A thioglucose derivative used as an antirheumatic and experimentally to produce obesity in animals.
Inorganic compounds that contain gold as an integral part of the molecule.
An oral chrysotherapeutic agent for the treatment of rheumatoid arthritis. Its exact mechanism of action is unknown, but it is believed to act via immunological mechanisms and alteration of lysosomal enzyme activity. Its efficacy is slightly less than that of injected gold salts, but it is better tolerated, and side effects which occur are potentially less serious.
A FLAVOPROTEIN enzyme that catalyzes the oxidation of THIOREDOXINS to thioredoxin disulfide in the presence of NADP+. It was formerly listed as EC 1.6.4.5
A non-steroidal anti-inflammatory drug. Oxyphenbutazone eyedrops have been used abroad in the management of postoperative ocular inflammation, superficial eye injuries, and episcleritis. (From AMA, Drug Evaluations Annual, 1994, p2000) It had been used by mouth in rheumatic disorders such as ankylosing spondylitis, osteoarthritis, and rheumatoid arthritis but such use is no longer considered justified owing to the risk of severe hematological adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p27)
The design or use of pharmaceutical agents that act on multiple targets or disease pathways.
A non-steroidal anti-inflammatory agent (ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL) similar in mode of action to INDOMETHACIN.
A butyl-diphenyl-pyrazolidinedione that has anti-inflammatory, antipyretic, and analgesic activities. It has been used in ANKYLOSING SPONDYLITIS; RHEUMATOID ARTHRITIS; and REACTIVE ARTHRITIS.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Databases devoted to knowledge about PHARMACEUTICAL PRODUCTS.
Drugs used by veterinarians in the treatment of animal diseases. The veterinarian's pharmacological armamentarium is the counterpart of drugs treating human diseases, with dosage and administration adjusted to the size, weight, disease, and idiosyncrasies of the species. In the United States most drugs are subject to federal regulations with special reference to the safety of drugs and residues in edible animal products.

Anti-rheumatic compound aurothioglucose inhibits tumor necrosis factor-alpha-induced HIV-1 replication in latently infected OM10.1 and Ach2 cells. (1/74)

NF-kappaB is a potent cellular activator of HIV-1 gene expression. Down-regulation of NF-kappaB activation is known to inhibit HIV replication from the latently infected cells. Gold compounds have been effectively used for many decades in the treatment of rheumatoid arthritis. We previously reported that gold compounds, especially aurothioglucose (AuTG) containing monovalent gold ion, inhibited the DNA-binding of NF-kappaB in vitro. In this report we have examined the efficacy of the gold compound AuTG as an inhibitor of HIV replication in latently infected OM10.1 and Ach2 cells. Tumor necrosis factor (TNF)-alpha-induced HIV-1 replication in OM10.1 or Ach2 cells was significantly inhibited by non-cytotoxic doses of AuTG (>10 microM in OM10.1 cells and >25 F.M in Ach2 cells), while 25 microM of the counter-anion thioglucose (TG) or gold compound containing divalent gold ion, HAuCl3, had no effect. The effect of AuTG on NF-kappaB-dependent gene expression was confirmed by a transient CAT assay. Specific staining as well as electron microscopic examinations revealed the accumulation of metal gold in the cells, supporting our previous hypothesis that gold ions could block NF-kappaB-DNA binding by a redox mechanism. These observations indicate that the monovalent gold compound AuTG is a potentially useful drug for the treatment of patients infected with HIV.  (+info)

Inhibition of IL-6 and IL-8 induction from cultured rheumatoid synovial fibroblasts by treatment with aurothioglucose. (2/74)

Gold compounds have long been used in the treatment of rheumatoid arthritis (RA). However, their actions in RA have not been clarified. In this study, we examined the effect of one of the monovalent gold compounds, aurothioglucose (AuTG), on the IL-1-induced production of IL-6, IL-8 and granulocyte macrophage colony stimulating factor (GM-CSF) from rheumatoid synovial fibroblasts (RSF) isolated from three RA patients. IL-6 and IL-8 induction but not GM-CSF induction was inhibited in most of the RSF after pretreatment with AuTG. Since gene expression of these cytokines is known to be under the control of a common transcription factor, NF-kappaB, the effect of AuTG on the cellular localization of NF-kappaB (p65 subunit) and on NF-kappaB-DNA binding was examined. Although AuTG treatment did not prevent NF-kappaB nuclear translocation, AuTG blocked the DNA-binding activity of NF-kappaB when examined in vitro. Morphologically, both metal-specific cell staining using p-dimethylaminobenzylidene rhodamine and transmission electron microscopic examinations demonstrated the accumulation of metal gold in the cytoplama and some organella (mitochondria and lysosomes) of the AuTG-treated RSF. These results indicate that one of the anti-rheumatic actions of AuTG might be through its inhibitory action on NF-kappaB.  (+info)

The effect of goldthioglucose on peroxidative processes in mice. (3/74)

Experiments were conducted to study the effect of goldthioglucose (GTG) upon the processes associated with lipid peroxidation. The glucose-6-phosphate dehydrogenase activity (G6PD; E.C. 1. 1.1.49) in red blood cells (RBC) and the amount of malonaldehyde precursors (MDA) per gram of brain, liver and kidney were determined. Adult mice received i.p. injections for three consecutive days of either saline (controls) or GTG dissolved in saline, in a dose of 0.10 mg.g(-1) or 0. 15 mg.g(-1) b.w. In mice receiving higher dose of GTG the G6PD activity was significantly increased (349.38+/-17.46 mU.10(-9) RBC compared to 258.2+/-14.46 mU.10(-9) RBC in control animals). The content of MDA precursors rose significantly from 4.8+/-0.81 micromol.g(-1) of the liver in controls to 8.12+/-1.41 micromol.g(-1) and 7.88+/-0.51 micromol.g(-1) and from 18.71+/-1.01 micromol.g(-1) of the kidneys in controls to 24.25+/-1.25 micromol.g(-1) and 24.88+/-1.7 micromol.g(-1) respectively. The GTG-induced higher levels of MDA precursors and increased G6PD activity in RBC corresponds to the rise in lipid peroxidation and its participation in producing the lesions after experimental and therapeutic use of gold-containing substances seems possible.  (+info)

Leptin has acute effects on glucose and lipid metabolism in both lean and gold thioglucose-obese mice. (4/74)

Leptin is reported to have effects in peripheral tissues that are independent of its central effects on food intake and body weight. In this study, the acute effects of a single dose of recombinant mouse leptin on lipid and glucose metabolism in lean and gold thioglucose-injected obese mice were examined. Changes were measured 2 h after leptin injection. In lean mice, liver and white adipose tissue (WAT) lipogenesis was inhibited. The activity of the pyruvate dehydrogenase complex (PDHCa), the rate-determining step for glucose oxidation, was reduced in heart, liver, quadriceps muscle, and both brown and white adipose tissues. Muscle and liver glycogen and liver triglyceride (TG) content was unchanged, but muscle TG was decreased. In obese mice, liver and WAT lipogenesis was inhibited and PDHCa reduced in heart and quadriceps muscle. Muscle and liver glycogen was decreased but not TG. Serum insulin was reduced in obese but not lean mice. These results are consistent with a role for leptin in the maintenance of steady-state energy stores by decreasing lipid synthesis and increasing fat mobilization, with decreased glucose oxidation occurring as a result of increased fatty acid oxidation.  (+info)

Aggressive treatment in early rheumatoid arthritis: a randomised controlled trial. On behalf of the Rheumatic Research Foundation Utrecht, The Netherlands. (5/74)

OBJECTIVES: To compare three therapeutic strategies using slow acting antirheumatic drugs (SAARDs) in early rheumatoid arthritis (RA), for their disease modifying properties, toxicity, and lag time until treatment effect. METHODS: Patients with recent onset RA from six hospitals were randomly assigned to immediate initiation of one of three treatment strategies: (I) a "mild SAARD with a long lag time" (hydroxychloroquine, if necessary replaced by auranofin); (II) a "potent SAARD with a long lag time" (intramuscular gold, if necessary replaced by D-penicillamine); (III) a "potent SAARD with a short lag time" (methotrexate, if necessary replaced by sulfasalazine). Comparisons included two years of follow up. RESULTS: All SAARD strategies reduced mean disease activity. A greater percentage of patients improved clinically with strategies II and III than with strategy I: percentages of patients improved on joint score with strategies II and III (79% and 82%, respectively), which was statistically different from strategy I (66%). The same was true for remission percentages: 31% and 24% v 16%, respectively). Longitudinal analysis showed significantly less disability with strategy III, and a lower erythrocyte sedimentation rate with strategy II than with strategy I. In addition, radiological damage after one and two years, was significantly lower in strategies II and III (at two years median scores were 11 and 10 v 14 in strategy I, p<0.05). Toxicity was increased in strategy II compared with the other strategies. CONCLUSION: Strategy III, comprising methotrexate or sulfasalazine, produced the best results weighing effectiveness and toxicity. Strategy I (hydroxychloroquine or auranofin) was slightly less effective, and strategy II (intramuscular gold or D-penicillamine) was associated with increased toxicity.  (+info)

Accumulation of gold in various organs of mice injected with gold thioglucose. (6/74)

The response of either male or female mice to the administration of gold thioglucose (GTG) was observed in food intake, in body and organ weights, and in gold accumulation in respective organs. Male mice were more sensitive to GTG toxicity than females. During 103 days after GTG administration, the adipose tissues of the females and males increased in weight 15 times and 2.5 times as high as those of control mice, respectively. The weights of heart, lung, and brain were not affected by GTG administration. In the respective organs, gold concentrations, which were determined by neutron activation analysis, were high in liver, kidney, spleen, adrenal, and adipose tissue (especially in female) within a shorter time after the GTG injection. In various organs of nonobese mice, the concentrations of GTG were significantly less than those in the typical obese mice. Even after more than 100 days after injection, gold was detected in the respective organs. In the control mice without any GTG administration, no gold could be detected.  (+info)

Apoprotein C-III deficiency markedly stimulates triglyceride secretion in vivo: comparison with apoprotein E. (7/74)

Apoprotein (apo) C-III plays an important role in the development of hypertriglyceridemia by inhibiting triglyceride (TG) removal. However, the effect of apo C-III on TG production remains unclear. We measured TG secretion rate (TGSR) in apo C-III gene-disrupted (apo C-III-null) mice to investigate the influence of this protein on TG turnover. TGSR measured by the Triton WR-1339 method was increased twofold in these mice compared with wild-type (WT) mice. Obesity was induced by the injection of gold-thioglucose (GTG), which made the WT mice hypertriglyceridemic due to a threefold increase of TGSR. However, GTG-induced obesity failed to increase TG in apo C-III-null mice, although TGSR was increased 10-fold, suggesting substantial stimulation of TG removal. Apo E-null mice were severely hypercholesterolemic but were not hypertriglyceridemic, and TGSR was rather decreased. GTG-induced obesity made these mice hypertriglyceridemic because of TG overproduction to an extent similar to that seen in WT mice. These results suggest that apo C-III deficiency potently enhances TG turnover, especially when TG production is stimulated, and that apo E deficiency is not always rate limiting for TG production.  (+info)

A novel, enzymatically active conformation of the Escherichia coli NADH:ubiquinone oxidoreductase (complex I). (8/74)

Electron microscopy has demonstrated the unusual L-shaped structure of the respiratory complex I consisting of two arms, which are arranged perpendicular to each other. We found that the Escherichia coli complex I has an additional stable conformation, with the two arms arranged side by side, resulting in a horseshoe-shaped structure. The structure of both conformations was determined by means of electron microscopy of gold thioglucose-stained single particles. They were distinguished from each other by titration of the complex with polyethylene glycol and by means of analytical ultracentrifugation. The transition between the two conformations is induced by the ionic strength of the buffer and is reversible. Only the horseshoe-shaped complex I exhibits enzyme activity in detergent solution, which is abolished by the addition of salt. Therefore, it is proposed that this structure is the native conformation of the complex in the membrane.  (+info)

Aurothioglucose is a gold-containing medication that has been used in the treatment of rheumatoid arthritis. It works by modulating the immune system and reducing inflammation in the joints. The medication is administered via injection, usually into a muscle (intramuscularly).

The use of aurothioglucose has declined in recent years due to the availability of newer and more effective medications for rheumatoid arthritis. Additionally, aurothioglucose can have significant side effects, including kidney damage, skin reactions, and blood disorders. It is important to be monitored by a healthcare provider while taking this medication to ensure that it is safe and effective for use.

Gold compounds refer to chemical combinations in which gold atoms are bonded with other elements. In the context of medicine, particularly in the field of rheumatology, gold compounds have been used as disease-modifying antirheumatic drugs (DMARDs) for the treatment of conditions such as rheumatoid arthritis.

The most commonly used gold compound is auranofin, which contains gold in the +1 oxidation state. Auranofin is an oral medication that can help reduce inflammation and slow down joint damage caused by rheumatoid arthritis. It works by inhibiting certain enzymes involved in the inflammatory response.

Other gold compounds, such as sodium aurothiomalate and gold thioglucose, are administered parenterally (usually intramuscularly) and contain gold in the +3 oxidation state. These medications also have anti-inflammatory properties and can help alleviate symptoms of rheumatoid arthritis.

It is important to note that the use of gold compounds as a treatment for rheumatoid arthritis has declined over time due to their side effects, which may include kidney damage, skin reactions, mouth ulcers, and bone marrow suppression. They are generally reserved for patients who have not responded well to other DMARDs or biologic agents.

Auranofin is a medication that contains gold and is used in the treatment of rheumatoid arthritis. It belongs to a class of drugs called gold-containing compounds, which are used to reduce inflammation and joint damage caused by rheumatoid arthritis.

Auranofin works by inhibiting certain enzymes that play a role in the inflammatory response, which can help to reduce swelling, pain, and stiffness in the joints. It is taken orally, usually in the form of a tablet, and is typically prescribed for use in combination with other medications used to treat rheumatoid arthritis.

It's important to note that auranofin can have serious side effects, including kidney damage, mouth sores, and skin rashes, and it should only be used under the close supervision of a healthcare provider. Additionally, regular monitoring of blood and urine tests is necessary while taking this medication to ensure that it is not causing any harmful effects on the body.

Thioredoxin-disulfide reductase (Txnrd, TrxR) is an enzyme that belongs to the pyridine nucleotide-disulfide oxidoreductase family. It plays a crucial role in maintaining the intracellular redox balance by reducing disulfide bonds in proteins and keeping them in their reduced state. This enzyme utilizes NADPH as an electron donor to reduce thioredoxin (Trx), which then transfers its electrons to various target proteins, thereby regulating their activity, protein folding, and antioxidant defense mechanisms.

Txnrd is essential for several cellular processes, including DNA synthesis, gene expression, signal transduction, and protection against oxidative stress. Dysregulation of Txnrd has been implicated in various pathological conditions, such as cancer, neurodegenerative diseases, and inflammatory disorders. Therefore, understanding the function and regulation of this enzyme is of great interest for developing novel therapeutic strategies.

Oxyphenbutazone is a non-selective non-steroidal anti-inflammatory drug (NSAID) that has been used in the past for its analgesic, anti-inflammatory, and antipyretic properties. It works by inhibiting the enzyme cyclooxygenase (COX), which is involved in the synthesis of prostaglandins, chemicals that mediate inflammation, pain, and fever.

However, due to its potential for serious side effects such as gastrointestinal ulcers, bleeding, and kidney damage, as well as interactions with other medications, oxyphenbutazone is no longer commonly used in many countries. It has been largely replaced by newer NSAIDs that have a more favorable safety profile.

It's important to note that the use of oxyphenbutazone should be under the strict supervision of a healthcare professional and should only be taken as directed, as it can cause potentially serious side effects even at therapeutic doses.

Polypharmacology is the practice of using multiple drugs or pharmaceutical agents to treat a single medical condition, or to target multiple disease-related targets (proteins, enzymes, etc.) simultaneously. This approach can be used for various reasons, such as increasing therapeutic efficacy, improving drug response rates, or overcoming resistance to monotherapy. It is also employed in the treatment of complex diseases like cancer, neurological disorders, and infectious diseases where multiple pathways are involved.

In contrast to traditional pharmacological approaches that focus on developing drugs with high selectivity for a single target (single-target therapy), polypharmacology acknowledges the inherent promiscuity of many drug molecules and harnesses this property to design more effective therapeutic strategies. However, it is crucial to carefully consider potential drug-drug interactions, side effects, and toxicities when implementing polypharmacological interventions.

Tolmetin is a non-steroidal anti-inflammatory drug (NSAID) that is used to relieve pain, inflammation, and fever. It works by inhibiting the production of prostaglandins, which are hormone-like substances that cause pain and inflammation in the body. Tolmetin is available in immediate-release and sustained-release forms, and it is typically prescribed to treat conditions such as osteoarthritis, rheumatoid arthritis, and juvenile rheumatoid arthritis.

The medical definition of Tolmetin can be found in various pharmaceutical and medical references, including the Merck Manual, the American Hospital Formulary Service (AHFS) Drug Information, and the National Library of Medicine's MedlinePlus. According to these sources, the chemical name for Tolmetin is (3R,5S)-3-(4-methylbenzoyl)-5-(3-methoxy-4-hydroxyphenyl)-1H-indole-2-one, and its molecular formula is C19H16NO3.

Tolmetin has a number of potential side effects, including stomach pain, nausea, vomiting, diarrhea, gas, dizziness, and headache. It can also increase the risk of serious gastrointestinal side effects, such as bleeding, ulcers, and perforations in the stomach or intestines, especially in people who are over the age of 65 or have a history of stomach ulcers or other gastrointestinal problems. Tolmetin can also increase the risk of heart attack, stroke, and other cardiovascular events, particularly in people who take it for a long time or at high doses.

Tolmetin is available only by prescription, and it should be taken exactly as directed by a healthcare provider. It is important to follow the instructions on the label carefully and to talk to a doctor or pharmacist if there are any questions about how to take Tolmetin or what the potential side effects may be.

Phenylbutazone is a non-steroidal anti-inflammatory drug (NSAID) that was commonly used in the past to treat pain and inflammation associated with conditions such as rheumatoid arthritis, osteoarthritis, and gout. It works by inhibiting the activity of cyclooxygenase (COX) enzymes, which are involved in the production of prostaglandins, chemicals that mediate inflammation and pain.

However, due to its potential for serious side effects, including bone marrow suppression, liver toxicity, and increased risk of heart attack and stroke, phenylbutazone is no longer commonly used in human medicine in many countries, including the United States. It may still be used in veterinary medicine under strict supervision.

An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.

Pharmaceutical databases are collections of information related to pharmaceuticals and medications. These databases can contain a variety of data types, including:

1. Drug information: This includes details about the chemical properties, therapeutic uses, dosages, side effects, interactions, and contraindications of medications.
2. Clinical trials data: Information on ongoing or completed clinical trials, including study design, participant demographics, outcomes, and safety data.
3. Prescription data: Data related to prescribing patterns, medication utilization, and adherence.
4. Pharmacoeconomic data: Cost-effectiveness analyses, budget impact models, and other economic evaluations of medications.
5. Regulatory information: Details about drug approvals, labeling changes, and safety alerts from regulatory agencies such as the US Food and Drug Administration (FDA) or the European Medicines Agency (EMA).
6. Pharmacovigilance data: Information on adverse events, medication errors, and other safety concerns reported to pharmacovigilance databases.
7. Literature databases: Citations and abstracts from medical literature related to pharmaceuticals and medications.

Pharmaceutical databases can be used by healthcare professionals, researchers, regulatory agencies, and the pharmaceutical industry for a variety of purposes, including drug development, clinical decision making, post-marketing surveillance, and health policy planning.

Veterinary drugs, also known as veterinary medicines, are substances or combinations of substances used to treat, prevent, or diagnose diseases in animals, including food-producing species and pets. These drugs can be administered to animals through various routes such as oral, topical, injectable, or inhalation. They contain active ingredients that interact with the animal's biological system to produce a therapeutic effect. Veterinary drugs are subject to regulatory control and must be prescribed or recommended by a licensed veterinarian in many countries to ensure their safe and effective use.

In 2001, aurothioglucose was withdrawn from the Dutch market, where it had been the only injectable gold preparation available ... Aurothioglucose, also known as gold thioglucose, is a chemical compound with the formula AuSC6H11O5. This derivative of the ... Media related to Aurothioglucose at Wikimedia Commons (Articles with short description, Short description is different from ... Aurothioglucose has an interaction with the antimalarial medication hydroxychloroquine. Auranofin Shaw, III C. F. (1999). "Gold ...
"Aurothioglucose Suspension adverse effects". Health Digest. "Gold sodium thiomalate (gold)". Archived from the original on 28 ... Beck RK (2002). "Auranofin and Aurothioglucose side effects & overdose". Drug Reference for EMS Providers. pp. 164-165. " ... "Aurothioglucose is a gold salt used in treating inflammatory arthritis". MedicineNet.com "About gold treatment: What is it? ... Aurothioglucose (Gold thioglucose) (US) Shaw CF (September 1999). "Gold-based therapeutic agents". Chemical Reviews. 99 (9): ...
The structure of the related drug Aurothioglucose is also polymeric with two-coordinate gold(I) centers. In such compounds, the ... Auranofin Aurothioglucose Gold salts Sodium aurothiomalate Shaw III CF (September 1999). "Gold-based therapeutic agents". ...
Care should be taken if combined with medication altering liver function as well as aurothioglucose (Solganal), cimetidine ( ...
It was recently discontinued from the US market along with aurothioglucose leaving only auranofin as the only gold salt on the ...
M01CA03 Oxycinchophen M01CB01 Sodium aurothiomalate M01CB02 Sodium aurothiosulfate M01CB03 Auranofin M01CB04 Aurothioglucose ...
Historically, injectable gold salts such as gold sodium thiomalate and aurothioglucose were considered by many to be the most ...
... aurothioglucose MeSH D02.691.675.249.150 - auranofin MeSH D02.691.675.500 - gold sodium thiomalate MeSH D02.691.750.100 - ...
Anthanthrene Anthracene Anthranilic acid Antimony trisulfide Apholate para-Aramid fibrils Atrazine Aurothioglucose (Auranofin) ...
In 2001, aurothioglucose was withdrawn from the Dutch market, where it had been the only injectable gold preparation available ... Aurothioglucose, also known as gold thioglucose, is a chemical compound with the formula AuSC6H11O5. This derivative of the ... Media related to Aurothioglucose at Wikimedia Commons (Articles with short description, Short description is different from ... Aurothioglucose has an interaction with the antimalarial medication hydroxychloroquine. Auranofin Shaw, III C. F. (1999). "Gold ...
Get up-to-date information on Aurothioglucose side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more ... How was your experience with Aurothioglucose?. First, a little about yourself. Male Female ... Aurothioglucose falls into category C:. In animal studies, pregnant animals were given this medication and had some babies born ... Aurothioglucose should be used during pregnancy only if the possible benefit outweighs the possible risk to the unborn baby. ...
Find information on Aurothioglucose (Solganol) in Daviss Drug Guide including dosage, side effects, interactions, nursing ... "Aurothioglucose." Daviss Drug Guide, 18th ed., F.A. Davis Company, 2023. Medicine Central, im.unboundmedicine.com/medicine/ ... view/Davis-Drug-Guide/109103/5/aurothioglucose. Vallerand AHA, Sanoski CAC, Quiring CC. Aurothioglucose. Daviss Drug Guide. F. ... Vallerand, A. H., Sanoski, C. A., & Quiring, C. (2023). Aurothioglucose. In Daviss Drug Guide (18th ed.). F.A. Davis Company. ...
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above. ...
Exfoliative dermatitis (ED) is a definitive term that refers to a scaling erythematous dermatitis involving 90% or more of the cutaneous surface. Exfoliative dermatitis is characterized by erythema and scaling involving the skins surface and often obscures the primary lesions that are important clues to understanding the evolution of the dis...
229960001799 aurothioglucose Drugs 0.000 description 1 * VSRXQHXAPYXROS-UHFFFAOYSA-N azanide;cyclobutane-1,1-dicarboxylic acid; ... XHVAWZZCDCWGBK-WYRLRVFGSA-M Aurothioglucose Chemical compound OC[C@H]1O[C@H](S[Au])[C@H](O)[C@@H](O)[C@@H]1O XHVAWZZCDCWGBK- ... aurothioglucose, gold sodium thiomalate); immunosuppressives (cyclosporine, tacrolimus (FK-506), sirolimus (rapamycin), ...
Be sure to mention any of the following: gold compounds such as auranofin (Ridaura) and aurothioglucose (Solganol); ...
Aurothioglucose can be used in the hyperresponsive patient. Gold compounds stabilise lysosomal enzymes, inhibit neutrophil and ...
There are two injectable forms of gold: gold sodium thiomalate (Myochrysine, generic) and aurothioglucose (Solganal, generic). ...
M01CA03 Oxycinchophen M01CB01 Sodium aurothiomalate M01CB02 Sodium aurothiosulfate M01CB03 Auranofin M01CB04 Aurothioglucose ...
AUROTHIOGLUCOSE 50440 AZATADINE 50444 AZTREONAM 50445 AZATHIOPRINE 50446 AZLOCILLIN SODIUM 50447 BACAMPICILLIN 50450 BACITRACIN ...
Chloroquine and hydroxychloroquine are anti-malarial medications also used against some auto-immune diseases.[64] Chloroquine, along with hydroxychloroquine, was an early experimental treatment for COVID-19.[65] Neither drug has been useful to prevent or treat SARS-CoV-2 infection.[66][67][68][69][70][71] Administration of chloroquine or hydroxychloroquine to COVID-19 patients has been associated with increased mortality and adverse effects, such as QT prolongation.[72][73] Researchers estimate that off-label use of hydroxychloroquine in hospitals during the first phase of the pandemic caused 17,000 deaths worldwide.[74] The widespread administration of chloroquine or hydroxychloroquine, either as monotherapies or in conjunction with azithromycin, has been associated with deleterious outcomes, including QT interval prolongation. As of 2024,[update] scientific evidence does not substantiate the efficacy of hydroxychloroquine, with or without the addition of azithromycin, in the therapeutic ...
Aurothioglucose injections help in dealing with rheumatoid arthritis. Gold is also applied in life-support devices and some ...
AUROTHIOGLUCOSE 50 MG/ML; 21. Auditory Canal, External [That part of the ear canal external to the ear drum ( NCI )] (UMLS (NCI ... 70. aurothioglucose [monovalent gold salt sometimes used in treatment of early active rheumatoid arthritis. ( CSP )] (UMLS (CSP ...
➥Inorganic Chemistry (Synonyms) - Flashcards 🎓 Get access to high-quality and unique 50 000 college essay examples and more than 100 000 flashcards and test answers from around the world!
Neuroprotective Effect of Aurothioglucose-Loaded PLGA Nanoparticles in an Aluminum Chloride-Induced Rat Model of Alzheimers ... Neuroprotective Effect of Aurothioglucose-Loaded PLGA Nanoparticles in an Aluminum Chloride-Induced Rat Model of Alzheimers ...
For aurothioglucose, ammonium molybdate- and phosphotungstate-stained molecules, the dimensions measured are consistent. In ...
Solganal Forte (Aurothioglucose) * Solganal (Aurothioglucose) * Soflax (Bisacodyl Laxative) * Sofracort (Framycetin Sulfate- ...
Traber KE, Okamoto H, Kurono C, Baba M, Saliou C, Soji T, Packer L, Okamoto T: Anti-rheumatic compound aurothioglucose inhibits ...
... auranofin and aurothioglucose) one antiviral (zidovudine) one antimalarial (artesunate) ARHGAP1 one anticancer (bleomycin) and ...
The gold drugs, gold sodium thiomalate (Myocrisin), aurothioglucose (Solganal), and the orally administered auranofin (Ridaura ...
","grey",0 46013,"Aurothioglucose","12192-57-3","C12192573","cheminventory_sample,tox21:all_plated,tox21:ncgc_all_plated,tox21: ...
D1.632.675.249.150 Aurothioglucose D1.632.675.249 Autonomic Nerve Block E4.525.210.550.500 Autopsy E1.370.60 Autoradiography ...
D1.632.675.249.150 Aurothioglucose D1.632.675.249 Autonomic Nerve Block E4.525.210.550.500 Autopsy E1.370.60 Autoradiography ...
Quinolines (Oxycinchophen) - Gold preparations (Sodium aurothiomalate, Sodium aurothiosulfate, Auranofin, Aurothioglucose, ...
[transmission electron microscopy (TEM); larval Hugin neuron of the pharynx; hugin-PH right 1 (L1EM:2811369); VFB CATMAID L1 CNS; L1 larval CNS ssTEM - Cardona/Janelia]
Catalysis of the reaction: a (3R)-hydroxyacyl-[acyl-carrier-protein] = a (2E)-enoyl-[acyl-carrier-protein] + H2O.
Artemether/Lemefantrine answers are found in the Johns Hopkins ABX Guide powered by Unbound Medicine. Available for iPhone, iPad, Android, and Web.
  • Only one gold drug remains in active clinical use for this purpose in the United States: auranofin although sodium aurothiomalate (gold sodium thiomalate) and aurothioglucose were still used until recently. (wikipedia.org)
  • Aurothioglucose has an interaction with the antimalarial medication hydroxychloroquine. (wikipedia.org)
  • In 2001, aurothioglucose was withdrawn from the Dutch market, where it had been the only injectable gold preparation available since 1943, forcing hospitals to change medication for a large number of patients to aurothiomalate. (wikipedia.org)
  • Aurothioglucose, also known as gold thioglucose, is a chemical compound with the formula AuSC6H11O5. (wikipedia.org)
  • Medicine Central , im.unboundmedicine.com/medicine/view/Davis-Drug-Guide/109103/5/aurothioglucose. (unboundmedicine.com)