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We have determined the nucleotide sequence of ribosomal 5S RNA from bovine liver. The comparison of this sequence with those from other cukaryotic sources shows that a common secondary structure model for all eukaryotic 5S rRNAs may exist Analysis of the evolution­ary conserved nucleotides in metazoan 5S rRNAs suggests that the tertiary interactions, proposed earlier for plant 5S rRNA, are also possible.
Recent studies on the structure and function of the tartrate-resistant acid phosphatase (Mr 38 000) of the frog liver arc reviewed. The nature of the enzyme heterogeneity is elucidated on a molecular and physiologi­cal basis. The following structure-activity relationship is proposed: the enzyme protein is modified by glycosylation processes leading to forma­tion of the different enzyme forms. The oligosaccharide chain stabilizes the final structure of the enzyme forms with altered conformation causing different exposure of the essential functional groups (e.g. sulfliydryl residues, antigen determinants). This leads to different physiological events necessary for fulfillment of metabolic requirements of the cell.
Pathomorphological Changesin the Small Intestine and Liver of the European Beaver (Castor fiber L. 1758): a case study.The aim of thestudy was to examine and describe the morphology and patomorphology of small intestine and liver of European beaver (Castor fiber). In natural environment beavers are in constant contact with various both internal and external parasites. Histological analysis revealed the pathological changes within the digestive track and liver indicating long-term inflammation. It was hypothesized that the observed inflammation was caused by the parasites not related to beavers so far.
The apoptotical effect of nitric oxide on effector apoptotical caspase 3 in rats' hepatocytes was examined. The experiment was performed on 16 white Wistar female rats divided into two equal groups. The rats from the experimental group received orally L-arginine in a dose of 40 mg/kg b.w. every other day for 2 weeks. The rats from the control group received orally 2 ml of distilled water in the same manner as the experimental group. All the rats were decapitated after 3 weeks of the experiment. After decapitation, specimens from the liver were collected, fixed in 10% formalin, and then embedded in paraffin blocks. Protein caspase 3 on slides was detected using the standard three-step immunohistochemical method. The quantitative evaluation of caspase 3 expression showed that the area occupied by positive caspase 3 reaction in the liver of the experimental group (128.11 µm²±96.54) was comparable to that in the control group (212.18 µm² ±1 16.59) (P=0.25). The dose of L-arginine used was similar to that applied in pregnant women treated for gestosis. The study shows that L-arginine as a donor of exogenous nitric oxide has no an apoptotic effect on rats' hepatocytes.
The experiment was carried out on 90 Swiss male mice divided into 9 groups (n=10). Over 4, 10 and 14 days mice of three control groups (I-III) were injected with 250 μl 0.9% NaCl solution daily, and those from six experimental groups (A-F) with 250 μl 0.9% NaCl solution containing 20 or 30 mg morphine hydrochloride per kg body weight. The injections were given intramuscularly once a day between 9:00-10:00 a.m. for 4, 10 and 14 days. In the lysosomal fraction of the liver and kidney the activities of acid phosphatase, lysosomal esterase, β-glucuronidase, β-galactosidase, and β-N-acetyl-hexosaminidase were estimated. Morphine increased the activity of all examined enzymes except EL, which activity was statistically proven to decrease in liver and kidneys after 10 days morphine administration in both doses.
Hepatic stellate cells play a crucial role in the development of liver fibrosis. In a damaged liver, stellate cells undergo activation, which is manifested as a change of their phenotype: differentiation of stellate cells to myofibroblast-type cells, expression of alpha-Smooth Muscle Actin, their proliferation and a reduction in the size of cytoplasmic lipid droplets. The aim of this study was to determine the number and morphology of stellate cells in the canine liver affected by congenital portosystemic shunt (PSS) and portal vein hypoplasia – hepatic microvascular dysplasia (PVH-HMD). The material for investigation were archived paraffin blocks with liver samples collected supravitally from six dogs with PSS, six dogs with PVH-HMD and six healthy dogs. On the HE-stained sections, the number of stellate cells per 100 hepatocytes was counted (Sztark method) and the diameter of veins in the hepatic triads was measured (light microscope Olympus BX 43, SC30 camera, CellSens Entry 2011 Olympus). In addition, the diameter of lipid droplets in stellate cells was measured (computed image analysis system LUCIA 4.21). The results were analysed statistically (the Kruskal-Wallis test followed by Dunn’s post-hoc procedure; significance level (α) at 0.05; Statistica 12 StatSoft Inc.). The degree of liver fibrosis was determined (Masson’s method of slide stain; Scheuer scale). The liver samples from the dogs with PSS and PVH-HMD were stained immunohistochemically with Monoclonal Mouse Anti-Human Smooth Muscle Actin (α-SMA), clone 1A4, antibodies (DAKO). Portosystemic shunt and primary portal vein hypoplasia in the dog results in a reduction in the diameter of portal vein branches and in insufficient portal blood flow through the liver. In the material investigated, this was particularly evident in the animals affected by PSS: such dogs had a significantly smaller diameter of the veins than did the healthy dogs (p < 0.001) or the dogs with PVH-HMD (p = 0.023). Fibrosis and the expression of α-SMA were stronger in the dogs with PSS than in those with PVH-HMD. Moreover, the dogs with PSS had a significantly higher average number of stellate cells than the healthy animals (p = 0.007) did. However, the examination of the material revealed an enlargement of cytoplasmic lipid droplets: the dogs with PSS had a significantly larger diameter of lipid vacuoles in the cytoplasm of stellate cells than did the healthy animals (p < 0.001) or the dogs with PVH-HMD (p = 0.043); the dogs with PVH-HMD had lipid droplets with a significantly larger diameter than the healthy animals (p < 0.001) did. Hypoperfusion of the liver and the accompanying regressive lesions in hepatocytes result mainly in an increased number of stellate cells and stronger expression of α-SMA, while cytoplasmic lipid droplets in the stellate cells are not reduced in size. The present study indicates the need for detailed analyses of clinical cases and warrants further comprehensive studies of comparative hepatopathology because it demonstrates differences between humans and dogs in the morphological indicators of hepatic stellate cell activation in chronic liver damage.
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