NUTRITIONAL LIPID LIVER DISEASE OF GRASS CARP CTENOPHARYNGODON IDULLUS(C.et V.)

The inadequate nutrient content of pellet feeds widely used in recent years in China for grass carp forming led to lipid liver degeneration in the fish. The present studies show that the pathological features of lipid liver disease are anaemia and hepatic ceroidosis. Other clinical features are: the ratio of liver to body weight exceeds 3% and lipid content exceeds 5%. Extreme infiltration of hepaiocytes by lipid results in the following deteriorative effects: swelling of the liver cells, increase of lipid droplets in the cytoplasm and dislocation of the nucleus, loss of cytoplasm staining affinity, and increased activities of GOT and GPT in serum. Lipid liver degeneration of grass carp can be divided into three stages: 1) deposition of liver lipid; 2) lipid infiltration of hepatic parenchyma; 3) atrophy of liver nucleus. The causes of lipid liver degeneration are complicated, but the main cause is assumed to be an imbalance of nutrients in daily feed and the lack of some lipotropic substances.

Induction of apoptosis by TPA and VP-16 is through translocation of TR3

AIM: To investigate the role of TR3 in induction of apoptosis in gastric cancer cells. METHODS: Human gastric cancer cell line, MGC80-3, was used. Expression of TR3 mRNA and its protein was detected by Northern blot and Western blot. Localization of TR3 protein was showed by immunofluorescence analysis under laser-scanning confocal microscope. Apoptotic morphology was observed by DAPI fluorescence staining, and apoptotic index was counted among 1000 cells randomly. Stable transfection assay was carried out by Lipofectamine. RESULTS: Treatment of MGC80-3 cells with TPA and VP-16 resulted in apoptosis, accompanied by the repression of Bcl-2 protein in a time-dependent manner. At the same time, TPA and VP-16 also up-regulated expression level of TR3 mRNA in MGC80-3 cells that expressed TR3 mRNA. When antisense-TR3 expression vector was transfected into the cells, expression of TR3 protein was repressed. In this case, TPA and VP-16 did not induce apoptosis. In addition, TPA and VP-16-induced apoptosis involved in translocation of TR3. In MGC80-3 cells, TR3 localized concentrative in nucleus, after treatment of cells with TPA and VP-16, TR3 translocated from nucleus to cytosol obviously. However, when this nuclear translocation was blocked by LMB, apoptosis was not occurred in MGC80-3 cells even in the presence of TPA and VP-16. CONCLUSION: Induction of apoptosis by TPA and VP-16 is through induction of TR3 expression and translocation of TR3 from nucleus to cytosol, which may be a novel signal pathway for TR3, and represent the new biological function of TR3 to exert its effect on apoptosis in gastric cancer cells.

CYTOPLASMIC EFFECT OF Xenopus laevis ON NUCLEAR FUNCTION OF ITS ALBINO MUTANT

The nucleo-cytoplasmic interactions have been studied by many investigators and it is well established that nucleus and cytoplasm are interdependent and interacting. We have studied the effects of the cytoplasm of wild-type Xenopus

ULTRASTRUCTURAL EVIDENCE OF THE CYTO PLASMIC ASSEMBLY OF NUCLEOCAPSIDS OF HERPES SIMPLEX VIRUS TYPES 1 AND 2 BYTHIN SECTION AND IMMUNOFERRITIN ELECTRON MICROSCOPY

There is general agreement that herpesvirus nucleocapsid assembly occurs in the nucleus of infected cells.However, we have seen ultrastructural evidence suggestive of concurrent cytoplasmic assembly ofherpes simplex virions by bothroutine and immunoferritin electron microscopy.Complete and incomplete particles-resembling nucleocapsids formed in the nucleus were observedin the cytoplasm.

FoxO mediates APP-induced AICD-dependent cell death

Supported financially by the National Natural Science Foundation of China,Prof.Xue Lei’s group at Shanghai Key Laboratory of Signaling and Disease Research,School of Life Science and Technology,Tongji University published a research article in Cell Death and Disease(2014,5:e1233),entitled"FoxO mediates APP-induced AICD-dependent cell death".

Impaired XPO5 function leads to transportation failure of microRNA precursor

MicroRNAs（miRNAs）constitute a class of small non-coding RNAs that participate in various biological processes by repressing protein translation or destabilizing target mRNAs.miRNA biogenesis begins with the transcription of primary miRNAs（pri-miRNAs）in the cell nucleus,which are then cleaved by the Drosha/DGCR complex into precursor miRNAs（pre-miRNAs）.The pre-miRNAs are transported by exportin-5（XPO5）from the nucleus to the cytoplasm,