis.com)
- 4 Other cannabinoids, which are normally present at low or very low concentrations in the cannabis plant, are being actively studied. (wecare-medicalcannabis.com)
- The ECS is also the target of cannabinoids found in the cannabis plant, such as THC and CBD, which can interact with the ECS to produce various effects. (thehappycampers.com)
- 9. ERK/MAPK regulates ERRγ expression, transcriptional activity and receptor-mediated tamoxifen resistance in ER+ breast cancer. (nih.gov)
- β-CGRP, human (Human β-CGRP) is one of calcitonin peptides, acts via the complex of calcitonin-receptor-like receptor (CRLR) and receptor-activity-modifying protein (RAMP), with IC 50 s of 1 nM and 300 nM for CRLR/RAMP1 and CRLR/RAMP2 in cells  . (medchemexpress.com)
- It's more of a modulator, tweaking the activity of those receptors and keeping them on their toes. (thehappycampers.com)
- partial agonist) receptors, 7 while its psychotropic effects are typically mediated by CB 2 . (wecare-medicalcannabis.com)
- Delta-8 https://optimisticmommy.com/can-hhc-gummies-be-bad-for-your-health/ and CBD are both naturally occurring cannabinoids present in cannabis (hemp and cannabis). (onlinesrs.co)
- They exert their effects through two receptor types: CB1, primarily located in the brain, and CB2, primarily located in the immune system. (medicalmarijuana411.com)
- This bad boy goes straight for the CB1 receptors in your brain and nervous system, giving you that trippy, mind-altering experience we all know and love. (thehappycampers.com)
- Think of your brain as an ocean, an ecosystem inhabited by numerous species of fish-like neurotransmitters and their receptors, with currents of electricity connecting and delicately balancing all the different components. (ultimatehealthreport.com)
- In 1988, Allyn Howlett and William Devane (Johns Hopkins University) discovered the first cannabinoid receptor in the brain of a rat. (lipocanna.com)
- in 1990, Lisa Matsuda (National Institute of Mental Health) mapped the DNA sequence responsible for the expression of THC-sensitive receptors in a rat's brain. (lipocanna.com)
- Dual Inhibition of CB1 Receptors and iNOS as a Potential Novel Approach to the Pharmacological Management of Acute and Long COVID-19. (nih.gov)
- MINNESOTA - A University of Minnesota Medical School research team led by Kalpna Gupta, Ph.D., has discovered that cannabinoids offer a novel approach to ease the chronic and acute pain caused by sickle cell disease (SCD). (medicalmarijuana411.com)
- To test this hypothesis, we examined effects of AM2201 on 5-HT 1A R agonist-activated G protein-coupled inwardly rectifying potassium channel currents in neurons in vitro and on the hypothermic response to 5-HT 1A R stimulation in mice lacking the cannabinoid receptor 1. (nih.gov)
- Four hundred and nine people with a specified condition of insomnia completed 1056 medical cannabis administration sessions using the Releaf App TM educational software during which they recorded real-time ratings of self-perceived insomnia severity levels prior to and following consumption, experienced side effects, and product characteristics, including combustion method, cannabis subtypes, and/or major cannabinoid contents of cannabis consumed. (mdpi.com)
- This is because CBD interacts with the CB1 and CB2 receptors. (verdeskin.co)
- The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and HIV dementia. (medicalmarijuana411.com)
- produced in post-synaptic neurons, then travel backwards to pre-synaptic neurons in the CB1 receptor (retrograde signaling) to inhibit neurotransmitter release, which influences other chemical reactions, producing a cascade effect. (lipocanna.com)
- They were able to alter the genetics of rats, producing "knock out" rats that lacked CB1 receptors. (lipocanna.com)
- Cannabinoids in CBD help regulate emotions and appetite. (verdeskin.co)
- Seven-transmembrane receptors signal via G-protein- and β-arrestin-dependent pathways. (nih.gov)