Hepatoprotective effects of 6(5H)-phenanthridinone from chemical-induced centrilobular necrosis.

Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme involved in the detection of DNA strand termini. Extensive cellular damage can overactivate PARP-1, which rapidly depletes the cellular stores of NAD+ and ATP, resulting in necrotic cell death. The purpose of the present study was to determine whether 6(5H)-phenanthridinone, a potent inhibitor of PARP-1, could attenuate the hepatotoxicity of carbon tetrachloride (CCl4).

Somatostatin receptor profiling in hepatic metastases from small intestinal and pancreatic neuroendocrine neoplasms: immunohistochemical approach with potential clinical utility.

Background: The expression of somatostatin receptors (SSTRs) on endocrine tumor (ET) cells forms the basis for somatostatin analog treatment of patients with SSTR-positive, hormonally active ETs. In patients with SSTR-negative ETs, the clinical response is generally absent or suboptimal, while nonfunctioning ETs with SSTR positivity show a variable response to such therapy.

Methods: We retrospectively studied SSTR subtype expression in hepatic metastases from 14 adult patients with primary endocrine carcinomas (ECAs) of the small intestine and pancreas and compared SSTR subtype expression among the primary and metastatic ECAs.

Hepatocellular accumulation of poly(ADP-ribose) in male ICR mice treated with a necrogenic dose of carbon tetrachloride.

Overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) in response to oxidative stress has been shown to contribute to necrotic cell death by consuming NAD+ and ATP. In the present study, PARP-1 overactivation was determined by identifying the distribution and accumulation of poly(ADP-ribose) following intraperitoneal administration of a hepatotoxic dose of carbon tetrachloride (572 mg/kg). Treated animals exhibited lipid peroxide levels 16.

Development of flattening and apparent fragmentation following ischemic necrosis of the capital femoral epiphysis in a piglet model.

Background: The repair response that follows ischemic necrosis of the immature femoral head and the biological processes that are responsible for the development of femoral head deformity and fragmentation have not been clearly defined. A piglet model was used to study the radiographic and histopathologic changes that occur prior to and during the development of femoral head deformity and fragmentation following ischemic necrosis.

Methods: Twenty-five male piglets were studied.