Animals ; Cardiovascular Diseases ; Cardiovascular System ; Humans ; MicroRNAs

Background A stable diabetic cataract animal model is a premise for screening and evaluating the drug for cataract therapy.Galactose cataract model is widely used in relevant experimental study,but the onset,extent and the type of lens opacification may be different due to different modeling way.Objective This study was to investigate the manifestations and pathological characteristics of cataract induced by D-galactose.Methods Fifty-six SPF SD rats were randomly divided into cataract-model group and control group and 28 rats for each group.50% D-galactose feed was given daily in model group,and regular feed was given in control group.Lenses of rats were examined under the slit lamp through the 30-day period at a 2-day interval,and then the opacity of lenses was graded on the modified Suryanarayana criteria.The body weight of rats was recorded and compared between two groups at day 5,10,15,20,25 and 30.The lenses samples were obtained for the histopathological examination by hemotoxylin and eosin staining.The wet weight,dry weight of the lenes and their ratio were detected and compared between these two groups.The use of animals followed the Regulation for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission.Results The body weight was reduced in model rats compared with control rats with the statistically significant difference from 10 days through 30 days(P＜0.05).The different grades of opacification of lens cortical and nuclear progressed in model rats throughout the experiment duration,but the lenses were clear in control rats.The slit-lamp microscopy and pathological examinations revealed that lenses opacity in model rats started from the cortex at the equator zone and developed towards central zone gradually with the lapse of experimental time.Following the entire opacity of lens cortex,lens nucleus were cloudy and expanded.The swelling and degeneration of the fiber cells in lens cortex,the differentiation,migration and denuclearation delay of lens epithelial cells were seen in model rats under the light microscope.The wet weight of lenses was increased and the dry weight was decreased in model rats in comparison with control rats in experimental 30 days,showing significant difference between two groups(t=138.571,t=52.468,P＜0.05).Conclusion The development of galactose-induced cataract animal model resemble one of age-related cortical cataract in human with the similar generating mechanism.This cataract model is reproducible and classifiable.

Janus kinase 2,myeloproliferative leukemia virus and tet encogene family member2 mutations affect a variety of cytokines signal transduction pathway in BCR/ABL-negative myeloproliferative neoplasms (MPN). In the influence of mutation load,co-mutation and genetic susceptibility,these mutations can induce different MPN phenotypes,and affect the characteristics of patients,the distribution of peripheral blood cells and prognosis. But how these mutations contribute to disease initiation,development,and transformation needs further reseach.

Female ; Humans ; Infant ; Mutation ; Pain Insensitivity, Congenital ; complications ; genetics ; pathology ; Receptor, trkA ; genetics

Background Sugar cataract is one of the major diabetic complications in the eye,but there is not effective medicine to prevent or delay development of cataract. Objective The goal of this study was to investigate the effects and the potential mechanism of aldose reductase (AR) inhibitor,AL-1576 on prevention of galactose cataract in rats. Methods Forty-two SD rats were randomly and equally divided into 7 groups.The cataracts were induced by feeding with 50％ galactose.At the day of feeding galactose and the day 5,10 and 15 after feeding galactose,AL-1576 was added into the feeds.The rats were divided AL-1576 prevention group and early-,intermediate-or late-stage intervention groups.For another group,the withdrawing AL-1576 group,AL-1576 was added into the feeds at the day of feeding galactose,then was removed after 10 days.The lenses of the rats were examined under the slit-lamp microscope before and after given AL-1576 every 5 days.At the day 35,the lenses were obtained.The wet and dry weight of the lenses were weighted,respectically,to calculate the water content of the lenses.Activities of AR and superoxidedismutase (SOD) and contents of glutathione (GSH) of the lenses were measured by their commercial detecting kits.The care and use of the animals complied with the Regulations for the Administration of Affairs Concerning Experimental Animals by State Science and Technology Commission. Results In AL-1576 prevention group,all lenses maintained clear.Opacification of the lenses were significantly attenuated in all three AL-1576 intervention groups and withdrawing AL-1576 group compared with the cataractous model group ( P＜0.05),but the inhibiting role was weaken with late intervention.The water contents and the activities of AR of the lenses were decreased,the contents of SOD and GSH were dramatically increased in all different AL-1576 treated groups compared with the cataractous model group (P＜0.05).Moreover,AL-1576 prevention group showed the best effect on all indexes (P＜0.05). Conclusions The activity of AR can be inhibited by AL-1576 at the different stages of development of cataract induced by galactose.By blocking and attenuating formation of the edema and elevating antioxdative capacity in the lenses,AL-1576 prevents and delays the formation of galactose cataract.

Aortic dissection is a dangerous and critical disease with extremely high mortality and disability rate.In clinical practice,aortic dissection should be highly suspected when patients developed dying-like severe chest and back pain.CT and MRI have been the reliable tools for diagnosing aortic dissection.In recent years,endovascular therapy has become the preferred treatment for Stanford type B aortic dissection,and some patients with Stanford type A dissection who cannot receive open surgery may also be treated with endovascular therapy.In order to improve endovascular treatment,to develop new instruments and to study the pathogenesis of aortic dissection,the preparation of stable and reliable animal models is very necessary.This paper aims to make a brief review about the research status concerning the preparation of animal models of aortic dissection.

Objective:To investigate the possibility and feasibility of the simultaneous coronary artery bypass grafting (CABG) with tumor excision in patients suffering from tumor combined with coronary artery disease(CAD). Methods:From August 2000 to July 2006, ten patients who were suspected of tumor (four patients suffered from urinary system tumor, two digestive system tumor, and four pulmonary tumor) with coronary artery disease were successfully treated by simultaneous surgeries. Surgical incisions were chose by the different tumor position. All carried on the CABG before tumor excision except one case. The two cases had cardiopulmonary bypass CABG, the rest eight had off-pump CABG. Follow-up was conducted after operation. Results:The combined operations were satisfied. There was no in-hospital mortality, no postoperative hemorrhage, no myocardial ischemia or infarction, with few complications. Postoperative in-hospital stay was 10-34 days, average 22.4 days. All discharged in cure. One patient lost the follow-up. Nine patients were followed up from six months to seven years three months. Two patients died from metastasis, and the others survived with satisfied follow-up without cardiovascular events. Conclusion:The simultaneous coronary artery bypass grafting with tumor excision for patients who suffer from either CAD with benign or malignant tumor is safe and feasible with satisfied short-and long-term survival.

B cell maturation antigen (BCMA) is a receptor of B lymphocyte stimulator (BLyS). Human IgG1Fc fusion proteins with the extracellular domain of BCMA(eBCMA), also called decoy receptors, have beenused as a potential BLyS antagonists to block BLyS activities. In order to design novel BLyS antagonistpeptides, computer-aided homologue modeling was used to construct an eBCMA-Fc fusion protein based on thecrystal structures of BCMA and Fc fragmant. To ensure the activity of eBCMA not to be interfered by Fcfusion, the root mean square distance (RMSD) for eBCMA and Fc were calculated to be 0.036 nm and 0.064nm, respectively, based on molecular docking modeling. An eBCMA-Fc fusion gene was constructed andintroduced into E. coli for expression. As expected, the purified 36 kD eBCMA-Fc fusion protein was able tobind BLyS in vitro at a dosage-dependent manner and demonstrated an anti-proliferative activity induced byBLyS in Daudi cells. The results have provided useful information on the evaluation of computer modeling andthe in vitro biological activity for the design of potential BLyS antagonist peptides.

AIM:To observe the clinical effect of femtosecond laser assisted penetrating keratoplasty.
METHODS: Twenty-four cases ( 24 eyes ) with corneal lesions were performed with femtosecond laser assisted penetrating keratoplasty. Preoperative and postoperative endothelial cell density and visual quality were compared.RESULTS: One week after operation, corneal grafts were clear in 21 eyes (87. 5%), mild cloudy in 3 eyes (12.5%);visual acuity ≥0. 5 in 18 eyes (75. 0%), 0. 2 ~0.4 in 6 eyes ( 25. 0%). After 3mo the mean corneal astigmatism was 2. 16±0. 21D ( range 2. 25 ~ 3. 09D). Compared to conventional penetrating keratoplasty which mean corneal astigmatism was average 3. 67±0. 38D after operation, there was significant difference between two groups ( P< 0. 05 ). There were significant differences between preoperative and postoperative visual acuity and astigmatism (both P<0. 05).
CONCLUSION: Femtosecond laser assisted penetrating corneal transplantation operation can improve patient's visual quality. And compared to traditional penetrating keratoplasty astigmatism decreased significantly, incision can be made in individual shape more precisely and neatly.

Objective To detect the mutations of Von Hippel-Lindau (VHL) gene via analyzing the prevalence of family members of VHL syndrome,clinical diagnosis and treatment,and gene analysis of patients with hemangioblastoma.methods All members of the VHL syndrome family members improved all relevant tests and plotted the family map.5 ml peripheral blood was extracted for gene sequencing,and the sequencing Result s were compared with the reported mutations of VHL gene in NCBI database.Result s(1)Analysis of clinical data of four members of the family:Ⅰ-2,Ⅱ-1,Ⅱ-5 suffering from central nervous system hemangioblastoma, Ⅱ-3 with pancreatic,retinopathy and pheochromocytoma,and Ⅱ-5 also combined with kidney,pancreatic lesions.The second generation of patients in the family have been treated surgically.(2)Gene sequencing Result s showed that all subjects in the test had the same mutation:exon2 109 sequence ATATCACACTGCCA was deleted and termination codon UGA appeared in exon 502.Conclusion Through the mutations of the VHL syndrome family,it is found that the family mutation type is a new mutation.For patients with central nervous system hemangioblastoma-based should be suspected of the disease and improve the family history survey.Once the diagnosis of familial VHL syndrome patients are confirmed,it is necessary to inform the other members of the family for clinical screening,and carry out genetic testing to reduce the harm of the disease to the greatest extent.