Liver enzymes of 191 dengue cases with fatty liver / 中国人兽共患病学报

We explored the liver enzymes characteristics of dengue patients with fatty liver in Xishuangbanna,providing evi-dences for local dengue fever effective treatment program.The clinical data of 1 9 1 dengue patients with fatty liver and 1 9 1 ran-domized controls was retrospectively analyzed on the patients'mainly liver enzymes indicators in Xishuangbanna Prefecture from 2013 to 2015.Results showed that the 191 cases with fatty liver,the growth rate of such as alanine aminotransferase was 84.8%,aspartate aminotransferase was 90.1%,gamma glutamyltransferase was 76.8% and bilirubin index was 20.4%,except bilirubin index,the other 3 indicators in dengue patients with fatty liver were higher than those in the control group (P<0.05). The liver injury was serious for the dengue cases with fatty liver in Xishuangbanna,of those alanine aminotransferase,aspar-tate aminotransferase and gamma glutamyltransferase were significantly increased.These results suggested that doctors should pay attention to above 3 enzymes changes and take related treatments immediately as soon as dengue cases with fatty liver were detected.

In vitro studies of Raf-CREB, Akt-CREB, and CaMK II -CREB signal transduction pathway regulated by ginsenosides Rb1, Rg1 and Re / 中国中药杂志

<p><b>OBJECTIVE</b>Effects of ginsenoside Rb1, Rg1 and Re on neurotrophic factor signal transduction pathway using liposome-mediated transfection of eukaryotic cells approach.</p><p><b>METHOD</b>The injury model was established by treating SH-SY5Y cells with 0.6 mmol x L(-1) of corticosterone (CORT) by 24 h. SH-SY5Y cell were pretreated with CORT for 30 min followed by co-treated with 120,60 and 20 micromol x L(-1) of Rb1, 120, 80 and 40 micromol x L(-1) of Rg1 and 120, 80 and 40 micromol x L(-1) of Re for 24 h. Cells viability was determined by Cell Counting Kit (CCK) assay. CREB expressing Luciferase reporter gene was constructed and transfected with plasmid containing hRaf, hcAMP, hAkt, hCaMK gene into human embryonic kidney (HEK293) cells using liposornal transfection reagent lipofection 2000. The expression of CREB before and after it addion of Rb1, Rg1 and Re was examined by Luc assay system and Western blotting.</p><p><b>RESULT</b>Compared with normal control group, CORT significantly decreased the viability of SH-SY5Y cells to 67.21% (P < 0.01). CCK results show that Rb1 (60 micromol x L(-1)), Rg1 (80 micromol x L(-1)) and Re (80 micromol x L(-1)) on SH-SY5Y cells have significant protective effect (P < 0.01). Lucassay and Western blotting results show that the gene and protein levels of CREB increased significantly through the pathway of Raf and Akt with Rb1 and Rg1 (P < 0.01), Re can increase significantly the gene and protein levels of CREB through the pathway of Raf and CaMK II.</p><p><b>CONCLUSION</b>Rb1, Rg1 and Re protects SH-SY5Y cells from CORT-induced damage and the neuroprotective mechanism may be associated with the Raf-CREB, Akt-CREB and CaMK II -CREB pathways.</p>

FHL2 inhibits the Id3-promoted proliferation and invasive growth of human MCF-7 breast cancer cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Id3 plays a key role in the progression of breast cancer. Previously, four and a half LIM protein (FHL2) was identified as a repressor of Id family proteins by interacting with them. This study aimed to investigate the effects of FHL2 on the transcriptional regulation and oncogenic activities of Id3 in human breast cancer cells.</p><p><b>METHODS</b>Cell transfection was performed with SuperFect reagent. Stable transfectants that overexpressed Id3 were obtained by selection on G418. The level of Id3 protein was determined by Western blotting analysis. Dual luciferase assays were used to measure the effect of Id3 and FHL2 on E47-mediated transcriptional activity in MCF-7 human breast cancer cells. The MTT assay was used to measure cell proliferation. The transwell assay was used to measure the invasive capacity of MCF-7 cancer cells.</p><p><b>RESULTS</b>Id3 markedly repressed transcription mediated by the basic helix-loop-helix (bHLH) factor E47 in MCF-7 cells. This Id3-mediated repression was effectively antagonized by FHL2. Overexpression of Id3 markedly promoted the proliferation and invasive capacity of MCF-7 cells; however, these effects were significantly suppressed by the overexpression of FHL2.</p><p><b>CONCLUSIONS</b>FHL2 can inhibit the proliferation and invasive growth of human breast cancer cells by repressing the functional activity of Id3. The functional roles of FHL2-Id3 signaling in the development of human breast cancer need further research.</p>

Calcineurin is involved in cardioprotection induced by ischemic postconditioning through attenuating endoplasmic reticulum stress / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Ischemic postconditioning (I-postC) is a newly discovered and more amenable cardioprotective strategy capable of protecting the myocardium from ischemia/reperfusion (I/R) injury. Endoplasmic reticulum (ER) is a principal site for secretary protein synthesis and calcium storage. Myocardial I/R causes ER stress and emerging studies suggest that the cardioprotection has been linked to the modulation of ER stress. The aim of the present study was to determine whether cardioprotection of I-postC involves reduction in ER stress through calcineurin pathway.</p><p><b>METHODS</b>In the in vivo model of rat myocardial I/R, myocardial infarct size was measured by triphenyltetrazolium chloride (TTC) staining and apoptosis was detected using terminal eoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. Expression of calreticulin, C/EBP homologous protein (CHOP), caspase-12, and activation of caspase-12 in myocardium were detected by Western blotting. The activity and expression of calcineurin in myocardium were also detected.</p><p><b>RESULTS</b>I-postC protected the I/R heart against apoptosis, myocardial infarction, and leakage of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB). I-postC suppressed I/R-induced ER stress, as shown by a decrease in the expression of calreticulin and CHOP, and caspase-12 activation. I-postC downregulated calcineurin activation in myocardium subjected to I/R.</p><p><b>CONCLUSION</b>I-postC protects myocardium from I/R injury by suppressing ER stress and calcineurin pathways are not associated with the I-postC-induced suppression of ER stress-related apoptosis.</p>

Biochemical metabolic changes detected by phosphorus-31 MR spectroscopy in liver of fasting rabbits / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the biochemical metabolic changes detected by phosphorus-31 MR spectroscopy ((31)P MRS) with pathologic changes in the liver of fasting rabbits.</p><p><b>METHODS</b>A total of 22 rabbits were under the starvation up to death to establish animal models. Hepatic (31)P MRS was performed in different period of 10 rabbits including normal condition, over-starvation, agonal condition and death after 30 min. Other 9 rabbits were divided into three type including over-starvation, agonal condition and death group with 3 rabbits in each group, and 3 healthy rabbits served as controls. All the 12 rabbits were sacrificed for the hepatic pathological examination. The MR examination was performed on a 1.5 T imager using a 1H/31P surface coil by the 2D chemical shift imaging technique. The relative quantities of phosphomonoesters (PME), phosphodiesters (PDE), inorganic phosphate (Pi) and adenosine triphosphate (ATP) were measured.</p><p><b>RESULTS</b>All the relative quantification of phosphorus metabolites were changed significantly from starvation to death (X(2)=23.13-35.41, P<0.01). The relative quantifications of ATP of normal condition, over-starvation, agonal condition and death were 2.54 +/-0.53, 1.73 +/-0.14, 0.88 +/-0.23 and 0.05 +/-0.08, respectively (rs=1.0, P<0.01). The relative quantifications of PDE from normal to death were 1.25 +/-0.54, 2.76 +/-0.23, 3.33 +/-0.49 and 3.87 +/-0.43, respectively, and those of Pi were 0.42 +/-0.02, 0.65 +/-0.05, 0.89 +/-0.15 and 0.99 +/-0.08, respectively (rs=1.0, P <0.01). The relative quantifications of PME were also significantly changed (rs=0.4, P=0.6). The pathologic changes of normal condition, over-starvation, agonal condition and death: decreased size of hepatocytes, loss of cell number, cellular swelling, degeneration and cell necrosis or hepatic hemorrhage became more and more pronounced.</p><p><b>CONCLUSION</b>(31)P MRS can monitor dynamic changes of relative quantification of phosphorus metabolites, which are correlated with the pathological severity of acute hepatic injury by fasting.</p>

Stimulating effect of catechin, an active component of Spatholobus suberectus Dunn, on bioactivity of hematopoietic growth factor / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Hematopoietic growth factor (HGF) is indispensable to hematopoiesis in the body. The proliferation and differentiation of hematopoietic cells must rely on the existence and stimulation of HGF. This study investigated the effect of catechin, an active component extracted from Spatholobus suberectus Dunn (SSD), on bioactivity of granulocyte-macrophage colony-stimulating activity (GM-CSA), burst-promoting activity (BPA) and megakaryocyte colony-stimulating activity (MK-CSA) in spleen condition medium (SPCM) of mice to clarify the hematopoietic mechanism of catechin and SSD.</p><p><b>METHODS</b>Spleen cells of mice were separated and spleen condition medium (SPCM) was prepared from spleen cell culture. Bone marrow cells of mice were separated and cultured in a culture system including 10% (v/v) SPCM (induced by catechin in vivo or ex vivo) for 6 days. Granulocyte-macrophage colony forming units (CFU-GM), erythrocyte burst-colony-forming units (BFU-E) and megakaryocyte colony-forming units (CFU-Meg) formation were employed to assay the effects of different treatment on the bioactivity of GM-CSA, BPA and MK-CSA in SPCM.</p><p><b>RESULTS</b>SPCM induced by 100 mg/L catechin ex vivo could promote the growth of CFU-GM, BFU-E and CFU-Meg, which indicated that catechin could stimulate the production of GM-CSA, BPA and MK-CSA in SPCM. SPCM prepared at the fourth day of spleen cell culture showed the best stimulating activity. The bioactivity of GM-CSA, BPA and MK-CSA in the SPCM prepared after intraperitoneally injecting catechin into mice was also increased. The number of CFU-GM, BFU-E and CFU-Meg gradually increased as the dose of catechin increased and the time of administration prolonged. CFU-GM, BFU-E and CFU-Meg of the high-dose catechin group were significantly higher than those of the control group (P < 0.01) and reached the maximum at the seventh day after administration.</p><p><b>CONCLUSIONS</b>This study suggests that catechin extracted from the active acetic ether part of Spatholobus suberectus Dunn can regulate hematopoiesis by inducing bioactivity of GM-CSA, BPA and MK-CSA in SPCM of mice. This may be one of the mechanisms for the hematopoietic-supportive effect of catechin and Spatholobus suberectus Dunn.</p>

Post-coital gross hematuria: an unusual presentation of benign prostatic hyperplasia / 亚洲男科学杂志(英文版)

<p><b>AIM</b>To describe an unusual symptom of benign prostatic hyperplasia (BPH).</p><p><b>METHODS</b>A patient presented to our urology clinic having experienced post-coital gross hematuria for 2 years. He had not experienced lower urinary tract symptoms (LUTS). A series of examinations were performed to determine the source of bleeding.</p><p><b>RESULTS</b>The prostate was defined as the active bleeding source responsible for the patient's post-coital hematuria. Endoscopic fulguration did not alleviate the symptom. The use of dutasteride, a dual inhibitor of 5alpha-reductase, solved the problem.</p><p><b>CONCLUSION</b>This study reports for the first time that post-coital gross hematuria is one of the clinical presentations of BPH, which can be successfully treated with 5alpha-reductase inhibitor.</p>