Roles of smooth muscle 22α in vascular homeostasis and vascular remodeling / 生理学报

The research on the molecular mechanism of vascular injury has been a hot topic in recent years since the mechanism can be targeted for the treatment of vascular injury diseases. A large number of studies have found that vascular injury, repair and pathological remodeling are closely related to phenotype switching, abnormal proliferation and migration, and apoptosis of vascular smooth muscle cells (VSMCs). Smooth muscle 22α (SM22α) is a shape change and transformation sensitive F-actin-binding protein. SM22α decorates the contractile filament bundles within cultured VSMCs exhibiting differentiated phenotypes. In addition, SM22α is involved in regulation of cell signaling pathways related to vascular homeostasis and vascular remodeling. Here, we reviewed the recent research progress of SM22α in vascular homeostasis and remodeling.

FAK-related non-kinase plasmid transfection inhibited hepatic stellate cells proliferation / 中国应用生理学杂志

<p><b>AIM</b>To observe the effect of FAK-related non-Kinase (FRNK) plasmid on hepatic stellate cell (HSC) proliferation stimulated by fibronectin (FN).</p><p><b>METHODS</b>FRNK plasmid was transfected into HSC with transient liposomal transfection. The proteins of FRNK, FAK and p-FAK(Tyr397) were assayed by Western blotting analysis. The proliferation of HSC was evaluated by improved MTT assay, and cell cycle pattern was determined by flow cytometry (FCM).</p><p><b>RESULTS</b>(1) The expression of FRNK protein increased after FRNK transfected HSC, and it was at 48 h that the expression of FRNK protein was the highest (P < 0.01). The protein level of FAK was no significant difference between before FRNK plasmid transfection and after transfection (P > 0.05). The expression of p-FAK(Tyr397) protein was down-regulated after FRNK had been transfected in HSC, (P < 0.01). (2) The HSC proliferation inhibition rates at 12 h, 24 h and 48 h after FRNK transfection were 20.07%, 26.16%, 29.77%, respectively (P < 0.01). (3) Compared with the non-FRNK plasmid group, the FRNK-transfected HSCs almost arrested in G0/G1 phase (71.4 +/- 2.81 vs 48.9 +/- 1.66, P < 0.01).</p><p><b>CONCLUSION</b>After FRNK were transfected successfully in HSCs using lipofectamine, the phosphorylation of FAK was inhibited. The HSC proliferation was restrained in a time-dependent manner and the HSC was arrested in G0/G1 phase.</p>

Clinical characteristics of patients with hemorrhagic fever with renal syndrome / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>Patients with typical clinical manifestations of Hemorrhagic fever with renal syndrome (HFRS) are becoming fewer. We conducted analysis on clinical features of HFRS in order to reduce the mistakes in diagnosis.</p><p><b>METHODS</b>64 patients were diagnosed as HFRS during May, 2000 to June, 2006 in our hospital. All the patients' serological tests (HFRS-NP-specific IgM, IgG antibody) by ELISA method were positive. We collected their clinical manifestations and test results. SPSS 12.0 was used in our statistical analysis.</p><p><b>RESULTS</b>Among the 64 patients, 71.6% of all the cases occurred from Feb. to June. Most of patients were admitted to the hospital with untypical manifestation. Only 30.6% patients appeared headache, lumbago, and pain of orbital cavity. 32.8% patients had obviously signs of injection and hemorrhage. However, there were 90.6% patients with headache and 84.4% patients with nausea or vomit. Hypotensive or oliguric phases were absent in 56.3% patients. There were only 31.3% patients with all five stages. Thrombocytopenia (79.7%) and heavy proteinuria (71.9%) were common. But 54.7% of patients shown normal or even decreased white blood cell count. Only 2/3 of patients had elevated serum creatinine (Cr). Liver involved was common showing as elevated aminotransferase. ALT level was not always parallel to Cr level. There was an opposite trend between them.</p><p><b>CONCLUSION</b>We must recognized the untypical manifestations of HFRS. Further study focus on pathogenesis was useful for diagnosis and therapy.</p>

Study on anti-endotoxin of baicalin / 华西口腔医学杂志

<p><b>OBJECTIVE</b>To study the anti-endotoxin of different concentration baicalin.</p><p><b>METHODS</b>6.250 microg/mL, 3.125 microLg/mL, 1.562 microg/mL and 0.781 microg/mL baicalin solutions were mixed with I EU/mL endotoxin, respectively. The mixtures were put into water of (37+/-1) degrees C for 15 min, 30 min and 60 min. The degrading effects were determined by using limulus amebocyte lysate test (LAL test).</p><p><b>RESULTS</b>1) The degrading effect of 6.250 microg/mL, 3.125 microg/mL and 1.562 microg/mL baicalin solution on I EU/mL endotoxin was degraded completely in 15 min, 30 min and 60 min, respectively. 2)The degrading effect of 3.125 microg/mL, 1.562 microg/mL and 0.781 microg/mL baicalin solution on 1 EU/mL endotoxin after these mixtures had been incubated for 15 min. Endotoxin values were (0.155 5 +/- 0.002 8) EU/mL, (0.212 1+/-0.004 9) EU/mL, (0.355 9+/-0.013 9) EU/mL, respectively. These differences among them were statistically significant (P<0.01). 3) The degrading effect of 1.562 microg/mL and 0.781 microg/mL baicalin solution on 1 EU/mL endotoxin after these mixtures had been incubated for 30 min. Endotoxin values were (0.1640+/-0.0025) EU/mL and (0.2094+/-0.004 4) EU/mL, respectively. These differences between them were statistically significant (P<0.01).</p><p><b>CONCLUSION</b>The action of anti-endotoxin of baicalin is dose-dependent and time-dependent. The results show that baicalin has the stronger anti-endotoxin effect.</p>