Physical cleansing reduces the mindset effect in problem-solving.

The present study investigated whether physical cleansing can reduce the mindset effect in problem-solving in two experiments. Both experiments followed the same procedure. In the first stage, participants formed a mindset through the Luchins' water-jar task (Experiment 1) or the idiom maze task (Experiment 2). The second stage is cleansing manipulation. In Experiment 1, participants were asked to clean their hands with wipes (cleansing condition) or examine the packaging of the wipes (no-cleansing condition). In Experiment 2, participants were asked to watch a washing-hands video (cleansing condition) or watch an examining-pen video (no-cleansing condition). At last, all participants completed the mindset effect test problems. The results showed that the participants in the cleansing condition were less affected by the mindset than those in the no-cleansing condition, indicating that physical cleansing reduced the mindset effect. Our results provide new evidence for the clean-slate effects and support the hypothesis that physical cleansing is an embodied process of psychological separation.

SIRT6 Inhibits Anoikis of Colorectal Cancer Cells by Down-Regulating NDRG1.

Anoikis, a form of apoptosis resulting from the loss of cell-extracellular matrix interaction, is a significant barrier to cancer cell metastasis. However, the epigenetic regulation of this process remains to be explored. Here, we demonstrate that the histone deacetylase sirtuin 6 (SIRT6) plays a pivotal role in conferring anoikis resistance to colorectal cancer (CRC) cells. The protein level of SIRT6 is negatively correlated with anoikis in CRC cells. The overexpression of SIRT6 decreases while the knockdown of SIRT6 increases detachment-induced anoikis. Mechanistically, SIRT6 inhibits the transcription of N-myc downstream-regulated gene 1 (NDRG1), a negative regulator of the AKT signaling pathway. We observed the up-regulation of SIRT6 in advanced-stage CRC samples. Together, our findings unveil a novel epigenetic program regulating the anoikis of CRC cells.

A panel of platelet-associated circulating long non-coding RNAs as potential biomarkers for colorectal cancer.

Evidence has suggested the potential of tumor-educated platelets as a biomarker trove for cancer diagnostics, but the difficulty in isolation limits its application. Since most of the circulating RNAs are derived from platelets, the change of RNA profile in platelets may lead to altered RNA expression in serum. Here, we identified a panel of platelet-associated long non-coding RNAs (lncRNAs) and evaluated its diagnostic capacity in serum of colorectal cancer (CRC) patients. Four lncRNAs, LNCAROD, SNHG20, LINC00534, and TSPOAP-AS1, were upregulated in both platelets and serum of CRC patients. A binary logistic model derived from them has validated area under roc curve of 0.78 indicating great performance. Furthermore, the expression levels of LNCAROD and TSPOAP-AS1 were correlated with cancer staging and tumor location. Together, our results add novel lncRNA biomarkers to the list of blood tests for CRC diagnostics and provide molecular evidence for the cross-talk between CRC platelets and serum.

Effects of Early Exposure to Isoflurane on Susceptibility to Chronic Pain Are Mediated by Increased Neural Activity Due to Actions of the Mammalian Target of the Rapamycin Pathway.

Patients who have undergone surgery in early life may be at elevated risk for suffering neuropathic pain in later life. The risk factors for this susceptibility are not fully understood. Here, we used a mouse chronic pain model to test the hypothesis that early exposure to the general anesthetic (GA) Isoflurane causes cellular and molecular alterations in dorsal spinal cord (DSC) and dorsal root ganglion (DRG) that produces a predisposition to neuropathic pain via an upregulation of the mammalian target of the rapamycin (mTOR) signaling pathway. Mice were exposed to isoflurane at postnatal day 7 (P7) and underwent spared nerve injury at P28 which causes chronic pain. Selected groups were treated with rapamycin, an mTOR inhibitor, for eight weeks. Behavioral tests showed that early isoflurane exposure enhanced susceptibility to chronic pain, and rapamycin treatment improved outcomes. Immunohistochemistry, Western blotting, and q-PCR indicated that isoflurane upregulated mTOR expression and neural activity in DSC and DRG. Accompanying upregulation of mTOR and rapamycin-reversible changes in chronic pain-associated markers, including N-cadherin, cAMP response element-binding protein (CREB), purinergic P2Y12 receptor, glial fibrillary acidic protein (GFAP) in DSC; and connexin 43, phospho-extracellular signal-regulated kinase (p-ERK), GFAP, Iba1 in DRG, were observed. We concluded that early GA exposure, at least with isoflurane, alters the development of pain circuits such that mice are subsequently more vulnerable to chronic neuropathic pain states.

Hyperhomocysteinemia-Induced Oxidative Stress Exacerbates Cortical Traumatic Brain Injury Outcomes in Rats.

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality among military service members and civilians in the United States. Despite significant advances in the understanding of TBI pathophysiology, several clinical reports indicate that multiple genetic and epigenetic factors can influence outcome. Homocysteine (HCY) is a non-proteinogenic amino acid, the catabolism of which can be dysregulated by stress, lifestyle, aging, or genetic abnormalities leading to hyperhomocysteinemia (HHCY). HHCY is a neurotoxic condition and a risk factor for multiple neurological and cardiovascular disorders that occurs when HCY levels is clinically > 15 µM. Although the deleterious impact of HHCY has been studied in human and animal models of neurological disorders such as stroke, Alzheimer's disease and Parkinson's disease, it has not been addressed in TBI models. This study tested the hypothesis that HHCY has detrimental effects on TBI pathophysiology. Moderate HHCY was induced in adult male Sprague Dawley rats via daily administration of methionine followed by impact-induced traumatic brain injury. In this model, HHCY increased oxidative stress, upregulated expression of proteins that promote blood coagulation, exacerbated TBI-associated blood-brain barrier dysfunction and promoted the infiltration of inflammatory cells into the cortex. We also observed an increase of brain injury-induced lesion size and aggravated anxiety-like behavior. These findings show that moderate HHCY exacerbates TBI outcomes and suggest that HCY catabolic dysregulation may be a significant biological variable that could contribute to TBI pathophysiology heterogeneity.

Implicit learning of semantic preferences of English words by Chinese learners.

The aim of the present study was to explore whether Chinese learners could implicitly learn the semantic preferences of novel English words. In training, participants learned four novel verbs and were exposed to a set of verb-noun phrases that included these new words. What the participants were not told was that the use of the verbs depended on the concreteness of the nouns (i.e., the semantic preference rule). In testing, participants were required to choose between two possible verbs (one of which violated the semantic preference rule) for nouns that never occurred in training. The results showed that participants acquired unconscious knowledge of semantic preferences under incidental learning conditions, as measured by verbal reports and structural knowledge attributions. Our results provide further evidence for implicit learning of semantic preferences, suggesting that implicit learning is an important mechanism in the acquisition of L2 collocations.

Environmental impacts of lithium production showing the importance of primary data of upstream process in life-cycle assessment.

Life-cycle assessment (LCA) emphasizes obtaining primary data from an on-site process to reduce uncertainties. However, data of the upstream process from secondary sources also yield significant uncertainties, which have not been drawn enough attention. This study aims to explore the importance of primary data of the upstream process in LCAs. Here, we choose lithium, a key component of lithium-ion (Li-ion) battery, as a case to present a cradle-to-gate LCA for its production by rock-based technology (LRT). Then, we compare the environmental impacts of lithium by LRT with that by brine-based technology (LBT) and the Li-ion battery using lithium by the two methods. The result shows that the impacts of rock-based lithium production are dominated by the leaching process, which has the highest levels of impacts for 8 of 10 environmental categories. Besides, all 10 impact categories of lithium produced by LRT are much larger than that by LBT, with differences up to 60.4 -fold. We also find that the Li-ion battery pack by rock-based lithium offers a 17-32% increase in acidification and global warming potential relative to that by brine-based lithium. Our results contribute by providing the first mass-produced life-cycle inventory of rock-based lithium and showing the importance of primary data of the upstream process in LCAs.

Nicotinamide N-methyltransferase enhances chemoresistance in breast cancer through SIRT1 protein stabilization.

BACKGROUND: Nicotinamide N-methyltransferase (NNMT) is overexpressed in various human tumors and involved in the development and progression of several carcinomas. In breast cancer, NNMT was found to be overexpressed in several cell lines. However, the clinical relevance of NNMT in breast cancer is not yet clear. METHODS: NNMT expression in breast carcinoma was examined by immunohistochemistry, and then, its relationship with patient clinicopathological characteristics was analyzed. The effects of NNMT on chemoresistance in breast cancer cells were assessed by cell viability, colony formation, and apoptosis assay. The NNMT, SIRT1, p53, and acetyl-p53 proteins, which are involved in NNMT-related chemoresistance, were examined by Western blotting. The SIRT1 mRNA was examined by real-time PCR, and its activity was measured by using the SIRT1 deacetylase fluorometric reagent kit. RESULTS: NNMT expression was significantly higher (53.9%) in breast carcinoma than in paracancerous tissues (10.0%) and breast hyperplasia (13.3%). A high level of NNMT expression correlated with poor survival and chemotherapy response in breast cancer patients who received chemotherapy. Ectopic overexpression of NNMT significantly inhibited the apoptotic cell death and suppression of colony formation induced by adriamycin and paclitaxel. Mechanistic studies revealed that NNMT overexpression increased SIRT1 expression and promoted its activity. Either inhibition of SIRT1 by EX527 or knockdown of SIRT1 by siRNA could reverse NNMT-mediated resistance to adriamycin and paclitaxel, which suggests that SIRT1 plays a critical role in NNMT-related chemoresistance in breast cancer. CONCLUSIONS: The results of this study demonstrate a novel correlation between the NNMT expression level and patient survival, suggesting that NNMT has the potential to become a new prognostic biomarker to predict the treatment outcomes of the clinical chemotherapy in breast cancer. Moreover, targeting NNMT or downstream SIRT1 may represent a new therapeutic approach to improve the efficacy of breast cancer chemotherapy.

PDE8 Is Expressed in Human Airway Smooth Muscle and Selectively Regulates cAMP Signaling by ß2-Adrenergic Receptors and Adenylyl Cyclase 6.

Two cAMP signaling compartments centered on adenylyl cyclase (AC) exist in human airway smooth muscle (HASM) cells, one containing ß2-adrenergic receptor AC6 and another containing E prostanoid receptor AC2. We hypothesized that different PDE isozymes selectively regulate cAMP signaling in each compartment. According to RNA-sequencing data, 18 of 24 PDE genes were expressed in primary HASM cells derived from age- and sex-matched donors with and without asthma. PDE8A was the third most abundant of the cAMP-degrading PDE genes, after PDE4A and PDE1A. Knockdown of PDE8A using shRNA evoked twofold greater cAMP responses to 1 µM forskolin in the presence of 3-isobutyl-1-methylxanthine. Overexpression of AC2 did not alter this response, but overexpression of AC6 increased cAMP responses an additional 80%. We examined cAMP dynamics in live HASM cells using a fluorescence sensor. PF-04957325, a PDE8-selective inhibitor, increased basal cAMP concentrations by itself, indicating a significant basal level of cAMP synthesis. In the presence of an AC inhibitor to reduce basal signaling, PF-04957325 accelerated cAMP production and increased the inhibition of cell proliferation induced by isoproterenol, but it had no effect on cAMP concentrations or cell proliferation regulated by prostaglandin E2. Lipid raft fractionation of HASM cells revealed PDE8A immunoreactivity in buoyant fractions containing caveolin-1 and AC5/6 immunoreactivity. Thus, PDE8 is expressed in lipid rafts of HASM cells, where it specifically regulates ß2-adrenergic receptor AC6 signaling without effects on signaling by the E prostanoid receptors 2/4-AC2 complex. In airway diseases such as asthma and chronic obstructive pulmonary disease, PDE8 may represent a novel therapeutic target to modulate HASM responsiveness and airway remodeling.

Genome-wide expression profiling analysis to identify key genes in the anti-HIV mechanism of CD4+ and CD8+ T cells.

Comprehensive bioinformatics analyses were performed to explore the key biomarkers in response to HIV infection of CD4+ and CD8+ T cells. The numbers of CD4+ and CD8+ T cells of HIV infected individuals were analyzed and the GEO database (GSE6740) was screened for differentially expressed genes (DEGs) in HIV infected CD4+ and CD8+ T cells. Gene Ontology enrichment, KEGG pathway analyses, and protein-protein interaction (PPI) network were performed to identify the key pathway and core proteins in anti-HIV virus process of CD4+ and CD8+ T cells. Finally, we analyzed the expressions of key proteins in HIV-infected T cells (GSE6740 dataset) and peripheral blood mononuclear cells(PBMCs) (GSE511 dataset). 1) CD4+ T cells counts and ratio of CD4+ /CD8+ T cells decreased while CD8+ T cells counts increased in HIV positive individuals; 2) 517 DEGs were found in HIV infected CD4+ and CD8+ T cells at acute and chronic stage with the criterial of P-value <0.05 and fold change (FC) ≥2; 3) In acute HIV infection, type 1 interferon (IFN-1) pathway might played a critical role in response to HIV infection of T cells. The main biological processes of the DEGs were response to virus and defense response to virus. At chronic stage, ISG15 protein, in conjunction with IFN-1 pathway might play key roles in anti-HIV responses of CD4+ T cells; and 4) The expression of ISG15 increased in both T cells and PBMCs after HIV infection. Gene expression profile of CD4+ and CD8+ T cells changed significantly in HIV infection, in which ISG15 gene may play a central role in activating the natural antiviral process of immune cells.

Glucose potentiates ß-cell function by inducing Tph1 expression in rat islets.

Impaired pancreatic ß-cell function is the primary defect in type 2 diabetes. Glucose is an important regulator of ß-cell growth and function; however, the mechanisms that are involved in the chronic adaptation of ß cells to hyperglycemia remain largely unknown. In the present study, global gene expression patterns revealed that tryptophan hydroxylase 1 (Tph1) was the most profound of genes that are up-regulated in rat islets exposed to high glucose. Calcium and cAMP signals synergistically mediated glucose-stimulated Tph1 transcription in ß cells by activating cAMP-responsive element-binding protein and promoting its binding with a Tph1 promoter. Similar to in vitro results, in vivo infusion of high glucose also strongly induced Tph1 expression and serotonin production in rat islets, along with enhanced islet function. Inhibition or knockdown of Tph1 markedly decreased glucose-potentiated insulin secretion. In contrast, overexpression of Tph1 augmented glucose-stimulated insulin secretion in rat islets by up-regulating the expression of genes that are related to islet function. In addition, the long-acting glucagon-like peptide 1 receptor agonist, exendin-4, stimulated Tph1 expression in a glucose-dependent manner. Knockdown of Tph1 inhibited exendin-4-potentiated insulin secretion in rat islets. These findings suggest that Tph1 mediates the compensation of islet function induced by glucose, and that promoting Tph1 expression in pancreatic ß cells will provide a new strategy for the treatment of type 2 diabetes mellitus.-Zhang, Y., Deng, R., Yang, X., Xu, W., Liu, Y., Li, F., Zhang, J., Tang, H., Ji, X., Bi, Y., Wang, X., Zhou, L., Ning, G. Glucose potentiates ß-cell function by inducing Tph1 expression in rat islets.

Measurement of HE4 and CA125 and establishment of reference intervals for the ROMA index in the sera of pregnant women.

INTRODUCTION: Cancer antigen 125 (CA125) and human epididymis protein 4 (HE4) are biomarkers for ovarian cancer. Their specificity and sensitivity are often limited during pregnancy as a result of great fluctuations. The risk of ovarian malignancy algorithm (ROMA) score, which combines CA125, HE4, and menopausal status, may improve diagnostic performance. There are no reports regarding the ROMA index in pregnant women. Therefore, the aim of our study was to establish appropriate reference intervals (RIs) for the ROMA index in pregnant Chinese women and compare them with those of CA125 and HE4 during pregnancy. METHODS: Serum concentrations of CA125 and HE4 were simultaneously measured in healthy pregnant women via electrochemiluminescence immunoassay (ECLIA). The ROMA index was calculated using premenopausal algorithms. RESULTS: The RIs for the ROMA index calculated by premenopausal algorithms were substantially closer to the normal range in the first 2 trimesters. For pregnant women, the great misclassifications identified in CA125 may be reversed by the use of ROMA index. CONCLUSIONS: We established the RIs for HE4 and CA125, as well as the ROMA index, in pregnant women at different gestational periods. The ROMA index is suggested to be a more promising tumor marker for pregnant women diagnosed with malignance.

CD11b regulates obesity-induced insulin resistance via limiting alternative activation and proliferation of adipose tissue macrophages.

Obesity-associated inflammation is accompanied by the accumulation of adipose tissue macrophages (ATMs), which is believed to predispose obese individuals to insulin resistance. CD11b (integrin αM) is highly expressed on monocytes and macrophages and is critical for their migration and function. We found here that high-fat diet-induced insulin resistance was significantly reduced in CD11b-deficient mice. Interestingly, the recruitment of monocytes to adipose tissue is impaired when CD11b is deficient, although the cellularity of ATMs in CD11b-deficient mice is higher than that in wild-type mice. We further found that the increase in ATMs is caused mainly by their vigorous proliferation in the absence of CD11b. Moreover, the proliferation and alternative activation of ATMs are regulated by the IL-4/STAT6 axis, which is inhibited by CD11b through the activity of phosphatase SHP-1. Thus, CD11b plays a critical role in obesity-induced insulin resistance by limiting the proliferation and alternative activation of ATMs.

Use of portable X-ray fluorescence spectroscopy and geostatistics for health risk assessment.

Laboratory analysis of trace metals using inductively coupled plasma (ICP) spectroscopy is not cost effective, and the complex spatial distribution of soil trace metals makes their spatial analysis and prediction problematic. Thus, for the health risk assessment of exposure to trace metals in soils, portable X-ray fluorescence (PXRF) spectroscopy was used to replace ICP spectroscopy for metal analysis, and robust geostatistical methods were used to identify spatial outliers in trace metal concentrations and to map trace metal distributions. A case study was carried out around an industrial area in Nanjing, China. The results showed that PXRF spectroscopy provided results for trace metal (Cu, Ni, Pb and Zn) levels comparable to ICP spectroscopy. The results of the health risk assessment showed that Ni posed a higher non-carcinogenic risk than Cu, Pb and Zn, indicating a higher priority of concern than the other elements. Sampling locations associated with adverse health effects were identified as 'hotspots', and high-risk areas were delineated from risk maps. These 'hotspots' and high-risk areas were in close proximity to and downwind from petrochemical plants, indicating the dominant role of industrial activities as the major sources of trace metals in soils. The approach used in this study could be adopted as a cost-effective methodology for screening 'hotspots' and priority areas of concern for cost-efficient health risk management.

Expression of AQP2, AQP4 and AQP 8 in mouse intestine induced by unprocessed and processed Euphorbia lathyris.

The present research was designed to study expression of AQP2, AQP4 and AQP8 in mouse intestines induced by unprocessed and processed Euphorbia lathyris. KM mice were given by different dose lavage of unprocessed and processed Euphorbia lathyris, Euphorbia factor L1, Euphorbia factor L2, Euphorbia factor L3. Samples of mouse intestine were collected for protein levels of AQP2, AQP 4 and AQP 8 which were assessed by immunohistochemical staining and mRNA expression of AQP2, AQP 4 and AQP 8 which were quantified by Real Time-PCR. Comparing to the normal control group, the protein levels of AQP2, AQP 4 and AQP 8 were significantly decreased (P<0.05)by Semen Euphorbiae group and Semen Euphorbiae Pulveratum group (unprocessed and processed Euphorbia lathyris) induced. Protein expression of AQP2, AQP 4 and AQP 8 in the Euphorbia factor L1, Euphorbia factor L2 and Euphorbia factor L3 group were not significantly lower than normal control group. There had no differences on the levels of AQP2 and AQP 8 mRNA expressions between the high-dose group of semen Euphorbiae group, semen Euphorbiae Pulveratum group and positive control group, while significantly lower than normal control group (P<0.05). Expression of AQP4 mRNA in the Semen Euphorbiae group and Semen Euphorbiae Pulveratum group has not significantly decreased. But levels of AQP2, AQP 4 and AQP 8 mRNA in the Euphorbia factor L1 group had no significant differences in normal control group and positive control group. These findings suggest that semen Euphorbiae could regulate expression of AQP2, AQP 4 and AQP 8 protein and mRNA, which may be the possible one reason of semen Euphorbiae induces diarrhea. The semen Euphorbiae group has more significant effects on the levels of AQP2, AQP 4 and AQP 8 protein and mRNA than semen Euphorbiae Pulveratum group, which may be one of the mechanisms of processing attenuation.

Acupuncture for the treatment of obesity in adults: a systematic review and meta-analysis.

OBJECTIVE: Meta-analysis was used to assess the clinical efficacy of acupuncture treatment for simple obesity and to provide evidence-based medical data for treating obesity with acupuncture. METHODS: A comprehensive search of studies on MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials and Chinese databases (Wan Fang,CNKI and VIP) from 1 January 1915 through 30 November 2015 (MEDLINE search updated through 31 December 2015) was performed. We included only randomised controlled trials (RCTs) that used acupuncture and sham acupuncture to treat simple obesity. The effect of acupuncture on simple obesity was measured using body mass index (BMI), body fat mass (BFM), waist circumference (WC), hip circumference (HC), and body weight (BW). The Jadad scale was used to assess methodological quality. The random effects model was used in the pooled analysis to adjust for the heterogeneity of the included studies, and funnel plots were used to examine publication bias. The differences between treatment groups were reported as mean differences (MD). RESULTS: Eleven RCTs were selected after all relevant literature from the electronic databases had been screened. There were 338 and 305 participants in the acupuncture and sham acupuncture groups, respectively. Auricular and electro acupuncture were both able to reduce BMI in obese patients (MD 0.47 kg/m2, 95% CI 0.35 to 0.58, p<0.001; MD 0.50 kg/m2, 95% CI 0.38 to 0.62, p<0.001). BFM change after acupuncture treatment compared with sham treatment was statistically significant (MD 0.66 kg, 95% CI 0.51 to 0.80, p<0.001). There were also significant differences in WC and HC between the acupuncture and sham acupuncture groups (MDwc2.02 cm, 95% CI 0.21 to 3.83, p=0.03; MDHC2.74 cm, 95% CI 1.21 to 4.27, p=0.0004). BW was not statistically significantly different between the acupuncture and sham acupuncture groups (MD 0.60 kg, 95% CI -0.20 to 1.39, p=0.14). Begg's test and funnel plots showed that the potential publication bias of the included studies was very slight (p>0.05). CONCLUSION: Acupuncture for simple obesity appeared to be an effective treatment, but more studies on the safety of acupuncture used to treat simple obesity are required.

Application of decomposition-ensemble learning paradigm with phase space reconstruction for day-ahead PM2.5 concentration forecasting.

PM2.5 concentration have received considerable attention from meteorologists, who are able to notify the public and take precautionary measures to prevent negative effects on health. Therefore, establishing an efficient early warning system plays a critical role in fostering public health in heavily polluted areas. In this study, ensemble empirical mode decomposition and least square support vector machine (EEMD-LSSVM) based on Phase space reconstruction (PSR) is proposed for day-ahead PM2.5 concentration prediction, according to the application of a decomposition-ensemble learning paradigm. The main methods of the proposed model mainly include: first, EEMD is presented to decompose the original data of PM2.5 concentration into some intrinsic model functions (IMFs); second, PSR is applied to determine the input form of each extracted component; third, LSSVM, an effective forecasting tool, is used to predict all reconstructed components independently; finally, another LSSVM is employed to aggregate all predicted components into ensemble results for the final prediction. The empirical results show that this proposed model can outperform the comparison models and can significantly improve the prediction performance in terms of higher predictive and directional accuracy.

Time Series Models for Short Term Prediction of the Incidence of Japanese Encephalitis in Xianyang City, P R China△.

Objective To construct a model of Seasonal Autoregressive Integrated Moving Average (SARIMA) for forecasting the epidemic of Japanese encephalitis (JE) in Xianyang, Shaanxi, China, and provide valuable reference information for JE control and prevention. Methods Theoretically epidemiologic study was employed in the research process. Monthly incidence data on JE for the period from Jan 2005 to Sep 2014 were obtained from a passive surveillance system at the Center for Diseases Prevention and Control in Xianyang, Shaanxi province. An optimal SARIMA model was developed for JE incidence from 2005 to 2013 with the Box and Jenkins approach. This SARIMA model could predict JE incidence for the year 2014 and 2015. Results SARIMA (1, 1, 1) (2, 1, 1)12 was considered to be the best model with the lowest Bayesian information criterion, Akaike information criterion, Mean Absolute Error values, the highest R2, and a lower Mean Absolute Percent Error. SARIMA (1, 1, 1) (2, 1, 1)12 was stationary and accurate for predicting JE incidence in Xianyang. The predicted incidence, around 0.3/100 000 from June to August in 2014 with low errors, was higher compared with the actual incidence. Therefore, SARIMA (1, 1, 1) (2, 1, 1)12 appeared to be reliable and accurate and could be applied to incidence prediction. Conclusions The proposed prediction model could provide clues to early identification of the JE incidence that is increased abnormally (≥0.4/100 000). According to the predicted Results in 2014, the JE incidence in Xianyang will decline slightly and reach its peak from June to August.

Performance of the Sysmex UF-1000i urine analyser in the rapid diagnosis of urinary tract infections in hospitalized patients.

BACKGROUND: Urinary tract infections (UTIs) are the second most frequently encountered nosocomial infectious diseases, and they greatly increase the cost of medical care and prolong the duration of hospital stays. AIM: We aimed to evaluate the performance of the Sysmex UF-1000i analyser for the rapid prediction of UTIs in hospitalized patients with or without indwelling catheters at a comprehensive teaching hospital that encounters complex disease types. METHODS: Urine specimens (n = 1016) were cultured and examined for WBC, RBC, bacteria (BACT) and yeast-like cell (YLC) count using the Sysmex UF-1000i. The results were compared with the urine culture results. Receiver operating characteristic curve analysis was applied to determine BACT and YLC cutoff values for bacterial and fungal UTIs independently. The diagnostic ability of the UF-1000i was also compared for patients with and without indwelling catheters. FINDINGS: A cutoff value of 38.7/µL was acceptable for ruling out bacterial UTIs. In this setting, we achieved a sensitivity of 90%, a negative predictive value of 94.5%, a false negative rate of 2.85% (29 cases), and avoided culturing in 52% of the samples. The BACT count presented a larger area under the curve for patients with indwelling catheters than for those without (0.939 vs. 0.861); however, no significant difference in the diagnostic ability of the two curves was found. CONCLUSION: The Sysmex UF-1000i analyser could be a reliable method for excluding bacterial UTIs in hospitalized patients with or without urinary catheters and could help clinicians determine whether antibiotic therapy is necessary.

Acute exposure of beta-cells to troglitazone decreases insulin hypersecretion via activating AMPK.

BACKGROUND: It has been recognized that insulin hypersecretion can lead to the development of insulin resistance and type 2 diabetes mellitus. There is substantial evidence demonstrating that thiazolidinediones are able to delay and prevent the progression of pancreatic ß-cell dysfunction. However, the mechanism underlying the protective effect of thiazolidinediones on ß-cell function remains elusive. METHODS: We synchronously detected the effects of troglitazone on insulin secretion and AMP-activated protein kinase (AMPK) activity under various conditions in isolated rat islets and MIN6 cells. RESULTS: Long-term exposure to high glucose stimulated insulin hypersecretion and inhibited AMPK activity in rat islets. Troglitazone-suppressed insulin hypersecretion was closely related to the activation of AMPK. This action was most prominent at the moderate concentration of glucose. Glucose-stimulated insulin secretion was decreased by long-term troglitazone treatment, but significantly increased after the drug withdrawal. Compound C, an AMPK inhibitor, reversed troglitazone-suppressed insulin secretion in MIN6 cells and rat islets. Knockdown of AMPKα2 showed a similar result. In MIN6 cells, troglitazone blocked high glucose-closed ATP-sensitive K(+) (KATP) channel and decreased membrane potential, along with increased voltage-dependent potassium channel currents. Troglitazone suppressed intracellular Ca(2+) response to high glucose, which was abolished by treatment with compound C. CONCLUSION: Our results suggest that troglitazone provides ß-cell "a rest" through activating AMPK and inhibiting insulin hypersecretion, and thus restores its response to glucose. GENERAL SIGNIFICANCE: These data support that AMPK activation may be an important mechanism for thiazolidinediones preserving ß-cell function.