Objective To explore the mechanism of mesenchymal stem cells （MSCs） transplantation for chronic hindlimb ischemia in Lewis rats by using cell tracer technique. Methods MSCs were isolated and cultured by using density gradient centrifugation and adherence method respectively， then labeled by 5-bromo-2-deoxyuridine （BrdU）. Eight chronic hindlimb ischemia models of Lewis rats were prepared by using suture-occluded method and then divided randomly to MSCs transplantation group and control group， each group enrolled 4 rats， accepting MSCs transplantation and saline respectively. Then on 7 days and 14 days after transplantation， clinical observation， determination of blood flow， and angiography were performed on rats of the 2 groups. At the same time points after previous tests， rats of the 2 groups were sacrificed to get quadriceps tissues and gastrocnemius tissues to perform HE staining and BrdU immunohis-tochemistry. Results The 8 rats were all survived on 14 days after transplantation， with no tumor happened and necroses in the transplanted area. On 14 days after transplantation， the blood flow ratio of operated side to un-operated side in the hindlimb （1.773 vs. 1.279） of rats in MSCs transplantation group and control group increased， and the angiography results showed that there were no much increase in ratio of collateral vessels number （0.908 vs. 0.835）. There were no significant change in the quadriceps tissues and gastrocnemius tissues by HE staining. The BrdU positive kernels located in the inter-stitial substance cells and vascular endothelia cells， and divided differently in different parts of hindlimb at different time points， that the ratio of positive cells in gastrocnemius tissue was higher than those of quadriceps tissue on 7 days after transplantation， but lower on 14 days. Conclusions MSCs transplantation can increases the blood perfusion of hindlimb in the early stage of chronic hindlimb ischemia model， and the possible mechanism may be the paracrine effect of MSCs but not the number increase of collateral vessels.
Obesity is a prevalent metabolic disorder,which seriously affects human health and has become the world's public health problem. Kinase S6K1, an important downstream effector of mammalian target of rapamycin (mTOR), influences specific pathological responses, including obesity, type 2 diabetes and cancer. Presently, S6K1 has become an attractive therapeutic target in the treatment of these disorders. Here, the functions of kinase S6K1, its molecular regulation mechanisms, related pathogenesis of disease and relevant small molecular inhibitors are reviewed. Finally, the prospect of research toward S6K1 is expected as well.
ObjectiveTo explore the effect of hydroxyapatite nanoparticle (nHAP) on hepatocellular carcinoma (HCC) and its mechanisms. MethodsThe literatures about the effect of nHAP on HCC were reviewed and summarized. ResultsAs a new nanoparticle, nHAP could suppress the DNA synthesis and subsequent division and proliferation of HCC cells through the inhibition of proliferating cell nuclear antigen (PCNA) and telomerase gene expression and increase of intracellular Ca2+. Moreover, nHAP was able to suppress the differentiation and metastases of HCC cells through the effect on the expressions of Paxillin and P130cas and the decrease of expressions of multiple drug resistance gene protein, microvessel density, and vascular endothelial growth factor. Finally, nHAP induced the apoptosis of HCC tumor cells by the regulation of bcl-2 and bax protein expressions. The combined use of nHAP and chemoembolization drugs could enhance the efficacy, prolong drug duration and reduce toxicity. ConclusionnHAP can inhibit the division, proliferation, differentiation, and metastases, and promote the apoptosis of HCC cells and combined use with chemoembolization drugs can enhance the efficacy and reduce toxicity.
ObjectiveTo explore and hypothesize the potential mechanisms of cancer stem cell(CSC) in peritoneal metastasis of gastric cancer. MethodsThe databases of PubMed and CNKI were searched, and relevant literatures were reviewed to draw out systematic hypotheses. ResultsMetastatic cancer stem cell(MCSC) was the subpopulation of CSC with the capacity of metastasis, had still not been well investigated. MCSC transfer was the tendency of migration and planting to specific target tissue by multi-steps of "homing" process. Peritoneal metastasis of gastric cancer was a simplified "homing" process, and we thinked that the key steps were adhesion, migration, and niche establishment of MCSC in peritoneum. That capturing human MCSC of peritoneal metastases in gastric cancer and identifying its stemness feature to determine high tumorigenicity and high invasive ability of it were the important research fields. ConclusionMCSC might play certain role in multiple processes in peritoneal metastasis of gastric cancer, but currently it's lack of relevant researches.
The synthesis and secretion of inflammatory cytokines in the monocytes of 68 cases of multiple system organ failure (MSOF) patients was investigated by the method of MTT stained in cytokines dependent defferential cell strain. The data showed that the serum levels of tumor necrosis factor, interleukine 1 and interleukine 6 were increased (Ｐ＜0.01) in the monocytes of MSOF patients. The synthesis and secretion of these inflammatory cytokines gradually increased in the monocytes after onset of MSOF. After 5 days of treatment with antibiotics and electrolytes intravenous infusion, the secretion of TNF, IL-1 and IL-6 were decreased respectively. These results suggested that the TNF, IL-1 and IL-6 are integrated into system inflammatory responese and caused the injury to the tissues and organs. The production levels of these cytokines can be regarded as the index of MSOF and its severity.
The study of relation between hepatogenic peptic ulcer and portal hypertension,transmitter metabolic disturbance,hepatic insufficiency and infection;and the therapeutic principles of complications of peptic ulcer are described.Twenty four of 58 patients with hepatogenic peptic ulcer were examined by color Doppler ultrasound.Portal venous flow volume (24 cases) was 1060.9±96ml/min.Portal venous pressure(8 cases)was 3.77±2.51kPa tested during operation.Histamine concentration (8 cases) was 0.70±0.31μmol/L in peripheral blood.The gastrin contents of 9cases tested 3cm,5cm away from the ulcer were 2195.6±1043.89ng/L and 2140.3±978.5ng/L respectively. H pylori positive rate was 80% in 58 cases.The therapeutic results were satisfactory with no death.The results suggest that pathogenesis of hepatogenic peptic ulcer is closely related to these factors foresaid.The treatment is nonsurgical and massive hemorrhage or perforation once occurs,surgical treatment is necessary.
Objective To study the relation between expressions of transforming growth factor β1 （TGF-β1）, transforming growth factor receptor type Ⅰ (TβRⅠ) and cell proliferation, cell cycle in gallbladder carcinomas, to disclose the mechanism of TGF-β1 and TβRⅠin the gallbladder carcinogenesis，and to evaluate their values in the prognosis of gallbladder carcinomas. Methods Thirty five gallbladder carcinomas 〔age （57.94± 4.61） years, 14 male cases and 21 female cases〕 comprised 32 adenocarcinomas, 2 adenosquamous carcinoma and 1 squamous cell carcinomas. Formalin fixed, paraffin embedded sections from gallbladder carcinomas were immunostained with TGF-β1, TβRⅠ, PCNA, cyclin E antibodies by immunochemical assays. Gallbladder adenoma and chronic cholecystitis were collected as non-malignant controls. Patients of gallbladder carcinomas were followed up. Results Positive immunostaining rate of TGF-β1 was 57.14% in gallbladder carcinomas, which was significantly higher than that in gallbladder adenomas and chronic cholecystitis (P＜0.01, respectively). Expression of TGF-β1 was associated with Nevin stage, lymph nodes and distant metastasis (P＜0.05, P＜0.01, respectively). Expression of TGF-β1 was positively correlated with expression of PCNA LI and cyclin E (r=0.523 2, P=0.001 3; r=0.406 5, P=0.015 4), and 34.29% of gallbladder carcinomas were immunostained positively for TβRⅠ. Expression of TβRⅠwas significantly lower in gallbladder carcinomas than that in gallbladder adenomas and cholecystitis (P＜0.05, respectively). It was significantly lower in gallbladder carcinomas patients with lymph nodes and distant metastases than in those without (P＜0.05). Expression of TβRⅠwas negatively correlated with PCNA LI (r=-0.402 4, P=0.016 6). Patients with negative expression of TGF-β1 and/or positive expression of TβRⅠ had significant longer survival rates than those with positive expression of TGF-β1 and/or negative expression of TβRⅠ(P＜0.01, P＜0.05, respectively). Expressions of TGF-β1 and TβRⅠ correlated with prognosis of gallbladder carcinomas closely. Conclusion TGF-β1 and TβRⅠ have close correlation with cell proliferation, cell cycle of gallbladder carcinomas and are important biological markers of carcinogenesis and progress of gallbladder carcinomas. The escape of growth inhibition of TGF-β1 due to low expression of TβRⅠand carcinogenesis of TGF-β1 may play an important role in gallbladder carcinogenesis. TGF-β1 and TβRⅠare valuable indices for judging the prognosis of gallbladder carcinoma.