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We report a two-step approach to bicyclic and monocyclic 5-(1-alkoxyalkylidene)tetronates starting from lactones/esters. The method features the use of thionolactones and thionoesters as activated forms of lactones/esters that allows the direct condensation with tetronates

Esophageal squamous cell carcinoma (ESCC) is a lethal disease due to its high aggressiveness. The aim of the present study was to investigate the role of xeroderma pigmentosum complementation group D (XPD) in the growth and invasion of ESCC and to elucidate the potential underlying molecular mechanisms. Western blot analysis and RT‑qPCR were used to detect the expression level of XPD in ESCC tissue samples and adjacent normal esophageal tissue samples. The pEGFP‑N2/XPD plasmid was transfected into human ESCC cell lines (EC9706 and EC109). The proliferation, apoptosis, migration and invasion of EC9706 or EC109 cells were assessed following transfection with the XPD overexpression plasmid. The chemosensitivity of EC9706 or EC109 cells to cisplatin or fluorouracil was evaluated by CCK‑8 assay. The expression levels of phosphoinositide 3‑kinase (PI3K)/AKT, nuclear factor (NF)‑κB, Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and mitogen‑activated protein kinase (MAPK) signaling pathway‑related genes were detected by RT‑qPCR and western blot analysis. The results demonstrated that the expression level of XPD was markedly lower in ESCC tissue samples than in adjacent normal esophageal tissue samples. The pEGFP‑N2/XPD plasmid was successfully transfected into EC9706 or EC109 cells, inducing XPD overexpression. A High XPD expression markedly suppressed cell proliferation, migration and invasion, and increased the apoptotic rate of EC9706 and EC109 cells. Furthermore, the overexpression of XPD significantly increased the chemosensitivity of EC9706 and EC109 cells to cisplatin or fluorouracil. Following XPD overexpression, the expression levels of PI3K, p‑AKT, c‑Myc, Cyclin D1, Bcl‑2, vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)‑9 were markedly downregulated, while the expression level of p21 was markedly upregulated. On the whole, the findings of the present study demonstrate that XPD inhibits the growth and invasion of EC9706 and EC109 cells, whilst also enhancing the chemosensitivity of EC9706 and EC109 cells to cisplatin or fluorouracil by regulating the PI3K/AKT signaling pathway. XPD may thus be an underlying target for ESCC treatment and drug resistance.

Objective To explore the small-world properties of brain functional networks in patients with obstructive sleep apnea−hypopnea syndrome (OSAHS) to aid diagnosis. Methods A total of 29 OSAHS patients and 26 matched healthy volunteers were scanned with blood oxygen level−dependent functional magnetic resonance imaging (BOLD-fMRI) separately, and the whole brain was divided into 90 districts via automated anatomical labeling. The matrix Z was then built through a Fisher Z transformation. Two-sample t tests were applied to evaluate the changes in small-world properties in OSAHS patients compared to the control group. The properties included Eglobal, Elocal, and small-world parameters Lp, Cp, γ, λ, and σ. Results Both groups satisfied the small-world properties (σ > 1) within the sparsity range of 0.1–0.2. However, compared with the control group, the OSAHS group performed significantly lower in Cp, Elocal, and Eglobal (p Conclusion Both healthy and OSAHS patients exhibited small-world properties in functional networks, but a subset of these small-world properties in OSAHS patients performed differently. These changes will not only provide a new perspective for pathophysiological mechanisms of OSAHS but will also help in understanding the disease in terms of whole-brain functional networks.

ObjectiveTo determine the changes in interhemispheric functional coordination in patients with obstructive sleep apnea–hypopnea syndrome (OSAHS) relative to controls, using a recently introduced method of analysis: voxel-mirrored homotopic connectivity (VMHC).MethodsTwenty-nine patients with OSAHS and twenty-six normal sex-, age-, and education-matched controls were recruited and resting-state functional magnetic resonance imaging data were obtained. We employed VMHC to analyze the interhemispheric functional connectivity differences between groups. The z-values of alterations in VMHC in brain region were correlated with clinical characteristics.ResultsCompared with controls, patients with OSAHS had significantly higher scores for body mass index (t = 5.749, P

Objectives The aim of this meta-analysis was to investigate whether an association existed between green tea consumption and the risk for liver cancer in prospective cohort studies in Asian populations. Methods Relevant studies were identified by searching PubMed, EMBASE, ISI Web of Science, and the Chinese Bio-medicine Database published before April 2015. Study-specific risk estimates for the highest versus non- or lowest and increment of daily cup of green tea consumption levels were combined based on fixed- or random-effects models. STATA 11.0 (Stata Corporation, College Station, TX, USA) software was used for statistical analysis. Results Nine prospective cohort articles involving 465,274 participants and 3694 cases of liver cancer from China, Japan, and Singapore were included. The summary relative risk (RR) indicated a significant association between the highest green tea consumption and reduced risk for liver cancer (summary RR, 0.88; 95% confidence interval [CI], 0.81-0.97). However, no statistically significant association was observed when analyzing daily consumption of one cup (summary RR, 0.97; 95% CI, 0.95-1.00). When stratified by sex, the protective effect of green tea consumption on risk for liver cancer was observed only in the group of women (summary RR, 0.78; 95% CI, 0.64-0.96), but not in men (summary RR, 0.89; 95% CI, 0.79-1.00). Conclusions The present analysis indicated the preventive effects of green tea intake on the risk for liver cancer in female Asian populations. However, additional studies are needed to make a convincing case for this association.

This study examined the toxic effects of cadmium on the function of sexual hormone release in the ovaries of rats and the mechanism of this dysregulation. In vivo , adult female rats were randomly assigned to four groups based on weight. Cadmium was given ip 5 days/week for 6 weeks at doses of 1.0, 0.5, 0.25 and 0 mg/kg. Following euthanasia, the ovaries were removed and placed into culture medium for 3 h. The levels of progesterone (P) and estadiol (E) in the culture medium were then measured by radioimmunoassay. In vitro studies were done using the ovaries of adult rats in different stages of estrous (proestrus, estrus, metestrus and diestrus). Individual ovaries were collected, placed into culture medium and exposed to 0, 0.1, 1, or 2 mM of CdCl 2 for 3 h, at which time the levels of P and E in the ovary culture serum were determined by radioimmunoassay. The in vivo results showed that the levels of P and E in the ovary culture serum (5.3 ± 1.4 ng/ml and 1.4 ± 0.4 pg/ml, respectively) decreased significantly in the high dose group compared to the control (9.2 ± 0.9 ng/ml and 3.9 ± 0.7 pg/ml, respectively). In vitro , there were significant differences in P and E in between the different concentrations of cadmium and also between the different stages of the estrous cycle. These data suggest that cadmium can inhibit P and E release in ovaries. This may represent an important mechanism of endocrine disruption.

The possible use of activated carbon (COASAC) prepared from camellia oleifera abel shells (COAS) by phosphoric acid activation as a biosorbent in the removal of Cr from aqueous solution was demonstrated. The effect of different parameters such as initial concentration of Cr , dose of adsorbent, pH and temperature on Cr adsorption were investigated. The results showed that the maximum uptake of Cr was up to 165.0 mg/g at pH of around 2.0, under the initial Cr concentration of 250 mg/L and the temperature of 293K. The adsorption kinetics was found to follow a pseudo-second order kinetic model. The extent of the Cr removal increased with increasing initial Cr concentration and the equilibrium data fitted well to the Freundlich model.

To investigate the effect of cadmium (Cd) on estrogen receptor and to assess its endocrine disrupting action.The estrogen receptor rich supernatant was prepared from the ovariectomized Sprague-Dawley rats. The effects of cadmium on estrogen binding were performed using a sing-dose ligand-binding assay. Extract from uterus were treated with various concentrations of cadmium (0, 10(-3), 10(-5) or 10(-7) mol/L) for various pre-incubation time (0, 30, 60, 90 min) by means of orthogonal experimental design with orthogonal layout of L16(4(5)) (the experiment was repeated for 5 times). In addition to the radioinert competitor, each assay included a zero tube and a DES standard curve for quality control purpose. Data for cadmium and the DES standard curve were plotted as percent [3H]-E2 bound versus log (molar concentration), and the IC50 for cadmium was determined. The RBA for cadmium was calculated by dividing the IC50 of DES in terms of the IC50 of cadmium.Cadmium could not block the binding of estradiol to the receptor because hormone binding did not change with increasing cadmium concentration or increasing preincubation time. The results showed that the binding of [3H]-estradiol to uterine cytosols was not significant (P0.05). The Bmax (its unit is pmol/mg protein) of various concentrations of cadmium (0, 10(-3), 10(-5) or 10(-7) mol/L) for pre-incubating 0 min is 203.15 +/- 75.16, 203.41 +/- 22.78, 220.82 +/- 45.35, 209.10 +/- 49.66 respectively; The Bmax of them for pre-incubating 30 min is 215.67 +/- 92.97, 139.79 +/- 53.78, 205.27 +/- 23.60, 172.63 +/- 55.09 respectively. The Bmax of them for pre-incubating 60 min is 197.11 +/- 50.68, 203.24 +/- 66.33, 183.92 +/- 31.89, 183.33 +/- 32.70, respectively. The Bmax of them for pre-incubating 90 min is 229.69 +/- 76.88, 175.70 +/- 70.28, 164.26 +/- 24.46, 150.78 +/- 65.97 respectively. Mean IC50 for cadmium is 10(-4) - 10(-3) M. If the affinities of DES binding to estrogen receptors was taken to be 100%, the relative binding affinities of cadmium was 10(-6) - 10(-7). The results indicated that cadmium had only a very poor affinity with estrogen receptor.In vitro assay cadmium did not have distinct disrupting effect on binding of estradiol to estrogen receptors from rat uterine.