Objective To investigate the possibility of bone marrow mesenchymal stem cells to transdifferentiate into insulinf-secreting cells or islet progenitors,and to demonstrate whether these islet-like cells can generate insulin and glucagon. Methods BMSCs were isolated from tibia or thighbone of 6-8 weeks normal SD rat,purified on the basis of their ability to adhere to matrix,and expanded through their self-renewal.Two-step strategy was adopted,BMSCs were induced to generate nestin-positive cells under diffferentiation culture medium 1(added 20??g/L bFGF,10??g/L EGF and 2% B-(27) in DMDM/F-(12) medium) in step one;Nestin-positive cells were differentiated and developed into islet-like cells or islet progenitors under complexed culture medium 2(added 10??g/L Betacellulin,10??g/L HCF,10??g/L Activin A,10?mmol/L nicotide and 2% B27 serum-free in HG-DMEM medium) in step two.The differentiated cells were tested by Dithiazone staining;Immunocytochemistry was carried out using standard protocols in which the cells were incubated with Rb-Rat insulin monoclone antibody,mouse-human glucogan polyclone antibody and Rb-Rat nestin monoclone antibody and assessed by examining the cells under a Zeiss microscope.Insulin secretion in response to insulin secretagogues(glucose) was assayed by radioimmunoassay(RIA). Results After 5 days,BMSCs were expressing nestin,a marker shared with neural stem cells and pancreatic stem cells.Dithiazone staining was positive(bright orange).The differentiated cell masses were containing insulin and glycagon as indicated by immunocytochemistry.RIA demonstrated that these cell mass could generate insulin,the responsibility to glucose was weak.Conclusion BMSCs can be induced to differentiate into insulin-secreting cells or islet progenitors by adding various different cell growth factors and the strategy is repeatable.This study may present a potential approach for the treatment of insulin-depended diabetes by interventional therapy.

Type I diabetes mellitus (T_1DM) is a chronic metabolic disease liable to teenagers all over the world. Its mechanism is due to the attack of auto-immune system on the body's own islet cells leading to hyperglycemia with great damages to the body. The implantation of islet cells is an effective way of curing T_1DM. The authors reviewed in detail the research advancement of islet cell source from stem cells of the bone marrow interstitial substance.

Objective To explore the relationship between N-acetyltransferase-2(NAT2)alleles polymorphism and type 2 diabetes mellitus(T2DM).Methods Polymerase chain reaction and sequence determination technique were used to identify NAT2 alleles in 174 patients with T2DM(T2DM group)and 174 unrelated healthy individuals(control group).Results Compared with control group,the allelic frequency of NAT2 mutation was no significant difference in T21DM group(x2=7.38,P＞0.05).The frequencies of the NAT2 genotypes(Wt/Wt,Wt/M1,Wt/M2,Wt/M3,M1/M1,M1/M2,M1/M3,M2/M2,M2/M3,M3/M3)were 39.08％(68/174),3.45％(6/174),22.99％(40/174),14.94％(26/174),0.57％(1/174),2.30％(4/174),1.15％(2/174),4.60％(8/174),9.20％(16/174),1.72％(3/174)and 44.83％(78/174),2.60％(8/174),27.59％(48/174),17.24％(30/174),0.57％(1/174),0.57％(1/174),0.57％(1/174),1.15％(21174),2.30％(4/174),0.57％(1/174)respectively,and significant differences showed between T2DM group and control group(x2=13.92,P＜0.01).The proportion of fast acetylate in T2DM group was significantly higher than that in control group[94.25％(164/174)vs.80.46％(140/174)],and the propoaion of slow acetylate in T2DM group was significantly lower than that in control group[5.75％(10/174)vs.19.54％(34/174)](P＜0.05),The risk of T2DM in people who were fast acetylate had 3.98 times(95％ CI:1.90-8.35)more than that in people who were slow acetylate.Conclusion It shows that the fast acetylate may be one of the genetic factors that influencing the susceptibility to T2DM,and slow acetylate may be one of the protecting factors.

Atherosclerosis,as a chronic inflammatory vascular disease,involves many cellular and molecular events in its formation and progression from an early fatty streak lesion to a highly dangerous rupture-prone plaque.The vulnerability or destabilization of atherosclerotic plaques is closely associated with plaque composition.Such imaging modality as magnetic resonance imaging(MRI),which allows of the evaluation of the plaque composition at the cellular and molecular level,may differentiate vulnerable and destabilized plaques and monitor the efficacy of antiatherosclerotic therapies.This paper gives an overview of molecular imaging strategies currently used for targeting the inflammation markers of atherosclerotic plaque vulnerability.

Pioglitazone treatment significantly improved the euglycemic clamp-determined insulin sensitivity (IS), raised adiponectin level, decreased TNF-α and FFA levels in rats with obese and hyperglycemia.

[Objective]To observe the expression of osteogenic growth peptide(OGP) gene,which had been transfected into rabbit bone marrow stromal cells(BMSC) by adenovirus,and detect the proliferation and differentiation of rabbit bone marrow stromal cells after gene transfection in vitro.[Methods]pcDNA3.1-OGP was constructed by using gene clone and recombined technique.With the help of lipofectamine 2000,BMSC were transfected with pcDNA3.1-OGP.The positive cell clones were selected with G418.The expression of OGP gene was observed by RT-PCR.Alkaline phosphatase(ALP) activity and type I collagen in pcDNA3.1-OGP transfected bone marrow stromal cells were measured to observe the differentiation from bone marrow stromal cells into osteoblast lineage.[Results]The pcDNA3.1-OGP vector was constructed successful.According to analysis of RT-PCR,alkaline phosphatase(ALP) and type I collagen assay showed that OGP gene could be expressed in BMSC,and could induce bone marrow stromal cells differentiation into osteoblast lineage.[Conclusion]The pcDNA3.1-OGP vector can be constructed successfully and its expression is confirmed in BMSC.The expression of OGP in bone marrow stromal cells can induce BMSC differentiation into osteoblast lineage.

Prostate cancer is one of the most common malignancies threatening men's health, and the mechanisms underlying its initiation and progression are poorly understood. Last decade has witnessed encouraging progress in the studies of prostate cancer stem cells (PCSCs), which are considered to play important roles in tumor initiation, recurrence and metastasis, castration resistance, and drug resistance. Therefore, a deeper insight into PCSCs is of great significance for the successful management of prostate cancer. This article presents an overview on the location, origin, and markers of PCSCs as well as their potential correlation with tumor metastasis and castration resistance.
Disease Progression ; Humans ; Male ; Neoplasm Recurrence, Local ; Neoplastic Stem Cells ; pathology ; Prostatic Neoplasms ; etiology ; pathology ; Prostatic Neoplasms, Castration-Resistant ; etiology ; pathology

This study is to investigate the protective effect of mangiferin on NF-kappaB (P65) and IkappaBalpha expression in peripheral blood mononuclear cell (PBMC) in rats with cigarette smoke induced chronic bronchitis. The rat model with chronic bronchitis was established by cigarette smoke. Real-time fluorescence RT-PCR was executed for evaluating the NF-kappaB (P65) and IKkappaBalpha gene expression in mononuclear cell, and flow cytometry for their protein expression. The serum hs-CRP (high-sensitivity C-reactive proteins) and TNF-alpha (tumor necrosis factor-alpha) were detected by enzyme-linked immunosorbent assay. The histopathological score was obtained from lung tissue HE staining slides of lung tissue. The results showed that mangiferin could markedly suppress the NF-kappaB (P65) mRNA and protein expression in mononuclear cell, while promote the IkappaBalpha mRNA and protein expression. Furthermore, mangiferin could lower serum hs-CRP and TNF-alpha level, and reduce the chronic inflammatory damage of bronchiole. These results suggested that mangiferin could notably ameliorate chronic bronchiole inflammation induced by cigarette smoke, and this protective effect might be linked to the regulation of NF-kappaB (P65) and IkappaBalpha expression in mononuclear cell.
Animals ; Bronchi ; pathology ; Bronchitis, Chronic ; blood ; etiology ; metabolism ; pathology ; C-Reactive Protein ; metabolism ; I-kappa B Kinase ; genetics ; metabolism ; Leukocytes, Mononuclear ; metabolism ; pathology ; Male ; Mangifera ; chemistry ; Plants, Medicinal ; chemistry ; RNA, Messenger ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tobacco Smoke Pollution ; Transcription Factor RelA ; genetics ; metabolism ; Tumor Necrosis Factor-alpha ; blood ; Xanthones ; isolation & purification ; pharmacology

This paper introduces the risk classification and listing way of medical devices in the United States, and according to the contents in various situations, FDA provides the requirements for clinical evaluation. At the same time, through the comparative study on the similarities and differences between USA and our country of the clinical evaluation, the paper puts forward some suggestions.
Equipment and Supplies ; standards ; Risk Assessment ; United States ; United States Food and Drug Administration

Objective To investigate the expression of neurotrophins receptor 75NTR in human breast cancer resistant cell line and its correlation with multidrug resistance. Methods Western blot was used to detect the expression level of p75NTR protein in various breast cancer cell lines and multidrug resistant cell lines. The over-expression vector and siRNA vector of p75NTR were constructed by gene recombination method. Western blot was used to detect the expression levels of p75NTR protein in transfected p75NTR and p75NTR - siRNA breast cancer resistant cell line MDA-MB-231/ADR;the sensitivity of MDA-MB-231 and MDA-MB-231/ADR to different chemotherapeutic anticancer drug (PTX ,ADM ,GEM ,DDP ,OXA) and the multi-drug resistance effects in over-expression and knock-down p75NTR MDA-MB-231/ADR were detected by CCK-8 assay. Results Western blot result showed that the expressions of p75NTR protein in the multidrug-resistant breast cancer cell lines MDA-MB-231/ADR and MCF-7/5-FU were higher than that of other breast cancer cell lines. Over-expression of p75NTRcan up-regulate the expression of p75NTR protein in MDA-MB-231/ADR;the CCK-8 assay indicated that over-expression of p75NTR can effectively enhance the resistance of MDA-MB-231/ADR cells to ADM,GEM and OXA. Conclusion The expression of p75NTR in breast cancer resistant cell line is higher than that of its parental cell line;over-expression of p75NTR can reduce the sensitivity to chemotherapeutic drugs and promote its multidrug resistance.