Modern Medicine in Digital format

* Gait Apraxia is related to dementia and alzheimer disease, and has symptoms including waddling gait, gait ataxia and gait dyspraxia. An important gene associated with Gait Apraxia is GRN (Granulin Precursor), and among its related pathways/superpathways are Neuroscience and A-beta Signaling Pathways. The drugs Vitamin D and Ergocalciferol have been mentioned in the context of this disorder. Affiliated tissues include brain and bone, and related phenotypes are nervous system and no phenotypic analysis. It is characterised by an inability to initiate the process of walking, despite the power and coordination of the legs being normal when tested in the seated or lying position. The gait is broad-based with short steps with a tendency to fall backwards.

* Galanin Peptide contracts the smooth muscle of the gastrointestinal and genito-urinary tract, regulates growth hormone, insulin release, and controls adrenal secretion.

* Galantide Peptide is a galanin antagonist consisting of aa 1-13 of galanin and the C-terminal fragment of bradykinin. Galantide reversibly blocks the neuronal activities of galanin. Galanin has different activities such as contraction of smooth muscle of the gastrointestinal and genito-urinary tract, regulation of growth hormone and insulin release, and control of adrenal secretion.

* Gantenerumab is a monoclonal antibody for the treatment of Alzheimer's disease.

* Gap junction beta-2 protein GJB2 (Connexin 26). A mutation causes a syndrome of sensorineural hearing loss and palmoplantar hyperkeratosis. The bilateral hearing loss is moderate to severe in the high frequencies and progresses slowly after onset in early child-hood. The hyperkeratosis of the palms and soles does not develop until mid childhood and is exacerbated by trauma.

* GAP-26 and GAP-27 connexin mimetic peptides correspond to specific sequences in the extracellular loops of connexins 37, 40 and 43. These pepties inhibit Cx43 hemichannel opening triggered by voltage and intracellular Ca2+ elevation. They were first used to inhibit gap-junctional coupling in a wide range of mammalian cells and tissues. Currently, they are also being examined as therapeutic agents that accelerate wound healing, in early treatment of spinal cord injury, and cardiac arrhythmia.

* Gastrin releasing peptide elicits gastrin release and regulates gastric acid secretion and enteric motor function. GRP is also involved in the biology of the circadian system, playing a role in the signaling of light to the master circadian oscillator in the suprachiasmatic nuclei of the hypothalamus. Furthermore, GRP seems to mediate certain aspects of stress.

* Gastrointestinal System Disease, also known as gastrointestinal diseases, is related to lymphocytic gastritis and celiac disease, and has symptoms including abdominal pain, constipation and diarrhea. An important gene associated with Gastrointestinal System Disease is TRPV1 (Transient Receptor Potential Cation Channel Subfamily V Member 1), and among its related pathways are Secretion of Hydrochloric Acid in Parietal Cells and Gastric acid production. The drugs sacrosidase and belladonna extract, usp have been mentioned in the context of this disorder. Affiliated tissues include the gastrointestinal tract, liver and small intestine, and related mouse phenotypes are digestive/alimentary and homeostasis/metabolism. A disease involving the gastrointestinal tract, namely the esophagus, stomach, small intestine, large intestine and rectum, and the accessory organs of digestion, the liver, gallbladder, and pancreas.

* GBA factor or beta-glucocerebrosidase is an enzyme with glucosylceramidase activity that is needed to cleave, by hydrolysis, the beta-glucosidic linkage of the chemical glucocerebroside, an intermediate in glycolipid metabolism. Mutations in the glucocerebrosidase gene cause Gaucher's disease, a lysosomal storage disease characterized by an accumulation of glucocerebrosides. Mutations in the glucocerebrosidase gene are also associated with Parkinson's disease. (Among the top most expensive meds - Ceredase/Cerezyme)

* GC factor. Cancers and viruses disable the immune system by destroying (deglycosylating) the Gc protein that is the precursor of GcMAF. With little or no Gc protein, there is little or no GcMAF. With little or no GcMAF there is little or no activation of the macrophages. Biochemically, Gc-MAF results from sequential deglycosylation of the vitamin D-binding protein (the Gc protein), which is naturally promoted by lymphocytes (B and T cells). The resulting protein may be a macrophage activating factor (MAF). MAFs are lymphokines that control the expression of antigens on the surface of macrophages, and one of their functions is to make macrophages become cytotoxic to tumors. Gc-MAF may play a role in various diseases. Gc-MAF results in high levels of TNF-alpha production and other cytokines which in effect cause side effects such as severe fatigue, fevershness, and depression in some patients.

* GC376 is a broad-spectrum antiviral medication under development for therapeutic uses in humans and animals. As of 2020, GC376 is being investigated as treatment for COVID-19. GC376 shows activity against many human and animal viruses including coronavirus and norovirus; the most extensive research has been multiple in vivo studies in cats treating a coronavirus which causes deadly feline infectious peritonitis. Other research supports use in porcine epidemic diarrhea virus. Since GC376 shows broad-spectrum activity against coronavirus, early on during the pandemic of 2020 it was suggested as a potential treatment for COVID-19. In response to the crisis, researchers published in vitro research indicating GC376 is highly active against 3CLpro in SARS-CoV-2 (the coronavirus which causes COVID-19). Another group of virologists at the University of Alberta lead then released a separate publication confirming GC376's activity against 3CLpro in SARS-CoV-2 and also indicating GC376 had a potent antiviral effect.

* G-CSF or granulocyte-colony stimulating factor is a glycoprotein that stimulates the bone marrow to produce granulocytes and stem cells and release them into the bloodstream. Functionally, it is a cytokine and hormone, a type of colony-stimulating factor, and is produced by a number of different tissues. G-CSF also stimulates the survival, proliferation, differentiation, and function of neutrophil precursors and mature neutrophils. G-CSF factor expression may lead to significant reduction in deaths, cerebral atrophy, and neurological deficits following ischemia. G-CSF holds a promise as a potential treatment for brain disorders including stroke, Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis. G-CSF when given early after exposure to radiation may improve white blood cell counts, and is stockpiled for use in radiation incidents. G-CSF is used with certain cancer patients to accelerate recovery from neutropenia after chemotherapy. G-CSF is also used to increase the number of hematopoietic stem cells in donor's blood, and may also be given to the receiver in hematopoietic stem cell transplantation.

* GDNF Factor. The so called GAS1 protein accelerates the functional decline of muscle stem cells. The protein is found in only a small number of young muscle stem cells, but is present in all aged muscle stem cells. Tinkering with muscle stem cells to express GAS1 in the entire young stem cell population resulted in diminished regeneration. By contrast, removing GAS1 from aged muscle stem cells rejuvenated them to a youthful state that supported robust regeneration. They also discovered that GAS1 inhibits another protein, a cell-surface receptor called RET, which they showed to be necessary for muscle stem cell renewal. The more GAS1 protein is present, the more RET's function is reduced. The inhibition of RET by GAS1 could be reversed by the third protein called GDNF, which binds to and activates RET. Indeed, when the researchers injected GDNF directly into the muscles of aged mice, muscle stem cell function and muscle regeneration were restored.

* Gemeprost is an analogue of prostaglandin E1. It is used as a treatment for obstetric bleeding. It is used with mifepristone to terminate pregnancy up to 24 weeks gestation.

* Gevokizumab is a potent monoclonal antibody with unique allosteric modulating properties and the potential to treat patients with a wide variety of inflammatory and other diseases. Gevokizumab binds strongly to interleukin-1 beta (IL-1 beta), a pro-inflammatory cytokine, and modulates the cellular signaling events that produce inflammation. IL-1 beta has been shown to be involved in diverse array of disease states, including non-infectious uveitis (including Behçet's uveitis), cardiovascular disease, and other auto-inflammatory diseases. It's application is under study in moderate to severe inflammatory acne, active non-infectious anterior scleritis, erosive osteoarthritis of the hand, arterial wall inflammation in patients with marked atherosclerotic plaque inflammation, polymyositis/dermatomyositis, giant cell arteritis, and Schnitzler syndrome.

* GHK-Copper peptide has skin anti-inflammatory properties, also can reduce UV-induced erythema. GHK-Cu's has the ability to restore function of irradiated fibroblasts to that of intact cells after radioactive cancer treatment. GHK promotes nerve regeneration, increased axon count and proliferation of Schwann cells. Facilitates wound healing, causing better wound contraction, faster development of granular tissue and improved angiogenesis. It also elevates the level of antioxidant enzymes. It is able to recover epidermal stem cells and increase their ability to repair tissue. GHK-Cu is able to reverse the expression of certain genes involved in metastatic spreading of colon cancer. Genomic research suggests that GHK directly modulates gene expression, which may explain the diversity of its biological actions. In smokers, GHK can downregulate genes involved in lung destruction and inflammation, while upregulating genes involved in tissue repair, restorimg their ability to remodel collagen and assemble it into properly organized fibrils. Several controlled facial studies confirmed anti-aging, firming and anti-wrinkle activity of copper peptide GHK-Cu.

* Ghrelin peptide induces the release of growth hormone from the pituitary gland. Beyond regulating hunger, ghrelin also plays a significant role in regulating the distribution and rate of use of energy.

* Ghrelin210 is an endogenous host-defence peptide to treat airway inflammation, chronic respiratory infection and cystic fibrosis.

* Ginkgolide B is a diterpenoid compound belonging to the group of ginkgolides, isolated from Ginkgo biloba leaves, exhibiting a wide spectrum of pharmacological properties and is used for the treatment of Alzheimer′s disease, cerebral insufficiency and memory loss. Antiinflammatory activity of G. biloba extracts is due to the presence of ginkgolides B that inhibits the platelet activating factors. This extract plays an important role in the pathogenesis of asthma. Ginkgolide B effectively inhibits the increase of T-helper 2 cytokines (which are interleukin IL-13 and IL-5), in bronchovascular lavage fluid by decreasing eosinophils count. It also inhibited the mucus hypersecretion by goblet cell and ovalbumin-induced eosinophils in lung tissue in the airway. It was concluded in a previous study that ginkgolides B is the most effective component in asthma treatments. Platelet-activating factor (PAF), a potent phospholipid inflammatory mediator, enhances glutamatergic exdtatory synaptic transmission in the hippocampus, ginkgolide B demonstrates protective effects against glutamate neurotoxidty involving PAF. Ginkgolide B caused a dose-related protection against dysrhythmias; the antiarrhythmic effect of ginkgolide B was comparable to that of diltiazem and superior to the activity of metoprolol. Ginkgolide B also caused a significant increase in cell viability and a highly significant decrease in the numbers of both spontaneously occurring and some induced apoptoses. Ginkgolide B has potent neuroprotective, anti-arrhythmias, anti-inflammatory and anti-apoptotic effects, it might be a promising drug on inhibiting platelet function and reducing inflammation in atherosclerosis. Additionally, this compound has been reported to inhibit neutrophil degranulation in vitro. Inhibits superoxide production in vitro and inhibits bronchoconstriction and is neuroprotective following oral administration in vivo. Extensive evidences has shown the promising effects of Ginkgo biloba consumption on several diseases such as Alzheimer's and Parkinson’s diseases, and ischemic stroke, etc. Several studies also have reported its beneficial role on motor activity and cognitive functions. This species contain a unique class of diterpenes, namely Ginkgolide B, which possess several pharmacological activities such as protective effect against cardiovascular disease; the most important causes of death worldwide. The promising effects of Ginkgolide B on stroke, both ischemic and hemorrhagic, are suggested by an overwhelming body of scientific evidences.

* GLA factor or alpha-galactosidase is a glycoside hydrolase enzyme that hydrolyses the terminal alpha-galactosyl moieties from glycolipids and glycoproteins. It is encoded by the GLA gene. This enzyme is a homodimeric glycoprotein that hydrolyses the terminal alpha-galactosyl moieties from glycolipids and glycoproteins. It predominantly hydrolyzes ceramide trihexoside, and it can catalyze the hydrolysis of melibiose into galactose and glucose. A variety of mutations in this gene affect the synthesis, processing, and stability of this enzyme, which causes Fabry's disease, a rare lysosomal storage disorder and sphingolipidosis that results from a failure to catabolize alpha-D-galactosyl glycolipid moieties. (Among the top most expensive meds - Fabrazyme)

* GLP-2 or glucagon-like peptide-2 is created by specific post-translational proteolytic cleavage of proglucagon in a process that also liberates the related glucagon-like peptide-1 (GLP-1). GLP-2 is produced by the intestinal endocrine L cell and by various neurons in the central nervous system. Intestinal GLP-2 is co-secreted along with GLP-1 upon nutrient ingestion. GLP-2 produces a number of effects in humans and rodents, including intestinal growth, enhancement of intestinal function, reduction in bone breakdown and neuroprotection. GLP-2 may act in an endocrine fashion to link intestinal growth and metabolism with nutrient intake. GLP-2 and related analogs may be treatments for short bowel syndrome, Crohn's disease, osteoporosis and as adjuvant therapy during cancer chemotherapy.

* Glucagon like peptide-1. A potent stimulator of glucose-dependent insulin release. Plays important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferaton. Inhibits beta cell apoptosis.

* Glucagon-like peptide-1 (GLP-1) 7-36 stimulates insulin gene transcription and secretion in pancreatic beta-cells. Displays antiapoptotic effects in hippocampal neurons and reduces food intake. It also reduces the level of sugar (glucose) in the blood.

* Glucose is a primary source of energy for the brain, so its availability influences psychological processes. When glucose is low, psychological processes requiring mental effort (e.g., self-control, effortful decision-making) are impaired. Individuals with diabetes or other conditions where hypoglycemia (low blood sugar) may occur often carry small amounts of sugar in various forms. One sugar commonly used is glucose.

* Glucose Intolerance, also known as impaired glucose tolerance, is related to abdominal obesity-metabolic syndrome 1 and coronary heart disease 1. An important gene associated with Glucose Intolerance is MT-TL1 (Mitochondrially Encoded TRNA-Leu (UUA/G) 1), and among its related pathways/superpathways are Respiratory electron transport, ATP synthesis by chemiosmotic coupling, and heat production by uncoupling proteins. and Regulation of lipid metabolism Insulin signaling-generic cascades. The drugs Metformin and Saxagliptin have been mentioned in the context of this disorder. Affiliated tissues include ovary, testes and liver, and related phenotypes are adipose tissue and endocrine/exocrine gland. A group of metabolic conditions that result in higher than normal blood glucose levels.

* Glucose Metabolism Disease (update), also known as glucose metabolism disorders, is related to diabetes mellitus and uremia. An important gene associated with Glucose Metabolism Disease is PINK1-AS (PINK1 Antisense RNA), and among its related pathways/superpathways are Metabolism of proteins and Aldosterone synthesis and secretion. The drugs Zinc and Pramlintide have been mentioned in the context of this disorder. Affiliated tissues include heart, endothelial and kidney, and related phenotypes are homeostasis/metabolism and growth/size/body region. Pathological conditions in which the blood glucose cannot be maintained within the normal range, such as in Hypoglycemia and Hyperglycemia.

* Glucose Metabolism Disease, also known as glucose metabolism disorders, is related to diabetes mellitus, insulin-dependent and hemolytic anemia due to triosephosphate isomerase deficiency. An important gene associated with Glucose Metabolism Disease is INS (Insulin), and among its related pathways are Differentiation of white and brown adipocyte and Signaling events mediated by PTP1B. Related mouse phenotypes are adipose tissue and liver/biliary system. A pathological condition in which the blood glucose cannot be maintained within the normal range, such as in Hypoglicemia and Hyperglicemia.

* Glutathione GSH is an important antioxidant that prevents damage to important cellular components caused by reactive oxygen species such as free radicals, peroxides, lipid peroxides and heavy metals. It regulates the nitric oxide cycle which is critical for life, but can be problematic if unregulated. It has a vital function in iron metabolism. Finally, is used in metabolic and biochemical reactions such as DNA synthesis and repair, protein synthesis, prostaglandin synthesis, amino acid transport, and enzyme activation. Raising GSH level is clinically proven to be beneficial for a very wide array of health concerns. GSH is at the heart of all immune functions and low GSH levels are seen in many diseases such as AIDS, advanced diabetes, and cancers. Raising and maintaining GSH levels can help minimize the risk of diseases. The spectrum includes AIDS, Alzheimer’s, asthma, burns, all cancers, cataracts, chronic fatigue syndrome, diabetes, autoimmune disorders, diseases of liver, kidneys, lungs, heart, and digestive system, flu, fibromyalgia, glaucoma (open angle only, closed angle not effected), hepatitis, multiple sclerosis, Parkinson’s, physical trauma, skin disorders, seizures, tumours, and more.

* Glycine can have a cooling effect on the brain and body. Glycine has been associated with a decrease in the body’s core temperature. As body temperature declines, so does heat production, followed by an increase in heat loss. All three of these thermoregulation techniques are the body’s way of promoting sleep onset and slow brain wave activity. Conversely, the body’s core temperature begins to increase a few hours prior to waking. In a study on levels of glycine and sleep efficacy, researchers observed that glycine plays a significant role in alleviating symptoms of fatigue in people with poor sleep. Glycine may also be able to offer protection against the atherosclerotic process to boost heart health. Glycine modulates blood glucose levels in normal adults and those with blood glucose sensitivity problems. Glycine is widely used for treating schizophrenia, stroke, benign prostatic hyperplasia (BPH), and some rare inherited metabolic disorders. It is also used to protect kidneys from the harmful side effects of certain drugs used after organ transplantation as well as the liver from harmful effects of alcohol. Other uses include cancer prevention and memory enhancement.

* GNF-6702 is the name for a broad-spectrum antiprotozoal drug, with activity against leishmaniasis, Chagas disease and sleeping sickness. These three diseases are caused by related kinetoplastid parasites, which share similar biology. GNF6702 acts as a non-competitive proteasome inhibitor which was effective against infection with any of the three protozoal diseases in mice, while having little evident toxicity to mammalian cells.

* Gonadorelin (GnRH) increases levels of GnRH which leads women to increase libido and sexual activity. In men increase GnRH surge raises testosterone levels, accompanied by all the typical strong anabolic and androgenic effects. After a transient increase, continuous use of gonadorelin results in downregulation of LH and FSH levels followed by a suppression of ovarian and testicular steroid biosynthesis.

* Gossypol Acetate is a polyphenolic aldehyde that permeates cells and acts as an inhibitor for several dehydrogenase enzymes such as lactate dehydrogenase, NAD-linked enzymes. Gossypol, a known antispermatogenic agent from the cotton plant genus Gossypium, was found to inhibit yellow perch sperm motility in vitro and lactate dehydrogenase activity in spermatozoa when used in a dose-dependent manner. Gossypol has been approved to have antiproliferative and apoptosis-inducing effects on some kinds of cancer cell lines in vitro. Gossypol acetate is able to inhibit tumor growth in Wus1-bearing mice, but the survival of mice is not prolonged, and tumor grows rapidly after short inhibition. Gossypol has now been found to have inhibitory effects on proliferation or to induce apoptosis in ovarian cancer, endometrial cancer, adrenal cortical tumor, thyroid cancer, colon carcinoma, leukemia, pancreatic cancer, melanoma, lymphoma, lung cancer and, lung adenocarcinoma, especially the most malignant proximal-proliferative subtype without druggable protein kinase mutations. In addition, gossypol can increase the sensitivity of drug-resistant tumor cells to chemotherapy and radiotherapy. Some clinical trials showed gossypol is well-tolerated, and partial responses are observed in some patients.

* GPW-105 peptide induced activation of formyl peptide receptor 2 stimulates ischemic neovasculogenesis by promoting homing of endothelial colony forming cells. GPW-105 attenuates severe hind limb ischemia and promotes neovascularization in ischemic limb. GPW-105 is a selective agonist of the Formylpeptide receptors (FPR2 and FPR3) and was discovered by screening peptide libraries for their ability to stimulate inositol phosphates in lymphocyte cell lines. It is also an agonist of FPR11. FPR2 is expressed in the promyelocytic leukemia cell line HL-60 as well as in the chronic myelogenous leukemia cell line K562. GPW-105 also inhibits the infection of human peripheral monocyte–derived macrophages and CD41 T lymphocytes by strains of HIV-1, via sensitization of chemokine receptors (CXCR4 and CCR5), following FPR2 activation.

* Granisetron is antinauseant, antiemetic agent, slows colonic transit, and Rotavirus induced diarrhoea.

* Graying hair plays simultaneously the frequencies of methionine sulfoxide reductase A and B (MSR A and B), catalase (CAT) and l- methionine. Loss of methionine has been linked to senile greying of hair. Its lack leads to a buildup of hydrogen peroxide in hair follicles, a reduction in tyrosinase effectiveness, and a gradual loss of hair color. MSRA, MSRB and catalase are subject to deactivation by H2O2 mediated oxidative stress in a concentration-dependent manner despite two of these enzymes MSRA and MSRB play a critical role in protein repair. The human epidermis expresses high levels of anti-oxidant enzymes to keep the redox homeostasis under control. Low catalase expression/activities leads to hydrogen peroxide (H2O2) accumulation in the skin. Such high concentrations of H2O2 oxidize L-methionine residues in proteins and peptides to (R and S)-methionine sulfoxide diasteriomers. In normal healthy human skin, methionine sulfoxide reductases A and B specifically reduce methionine sulfoxides (S) and (R), H2O2-induced oxidative damage in the entire human hair follicle, inclusive of the hair shaft, affects human hair color by blunting methionine sulfoxide repair.

* Griffithsin is a virucide with a broad spectrum ability to bind to the glycoproteins of other viruses, such as the coronavirus. Griffithsin's three identical carbohydrate domains bind to specific oligosaccharides on the envelope of viral glycoproteins. This was demonstrated by in vitro and in vivo studies. For instance, it was shown that griffithsin binds to the SARS-CoV spike glycoprotein to inhibit entry of the SARS virus and thus inhibit infection. A 2014 study showed griffithsin to also possess useful antiviral activity against Ebolavirus. It has been shown in vitro to be a highly potent HIV entry inhibitor. It is currently being investigated as a potential microbicide for use in the prevention of the transmission of HIV.

* Growth Hormone Deficiency, also known as isolated somatotropin deficiency, is related to growth hormone insensitivity, partial and isolated growth hormone deficiency. An important gene associated with Growth Hormone Deficiency is GH1 (Growth Hormone 1), and among its related pathways/superpathways are G-Beta Gamma Signaling and Peptide hormone metabolism. The drugs Clonidine and Estradiol have been mentioned in the context of this disorder. Affiliated tissues include bone, testes and pituitary, and related phenotypes are endocrine/exocrine gland and adipose tissue. A medical condition, caused by problems arising in the pituitary gland, in which the body does not produce enough growth hormone (GH).

* GSHHRHVHSPFV peptide inhibits infectious bronchitis virus (IBV) infectivity in HeLa cells and blocks IBV haemagglutination.

* GSK-2795039 is a novel NOX2 inhibitor that is the first small molecule to demonstrate inhibition of the NOX2 enzyme in vivo. Oxidative stress, an excess of reactive oxygen species (ROS) production versus consumption, may be involved in the pathogenesis of different diseases. NOX inhibitors are the most promising therapeutic option for diseases associated with oxidative stress.Oxidative stress is a likely common underlying mechanism for multiple diseases such as cardiovascular diseases, neurodegenerative disorders, and cancer. The term oxidative stress describes the disturbance of the redox hemostasis in favor of increased levels of reactive oxygen species (ROS). It can be caused either by decreased antioxidant capacity due to low concentrations of antioxidants and impaired antioxidant enzyme activity, and/or by increased ROS production due to enhanced activity of ROS-producing entities. Since antioxidant supplementation proved to be non-effective or even detrimental, another therapeutic strategy to fight oxidative stress evolved: Targeting the sources of pathophysiological ROS rather than trying to scavenge ROS in a generalized fashion after they have been produced.

* GsMTx4 peptide from tarantula venom protects articular chondrocytes from mechanically induced cell death via inhibition of Piezo1/2. Piezo1 and Piezo2 channels' synergy confers high-strain mechanosensitivity to articular cartilage. Directed coexpression of Piezo1 and Piezo2 potentiates mechanically induced Ca2+ signals and transmembrane currents. Simple attenuation of Piezo expression leads to attenuation of mechanical sensitivity to injurious strain. Piezo1/2-mediated mechanotransduction pathway modulates chondrocyte injury, and blocking this pathway is protective. GsMTx4 is a potentially useful therapeutic agent for targeting Piezo1/2 so that progressive cartilage degeneration following joint trauma can hopefully be addressed more rationally. GsMTx4' potency is 20-fold increased by dynasore, a dynamin GTPase inhibitor. Chondrocyte death has been proposed as an important mechanism leading to posttraumatic arthritis following traumatic joint injury. PIEZO1/2, functionally expressed in joint cartilage, provide novel molecular targets for reducing cell death and mitigating injury-induced cartilage degeneration following joint trauma. Thus, targeting Piezos could potentially serve as a therapy for posttraumatic osteoarthritis. In this regard, GsMTx4 may be able to serve as a chondroprotective agent to prevent and treat osteoarthritis and other mechanically induced forms of the disease such as those caused by joint instability, misalignment, or obesity, by altering pathologic mechanical signal transduction pathways.

* GSTM1 factor genetic variations can change an individual's susceptibility to carcinogens and toxins as well as affect the toxicity and efficacy of certain drugs. GSTM1 is a glutathione S-transferase (GST) which plays a role in the detoxification of metabolites of environmental carcinogens including tobacco smoke. The body produces its own glutathione. However, poor diet, pollution, toxins, medications, stress, trauma, aging, infections and radiation all deplete glutathione. It is also the most critical and integral part of the detoxification system. All the toxins stick onto glutathione, which then carries them into the bile and the stool -and out of the body. And lastly, it also helps in reaching peak mental and physical function. Research has shown that raised glutathione levels decrease muscle damage, reduce recovery time, increase strength and endurance and shift metabolism from fat production to muscle development.

* GSTP1 factor or glutathione S-transferases (GSTs) are a family of enzymes that play an important role in detoxification by catalyzing the conjugation of many hydrophobic and electrophilic compounds with reduced glutathione. Glutathione S-transferase P or GSTP1 regulates cyclophosphamide cardiotoxicity, and prevents cyclophosphamide toxicity by detoxifying acrolein. Thus, humans with low cardiac GSTP levels or polymorphic forms of GSTP with low acrolein-metabolizing capacity may be more sensitive to cyclophosphamide toxicity. GSTP protects against the endothelial dysfunction induced by tobacco smoke exposure and this protection may be related to the detoxification of acrolein or other related cigarette smoke constituents.

* Guanabenz acts by temporarily blocking the reactivation of a protein known as eukaryotic translation initiation factor 2 (eIF2alfa). When deactivated, eIF2alfa initiates the stress response pathway. Blocking its reactivation results in a prolonged stress response and provides protection against cell death. The researchers hypothesize that guanabenz stimulates a protective cascade – because fewer oligodendrocytes die, less immune cells are recruited to the brain, which results in a decreased inflammatory response and preservation of myelin levels. Gunabenz is an alfa agonist of the alfa-2 adrenergic receptor that is used as an antihypertensive drug. It is used to treat high blood pressure (hypertension). Guanabenz also prevents myelin loss and alleviates clinical symptoms of multiple sclerosis (MS) in animal models. The drug appears to enhance an innate cellular mechanism that protects myelin-producing cells against inflammatory stress, and points to new avenues for the development of new, protective therapies against MS.

* GUCA2B or guanylate cyclase activator 2B is the endogenous activator of intestinal guanylate cyclase (see below). It is expressed in the stomach and intestine. This protein stimulates an increase in cyclic GMP, a key component of several intracellular signal transduction pathways. It maybe involved in salt and water secretion into the intestinal lumen as well as the renal tubules, and thus regulate electrolyte homeostasis in these tissues. It may be used for treatment of gastrointestinal functional disorders and diseases including colon polyps.

* Guineensine inhibits the cellular reuptake of anandamide and 2-arachidonoylglycerol in a mouse model. This causes an increase in the activity of the two neurotransmitters which are classified as endogenous cannabinoids. Guineesine can dose-dependently produce cannabimimetic effects in a mouse model which are indicated by potent catatonic, analgesic, hypo-locomotive and hypo-thermic effects. In addition, the analgesic and catatonic effects were reversed by the cannabinoid receptor type 1 (CB1) inverse agonist rimonabant. Guineesine is also a monoamine oxidase inhibitor (MAOI) in vitro. Recently researchers proposed that guineensine can be an efficient compound in the management of neuropathic pain resulting from the damage of neurons. Rearchers have reported the larvicidal activity of guineensine against larvae of Culex pipiens pallens, Aedes aegypti, and A. togoi, which are among the medically important mosquitoes. In another study, researchers found that guineensine significantly inhibits indomethacin-induced gastric lesions.

* GV1001 is a peptide derived from the human telomerase reverse transcriptase (hTERT) sequence that is reported to have anti-cancer effects. It is also an anti-inflammatory that downregulates the production of pro-inflammatory cytokines through the suppression of p38 MAPK and NF-κB activation following ENO1 stimulation. It was developed as an anti-cancer agent to treat advanced pancreatic cancer, non-small lung cancer, melanoma, and other cancers. Recent studies have reported that GV1001 penetrates cell membranes by binding with heat shock proteins (HSPs) and accumulates in the cytoplasm. Additionally, this peptide protects against renal ischemia reperfusion injury (IRI) in mice by reducing acute inflammatory responses and decreasing the proportion of apoptotic cells that can cause renal injury. GV1001 possesses neuroprotective effects against Beta amyloid 25–35 oligomer in Neural Stem Cells and these effects are mediated through mimicking the extra-telomeric functions of human telomerase reverse transcriptase, including the induction of cellular proliferation, anti-apoptotic effects, mitochondrial stabilization, and anti-aging and anti-oxidant effects.