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A placebo-controlled trial of pioglitazone in subjects with nonalcoholic steatohepatitis.
TLDR
In this proof-of-concept study, the administration of pioglitazone led to metabolic and histologic improvement in subjects with nonalcoholic steatohepatitis and larger controlled trials of longer duration are warranted to assess the long-term clinical benefit.
An official ATS statement: hepatotoxicity of antituberculosis therapy.
TLDR
Systematic steps for prevention and management of TB DILI are recommended, including patient and regimen selection to optimize benefits over risks, effective staff and patient education, ready access to care for patients, good communication among providers, and judicious use of clinical and biochemical monitoring.
Acute acalculous cholecystitis: a review.
Vitamin E and vitamin C treatment improves fibrosis in patients with nonalcoholic steatohepatitis
TLDR
Vitamin E and vitamin C, in the doses used in this study, were well tolerated and were effective in improving fibrosis scores in NASH patients and a larger, multicenter, longer-term trial with vitamin E anditamin C seems to be warranted.
Importance of changes in adipose tissue insulin resistance to histological response during thiazolidinedione treatment of patients with nonalcoholic steatohepatitis
TLDR
Amelioration of Adipo‐IR by pioglitazone is closely related to histological improvement and plays an important role during treatment of patients with NASH.
Ethanol‐induced oxidative stress precedes mitochondrially mediated apoptotic death of cultured fetal cortical neurons
TLDR
C cultured fetal rat cortical neurons are utilized to illustrate that oxidative stress and formation of a proapoptotic lipid peroxidation product, HNE, precede a cascade of mitochondrially mediated events in cultured fetal cortical neurons, culminating in apoptotic death.
Nonalcoholic steatohepatitis: what we know in the new millennium
TLDR
Current investigations are focusing on improving the underlying insulin resistance that has been associated with NASH as well as other therapies that decrease oxidative stress or improve hepatocyte survival.
In utero ethanol exposure causes mitochondrial dysfunction, which can result in apoptotic cell death in fetal brain: a potential role for 4-hydroxynonenal.
TLDR
It is illustrated that in utero ethanol exposure can elicit a cascade of events in the fetal brain that are consistent with mitochondrially mediated apoptotic cell death, and a potential role for HNE in the proapoptotic responses to ethanol is presented.
The effects of age and liver disease on the disposition and elimination of diazepam in adult man.
TLDR
The constancy of diazepam clearance indicates that drug plasma concentrations will not accumulate any more in the old than the young, and chronic dosage modifications based on pharmacokinetic considerations are unnecessary.
In utero ethanol exposure elicits oxidative stress in the rat fetus.
Prior studies in our laboratory have shown that exposure of cultured fetal rat hepatocytes to ethanol (E) blocks epidermal growth factor-dependent replication and that this is paralleled by cell
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