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.

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.

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.

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.

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 establish a cellulose acetate membrane electrophoretic method for separating the exogenous sulfated poly mannuguluronicate(911) from glycosaminoglycans.Methods 911 both in urine and ultrafiltrated urine were extracted with cetylpyridinium chloride (CPC), and then separated by two step electrophoretic method with two different buffer solutions. Results The results indicated that 911 was thoroughly separated from endogenous CSC and DS with its average recovery in urine approximately at 70%. Furthermore, the lowest sensitivity for determination of 911 in aquatic solution was 100 ?g?L -1 , whereas that in urine 250 ?g?L -1 and in ultrafiltrated urine 500 ?g?L -1 . And most importantly 911 in rat's urine was detectable after it's oral administration at dose of 200mg?kg -1 . Conclusions It is the first time for us to conduct the existence of 911 in urine by two step electrophoretic method with two different buffer solutions, suggestive of the feasibility to determine 911 in urine even following it's oral administration.