目的探讨辽宁省机关干部肥胖的患病率及其危险因素以及肥胖与其他代谢异常的关系。方法对辽宁省1680名机关干部随机抽样进行体格检查,并进行肥胖患病率的流行病学调查。结果本组人群肥胖患病率为20.42%,其中男性27.8%,女性21.9%,男女性之间有显著性差异(P<0.05);不同年龄组间肥胖患病率亦有显著性差异,其中以40～50岁中青年干部肥胖患病率最高,为26.25%;肥胖与生活方式及其他代谢异常密切相关。结论中青年机关干部的肥胖患病率明显高于中老年组,且与不良生活方式有关,同时合并有其他代谢紊乱。

AIM: To investigate the role of gene poly mo rphisms of insulin receptor substrate-1 (IRS-1) in northern Chinese Han pedigree s with type 2 diabetes mellitus (DM). METHODS: Polymorphisms in codon 804 and 971 of IRS-1 gene in 80 unrelated patients with type 2 DM and 80 control subjects were analyzed by polym erase chain reaction-sequence specific primer(PCR-SSP) technique followed by pol yacrylamide gel electrophoresis and silver staining. RESULTS: The frequencies (GCA→GCG) in codon 804 of IRS-1 gene w ere significantly higher in type 2 DM than normal subjects(0.200 vs 0.062, P

Objective To investigate the effects of human umbilical cord mesenchymal stem cells (hUCMSCs)transplantation on the treatment of hypoxic-ischemic encephalopathy(HIE). Methods A total of 25 HIE patients were randomly divided into stem cell transplantation group(15 case)and control group(10 cases). The patients in transplantation group were given intravenous infusion of hUCMSCs,which isolated under sterile condition in vitro and cultured, while in control group were treated with routine drug treatment. Neurological function( American National Institutes of Health Stroke Scale( NIHSS ),Barthel index (BI)),extrapyramidal function(Unified Parkinson's disease questionnaire(UPDRS)),cognition and emotional reaction(The mini mental state examination(MMSE),the 14 item Hamilton Depression Scale(HAMD14)and HAMD24)were all assessed before and after transplantation for 14 d,90 d and 180 d respectively to evaluate the clinical efficacy of hUCMSCs transplantation. Results There was no significant difference between two groups in terms of each function before transplantation. The scores of transplantation group were all obviously improved after treatment for 14 d,90 d and 180 d compared to that of before treatment,and the therapy effect in transplantation group was significantly better than that of the control group( NIHSS:Ftime =4. 372,P=0. 031;Ftime*group =4. 175,P=0. 038;Fgroup =3. 897,P=0. 045.BI:Ftime =4. 728,P=0. 044;Ftime*group =4. 894,P=0. 037;Fgroup =4. 284,P=0. 039.UPDRS:Ftime =5. 112,P=0. 047;Ftime*group =4. 895,P=0. 045;Fgroup=3. 879,P =0. 031.MMSE:Ftime =5. 135,P =0. 039;Ftime*group =3. 213,P =0. 036;Fgroup =4. 184,P=0. 045.HAMD14:Ftime =3. 977,P =0. 049;Ftime*group =4. 587,P =0. 038;Fgroup =4. 381,P =0. 041.HAMD24:Ftime =3. 845,P =0. 033;Ftime*group =4. 125,P=0. 035;Fgroup =3. 547,P=0. 034). Conclusion Transplantation of hUCMSCs is safe and effective for treatment of HIE,which can significantly improve the neurological function,extrapyramidal function,cognition and emotion.

Objective To investigate the effect of rapamycin (RAPA) on mitochondrial injury in a mouse model of aging Parkinson's disease (PD).Methods Forty senescence-accelerated prone mice 8 (SAMP8) (12-month old) were randomly divided into 5 groups:blank group,model group,and RAPA low-,middle-,and high-dose groups.Mice in the model group and three RAPA groups were administered a subcutaneous injection of MPTP to generate the PD model.RAPA at 1,2,and 4 mg· kg 1· d 1 was administered from 7 days before,5 days during,and 7 days after the PD model preparation to the RAPA groups;an equal volume of sterile saline was administered to the other two groups.After the administration,behavioral test scores,dopamine levels,transmembrane potential of mitochondria,and activity of mitochondrial complex Ⅰ in the 5 groups were evaluated.Results Behavioral scores,dopamine levels,transmembrane potential,mitochondrial complex Ⅰ activity of mice in the model group were significantly decreased compared with the blank group (P ＜ 0.05 respectively).All indexes in the RAPA groups were significantly improved compared to the model group (P ＜ 0.05 respectively).There was no significant difference among the three RAPA groups.Conclusion RAPA has a protective effect on aging PD model mice,and its mechanism may be related to the protection against mitochondrial damage.

Since there is a lack of obvious clinical symptoms in the early stage of hepatocellular carcinoma (HCC), most patients have progressed to the advanced stage at the time of confirmed diagnosis. There are limited treatment options for HCC patients who miss the opportunity for surgery, so it is of great importance to find new therapeutic targets. Tumor-associated macrophages (TAMs) are a group of macrophages existing in the tumor immune microenvironment and affect the malignant behaviors of HCC cells and the state of immune escape within the tumor. This article introduces the origin and classification of TAM, summarizes the role and mechanism of TAMs in vascular proliferation, invasion and metastasis, formation and maintenance of stemness, and anti-tumor immunity in HCC, and briefly describes the current research advances in therapeutic targets for TAM, and it is pointed out that targeting TAM may be a promising direction for clinical treatment.

ObjectiveTo investigate the effect of kinesin family member 15 （KIF15） on the proliferation of hepatocellular carcinoma （HCC） cells and its mechanism of action. MethodsTCGA and GEPIA datasets were analyzed to determine the expression of KIF15 in HCC and its effect on tumor stage and survival. Quantitative real-time PCR and Western blot were used to measure the expression level of KIF15 in human-derived HCC cell lines （HepG2， Hep3B， MHCC-97H， and LM3） and human normal liver cell line L02 cultured in vitro， and Hep3B and HepG2 were selected for subsequent studies. CCK-8 assay， plate colony formation assay， and EdU staining were performed for Hep3B cells transfected with shRNA-NC or shRNA-KIF15 and HepG2 cells transfected with LV-vector or LV-KIF15 to evaluate the viability and proliferative capacity of these cells. GSEA was used to analyze the potential signaling pathways associated with KIF15 in HCC， and Western blot was used for detection. The independent-samples t test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsThe analysis of TCGA and GEPIA datasets showed that in HCC patients， the expression of KIF15 in HCC tissue was significantly higher than that in normal tissue， and the HCC patients with high KIF15 expression tended to have a poorer prognosis. Compared with sh-NC-Hep3B， sh3-Hep3B showed significant reductions in the mRNA and protein levels of KIF15 （P<0.05）， cell viability， clone formation number， and EdU positive rate （all P<0.05）. Compared with vector-HepG2， LV-KIF15-HepG2 showed significant increases in the mRNA and protein levels of KIF15 （P<0.05）， cell viability， clone formation number， and EdU positive rate （all P<0.05）. Subcutaneous tumor assay showed that compared with sh-NC-Hep3B， sh3-Hep3B showed reductions in tumor volume and tumor weight， as well as a significant reduction in the immunohistochemical score of Ki67 and a significant increase in the immunohistochemical score of TUNEL （P<0.05）. GSEA analysis showed that the PI3K/AKT/mTOR pathway was positively correlated with KIF15 in HCC （NES=1.59， P<0.001）. Western blot showed that LY294002 could inhibit the PI3K/AKT/mTOR pathway upregulated in LV-KIF15-HepG2， and compared with LV-KIF15-HepG2， LY294002+LV-KIF15-HepG2 showed significant reductions in cell viability， clone formation number， and EdU positive rate （all P<0.05）. ConclusionKIF15 enhances the viability and proliferative capacity of HCC cells by upregulating the PI3K/AKT/mTOR signaling pathway.