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Unseld, E.; Klotz, Ulrich

doi:10.1023/a:1015848515036

Cited by 23 publications

(4 citation statements)

References 13 publications

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“…While these results are consistent with hypothesis that intestinal bacteria are, at least partially, a source of endogenous BZ [65,66,67], they suggest that this antibiotic – administered cyclically – could prevent the accumulation of both pathogenetic (i.e. ammonia) and precipitating (i.e.…”

Section: Rifaximin In the Treatment Of Hesupporting

confidence: 89%

Management of Hepatic Encephalopathy: Focus on Antibiotic Therapy

Festi

Vestito²,

Mazzella³

et al. 2006

Digestion

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Hepatic encephalopathy (HE) is a major neuropsychiatric complication of both acute and chronic liver failure. Symptoms of HE include attention deficits, alterations of sleep patterns and muscular incoordination progressing to stupor and coma. The pathogenesis of HE is still unknown, although ammonia-induced alterations of cerebral neurotransmitter balance, especially at the astrocyte-neurone interface, may play a major role. Treatment of HE is therefore directed at reducing the production and absorption of gut-derived neurotoxic substances, especially ammonia. The non-absorbable disaccharides lactulose and lactitol were long considered as a first-line pharmacological treatment of HE, but a recent systematic review questioned their efficacy, pointing out that there is insufficient high-quality evidence to support their use. Oral antibiotics are regarded as a suitable therapeutic alternative. However, the prolonged use of antimicrobials is precluded by the possible occurrence of adverse events. Rifaximin, a synthetic antibiotic structurally related to rifamycin, displays a wide spectrum of antibacterial activity against Gram-negative and Gram-positive bacteria, both aerobic and anaerobic, and a very low rate of systemic absorption. Available evidence suggests that rifaximin – thanks to its efficacy and remarkable safety – has the highest benefit-risk ratio in the overall treatment of HE.

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Section: Rifaximin In the Treatment Of Hesupporting

confidence: 89%

Management of Hepatic Encephalopathy: Focus on Antibiotic Therapy

Festi

Vestito²,

Mazzella³

et al. 2006

Digestion

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“…In clinical practice these drugs are widely prescribed for the treatment of insomnia and anxiety disorders. Benzodiazepines are central nervous system (CNS) depressants4, 5 and are characterized by a strong and specific interaction with local γ ‐aminobutyric acid chloride channel receptor (GABA A ) sites 6–10. Various benzodiazepine derivatives were originally marketed as an improvement over the then available barbiturates with regard to overdose effects, drug interactions, dependence development, and illicit abuse.…”

Section: Methodsmentioning

confidence: 99%

Gas‐phase fragmentation of protonated benzodiazepines

Risoli

Cheng

Verkerk

et al. 2007

Rapid Comm Mass Spectrometry

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Protonated 1,4-benzodiazepines dissociate in the gas phase by the common pathway of CO elimination and by unique pathways dictated by the substituents; the latter typically differentiate one benzodiazepine from another. Protonated 3-dihydro-5-phenyl-1,4-benzodiazepin-2-one, the base diazepam devoid of substituents, dissociates by eliminating CO, HNCO, benzene, and benzonitrile. Mechanisms of these reactions are proposed with ionic products being resonance stabilized. The abundant [MH-CO]+ ion dissociates to secondary products via elimination of benzene, benzonitrile, the NH2 radical, and ammonia, yielding again ionic products that are stabilized by resonance.

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“…This view of • NO changed in the 1980s when Robert Furchgott discovered that the endothelium released a labile factor, termed “endothelial-derived relaxing factor” (EDRF), which caused vascular relaxation when vascular smooth muscle cell preparations were stimulated with vasodilators (e.g., acetylcholine, histamine, and bradykinin) [16]. EDRF was also called “nitrovasodilator” because nitrovasodilators such as nitroglycerin, nitroprusside, other organic nitrites, cause vascular relaxation [17]. Subsequently, it was proposed that EDRF is • NO.…”

Section: Introduction To Reactive Oxygen and Nitrogen Species (Ros/rns)mentioning

confidence: 99%

Teaching the basics of redox biology to medical and graduate students: Oxidants, antioxidants and disease mechanisms

2013

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This article provides a succinct but limited overview of the protective and deleterious effects of reactive oxygen and nitrogen species in a clinical context. Reactive oxygen species include superoxide, hydrogen peroxide, single oxygen and lipid peroxides. Reactive nitrogen species include species derived from nitric oxide. This review gives a brief overview of the reaction chemistry of these species, the role of various enzymes involved in the generation and detoxification of these species in disease mechanisms and drug toxicity and the protective role of dietary antioxidants. I hope that the graphical review will be helpful for teaching both the first year medical and graduate students in the U.S. and abroad the fundamentals of reactive oxygen and nitrogen species in redox biology and clinical medicine.

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Untitled

Cited by 23 publications

References 13 publications

Management of Hepatic Encephalopathy: Focus on Antibiotic Therapy

Management of Hepatic Encephalopathy: Focus on Antibiotic Therapy

Gas‐phase fragmentation of protonated benzodiazepines

Teaching the basics of redox biology to medical and graduate students: Oxidants, antioxidants and disease mechanisms

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