Objective To investigate the alteration of chaperone hsp40 and its effects on the dealyed neuron death in the CAI neurons after transient cerebral ischemia.Method Twenty-minute transient global ischemia rat model was used.Following different repeffusion period,all the 28 wistar rats were divided into sham-operation group ,4-hour recovery group,24-honr recovery group and 72-hour recovery gronp,7 ratsin in each group,Immunochemistry and laser scanning confocal microscopy were used to observe the distributional alteration of hsp40 in the neurons.Differential centrifuge and westemblot analysis were used to analyze the quantitative alteration of hsp40 and its redistribution in the neurons.Results lnanunechemistry and laser scanning confocal microscopy showedthe reduction of hsp40 first in cytosol,then in the nucleus until all the neurons in the CAI region died.Differential centrifuge and westemblot analysis showed the quantity of hsp40 decreased from (1.00_+0.21) to (0.23±0.13)(P<0.01) after 24-hour repeffusion;the quantity of hsp40 in the protein aggregates increased from (1.00±0.18) to(8.61±1.89)(P<0.01) after24-hour reperfusion.Conclusions The reduction of hsp40 in the neurons of hippocampus CA1 region is an important factor resulting in protein aggregates formation.

Objective:To summarize the preliminary experience of endoscopically assisted mid-cheek benign tumor resection using a single preauricular or transoral incision and to evaluate its indications, advantages, and disadvantages.Methods:Thirty-six patients with benign mid-cheek tumors were prospectively enrolled, including 11 males and 25 females, aged (37.2± 15.9) years and ranged from 11 to 65 years old. The patients were randomly divided into two groups: endoscope-assisted tumor dissections through a single preauricular incision (preauricular group, 19 cases) or transoral incision (transoral group, 17 cases). Their surgical approaches were introduced, and the tumor long-axis length, incision length, operative time, estimated intraoperative bleeding, postoperative drainage amount and time, aesthetic satisfaction, perioperative complications, and follow-up were recorded and analyzed.Results:The difference between the tumor long-axis lengths in the preauricular group [(2.2±0.9) cm] and the transoral group [(2.1± 0.7) cm] was not statistically significant ( t=0.46, P=0.687), and all surgical procedures were completed as planned. There was no significant difference in the incision size ( t=1.57, P=0.100) or operative time ( t=0.44, P=0.736). Compared with the preauricular group [(30.8±8.7) ml], transoral group [(23.6±8.9) ml] significantly reduced intraoperative blood loss ( t=2.97, P=0.006) and improved aesthetic pleasure ( t=3.44, P=0.015). Two cases of earlobe numbness and one case of temporary facial palsy were observed in the preauricular group; two cases of postoperative effusion were noted in the transoral group, and no signs of nerve injury were detected. No tumor recurrence was found during the 1-54-month of follow-up. Conclusions:Endoscopic-assisted preauricular or transoral incision for dissecting mid-cheek benign tumors provides excellent aesthetic and minimally invasive results, reducing complications and obtaining satisfactory aesthetic results.

ObjectiveTo clarify the repair effect of Mume Fructus on the intestinal mucosal epithelial barrier in the mouse model of inflammatory bowel disease （IBD） and explore the repair mechanism. MethodsThirty-six male C57BL/6 mice were randomly assigned into six groups： normal， model， low-， medium-， and high-dose （200， 400， and 800 mg·kg^-1） Mume Fructus， and sulfasalazine （300 mg·kg^-1）. Except the normal group， the rest groups had free access to 2% dextran sulfate sodium （DSS） solution for seven days to establish the IBD model， followed by a seven-day drug intervention. The body weight change and disease activity index （DAI） were recorded. After the last administration， spleen and colon tissue samples were collected to analyze the differences in colon length and spleen index. Hematoxylin-eosin staining was used to observe the morphology of the colon tissue. The level of diamine oxidase （DAO） in the serum was measured by the DAO assay kit. Immunohistochemistry was employed to determine the expression of tight junction proteins such as Claudin-1， Occludin， and zonula occludens-1 （ZO-1） in the colon tissue. Real-time PCR was performed to measure the mRNA levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in the colon tissue. Finally， Western blot was employed to determine the protein levels of mitogen-activated protein kinase kinase （MEK）， extracellular signal-regulated kinase （ERK）， phosphorylated （p）-MEK， and phosphorylated ERK in the colon tissue. ResultsCompared with the normal group， the model group exhibited decreases in body weight and colon length （P<0.01）， increases in DAI， spleen index， and serum DAO level （P<0.01）， damaged colonic epithelium and goblet cells， and obvious infiltration of inflammatory cells. In addition， the model group exhibited higher positive expression of Claudin-1， Occludin， and ZO-1 （P<0.01）， higher mRNA levels of TNF-α and IL-1β （P<0.01）， and higher protein levels of p-MEK and p-ERK （P<0.05， P<0.01） than the normal group. However， sulfasalazine and three doses of Mume Fructus markedly decreased the body weight and DAI （P<0.05）， recovered the colon length and spleen index， alleviated colon tissue damage， lowered the level of DAO in the serum （P<0.01）， and down-regulated the mRNA levels of TNF-α and IL-1β （P<0.01） and the protein levels of p-MEK and p-ERK （P<0.05）. Sulfasalazine and low- and medium-dose Mume Fructus increased the positive expression of Occludin， Claudin-1， and ZO-1 （P<0.05， P<0.01）. Furthermore， high-dose Mume Fructus elevated the protein expression of Occludin （P<0.05）. ConclusionMume Fructus can restore the expression of intestinal epithelial tight junction proteins by inhibiting the phosphorylation of proteins in the MEK/ERK signaling pathway and down-regulating the levels of TNF-α and IL-1β， thus repairing the intestinal mucosal barrier in the mouse model of IBD.