Objective:To research expression and function of c-myc gene in hyperacute r ejection of xenotransplantation. 　　Method:Through the model of hyperacute rejection of xenotransplantation wit h isolated rat heart perfused with human plasma,we detected c-myc mRNA expressi on and cell localization with in situ hybridization in hyperacute rejection. 　　Result:c-myc mRNA increased expression in the endothelium cell of heart.Th e value of signal is 450.09±409.99.The value of signal of group of control is 1 74.40±51.50(p＜0.05)。 　　Conclusion:From these study findings,it would appear that hyperacute rejecti on is associated with the elevation of c-myc mRNA expression.

Cholangiocarcinoma (CCA) is a malignant neoplasm derived from cholangiocytes. The incidence of CCA is only lower than that of hepatocellular carcinoma and ranked the second in liver malignant cancers. The prognosis of CCA patients is poor and most patients will die within a few months after diagnosis. CCA is related to various risk factors, including primary sclerosing cholangitis, cirrhosis, certain chemical agents and liver fluke. Establishment of proper animal models of CCA can not only be helpful for understanding the mechanisms of incidence and development, but also lay a solid foundation for developing novel treatment strategies. Common animal models of CCA include carcinogen-induced models, implantation models, operation models, and genetically engineered models.

Matrix metalloproteinase-9 plays an important role in the blood-brain barrier disruption.Blood-brain barrier disruption may directly influence the neurovascuiar unit repair after cerebral ischemia.An in-depth study of matrix metalloproteinase-9-mediated ischemic brain damage and neurovascular remodeling is expected to open up a new way for the diagnosis and treatment of cerebral ischemia in clinical practice.

This article expounds the molecular biological characteristics and signaling pathw ay of Tol -like receptor 2 and investigates its advances in research on the roles of neuronal and blood brain barrier damage after cerebral ischemia.

Objective To investigate the relationship between the G20210A mutation of prothrombin gene and cerebral infarclion(CI) in young patients. Methods The frequency of G20210A gene mutation of prothrombin in 40 young CI patients and 48 controls were studied by polymerase chain reaction (PCR) followed by Mnl- I and Hind-Ⅲ restriction enzyme analysis. Results No prothrombin gene G20210A mutation was found in both patients and controls. Conclusion The G20210A gene mutation of prothrombin was not the risk factor of this group of young CI patients.

Objective To discuss the influence of conbercept intraocular injection to vitrectomy on diabetic retinopathy.Methods patients (100 cases) with diabetic retinopathy were divided into two groups according to whether use intraocular injection drug or not.The injection group (49 cases) was given conbercept intraocular injection before vitrectomy.The control group (51 cases) was only given vitrectomy.The influence of conbercept intraocular injection to vitrectomy on diabetic retinopathy was evaluated by surgery,prognosis,visual acuity before and after surgery.Results The surgery time of the injection group was shorter than that of the control group (P ＜ 0.05).There were six bleeding cases in the injection group and 20 cases in the control group.The number of bleeding of injection group was shorter than that of the control group (P ＜ 0.05).In addition,the electric coagulation,silicone oil use,iatrogenic macular holes number of injection group was smaller than of that of the control group (P ＜ 0.05).During 1 month follow-up,the number of small bleeding and large bleeding cases of injection group was smaller than of the control group (P ＜ 0.05).There was no statistical significance on vision between two groups.After 1 month surgery,the vision of two groups were increased.And the vision of injection group was significantly higher than that of the control group (P ＜ 0.05).Conclusion In summary,conbercept intraocular injection could help vitrectomy.It could reduce the difficulty of surgery and shorten the surgery time.It could reduce the bleeding symptoms during and after surgery.It could improve the vision of patients.

Objective To investigate the clinical safety of preoperative lymphatic chemotherapy in the treatment of reetal cancer.Methods The regional and systemic symptoms,postoperatwe stoma healing,haematogenesis.functions of hean,liver and kidney after lymphatic chemotherapy,and the level of CD3+,CD4+,CD8+,CD4+/CD8+,CD(16+56)+in blood 30 minutes before and 48 hours after lymphatic chemotherapv were detected.Results There were no significant effects of lymphatic chemotherapy on the regional and systemic symptoms,postoperative stoma healing,haematogenesis and the functions of heart,liver and kidney.The level of CD4+/CD8+48 hours after lymphatic chemotherapy was significantly increased(t=7.145,P＜0.05),while no significant changes of CD3+,CIM+,CD8+,CD(16+56)+were detected(t=1.782,1.151,1.184,0.955,P＞0.05),when compared with those 30 minutes before lymphatic chemotherapy.Conclusions Preoperative lymphatic chemotherapy is safe and can enhance patients'immunity in early stage.

Atrial Fibrillation ; surgery ; Catheter Ablation ; methods ; Humans

The pathophysiological mechanism of ischemic stroke is very complex.Many intracellular and extracellular factors play the important roles in it.Studies have shown that the expression of matrix metalloproteinase-9 (MMP-9) has the changes of quantity,time and space after stroke.These changes are closely associated with the occurrence and development of ischemic stroke.The experimental studies focusing on MMP-9 also have made corresponding effects.The in-depth study of the mechanism of action of MMP-9 is expected to provide a new approach for the diagnosis and treatment of ischemic stroke.

Objective To investigate the impact of hyperthermia on the expression of claudin-1 in focal cerebral ischemia-reperfusion injury in rats and its mechanism in ischemic cerebral injury.Methods A total of 100 male Sprague-Dawley rats were randomly divided into 3 groups:sham operation,normothermia and hyperthermia groups.Both the normothermia and hyperthermia groups were redivided into 3 time points:Ischemia (1 hour) and reperfusion for 3,6,and 24 h.A model of middle cerebral artery occlusion was induced by the intraluminal suture method.At 24 h after reperfusion,brain water content was measured by the wet and dry weight method.The volume of cerebral infarction was assessed by 2,3,5 triphenyl tetrazolium chloride staining.At 3,6,and 24 h after reperfusion,the claudin-1 expression in ischemic brain tissue was measured by Western blot and immunohistochemical staining Results At 24 h after reperfusion,the mean neurological function score in the normothermia group was significantly lower than that in the hyperthermia group (2.3 ± 0.48 vs.3.2 ± 0.63; t =3.576,P =0.002).The brain water content on the operated sides in the sham operation,normothermia and hyperthermia groups was 79.31％ ± 0.60％,81.13％ ± 0.12％,and 84.4％ ± 0.55％,respectively.There were significant differences (F=147.115,P=0.000).Western blot analysis showed that at 3,6,and 24 h after reperfusion,the expression levels of claudin-1 in the normothermia and hyperthermia groups were significantly lower than the sham operation group (all P =0.000),and the expression levels of claudin-1 progressively decreased with the extension of ischemia-reperfusion time (all P ＜ 0.05).At the same time point,the expression level of claudin-1 in the hyperthermia group was significantly lower than that in the normothermia group (all P ＜ 0.01).At 3 and 6 h after reperfusion,the positive expression of claudin-1 among the cerebrovascular endothelial cells was observed in the sham operation,normothermia and hyperthermia groups,while at 24 h after reperfusion,no claudin-1 positive cells were observed.Compared to the sham operation group,at 3 h after reperfusion,the numbers of claudin-1 positive cell and claudin-1 IOD/area (integrated optical density/accumulated positive cell area) in the normothermia and hyperthermia groups begin to decrease,they decreased significantly at 6 h and disappeared at 24 h (P=0.000).At 3 and 6 h after reperfusion,claudin-1 IOD/area in the hyperthermia group was significantly lower than that in the normothermia group (all P ＜ 0.01).Conclusions During cerebral ischemia-reperfusion,hyperthermia may aggravate ischemic brain edema and brain injury by down-regulating the expression of claudin-1 in blood-brain barrier.