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Cannabis in cancer care. Cannabinoids, the active components of Cannabis sativa, mimic the effects of the endogenous cannabinoids endocannabinoids , activating specific cannabinoid receptors, particularly CB1 found predominantly in the central nervous system and CB2 found predominantly in cells involved with immune function. This paper has 55 citations. From This Paper Figures, tables, and topics from this paper. Citations Publications citing this paper.
Showing of 28 extracted citations. Preliminary evaluation of the efficacy, safety, and costs associated with the treatment of chronic pain with medical cannabis Terrance Bellnier , Geoffrey W Brown , Tulio R Ortega.
Cannabis use among patients at a comprehensive cancer center in a state with legalized medicinal and recreational use Steven A Pergam , Maresa C. Nalini Vadivelu , Alice M. Bjorling , Zun-yi Wang. Citation Statistics 55 Citations 0 10 20 Semantic Scholar estimates that this publication has 55 citations based on the available data.
How do you define a highly subjective experience? As science advances, it may seem incomprehensible that more people will suffer from chronic pain in the future than they do now. But, paradoxically, as science advances, people live longer and survive conditions that previously would have ended their lives. Conditions such as cancer, severe injuries, HIV, that were once a death sentence are now treatable.
Legal medical marijuana is available to more than half of America. Given how widespread chronic pain is and how limited truly efficacious treatment options are, predictably, an increasing number of sufferers are turning to cannabis to treat their condition.
However, whether cannabis is right for you is a highly personal decision. What works for others, may not be appropriate for your situation. Likewise, deciding on whether cannabis should be an adjunctive therapy to your your current treatment protocol or a replacement, is yet another consideration. We have accumulated more evidence supporting a therapeutic role for cannabis to treat chronic pain than we have for most other conditions.
Broadly speaking, if you have pain that has persists for more than three months and has not been relieved by medical or surgical care, you may have a chronic pain condition. Chronic pain is a condition characterized by generalized muscle or nerve pain, that persists well beyond reasonable expectations of recovery; it affects million Americans — approximately two out of five adults.
Nociceptive - Caused by tissue damage or inflammation, it is usually described usually described as sharp, aching, or throbbing pain.
Neuropathic - Caused by nervous system damage or malfunction. Sufferers commonly describe the pain as causing numbness or a burning sensation. Anyone can develop chronic pain, although it most commonly affects older adults and people with health conditions like diabetes, arthritis, or back problems. There are also a number of specific diseases that associated with chronic pain, including shingles, diabetes, blood vessel problems, HIV, and most types of cancer.
Treatment may bring the disease under control, or even cure it completely, but the chronic pain persists. Similarly, in the event a pain-inducing disease may not be able to be cured, does not mean the pain cannot be mitigated.
Effective pain management requires ongoing attention in conjunction with a qualified medical professional. The downside of these treatments is that for many patients they are only nominally effective and can come with intolerable and potentially debilitating side effects, including:. Because of the unpredictable efficacy, often intolerable side effects, and risk of addiction, an increasing number of patients are turning to cannabis.
The endocannabinoid system ECS is responsible for a number of physiological functions related to health, including pain modulation and inflammation. Over studies have been conducted evaluating the efficacy of cannabis and cannabinoid-derived formulations to treat chronic pain conditions. One comprehensive systematic study conducted by Harvard professor and addiction psychiatrist, Dr.
Kevin Hill, reviewed 28 well-designed studies. Canadian researchers came to similar conclusions in their Review Study of 18 trials, identifying 15 trials that demonstrated efficacy in treating chronic non-cancer pain. They noted several trials reported significant improvements in sleep, with no serious side effects. Further, the studies found just a few adverse effects which were mild to moderate and well tolerated. In recent years, North America has been ravaged by an ever-growing epidemic: Since Purdue Pharma brought OxyContin to the market in the mid s, prescriptions have increased four-fold.
Following the increase in prescriptions, rates of heroin addiction and the number of opioid-related overdoses have skyrocketed. How could medical marijuana help? In patients with unilateral adrenal adenoma, the abnormal expression or function of GIP or vasopressin receptor has been found, but the presence of ectopic or abnormal hormone receptors appears to be less prevalent than in macronodular adrenal hyperplasia.
The identification of the presence of an abnormal adrenal receptor offers the possibility of a new pharmacological approach to control hypercortisolism by suppressing the endogenous ligands or by using specific antagonists for the abnormal receptors.
Over the past few years, increasing public and political pressure has supported legalization of medical marijuana. One of the main thrusts in this effort has related to the treatment of refractory epilepsy—especially in children with Dravet syndrome—using cannabidiol CBD. Despite initiatives in numerous states to at least legalize possession of CBD oil for treating epilepsy, little published evidence is available to prove or disprove the efficacy and safety of CBD in patients with epilepsy Cannabidiol regulation of learned fear: Phobias and post-traumatic stress disorder PTSD are characterized by abnormal and persistent memories of fear-related contexts and cues.
The effects of psychological treatments such as exposure therapy are often only temporary and medications can be ineffective and have adverse side effects. Growing evidence from human and animal studies indicates that cannabidiol , the main non-psychotomimetic phytocannabinoid present in Cannabis sativa, alleviates anxiety in paradigms assessing innate fear. More recently, the effects of cannabidiol on learned fear have been investigated in preclinical studies with translational relevance for phobias and PTSD.
Here we review the findings from these studies, with an emphasis on cannabidiol regulation of contextual fear. The evidence indicates that cannabidiol reduces learned fear in different ways: We also present novel data on cannabidiol regulation of learned fear related to explicit cues, which indicates that auditory fear expression is also reduced acutely by cannabidiol. We conclude by outlining future directions for research to elucidate the neural circuit, psychological, cellular, and molecular mechanisms underlying the regulation of fear memory processing by cannabidiol.
This line of investigation may lead to the development of cannabidiol as a novel therapeutic approach for treating anxiety and trauma-related disorders such as phobias and PTSD in the future. One of the main thrusts in this effort has related to the treatment of refractory epilepsy-especially in children with Dravet syndrome-using cannabidiol CBD.
Despite initiatives in numerous states to at least legalize possession of CBD oil for treating epilepsy, little published evidence is available to prove or disprove the efficacy and safety of CBD in patients with epilepsy.
This review highlights some of the basic science theory behind the use of CBD, summarizes published data on clinical use of CBD for epilepsy, and highlights issues related to the use of currently available CBD products. Cannabidiol is the major nonpsychoactive component of Cannabis sativa.
Over the centuries, a number of medicinal preparations derived from C. These preparations were widely employed as analgesics by Western medical practitioners in the 19 th century 1. More recently, there is clinical evidence suggesting efficacy in HIV-associated neuropathic pain, as well as spasms associated with multiple sclerosis 1. Cannabidiol -induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression.
In the current study, we examined the effects of the nonpsychoactive cannabinoid, cannabidiol , on the induction of apoptosis in leukemia cells. Exposure of leukemia cells to cannabidiol led to cannabinoid receptor 2 CB2 -mediated reduction in cell viability and induction in apoptosis. Furthermore, cannabidiol treatment led to a significant decrease in tumor burden and an increase in apoptotic tumors in vivo.
From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly ADP-ribose polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways. The role of the mitochondria was further suggested as exposure to cannabidiol led to loss of mitochondrial membrane potential and release of cytochrome c. It is noteworthy that cannabidiol exposure led to an increase in reactive oxygen species ROS production as well as an increase in the expression of the NAD P H oxidases Nox4 and p22 phox.
Finally, cannabidiol exposure led to a decrease in the levels of p-p38 mitogen-activated protein kinase, which could be blocked by treatment with a CB2-selective antagonist or ROS scavenger.
Together, the results from this study reveal that cannabidiol , acting through CB2 and regulation of Nox4 and p22 phox expression, may be a novel and highly selective treatment for leukemia. Cannabidiol CBD is a non-psychoactive constituent of Cannabis sativa with potential to treat neurodegenerative diseases. Its neuroprotection has been mainly associated with anti-inflammatory and antioxidant events; however, other mechanisms might be involved. CBD increased cell viability, differentiation, and the expression of axonal GAP and synaptic synaptophysin and synapsin I proteins.
Its neuritogenic effect was not dependent or additive to NGF, but it was inhibited by Ka trkA inhibitor. CBD did not induce neuritogenesis in this cellular model, which supports the involvement of trkA receptors. This is the first study to report the involvement of neuronal proteins and trkA in the neuroprotection of CBD. Full Text Available The defect of the melatonin signaling pathway has been proposed to be one of the key etiopathogenic factors in adolescent idiopathic scoliosis AIS.
The present study aimed to investigate whether the abnormal MT2 expression in AIS is quantitative or qualitative. Cultured osteoblasts were obtained from 41 AIS girls and nine normal controls. Anthropometric parameters were also compared and correlated with the protein expression and mRNA expression of the receptors.
No differences were found in the expression of MT1. The results of this study showed for the first time a quantitative change of MT2 in AIS that was also correlated with abnormal arm span as part of abnormal systemic skeletal growth. Familial defective apolipoprotein B Previous in vivo turnover studies suggested that retarded clearance of low density lipoproteins LDL from the plasma of some hypercholesterolemic patients is due to LDL with defective receptor binding.
The present study examined this postulate directly by receptor binding experiments. The LDL from a hypercholesterolemic patient G. LDL were much less effective than normal LDL in competing with I-labeled normal LDL for cellular uptake and degradation and in stimulating intracellular cholesteryl ester synthesis. The defect in LDL binding appears to be due to a genetic abnormality of apolipoprotein B Further, the defect in receptor binding does not appear to be associated wit an abnormal lipid composition or structure of the LDL.
Normal and abnormal LDL subpopulations were partially separated from plasma of two subjects by density-gradient ultracentrifugation, a finding consistent with the presence of a normal and a mutant allele.
The affected family members appear to be heterozygous for this disorder, which has been designated familial defective apolipoprotein B These studies indicate that the defective receptor binding results in inefficient clearance of LDL and the hypercholesterolemia observed in these patients. The Dravet syndrome is a complex childhood epilepsy disorder that is associated with drug-resistant seizures and a high mortality rate.
We studied cannabidiol for the treatment of drug-resistant seizures in the Dravet syndrome. In this double-blind, placebo-controlled trial, we randomly assigned children and young adults with the Dravet syndrome and drug-resistant seizures to receive either cannabidiol oral solution at a dose of 20 mg per kilogram of body weight per day or placebo, in addition to standard antiepileptic treatment. The primary end point was the change in convulsive-seizure frequency over a week treatment period, as compared with a 4-week baseline period.
The median frequency of convulsive seizures per month decreased from Adverse events that occurred more frequently in the cannabidiol group than in the placebo group included diarrhea, vomiting, fatigue, pyrexia, somnolence, and abnormal results on liver-function tests. There were more withdrawals from the trial in the cannabidiol group. The effects of leptin in combination with a cannabinoid receptor 1 antagonist, AM , or cannabidiol on food intake and body weight in rats fed a high-fat or a free-choice high sugar diet.
High intake of fats and sugars has prompted a rapid growth in the number of obese individuals worldwide. The hormone had no significant effects, however, on either caloric intake, body weight or food preferences in rats fed an FC diet. This drug combination, however, had no effect on the consumption of high-sucrose chow. None of the drug combinations affected water consumption. It is concluded that the concomitant treatment with leptin and AM attenuated markedly body weight gain in rats maintained on high-calorie diets rich in fat and carbohydrates but did not affect preferences for sweet food.
We describe the varied clinical features and mutations in nine patients examined at the National Institutes of Health who were compound heterozygotes for XPD mutations but had different clinical phenotypes: The vitamin D stimulation ratio of CYP24 and osteopontin was associated with specific pairs of mutations reduced in 5, elevated in 1 but not correlated with distinct clinical phenotypes.
Thyroid receptor stimulation ratio for KLF9 was not significantly different from normal. Prenatal exposure to phencyclidine produces abnormal behaviour and NMDA receptor expression in postpubertal mice. Several studies have shown the disruptive effects of non-competitive N-methyl-d-aspartate NMDA receptor antagonists on neurobehavioural development.
Based on the neurodevelopment hypothesis of schizophrenia, there is growing interest in animal models treated with NMDA antagonists at developing stages to investigate the pathogenesis of psychological disturbances in humans. Previous studies have reported that perinatal treatment with phencyclidine PCP impairs the development of neuronal systems and induces schizophrenia-like behaviour.
This study investigated the long-term effects of prenatal exposure to PCP in mice. The prenatal PCP-treated mice showed hypersensitivity to a low dose of PCP in locomotor activity and impairment of recognition memory in the novel object recognition test at age 7 wk. Meanwhile, the prenatal exposure reduced the phosphorylation of NR1, although it increased the expression of NR1 itself.
Furthermore, these behavioural changes were attenuated by atypical antipsychotic treatment. Taken together, prenatal exposure to PCP produced long-lasting behavioural deficits, accompanied by the abnormal expression and dysfunction of NMDA receptors in postpubertal mice.
It is worth investigating the influences of disrupted NMDA receptors during the prenatal period on behaviour in later life. Cannabidiol improves brain and liver function in a fulminant hepatic failure-induced model of hepatic encephalopathy in mice. Hepatic encephalopathy is a neuropsychiatric disorder of complex pathogenesis caused by acute or chronic liver failure. We investigated the effects of cannabidiol , a non-psychoactive constituent of Cannabis sativa with anti-inflammatory properties that activates the 5-hydroxytryptamine receptor 5-HT 1A , on brain and liver functions in a model of hepatic encephalopathy associated with fulminant hepatic failure induced in mice by thioacetamide.
Female Sabra mice were injected with either saline or thioacetamide and were treated with either vehicle or cannabidiol. Neurological and motor functions were evaluated 2 and 3 days, respectively, after induction of hepatic failure, after which brains and livers were removed for histopathological analysis and blood was drawn for analysis of plasma liver enzymes.
In a separate group of animals, cognitive function was tested after 8 days and brain 5-HT levels were measured 12 days after induction of hepatic failure. Neurological and cognitive functions were severely impaired in thioacetamide-treated mice and were restored by cannabidiol. Similarly, decreased motor activity in thioacetamide-treated mice was partially restored by cannabidiol.
Increased plasma levels of ammonia, bilirubin and liver enzymes, as well as enhanced 5-HT levels in thioacetamide-treated mice were normalized following cannabidiol administration. Likewise, astrogliosis in the brains of thioacetamide-treated mice was moderated after cannabidiol treatment.
Cannabidiol restores liver function, normalizes 5-HT levels and improves brain pathology in accordance with normalization of brain function. Therefore, the effects of cannabidiol may result from a combination of its actions in the liver and brain. The sporostatic effect of cannabidiolic acid. A study was undertaken to clarify whether cannabidiolic acid could be made to enhance the microbiological effect of food preservation by heat treatment or irradiation.
Cannabidiolic acid was found to have a high inhibiting effect on the spores of Bacillus cereus. Its sporostatic effect is roughly equivalent to that of the antibiotics nisin and tylosin.
In these combination treatments cannabidiolic acid added at the above concentration proved to be ineffective. On investigating the cause of this phenomenon, cannabidiolic acid was found to react with protein of peas prior to irradiation or heat treatment, or in an early phase of treatment loosing thereby its microbiological effect.
On the other hand, since cannabidiolic acid cannot react with proteins denatured by heat, it was found active in a sterilized nutrient medium containing denatured protein. Cannabidiol restores intestinal barrier dysfunction and inhibits the apoptotic process induced by Clostridium difficile toxin A in Caco-2 cells.
Clostridium difficile toxin A is responsible for colonic damage observed in infected patients. Drugs able to restore Clostridium difficile toxin A-induced toxicity have the potential to improve the recovery of infected patients. The purpose of this study was to evaluate a the anti-apoptotic effect and b the mechanisms by which cannabidiol protects mucosal integrity in Caco-2 cells exposed to Clostridium difficile toxin A.
Cytotoxicity assay, transepithelial electrical resistence measurements, immunofluorescence analysis and immunoblot analysis were performed in the different experimental conditions. Clostridium difficile toxin A significantly decreased Caco-2 cells' viability and reduced transepithelial electrical resistence values and RhoA guanosine triphosphate GTP , bax, zonula occludens-1 and occludin protein expression, respectively.
All these effects were significantly and concentration-dependently inhibited by cannabidiol , whose effects were completely abolished in the presence of the cannabinoid receptor type 1 CB1 antagonist, AM Cannabidiol improved Clostridium difficile toxin A-induced damage in Caco-2 cells, by inhibiting the apoptotic process and restoring the intestinal barrier integrity, through the involvement of the CB1 receptor.
Responding was maintained under a fixed ratio 5 schedule of stimulus-shock termination. Both training drugs dose-dependently increased the percentage of responses on the respective drug-associated levers. Cannabidiol up to Moreover, 8-OH-DPAT significantly attenuated the discriminative stimulus effects of rimonabant, whereas cannabidiol did not modify the rimonabant discriminative stimulus.
Results Both training drugs dose-dependently increased the percentage of responses on the respective drug-associated levers. Full Text Available Cannabis contains the psychoactive component delta9-tetrahydrocannabinol delta9-THC, and the non-psychoactive components cannabidiol CBD, cannabinol, and cannabigerol. It is well-known that delta9-THC and other cannabinoid CB1 receptor agonists are neuroprotective during global and focal ischemic injury.
Additionally, delta9-THC also mediates psychological effects through the activation of the CB1 receptor in the central nervous system. In addition to the CB1 receptor agonists, cannabis also contains therapeutically active components which are CB1 receptor independent.
In the past five years, an increasing number of publications have focused on the discovery of the anti-inflammatory, anti-oxidant, and neuroprotective effects of CBD. The cerebroprotective action of CBD is CB1 receptor -independent, long-lasting, and has potent anti-oxidant activity. Importantly, CBD use does not lead to tolerance.
In this review, we will discuss the therapeutic possibility of CBD as a cerebroprotective agent, highlighting recent pharmacological advances, novel mechanisms, and therapeutic time window of CBD in ischemic stroke. Imaging cerebral GABA A receptor density GRD with single-photon emission tomography SPET and iodine iomazenil is highly accurate in lateralizing epileptogenic foci in patients with complex partial seizures of temporal origin. We present a patient with complex partial seizures in whom MRI had identified an arachnoid cyst anterior to the tip of the left temporal lobe.
Contralaterally to this structural abnormality , interictal electroencephalography EEG performed after sleep deprivation disclosed an intermittent frontotemporal dysrhythmic focus with slow and sharp waves. These data suggest that iomazenil SPET may significantly contribute to the presurgical evaluation of epileptic patients even when MRI identifies potentialy epileptogenic structural lesions.
Nicotinic acid receptor abnormalities in human skin cancer: Full Text Available Chronic UV skin exposure leads to epidermal differentiation defects in humans that can be largely restored by pharmacological doses of nicotinic acid. Nicotinic acid increases epidermal differentiation in photodamaged human skin as judged by the terminal differentiation markers caspase 14 and filaggrin.
Both GPRA and GPRB genes are transcribed in human skin and in epidermal keratinocytes, but expression in dermal fibroblasts is below limits of detection. Receptor transcripts are greatly over-expressed in squamous cell cancers. Receptor protein in normal skin is prominent from the basal through granular layers of the epidermis, with cellular localization more dispersive in the basal layer but predominantly localized at the plasma membrane in more differentiated epidermal layers.
In normal human primary and immortalized keratinocytes, nicotinic acid receptors show plasma membrane localization and functional G i-mediated signaling.
In contrast, in a squamous cell carcinoma derived cell line, receptor protein shows a more diffuse cellular localization and the receptors are nearly non-functional. The results of these studies justify future genetic and pharmacological intervention studies to define possible specific role s of nicotinic acid receptors in human skin homeostasis. Full Text Available The Developmental Origins of Health and Disease DOHaD Theory proposes that the environment encountered during fetal life and infancy permanently shapes tissue physiology and homeostasis such that damage resulting from maternal stress, poor nutrition or exposure to environmental agents may be at the heart of adult onset disease.
Interference with endogenous developmental functions of the aryl hydrocarbon receptor AHR, either by gene ablation or by exposure in utero to 2,3,7,8-tetrachlorodibenzo-p-dioxin TCDD, a potent AHR ligand, causes structural, molecular and functional cardiac abnormalities and altered heart physiology in mouse embryos. To test if embryonic effects progress into an adult phenotype, we investigated whether Ahr ablation or TCDD exposure in utero resulted in cardiac abnormalities in adult mice long after removal of the agent.
Underlying these effects, genes in signaling networks related to cardiac hypertrophy and mitochondrial function were differentially expressed. The findings reported here underscore the conclusion that AHR signaling in the developing heart is one potential target of environmental factors associated with cardiovascular disease.
The anti-cancer effect of the plant-derived cannabinoid, cannabidiol , has been widely demonstrated both in vivo and in vitro. However, this body of preclinical work has not been translated into clinical use.
Key issues around this failure can be related to narrow dose effects, the cell model used and incomplete efficacy. A model of acute lymphoblastic disease, the Jurkat T cell line, has been used extensively to study the cannabinoid system in the immune system and cannabinoid-induced apoptosis. Using these cells, this study sought to investigate the outcome of those remaining viable cells post-treatment with cannabidiol , both in terms of cell size and tracking any subsequent recovery.
The phosphorylation status of the mammalian Target of Rapamycin mTOR signaling pathway and the downstream target ribosomal protein S6, were measured. The ability of cannabidiol to exert its effect on cell viability was also evaluated in physiological oxygen conditions. The remaining population of viable cells that were cultured in nutrient rich conditions post-treatment were able to proliferate, but did not recover to control cell numbers. However, the proportion of viable cells that were gated as small, increased in response to cannabidiol and normally sized cells decreased.
This proportion of small cells persisted in the recovery period and did not return to basal levels. In conclusion, these results indicate that cannabidiol causes a reduction in cell size, which persists post-treatment. However, resistance to cannabidiol under physiological normoxia for these cells would imply that cannabidiol may not be useful in the clinic as an anti-leukemic agent.
Short-term treatment with VEGF receptor inhibitors induces retinopathy of prematurity-like abnormal vascular growth in neonatal rats. Retinal arterial tortuosity and venous dilation are hallmarks of plus disease, which is a severe form of retinopathy of prematurity ROP.
In this study, we examined whether short-term interruption of vascular endothelial growth factor VEGF signals leads to the formation of severe ROP-like abnormal retinal blood vessels. The retinal vasculatures were examined on P9, P14, or P21 in retinal whole-mounts stained with an endothelial cell marker.
Prevention of vascular growth and regression of some preformed capillaries were observed on P9 in retinas of rats treated with KRN However, on P14 and P21, density of capillaries, tortuosity index of arterioles, and diameter of veins significantly increased in KRNtreated rats, compared to vehicle 0. Similar observations were made with axitinib-treated rats. These results suggest that an interruption of normal retinal vascular development in neonatal rats as a result of short-term VEGFR inhibition causes severe ROP-like abnormal retinal vascular growth in a VEGF-dependent manner.
Rats treated postnatally with VEGFR inhibitors could serve as an animal model for studying the mechanisms underlying the development of plus disease. Dopamine D3 receptor knockout mice exhibit abnormal nociception in a sex-different manner. Pain is a complex and subjective experience. Previous studies have shown that mice lacking the dopamine D3 receptor D3RKO exhibit hypoalgesia, indicating a role of the D3 receptor in modulation of nociception.
Given that there are sex differences in pain perception, there may be differences in responses to nociceptive stimuli between male and female D3RKO mice. In the current study, we examined the role of the D3 receptor in modulating nociception in male and female D3RKO mice. Acute thermal pain was modeled by hot-plate test.
The von Frey hair test was applied to evaluate mechanical pain. And persistent pain produced by peripheral tissue injury and inflammation was modeled by formalin test. In the hot-plate test, compared with wild-type WT mice, D3RKO mice generally exhibited longer latencies at each of the three temperatures.
In the formalin test, the male D3RKO mice displayed a similar nociceptive behavior as their sex-matched WT littermates, whereas significantly depressed late-phase formalin-induced nociceptive behaviors were observed in the female mutants. These findings indicated that the D3 receptor affects nociceptive behaviors in a sex-specific manner and that its absence induces more analgesic behavior in the female knockout mice.
Correlation between dopamine receptor D2 expression and presence of abnormal involuntary movements in Wistar rats with hemiparkinsonism and dyskinesia. Although the pathogenic mechanism of L-DOPA-induced dyskinesia is unclear, the condition has been associated with alterations in dopamine receptors , among which D2 receptors D2R have received little attention.
This study aims to: We allocated 21 male Wistar rats into 3 groups: Sensorimotor impairment was assessed with behavioural tests. Full Text Available Alterations in lipid metabolism have been found in several neurodegenerative disorders, including Alzheimer's disease.
Lipoprotein lipase LPL hydrolyzes triacylglycerides in lipoproteins and regulates lipid metabolism in multiple organs and tissues, including the central nervous system CNS. We interpret these findings to indicate that LPL regulates the availability of PUFA in the CNS and, this in turn, impacts the strength of synaptic plasticity in the brain of aging mice through the modification of AMPA receptor and its phosphorylation.
Cytogenetic evaluation of human glial tumors: Chromosome banding analysis of human glial tumors were performed using G- and Q-banding techniques in an attempt to establish recurring sites of chromosome change.
All tumors examined displayed numerical abnormalities , with the most common numeric change being a gain of chromosome 7. An attempt was then made to correlate the observed chromosome 7 changes with activation of the cellular proto-oncogene c-erb-B, whose produce is the epidermal growth factor receptor EGFR.
The results suggest that overexpression of the EGFR may be related to an alternative mechanism, other than gene amplification and elevated mRNA levels, such as the regulation of receptor biosynthesis and degradation.
In summary, findings indicate that alterations of chromosome 7 are the most prevalent chromosomal change in human glial tumors, and that these alterations may lead to overexpression of the protooncogene c-erb-B. Abnormal norepinephrine clearance and adrenergic receptor sensitivity in idiopathic orthostatic intolerance. Chronic orthostatic intolerance OI is characterized by symptoms of inadequate cerebral perfusion with standing, in the absence of significant orthostatic hypotension.
Possible underlying pathophysiologies include hypovolemia, partial dysautonomia, or a primary hyperadrenergic state. We tested the hypothesis that patients with OI have functional abnormalities in autonomic neurons regulating cardiovascular responses. Thirteen patients with chronic OI and 10 control subjects underwent a battery of autonomic tests.
Systemic norepinephrine NE kinetics were determined with the patients supine and standing before and after tyramine administration. In addition, baroreflex sensitivity, hemodynamic responses to bolus injections of adrenergic agonists, and intrinsic heart rate were determined. Resting supine NE spillover and clearance were similar in both groups. The decreased NE clearance with standing, resistance to the NE-releasing effect of tyramine, and increased sensitivity to adrenergic agonists demonstrate dramatically disordered sympathetic cardiovascular regulation in patients with chronic OI.
At date the major neuroreceptors i. Moreover these effects were linked to evident ultra-structural changes such as shrunken cell membranes and loss of cytoplasmic architecture. In contrast, MUS supplied a very low, if any, argyrophilic reaction in hypothalamic and mesencephalic regions plus a scarce level of ultra-structural damages. Overall it is tempting to suggest, for the first time, a neuroprotective role of GABA A R inhibitory actions against the overexcitatory ORXR-dependent neurodegeneration and consequently abnormal swimming events in fish.
Abnormalities in osteoclastogenesis and decreased tumorigenesis in mice deficient for ovarian cancer G protein-coupled receptor 1. We have shown that OGR1 functions as a tumor metastasis suppressor gene when it is over-expressed in human prostate cancer cells in vivo.
To examine the physiological functions of OGR1, we generated conditional OGR1 deficient mice by homologous recombination. OGR1 deficient mice were viable and upon gross-inspection appeared normal. Consistent with in vitro studies showing that OGR1 is involved in osteoclastogenesis, reduced osteoclasts were detected in OGR1 deficient mice. A pH-dependent osteoclasts survival effect was also observed. However, overall abnormality in the bones of these animals was not observed.
In addition, melanoma cell tumorigenesis was significantly inhibited in OGR1 deficient mice. OGR1 deficient mice in the mixed background produced significantly less peritoneal macrophages when stimulated with thioglycolate. These macrophages also showed altered extracellular signal-regulated kinases ERK activation and nitric oxide NO production in response to lipopolysaccharide. OGR1-dependent pH responses assessed by cAMP production and cell survival in macrophages or brown fat cells were not observed, presumably due to the presence of other proton sensing receptors in these cells.
Our results indicate that OGR1's role in osteoclastogenesis is not strong enough to affect overall bone development and its role in tumorigenesis warrants further investigation. The mice generated can be potentially used for several disease models, including cancers or osteoclast-related diseases. Correction of abnormal B-cell subset distribution by interleukin-6 receptor blockade in polymyalgia rheumatica.
The aim was to study lymphocyte subsets and circulating cytokines at diagnosis of PMR and after tocilizumab monotherapy. Eighteen untreated patients with PMR were included in a prospective study and received 3-monthly tocilizumab infusions without glucocorticoids.
Lymphocyte subset distribution was assessed by flow cytometry and serum cytokines were assayed by a cytokine array and ELISA, at baseline and during follow-up. Baseline data were also compared with age- and sex-matched controls. Circulating B-cell counts were positively correlated with the PMR activity score PMR-AS in untreated active patients at baseline, but subsequently increased to normal values while disease activity was controlled after tocilizumab therapy.
Among serum cytokines, IL-6 showed the largest concentration difference between patients and controls, and the serum IL-6 concentration was correlated with baseline PMR-AS. The effects of tocilizumab on serum IL-6 concentration were heterogeneous, and the patients whose serum IL-6 decreased after tocilizumab therapy exhibited a significant increase in circulating B-cell counts. In patients with PMR, B-cell lymphopenia and abnormal B-cell subset distribution are associated with disease activity and IL-6 concentration, and both are corrected by the IL-6 antagonist tocilizumab.
For Permissions, please email: Decreased striatal D2 receptor density associated with severe behavioral abnormality in Alzheimer's disease. Since patients manifesting behavioral and psychological symptoms of dementia BPSD are a burden for their families and caregivers, the underlying neurobiological mechanism of this condition should be clarified. Using positron emission tomography PET , we previously reported that wandering behavior in dementia was associated with a disturbed dopaminergic neuron system.
The tracer used was [ 11 C]raclopride D 2 antagonist. The uptake of [ 11 C]raclopride was calculated as the estimation of binding potential BP of the striatum to the cerebellum. Pharmacology and potential therapeutic role in epilepsy and other neuropsychiatric disorders. Objective To present a summary of current scientific evidence about the cannabinoid, cannabidiol CBD with regards to their relevance to epilepsy and other selected neuropsychiatric disorders.
Methods We summarize the presentations from a conference in which invited participants reviewed relevant aspects of the physiology, mechanisms of action, pharmacology and data from studies with animal models and human subjects. Results Cannabis has been used to treat disease since ancient times.
CBD is anticonvulsant in many acute animal models but there is limited data in chronic models. CBD has neuroprotective and anti-inflammatory effects. CBD appears to be well tolerated in humans but small and methodologically limited studies of CBD in human epilepsy have been inconclusive.
More recent anecdotal reports of high-ratio CBD: Significance CBD bears investigation in epilepsy and other neuropsychiatric disorders, including anxiety, schizophrenia, addiction and neonatal hypoxic-ischemic encephalopathy. However, we lack data from well-powered double-blind randomized, controlled studies on the efficacy of pure CBD for any disorder. Initial dose-tolerability and double-blind randomized, controlled studies focusing on target intractable epilepsy populations such as patients with.
The intellectual capacity of patients with Laron syndrome LS differs with various molecular defects of the growth hormone receptor gene. Correlation with CNS abnormalities. The correlation between the molecular defects of the GH receptor R , psychosocial development and brain abnormalities were evaluated in 10 patients with Laron syndrome LS , in whom all data were available.
Cannabis and Chronic Pain
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