Objective To investigate cadmium induced adaptive responses (AR) to either toxicant challenge or irradiation and also the role of PI3K family in the AR. Methods Cells were pre-treated with 0.1 or 1 μmol/L cadmium and then challenged by 50, 100 μmol/L cadmium or 1, 2 Gy γ-rays irradiation. Micronucleus induction was measured to evaluate the magnitude of AR. In some experiments, cells were treated with wortmannin during and after pretreatment. Results Cadmium of sub-lethal concentration could induce AR in all the cells toward 50 μmol/L cadmium or 1 Gy irradiation. When challenged by 50 μmol/L CdCl1, EM-C11 cells had an AR less apparent than the other two cell lines. Moreover, treatment of cells with wortmannin eliminated the AR in all three cell lines. Conclusions The magnitudes of AR in adapted cells may be related to multiple factors, such as DNA repair capacity, the priming and challenging dose of cadmium or irradiation. SSB rather than DSB repair is mainly involved in the cadmium induced AR and this cellular response may be mediated through ATM pathway.

Cumulative evidence demonstrated that the chromatin modification plays important roles in the processes of DNA replication,transcription,repair and recombination.Both of the generation of DNA lesions and the activation of DNA damage response (DDR) to ionizing radiation could be affected by the chromatin modifications.This paper reviewed the recent research progresses in the chromatin structure modifications and its role in DDR,especially the influence of characteristic chromatin structure and histone modification on the radiation sensitivity of tumor cells.

Recently,many researches showed that vitamin D was involved in the pathophysiological processes of cardiovascular diseases.The incidence of vitamin D deficiency was increased with aging,and might be associated with an increased prevalence of cardiovascular disease with aging.In this paper,the association of vitamin D with cardiovascular diseases and the possible mechanisms are reviewed.

Anopheles minimus collected from Yuanjiang, Yunnan Province, were bred with standard methods in lab. The ovarian nurse cells of A.minimus were separated and stained, and the whole polytene chromosomes were photographed under light microscope and compared with A.minimus from Guangxi. 365 samples of ovarian nurse cells were observed. The chromosomes included one telocentric sex-chromosome X, two submetacentric autosomes II(autosome II right arm, 2R and autosome II left arm, 2L) and two metacentric autosomes III(autosome III right arm, 3R, and autosome III left arm, 3L). The X is the shortest chromosome and the 2R is the longest one. In comparison with the pattern of polytene chromosomes of A. minimus from Guangxi, difference at 12 positions has been found at the parts of arms in banding sequences.

Objective To investigate the effects of photochemotherapy on the angiogenic ability of endothelial cells and expression of integrin. Methods In vitro angiogenesis assay ( UVA exposure dose: 0, 2.0, 5.0 J/cm~2) was used to detect the effects of photochemotherapy on the angiogenic ability of endothelial cells. Reverse polymerase chain reaction and flow cytometry were employed to determine the effects of photochemotherapy on the expression of integrin mRNA and protein, respectively. bFGF stimulation group and PMA stimulation group were divided according to the inductors, and subgroups were divided according to the UVA exposure doses of 0, 2. 0 and 5. 0 J/cm~2 in each group. Results Combination of UVA (2.0 and 5.0 J/cm~2) and 8-MOP (100 ng/mL) resulted in a decrease in the angiogenic ability of endothelial cells in vitro and the expression of integrin mRNA and protein. Conclusion Photochemotherapy may inhibit the angiogenic ability of endothelial cells through downregulating the expression of integrin.

Objective To explore the value of 64-slice multi-detector computed tomography coronary angiography (64SCTA) in detecting the coronary artery plaque and to analyze the risk factors for unstable plaque. Methods A total of 112 inpatients who had been diagnosed as coronary artery disease by 64SCTA received catheter coronary angiography (CAG). The levels of serum endothelin-1 (ET-1), matrix metalloproteinase-9 (MMP-9), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP) were measured. The effect of 64SCTA in detecting the coronary artery plaque was evaluated as compared with CAG. The patients were divided into the soft plaque group (n=51) and non-soft plaque group (n=61) according to the CT value of correctly detected plaque. The differences in the above detection indexes between two groups and the risk factors for soft plaque forming were analyzed. Results The 64SCTA had 87.4% sensitivity and 87.1% specificity in detecting coronary artery plaque, the positive predictive value was 82.2% and the negative predictive value was 91.0%. There were significant differences between soft plaque group and non-soft plaque group in the levels of MMP-9, IL-6, hs-CRP, the number of coronary lesions and the composition ratios of gender, diagnosis and diabetes. Logistic regression analysis showed that MMP-9>5.231 ng/L (P=0.0215, OR=2.33, 95%CI 1.13-4.79), hs-CRP>3.583 mg/L (P=0.0008, OR=4.32, 95%CI 1.84-10.15) and unstable angina pectoris (P=0. 0339, OR=4.33, 95% CI 1.12-16.77) were the risk factors for soft plaque formation. Conclusions 64SCTA has highervalue in detecting the coronary artery plaque, and is one of most reliable means in non-invasive methods. MMP-9, hs-CRP and unstable angina pectoris are independent risk factors of plaque instability.

Objective To study the expression of Survivin and the relationship with proliferative activity in pancreatic carcinoma(PC).Methods The expression of SurvivinmRNA was investigated by reverse(transcriptase) polymerase chain reaction(RT-PCR) in 62 cases of PC samples,12 cases of chronic(pancreatitis)(CP) samples,and 10 cases of normal pancreatic tissue samples.Meanwhile,the expression of proliferative cell nuclear antigen(PCNA) was detected by immunohistochemical assay.Results The(expression) of Survivin gene was detected in a significantly greater proportion in PC(74.2%) than CP(0/12) and normal pancreatic tissue(0/10)(P

Background The mitochondrial Na+/Ca2+exchanger, NCLX, plays an important role in the balance between Ca2+influx and efflux across the mitochondrial inner membrane in endothelial cells. Mitochondrial metabolism is likely to be affected by the activity of NCLX because Ca2+activates several enzymes of the Krebs cycle. It is currently believed that mitochondria are not only centers of energy produc-tion but are also important sites of reactive oxygen species (ROS) generation and nucleotide-binding oligomerization domain receptor 3 (NLRP3) inflammasome activation. Methods&Results This study focused on NCLX function, in rat aortic endothelial cells (RAECs), induced by glucose. First, we detected an increase in NCLX expression in the endothelia of rats with diabetes mellitus, which was induced by an injection of streptozotocin. Next, colocalization of NCLX expression and mitochondria was detected using confocal analysis. Suppression of NCLX expression, using an siRNA construct (siNCLX), enhanced mitochondrial Ca2+influx and blocked efflux induced by glucose. Un-expectedly, silencing of NCLX expression induced increased ROS generation and NLRP3 inflammasome activation. Conclusions These findings suggest that NCLX affects glucose-dependent mitochondrial Ca2+signaling, thereby regulating ROS generation and NLRP3 in-flammasome activation in high glucose conditions. In the early stages of high glucose stimulation, NCLX expression increases to compensate in order to self-protect mitochondrial maintenance, stability, and function in endothelial cells.

Objective To investigate the effects of long-term low-dose radiation (LDR) of γ-rays on the proliferation and radiosensitivity of human lymphoblast cells HMy2.CIR (HMy) and to elucidate the underlying mechanism.Methods HMy cells were divided into control group and long-term LDR group.For the long-term LDR treatment,HMy cells were fractionally exposed to a low dose of γ-rays,which could enhance cell proliferation,3 times per week for 4 weeks.After the long-term LDR exposure,part of the control and long-term LDR exposed cells were further irradiated with a challenging dose (2 Gy) of γ-rays.Then cell proliferation and radiosensitivity were assayed by CCK-8 kit,cell apoptosis,and γ-H2AX formation was measured by flow cytometry.Gene expressions of cyclinD1,PCNA,bcl-2 and bax were detected by RT-PCR.Results The long-term LDR significantly increased cell proliferation (t =9.607,P ＜ 0.01) accompanied with up-regulation of cell cycle regulation gene cyclinD1 (t =6.869,P ＜ 0.01),proliferation regulation gene PCNA (proliferating cell nuclear antigen) (t =9.229,P ＜ 0.01) and bcl-2 gene (t =2.662,P ＜ 0.05),but decreased the expression of pro-apoptotic gene bax (t =19.908,P ＜0.01) in HMy cells.Compared to untreated cells,the long-term LDR decreased cell radiosensitivity (t =8.896,P ＜ 0.01),including apoptosis induction (t =4.762,P ＜ 0.01) and γ-H2AX formation (t =10.264,P＜0.01).Conclusions The long-term LDR promoted cell proliferation by up-regulating cell cycle related genes,while it reduced the radiosensitivity of HMy cells with acquisition of apoptotic resistance.

Objective To evaluate the therapy effect of pneumatic lithotripsy treatment under ureteroscopic on urinary catheter encrustation(CE).Methods Eight patients with difficulty in pulling catheter tube crustcaused were enrolled as our subjects.They were performed pneumatic lithotripsy under ureteroscope operation.The information related to operation was recorded.Results Eight cases were successful in terms of crushing catheter encrustations,and the catheters were removed smoothly.Conclusion The therapy of pneumatic lithotripsy treatment under ureteroscopic is proved to be a minimally invasive treatment with small damage,and higher safety.