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1.
Indian J Pathol Microbiol ; 2022 Sept; 65(3): 572-580
Article | IMSEAR | ID: sea-223381

ABSTRACT

Background: Neonatal cholestasis is caused by a group of diseases that cause jaundice, which can be encountered in the neonatal period. Biliary atresia (BA) and idiopathic neonatal hepatitis (INH) are among neonatal cholestasis diseases. Aims: The aim of this study was to perform histopathological and ultra-structural examinations of liver biopsy tissue samples from BA and INH patients with liver biopsies taken during laparotomy to confirm the diagnosis of biliary atresia. Settings and Design: A total of patients undergoing Kasai surgery before the age of 60 days were included in an “early” group (n = 7), whereas patients undergoing surgery after the age of 60 days were included in a “late” group (n = 11). The control group (n = 11) included INH patients. Materials and Methods: For histopathological examinations, liver tissue samples obtained intra-operatively were subjected to routine histopathological procedures after being stained with caspase-3 and cytokeratin-7 antibodies. Ultra-structural evaluations were also performed. Statistical analysis used: For comparisons between the groups, a one-way analysis of variance (ANOVA) test and the Mann–Whitney U test were used for continuous variables. Results: Histopathological findings reflected the specific liver pathologic findings seen in biliary atresia. Although there was no significant difference between the BA groups, these parameters were not detected in the control group. The histopathological evaluations revealed no significant differences in the findings of liver parenchyma damage between the early, late, and control groups. Electron microscopic examinations showed that the patients in the late group had more severe signs of intra-cellular damage to the liver. Conclusions: Although the histopathological examination revealed no significant differences in liver damage between the three groups, in ultra-structural evaluation, intra-cellular damage was found to be less in groups with better prognosis. Electron microscopy evaluations of intra-cellular damage may be more useful in this respect.

2.
Braz. j. med. biol. res ; 42(9): 776-782, Sept. 2009. ilus, tab
Article in English | LILACS | ID: lil-524324

ABSTRACT

The aim of this study was to evaluate the role of oxidative damage in pancreatitis-induced hepatic injury. Thirty-five rats were divided into five groups (each of 7 rats): control, cerulein (100 µg/kg body weight), cerulein and pentoxifylline (12 mg/kg body weight), cerulein plus L-NAME (10 mg/kg body weight) and cerulein plus L-arginine (160 mg/kg body weight). The degree of hepatic cell degeneration differed significantly between groups. Mean malondialdehyde levels were 7.00 ± 2.29, 20.89 ± 10.13, 11.52 ± 4.60, 18.69 ± 8.56, and 8.58 ± 3.68 nmol/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Mean catalase activity was 3.20 ± 0.83, 1.09 ± 0.35, 2.05 ± 0.91, 1.70 ± 0.60, and 2.85 ± 0.47 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively, and mean glutathione peroxidase activity was 0.72 ± 0.25, 0.33 ± 0.09, 0.37 ± 0.04, 0.34 ± 0.07 and 0.42 ± 0.1 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Cerulein-induced liver damage was accompanied by a significant increase in tissue malondialdehyde levels (P < 0.05) and a significant decrease in catalase (P < 0.05) and GPx activities (P < 0.05). L-arginine and pentoxifylline, but not L-NAME, protected against this damage. Oxidative injury plays an important role not only in the pathogenesis of AP but also in pancreatitis-induced hepatic damage.


Subject(s)
Animals , Female , Rats , Lipid Peroxidation/drug effects , Liver Diseases/etiology , Pancreatitis/complications , Reactive Oxygen Species/metabolism , Acute Disease , Arginine/pharmacology , Ceruletide , Free Radical Scavengers/pharmacology , Liver Diseases/pathology , Liver Diseases/prevention & control , NG-Nitroarginine Methyl Ester/pharmacology , Pancreatitis/chemically induced , Pancreatitis/metabolism , Pentoxifylline/pharmacology , Rats, Wistar
3.
Indian J Exp Biol ; 2000 Oct; 38(10): 1020-5
Article in English | IMSEAR | ID: sea-56991

ABSTRACT

Mouse renal carcinoma (renca) cells growing exponentially in foetal bovine serum (1%) supplemented with selenium (1 microM, sodium selenite) were exposed to oxidative insult. It was found that glutathione peroxidase activity increased (44%), while the activities of catalase, glutathione disulfide reductase, and level of total glutathione did not change due to selenium supplementation. Selenium supplementation made renca cells susceptible to tert-butylhydroperoxide induced cell death, while it did not affect the viability when the cells were exposed to hydrogen peroxide. It suggested that the contribution of glutathione peroxidase in antioxidant defense mechanism of renca cells was possibly not crucial and the function of catalase might be important especially against hydrogen peroxide.


Subject(s)
Animals , Carcinoma, Renal Cell/pathology , Cell Survival/drug effects , Kidney Neoplasms/pathology , Mice , Selenium/administration & dosage , Tumor Cells, Cultured , tert-Butylhydroperoxide/toxicity
5.
JAMC-Journal of Ayub Medical College-Abbotabad-Pakistan. 1991; 4 (1): 23-8
in English | IMEMR | ID: emr-20122

ABSTRACT

One hundred and thirty cases over a period of five years are included in this study. Duration of the disease, duration of perforation, age, sex and various surgical treatments are analysed. Prognostic factors and causes of mortality and morbidity are discussed. Minimum surgical intervention is preferred, as mortality is increased in extensive surgical procedure, in already sick and toxic patients


Subject(s)
Ileum/physiopathology , Blood Transfusion , Biopsy , Chloramphenicol/administration & dosage
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