Objective To discuss the clinical value of procalcitonin (PCT) in guiding antibiotics use in children with severe diseases. Methods The clinical data of patients admitted to intensive care unit from January 2012 to July 2012 were retrospectively analyzed. The patients without antibiotics use before admission and with procalcitonin level less than 0.5 ng/ml on admission were selected. The body temperature, infection indicators and prognosis were compared between patients with and without antibiotics use during hospitalization. Results There was no difference in body temperature, PCT, C-reactive pro-tein (CRP), erythrocyte sedimentation rate (ESR) and white blood cell count (WBC) on admission between patients with and without antibiotics use during hospitalization. The PCT level was increased signiifcantly (P<0.05) on the day of starting the an-tibiotics when compared with that on admission in 60 patients while there was no change in the levels of WBC and CRP. Com-pared with the day of starting the antibiotics, body temperature declined (P<0.05) and PCT level in 56 patients reexamined was decreased (P<0.05) at 3 days after antibiotics use. Two hundred and eleven patients (98.14%) had favorable prognosis. Conclu-sions Monitoring PCT can guiding the clinical use of antibiotics.

Objective To investigate the effects of morroniside on the expression of vascular endothelial growth factor (VEGF) and fi-broblast growth factor-2 (FGF-2) in rat cortex after focal cerebral ischemia-reperfusion. Methods 30 male Sprague-Dawley rats were ran-domly divided into sham group, model group, morroniside-low group (30 mg/kg), morroniside-middle group (90 mg/kg) and morroni-side-high group (270 mg/kg). Middle cerebral arteries of rats were occluded for 30 minutes with Longa's method and re-perfused. The ex-pression of VEGF and FGF-2 in the ischemic ipsilateral cortex was detected with Western blotting 7 days after reperfusion. Results The ex-pression of both VEGF and FGF-2 increased in the ischemic ipsilateral cortexin in all the ischemic groups compared with the sham group (P<0.05). The expression of VEGF further increased in a dose-dependent manner in all the morroniside groups compared with that of model group (P<0.05), and the expression of FGF-2 increased in the morroniside-high group (P<0.001). Conclusion Morroniside could increase the expression of VEGF and FGF-2 after ischemia-reperfusion, which might promote angiogenesis.

Objective To explore the effects of morroniside on the expression of CD34 in ipsilateral cortex of rats after focal cerebral isch-emia-reperfusion. Methods 45 male Sprague-Dawley rats were divided into sham group (n=9), ischemia group (n=9), and morroniside groups (low, medium and high dosage groups, n=9). The middle cerebral artery were occluded for 30 minutes, and reperfused. Morroniside was administered intragastrically once a day at dose of 30 mg/kg, 90 mg/kg, 270 mg/kg after operation. The expression of CD34 in the isch-emic ipsilateral cortex were detected with immunohistochemistry (n=6) and Western blotting (n=3) 7 days after operation. Results The ex-pression of CD34 increased in the ischemia group compared with the sham group, and further increased in the morroniside groups of high dos-age compared with the ischemia group (F>14.865, P<0.001). Conclusion Morroniside could increase the expression of CD34 in the ischemic ipsilateral cortex after ischemia-reperfusion in rats, which may promote the angiogenesis and neurogenesis after ischemia.

Objective To evaluate the effect of dexmedetomidine pretreatment on the expression of mitochondrial transcription factor A ( TFAM) and succinate dehydrogenase ( SDHA) during lung ischemia-reperfusion ( I∕R) in mice. Methods Twenty-four clean-grade healthy male C57BL∕6J mice, aged 8-10 weeks, weighing 18-22 g, were divided into 3 groups ( n=8 each) using a random number table method:sham operation group ( group S ) , lung I∕R group ( group I∕R ) and dexmedetomidine pretreatment group ( group D) . In I∕R and D groups, lung I∕R was induced by clamping the left pulmonary hilum for 60 min followed by 120-min reperfusion in anesthetized mice. The chest was only opened, but the left pulmonary hilum was not occluded in group S. Dexmedetomidine 25μg∕kg was intraperitoneally injected at 30 min be-fore ischemia in group D, while the equal volume of normal saline was given instead of dexmedetomidine in I∕R and S groups. The mice were sacrificed at 120 min of reperfusion, and lungs were removed for determi-nation of wet∕dry weight ratio ( W∕D ratio) , cell apoptosis ( by TUNEL) and expression of TFAM and SDHA mRNA in lung tissues ( by real-time polymerase chain reaction ) and for examination of the pathological changes of lung tissues. The apoptosis index was calculated. Results Compared with group S, the W∕D ratio, apoptosis index and lung injury scores were significantly increased, and the expression of TFAM and SDHA mRNA was down-regulated in I∕R and D groups ( P<0. 05) . Compared with group I∕R, the W∕D ra-tio, apoptosis index and lung injury scores were significantly decreased, and the expression of TFAM and SDHA mRNA was up-regulated in group D ( P<0. 05) . Conclusion The mechanism by which dexmedeto-midine pretreatment attenuates lung I∕R injury is related to up-regulating the expression of TFAM and SDHA in mice.

Diabetic foot(DF)is one of the most severe chronic complications of diabetes mellitus(DM),and it is an important cause of disability and mortality inpatients with DM.Changes in proteins in the tissues,organs and circulation of organisms can serve as microscopic reflections of the disease development process.Proteomics is an important technologyto explore the pathogenesis and treatment mechanism of dis-ease,and to find potential therapeutic targets and prognostic biomarkers of diseases.This article reviews the progress of proteomics research in DF.

Objective To investigate the changes of sex hormone and androgen receptor levels and evaluate the relationship of the sex hormones and androgen receptor with coronary heart disease (CHD) in elderly men. Methods A cross-sectional study was performed in 539 elderly men, including 400 healthy people aged 62-92 years and 139 CHD patients aged 60-88 years. The plasma concentrations of total testosterone (TT), free testosterone (FT), dehydroepiandrosterone sulfate (DHEAS), sex hormone binding globulin (SHBG), estradiol (E2), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured. The androgen receptor (AR) level was tested by flow cytometry. Results The fluorescence intensity of DHEAS, TT, SHBG, FT and AR were significantly lower in CHD group than in healthy group (P<0.01);however, FSH and E2 in CHD group were higher(P(0.01). Age was negatively correlated with TT(r=-0.28,P<0.01) and FT (r=-0.17,P<0.05), and positively correlated with SHBG(r=0.14,P<0.05) and E2 (r=0.33, P<0.01). AR fluorescence intensity was negatively correlated with systolic blood pressure (r=-0.12,P<0.01). Logistic regression analysis indicated that TT (OR=1.065,9% CI: 1.012～1.121,P<0.05), SHBG(OR=0.994,95% CI:0.990～0.998,P<0.01) and AR (OR=0.971,95%CI:0.956～0.986, P<0.01)were significantly associated with CHD in elderly male patients. Conclusions The levels of DHEAS, TT, SHBG, FT and AR are lower in elderly men with CHD than in elderly healthy men;however, the FSH and E2 concentrations are higher. Low levels of TT, SHBG and AR may be the independent risk factors for CHD in elderly men.

Cardiovascular disease is a health hazard to humans and systolic heart failure due to myocardial infarction is a major cause of death.It was previously thought that myocardial cells of the adult mammalian heart possess a limited ability to proliferate and self-renew.However,it has been widely reported that mammals have the ability to regenerate the myocardium,which is restricted to early postnatal life,and that it is strong enough to repair damaged heart tissue.The discovery of myocardial regeneration in neonatal hearts has provided an ideal animal model to investigate the mechanisms that affect myocardial regeneration,and many mechanisms that reverse myocardial cell cycle arrest and promote myocardial regeneration have been revealed.In this article,we review the factors affecting gene expression for myocardial regeneration(e.g.,ncRNAs and transcription factors),myocardial regeneration-related signaling pathways,and the regulation of myocardial regeneration by non-myocardial cells(e.g.,extracellular matrix,immune response,and epicardium)to provide directions for achieving myocardial regeneration after myocardial injury in adult mammals.

Objective:To evaluate the cerebral infarct volume and the nerve fiber connectivity between cortical and neurogenesis-related regions in the mouse model of reperfusion after middle cerebral artery occlusion (MCAO) by 11.7 Tesla(11.7 T) magnetic resonance imaging (MRI).Methods:MCAO models were established in SPF grade adult male C57BL/6 mice using the suture-occluded method.MRI scans were performed at 3 days before and 1 day after modeling.Infarct volumes were calculated, and nerve fiber tracking was performed on specific brain regions to analyze the nerve fiber number and the parameters of fractional anisotropy(FA), mean diffusivity(MD), axial diffusivity (AD)and radial diffusivity(RD). SPSS 26.0 was used for statistical analysis, and paired t test was used to compare the data before and after modeling. Results:(1) After MCAO-induced ischemia, the infarct volume was up to (35.11±17.57)mm 3, and the FA value of the infarct area was significantly reduced compared with that of before modeling( t=4.73, P<0.01). (2) At the anterior-posterior(AP): + 1.2 mm section, the results of fiber tracking showed that compared with before modeling, the number of fiber bundles originating from the dorsal horn of the lateral sub-ventricle zone(SVZ)to the cortex reduced ((92 584.20±14 751.00) vs (59 815.60±6 752.46), t=4.87, P<0.01), and the number of fiber bundles projected to the infarcted area reduced ((107 671.40±10 497.57) vs (61 658.60±10 178.21), t=6.43, P<0.01). FA, AD, MD, and RD values were all decreased in different degrees( t=3.38-6.43, all P<0.05). (3) At the AP: -3.8 mm section, the number of fiber bundles originating from the dorsal horn of the SVZ to the cortex decreased (after modeling(96 944.00±18 331.09), before modeling(58 767.80±16 445.25), t=2.99, P<0.05), and the values of FA, AD, MD and RD decreased after ischemia ( t=7.30, 5.05, 6.74, 4.13, all P<0.05). Conclusion:The ultra-high field strength of 11.7 T MRI can accurately detect the following results that the number of nerve fiber bundles from the SVZ to the cortex or infarct area are both significantly reduced, and diffusion tensor parameters are consistently changed in mice after 1 day of ischemia-reperfusion.