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Find video protocols related to scientific articles indexed in Pubmed.
T-bet Is Critical for the Development of Acute Graft-versus-Host Disease through Controlling T Cell Differentiation and Function.
J. Immunol.
PUBLISHED: 11-19-2014
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T-bet is a master regulator for IFN-? production and Th1 differentiation. We evaluated the roles of T-bet and IFN-? in T cell responses in acute graft-versus-host disease (GVHD) and found that T-bet(-/-) T cells induced significantly less GVHD compared with wild-type or IFN-?(-/-) counterparts in both MHC-mismatched and MHC-matched but minor histocompatibility Ag-mismatched models driven by CD4 T cells. T-bet(-/-), but not IFN-?(-/-), CD4 T cells had a markedly reduced ability to cause tissue damage in liver and gut. This distinct outcome is reflected by the differential gene expression on donor CD4 T cells deficient for T-bet or IFN-?. At mRNA and protein levels, we defined several T-bet-dependent molecules that may account for the impaired ability of T-bet(-/-) T cells to migrate into target organs and to produce Th1-related cytokines. Moreover, these molecules were independent of either endogenous IFN-?, such as CXCR3 and programmed death-1, or systematic IFN-?, such as NKG2D, I-A(b), and granzyme B. Although both T-bet(-/-) and IFN-?(-/-) CD4 T cells are prone to differentiate into Th17 cells, polarized Th17 cells deficient for T-bet but not for IFN-? had a significantly reduced ability to cause GVHD. Finally, T-bet(-/-) T cells had a compromised graft-versus-leukemia effect, which could be essentially reversed by neutralization of IL-17 in the recipients. We conclude that T-bet is required for Th1 differentiation and migration, as well as for optimal function of Th17 cells. Thus, targeting T-bet or regulating its downstream effectors independent of IFN-? may be a promising strategy to control GVHD in the clinic.
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Small molecule inhibitor YM155-mediated activation of death receptor 5 is crucial for chemotherapy-induced apoptosis in pancreatic carcinoma.
Mol. Cancer Ther.
PUBLISHED: 10-26-2014
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Despite much effort, pancreatic cancer survival rates are still dismally low. Novel therapeutics may hold the key to improving survival. YM155 is a small molecule inhibitor which has shown anti-tumor activity in a number of cancers by reducing the expression of survivin. The aim of our study is to understand the mechanisms by which YM155 functions in pancreatic cancer cells. We established the anti-tumor effect of YM155 with in vitro studies in the cultured cells, and in vivo studies using a mouse xenograft model. Our data demonstrated that YM155 reduced the expression of survivin; however down-regulation of survivin itself is insufficient to induce apoptosis in pancreatic cancer cells. We showed for the first time that treatment with YM155 increased death receptor 5 (DR5) expression in pancreatic cancer cells. We found that YM155 induced apoptosis by broad-spectrum inhibition of IAP family member proteins (e.g. CIAP1/2 and FLIP) and induced pro-apoptotic Bak protein up-regulation and activation; the anti-tumor effect of YM155 treatment with either the DR5 agonist lexatumumab or gemcitabine on pancreatic cancer cells was synergistic. Our data also revealed that YM155 inhibit tumor growth in vivo, whilst had no apparent toxicity to the non-cancerous human pancreatic ductal epithelial cell line (HPDE). Together, these findings suggest that YM155 could be a novel therapeutic agent for pancreatic cancer.
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ADAPTIVE CONTROL OF PARKINSON'S STATE BASED ON A NONLINEAR COMPUTATIONAL MODEL WITH UNKNOWN PARAMETERS.
Int J Neural Syst
PUBLISHED: 10-24-2014
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The objective here is to explore the use of adaptive input-output feedback linearization method to achieve an improved deep brain stimulation (DBS) algorithm for closed-loop control of Parkinson's state. The control law is based on a highly nonlinear computational model of Parkinson's disease (PD) with unknown parameters. The restoration of thalamic relay reliability is formulated as the desired outcome of the adaptive control methodology, and the DBS waveform is the control input. The control input is adjusted in real time according to estimates of unknown parameters as well as the feedback signal. Simulation results show that the proposed adaptive control algorithm succeeds in restoring the relay reliability of the thalamus, and at the same time achieves accurate estimation of unknown parameters. Our findings point to the potential value of adaptive control approach that could be used to regulate DBS waveform in more effective treatment of PD.
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Epigenetic signatures of alcohol abuse and hepatitis infection during human hepatocarcinogenesis.
Oncotarget
PUBLISHED: 10-09-2014
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Hepatocellular carcinoma (HCC) is the second most common cause of cancer deaths worldwide. Deregulated DNA methylation landscapes are ubiquitous in human cancers. Interpretation of epigenetic aberrations in HCC is confounded by multiple etiologic drivers and underlying cirrhosis. We globally profiled the DNA methylome of 34 normal and 122 liver disease tissues arising in settings of hepatitis B (HBV) or C (HCV) viral infection, alcoholism (EtOH), and other causes to examine how these environmental agents impact DNA methylation in a manner that contributes to liver disease. Our results demonstrate that each 'exposure' leaves unique and overlapping signatures on the methylome. CpGs aberrantly methylated in cirrhosis-HCV and conserved in HCC were enriched for cancer driver genes, suggesting a pathogenic role for HCV-induced methylation changes. Additionally, large genomic regions displaying stepwise hypermethylation or hypomethylation during disease progression were identified. HCC-HCV/EtOH methylomes overlap highly with cryptogenic HCC, suggesting shared epigenetically deregulated pathways for hepatocarcinogenesis. Finally, overlapping methylation abnormalities between primary and cultured tumors unveil conserved epigenetic signatures in HCC. Taken together, this study reveals profound epigenome deregulation in HCC beginning during cirrhosis and influenced by common environmental agents. These results lay the foundation for defining epigenetic drivers and clinically useful methylation markers for HCC.
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Computed tomography-based study exploring the feasibility of endovascular treatment of type a aortic dissection in the chinese population.
J. Endovasc. Ther.
PUBLISHED: 10-08-2014
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Purpose : To characterize type A aortic dissection (TAAD) in the Chinese population using high-resolution computed tomography (CT) and explore potential candidacy for endovascular repair of TAAD. Methods : The imaging studies and medical records of all 302 patients presenting with TAAD at two Chinese hospitals from 2010 to 2013 were reviewed. Of these, 221 patients were excluded because of missing/inadequate preoperative CT scans. The remaining 91 patients (64 men; mean age 51.1±7.5 years) had CT data adequate to assess anatomical suitability for endovascular treatment. Entry tears were identified using multiplanar reconstructions, while morphological measurements were based on a centerline of flow (CLF) technique. Suitability for endovascular treatment was based on a proximal landing zone ?20 mm long, a true lumen aortic diameter ?38 mm, and a total aortic diameter ?46 mm; no coronary bypass grafts originating from the ascending aorta; no malfunctioning aortic valve; and good cerebral and cardiac perfusion. Results : In the 91 patients, the precise location of the primary proximal entry tear could be identified in only 34 (37.4%) patients; in these patients, the identifiable intimal tears were located 36.4±41.0 mm distal to the closest coronary artery. The CLF was successfully generated in the CT scans of all patients; the mean lumen and total aortic lumen diameters at the entry tear level were 37.6±6.3 and 44.3±13.3 mm, respectively. Based on the CT measurements, stent-graft repair would have been anatomically feasible in 35 (38.5%) patients. No proximal landing zone (n=23), large aortic diameter (n=15), abnormal aortic valve (n=10), previous coronary bypass graft surgery (n=5), and poor cerebral and cardiac perfusion (n=3) were obstacles that affected the suitability for this treatment. Conclusion : Based on high-resolution CT scans, our pilot study suggested that 38% of Chinese patients with TAAD could potentially be treated by stent-grafting based on the anatomical characteristics of the proximal dissection.
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[Treatment of obstructive sleep apnea-hypopnea syndrome for children refractory asthma].
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
PUBLISHED: 09-23-2014
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The aim of this study was to understand the effect of different treatment of obstructive sleep apnea-hypopnea syndrome (OSAHS) for refractory asthma in children.
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[Portable ECG measuring system with non-contact electrode].
Zhongguo Yi Liao Qi Xie Za Zhi
PUBLISHED: 09-23-2014
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Heart disease is the major disease that threaten human health. ECG is an important tool for the diagnosis of cardiac disease. As traditional ECG measurement devices have many disadvantages, a non-contact ECG measurement system was designed. With the non-contact electrode based on capacitive coupling, the signals were collected and then they were amplified and filtered. The conditioned analog signal was converted to digital data which was sent to the mobile terminal through bluetooth. Finally, the ECG data was analyzed to extract the key ECG parameters. The results showed that the precise ECG signals can be got with the non-contact electrode and the key ECG parameters can be acquired accurately.
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Autophagy gene atg16l1 prevents lethal T cell alloreactivity mediated by dendritic cells.
Immunity
PUBLISHED: 09-13-2014
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Atg16L1 mediates the cellular degradative process of autophagy and is considered a critical regulator of inflammation based on its genetic association with inflammatory bowel disease. Here we find that Atg16L1 deficiency leads to an exacerbated graft-versus-host disease (GVHD) in a mouse model of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Atg16L1-deficient allo-HSCT recipients with GVHD displayed increased T cell proliferation due to increased dendritic cell (DC) numbers and costimulatory molecule expression. Reduced autophagy within DCs was associated with lysosomal abnormalities and decreased amounts of A20, a negative regulator of DC activation. These results broaden the function of Atg16L1 and the autophagy pathway to include a role in limiting a DC-mediated response during inflammatory disease, such as GVHD.
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Blood Neutrophil-Lymphocyte Ratio Predicts Survival in Patients with Advanced Pancreatic Cancer Treated with Chemotherapy.
Ann. Surg. Oncol.
PUBLISHED: 08-26-2014
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Although a high neutrophil-to-lymphocyte ratio (NLR) has been reported to be a predictor of poor survival in patients with pancreatic cancers, its prognostic role in patients with advanced pancreatic cancer undergoing chemotherapy remains unclear. This study was performed to determine the prognostic role of NLR in patients with advanced pancreatic cancer undergoing chemotherapy.
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Berberine induces hERG channel deficiency through trafficking inhibition.
Cell. Physiol. Biochem.
PUBLISHED: 08-18-2014
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The human ether-a-go-go-related gene (hERG) encodes the ? subunit of the IKr, which plays an essential role in repolarization of action potentials. hERG channels are targeted by various pro-arrhythmic drugs. Berberine (BBR) was previously found to acutely inhibit hERG currents and prolong action potential duration. The present study aimed to determine long-term effects of BBR on the expression of 135kDa/155kDa hERG and the mechanism.
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Frequency-dependent changes in the amplitude of low-frequency fluctuations in subcortical ischemic vascular disease (SIVD): a resting-state fMRI study.
Behav. Brain Res.
PUBLISHED: 08-17-2014
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Resting-state functional magnetic resonance imaging (RS-fMRI) allowed researchers to detect intrinsic brain activity during rest and has been considered an analytical tool for evaluation of dementia. Previously, subcortical ischemic vascular disease (SIVD) has been found decreased amplitude low-frequency fluctuations (ALFF) in a widely frequency range (0.01-0.08Hz) in the bilateral precuneus and increased ALFF values in the bilateral anterior cingulate cortex (ACC), left insula and hippocampus, which showed significant correlations with the cognitive performance. In this study we analyzed the ALFF of 30 patients with SIVD in two different frequency bands (slow-5: 0.01-0.027Hz; slow-4: 0.027-0.073Hz). In the slow-5 band, SIVD patients compared with controls exhibited significant higher ALFF in the bilateral anterior cingulate cortex, right putamen and right supplementary motor area, while lower ALFF in the right precuneus and right angular gyrus. A close correlation was found between the ALFF value of the right angular gyrus and ADL scores. In the slow-4 band, SIVD patients only exhibited increased ALFF in the bilateral anterior cingulate cortex, right putamen, left fusiform gyrus, and no correlation with cognitive scores was found. Our data demonstrate that SIVD patients have widespread abnormal intrinsic neural oscillations, which are dependent on specific frequency bands. ALFF of right angular gyrus at slow-5 band is more specific for SIVD and may be a useful tool to help SIVD diagnosis.
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Local spectroscopy of silver nanowire in different environments excited with a halogen lamp.
Opt Lett
PUBLISHED: 08-15-2014
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We report a propagation spectrum detection system in which one end of a plasmonic silver nanowire is locally illuminated from a normal halogen lamp and the scattered light is recorded spectroscopically at the other end. The system is applied to investigate surface plasmon polariton-Fabry-Perot (SPP-FP) modes of silver nanowires with different lengths at air-glass and oil-glass interfaces. The generalized FP model is used to analyze the spectrum, which fits well with the experimental results. The influence of nanowire length and environment on the properties of the FP resonances is discussed. The propagation spectrum detection system will find applications for integrated optical circuits and plasmonic sensing.
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The rescuable function and mechanism of resveratrol on As2O 3-induced hERG K (+) channel deficiency.
Naunyn Schmiedebergs Arch. Pharmacol.
PUBLISHED: 08-10-2014
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Arsenic trioxide (As2O3) is used to treat acute promyelocytic leukemia. However, the cardiotoxicity of long QT syndrome restricts its clinical application. Previous studies showed that As2O3 can damage the human ether-a-go-go-related gene (hERG) current via disturbing its trafficking to cellular membrane. This study aimed to investigate whether the As2O3-insulted hERG channel can be rescued by resveratrol, a recognized cardioprotective agent. The whole-cell patch clamp technique was used to record the hERG current and action potential duration. Co-immunoprecipitation and Western blot assay were applied to determine the function of hERG-Hsp70/Hsp90 chaperone complexes and the expression alteration of protein-folding-related proteins, respectively. Compared with treatment of As2O3 alone, co-treatment with resveratrol successfully restored the current and surface expression of hERG and obviously shortened action potential duration in guinea pig ventricular myocytes. Further experiments demonstrate that resveratrol relieved As2O3-caused endoplasmic reticulum (ER) stress by restoring the function of hERG-Hsp70/Hsp90 chaperone complexes and downregulating the protein expression of ER chaperone proteins (calnexin and calreticulin) and activating transcription factor 6. In conclusion, resveratrol was able to rescue the trafficking deficiency and relieve the ER stress (ERS). Our findings suggest that resveratrol has a potential effect to alleviate the adverse effect of As2O3 on cardiotoxicity.
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CD4(+)CD25 (+) regulatory T cells are not required for mesenchymal stem cell function in fully MHC-mismatched mouse cardiac transplantation.
Cell Tissue Res.
PUBLISHED: 08-08-2014
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Although the immunomodulative properties of mesenchymal stem cells (MSCs) open up attractive possibilities in solid-organ transplantation, information concerning the optimal dose, route, timing of administration, major histocompatibility complex (MHC)-restriction and relevant mechanisms is currently lacking. Therefore, better characterization of MSC immunoregulatory activity and elucidation of its mechanisms are crucial. In this study, we confirmed that MSCs did not elicit proliferation by allogeneic CD4(+) T cells, suggesting that MSCs were not immunogenic. By using C57BL/6 mouse MSCs as donor-derived or recipient-derived or as third-party MSCs, we discovered that MSCs suppressed CD4(+) T cell proliferation and prolonged mouse cardiac allograft survival in a dose-dependent and non-MHC-restricted manner. We also found that intraperitoneal administration favored survival prolongation, although this prolongation was weaker than that via the intravenous route. Only infusion at earlier time points favored survival prolongation. Depletion of CD4(+)CD25(+) T cells did not affect the immunosuppression of MSCs on CD4(+) T cells. Moreover, MSCs did not induce regulatory T cells. The in vivo data revealed that MSCs did not increase the percentage of CD4(+)CD25(+) T cells and FoxP3 expression. More importantly, we demonstrated for the first time that depletion of CD4(+)CD25(+) T cells did not hinder MSC-induced survival prolongation, indicating that CD4(+)CD25(+) regulatory T cells were not essential for the prolongation of MSC-mediated allograft survival.
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Stathmin destabilizing microtubule dynamics promotes malignant potential in cancer cells by epithelial-mesenchymal transition.
HBPD INT
PUBLISHED: 08-08-2014
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Stathmin is a ubiquitous cytosolic regulatory phosphoprotein and is overexpressed in different human malignancies. The main physiological function of stathmin is to interfere with microtubule dynamics by promoting depolymerization of microtubules or by preventing polymerization of tubulin heterodimers. Stathmin plays important roles in regulating many cellular functions as a result of its microtubule-destabilizing activity. Currently, the critical roles of stathmin in cancer cells, as well as in lymphocytes have been valued. This review discusses stathmin and microtubule dynamics in cancer development, and hypothesizes their possible relationship with epithelial-mesenchymal transition (EMT).
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Profilin-1 suppresses tumorigenicity in pancreatic cancer through regulation of the SIRT3-HIF1? axis.
Mol. Cancer
PUBLISHED: 08-07-2014
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Tumor cells exhibit abnormal actin remodeling profiles, which involve the altered expressions of several important actin-binding proteins. Profilin1 (Pfn1), originally identified as an actin-associated protein, has been linked to several human malignancies. Our recent studies suggested that Pfn1 facilitates apoptosis in pancreatic cancer cells. Here, we investigated the exact role of Profilin1 (Pfn1) in pancreatic adenocarcinoma (PDAC) and the underlying mechanisms.
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The combination of HTATIP2 expression and microvessel density predicts converse survival of hepatocellular carcinoma with or without sorafenib.
Oncotarget
PUBLISHED: 07-11-2014
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Our previous studies have demonstrated that sorafenib can promote the dissemination of hepatocellular carcinoma (HCC) through downregulation of HTATIP2, a suppressor of tumor growth and metastasis that is associated with inhibition of angiogenesis. Here, we investigated the predictive values of the HTATIP2 level and microvessel density (MVD) with or without sorafenib administration for HCC. Three independent cohorts were included. Using tissue microarray, we assessed the relationship between HTATIP2 expression/MVD and overall survival. The results showed that high HTATIP2 expression and a low MVD value were independent protective prognostic factors after curative HCC resection (297 cases/cohort 1); however, both parameters were converted to independent negative prognostic indicators for patients with postsurgical sorafenib treatment (69/143 cases/cohort 2; P<0.05 for all). This same relationship was observed in patients that received sorafenib treatment for advanced HCC (83 cases/cohort 3; efficacy measures and survival analyses, P<0.05 for all). Moreover, the combination of HTATIP2 and MVD had better power to predict patient death and disease recurrence (P<0.001 for both). We conclude that the combination of HTATIP2 and MVD predicts the converse survival of HCC with or without sorafenib intervention. Our findings can assist in the selection of candidates for personalized treatment with sorafenib.
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Axl as a downstream effector of TGF-?1 via PI3K/Akt-PAK1 signaling pathway promotes tumor invasion and chemoresistance in breast carcinoma.
Tumour Biol.
PUBLISHED: 06-29-2014
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The invasion and chemoresistance are crucial causes of morbidity and death for cancer patients. Axl is closely associated with malignant phenotype of breast tumor cells, including invasiveness and metastasis. Both breast cancer cell line and tissue displayed increased expression of Axl, especially in highly metastatic breast cancer. On the contrary, experimental inhibition of Axl or transforming growth factor beta 1 (TGF-?1) by RNAi assay could suppress cell invasion ability and chemoresistance. Moreover, the up-regulation of Axl was induced by TGF-?1, further activated phosphatidylinositol 3-kinase (PI3K)/Akt and PAK1 translocation, and resulted in greater cell motility, invasion, and chemoresistance in vitro and in vivo. After the detection and statistics in human breast cancer specimens, we found that the Axl expression was closely correlated with TGF-?1 level, tumor differentiation, lymph node metastasis, and clinical stage (p?
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Association between ERCC2 polymorphisms and glioma risk: a meta-analysis.
Asian Pac. J. Cancer Prev.
PUBLISHED: 06-28-2014
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ERCC2 is an essential component of the nucleotide excision repair pathway which is involved in the effective maintenance of genome integrity. Association studies on ERCC2 polymorphisms and glioma risk have yielded inconclusive results. This meta-analysis was performed to gain a better insight into the relationship between ERCC2 polymorphisms and glioma risk. A systematic literature search updated to December 2, 2013 was performed in the Pubmed and EMBASE databases. Crude pooled odds ratios (ORs) with their corresponding 95% confidence intervals (95% CIs) were used to estimate the association between ERCC2 polymorphisms and glioma risk under a suitable effect model according to heterogeneity. All analyses were performed using Review Manager 5 (version 5.2) and STATA (version 12.0). The combined results demonstrated rs13181 to be significantly associated with glioma risk (G allele versus T allele: OR=1.15, 95% CI=1.05-1.26, P=0.002; dominant model: OR=1.22, 95% CI=1.07-1.39, P=0.002; recessive model: OR=1.18, 95% CI=0.98-1.41, P=0.070). We also found that rs13181 acts in an allele dose-dependent manner (GG versus TT: OR=1.30, 95% CI=1.07-1.57, P=0.009; TG versus TT: OR=1.20, 95%=CI 1.05-1.37, P=0.009; trend test, P=0.004). However, no evidence was found in analyses for the association between other 3 ERCC2 polymorphisms (rs238406, rs1799793, and rs1052555) and susceptibility to glioma development. Our meta-analysis suggests that rs13181 is significantly associated with glioma risk in an allele dose-dependent manner, whereas, 3 other ERCC2 polymorphisms (rs238406, rs1799793, and rs1052555) may have no influence.
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Recent trends in wastewater flow and pollutant load resulting from urbanization in Shanghai.
Water Environ. Res.
PUBLISHED: 06-26-2014
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To better control water pollution and to manage water resources, we used input-output analysis to examine structural changes in wastewater flows and pollutant loads following changes in socioeconomic activities in Shanghai. We found that the industrial structure has changed considerably and that total direct emission loads exhibited a decreasing trend between 1997 and 2007. Emission loads from secondary industries, especially from paper manufacturing, have decreased. However, wastewater from primary industries remained constant while wastewater from tertiary industries and domestic sources increased, acting as the largest sources of emission loads since 2002. Wastewater and pollutant loads from household consumption, including indirect sources from food manufacturing, clothing, and transportation, had an especially large influence on emission loads in 2007. These emissions were primarily generated through primary industries and food manufacturing sectors. With continued urbanization, wastewater and pollutants generated by household consumption should be factored into the control of water pollution in Shanghai.
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Residential preferences for river network improvement: an exploration of choice experiments in Zhujiajiao, Shanghai, China.
Environ Manage
PUBLISHED: 06-19-2014
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River networks have both ecological and social benefits for urban development. However, river networks have suffered extensive destruction as a result of urbanization and industrialization, especially in China. River restoration is a growth business but suffers poor efficiency due to a lack of social understanding. Assessing the benefits of river system restoration and recognizing public preferences are critical for effective river ecosystem restoration and sustainable river management. This study used a choice experiment with a multinomial logit model and a random parameter logit model to assess respondents' cognitive preferences regarding attributes of river networks, and their possible sources of heterogeneity. Results showed that riverfront condition was the attribute most preferred by respondents, while stream morphology was the least preferred. Results also illustrated that the current status of each of three river network attributes was not desirable, and respondents would prefer a river network with a "branch pattern," that is "limpid with no odor," and "accessible with vegetation." Estimated willingness to pay was mainly affected by household monthly income, residential location, and whether respondents had household members engaged in a water protection career. The assessment results can provide guidance and a reference for managers, sponsors, and researchers.
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Complete mitochondrial genome of Platevindex sp. (Gastropoda: Pulmonata: Systellommatophora: Onchidiidae).
Mitochondrial DNA
PUBLISHED: 06-19-2014
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Abstract The complete mitochondrial genome sequence of Platevindex sp. is firstly described in the article. The mitogenome (13,908?bp) contains 22 tRNA genes, 2 ribosomal RNA genes and 13 protein-coding genes, and 1 putative control region (CR). CR is not well characterized due to lack of discrete conserved sequence blocks. This characteristic is similar with CRs of other invertebrate mitochondrial genomes. The characteristic is the typical bivalvia mitochondrial gene composition.
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Id1 expression promotes T regulatory cell differentiation by facilitating TCR costimulation.
J. Immunol.
PUBLISHED: 06-11-2014
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T regulatory (Treg) cells play crucial roles in the regulation of cellular immunity. The development of Treg cells depends on signals from TCRs and IL-2Rs and is influenced by a variety of transcription factors. The basic helix-loop-helix proteins are known to influence TCR signaling thresholds. Whether this property impacts Treg differentiation is not understood. In this study, we interrogated the role of basic helix-loop-helix proteins in the production of Treg cells using the CD4 promoter-driven Id1 transgene. We found that Treg cells continued to accumulate as Id1 transgenic mice aged, resulting in a significant increase in Treg cell counts in the thymus as well as in the periphery compared with wild-type controls. Data from mixed bone marrow assays suggest that Id1 acts intrinsically on developing Treg cells. We made a connection between Id1 expression and CD28 costimulatory signaling because Id1 transgene expression facilitated the formation of Treg precursors in CD28(-/-) mice and the in vitro differentiation of Treg cells on thymic dendritic cells despite the blockade of costimulation by anti-CD80/CD86. Id1 expression also allowed in vitro Treg differentiation without anti-CD28 costimulation, which was at least in part due to enhanced production of IL-2. Notably, with full strength of costimulatory signals, however, Id1 expression caused modest but significant suppression of Treg induction. Finally, we demonstrate that Id1 transgenic mice were less susceptible to the induction of experimental autoimmune encephalomyelitis, thus illustrating the impact of Id1-mediated augmentation of Treg cell levels on cellular immunity.
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(18)F-FDG PET/CT can be used to detect non-functioning pancreatic neuroendocrine tumors.
Int. J. Oncol.
PUBLISHED: 06-10-2014
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18F-Fluorodeoxyglucose positron emission tomo-graphy and computed tomography (18F-FDG PET/CT) has limited value in well-differentiated neuroendocrine tumors. The value of 18F-FDG PET/CT in non-functioning pancreatic neuroendocrine tumors, which are often poorly differentiated, malignant, and present at an advanced stage, was also thought to be limited. This study was performed to evaluate the clinical value of 18F-FDG PET/CT in assessing non-functioning pancreatic neuroendocrine tumors. From January 2010 to February 2014, a comparable large cohort of patients (31 cases) with non-functioning pancreatic neuroendocrine tumors from Shanghai Cancer Center underwent 18F-FDG PET/CT scans. Demographics and clinical characteristics were retrospectively collected and analyzed for all the patients. Twenty-eight of 31 (90.3%) patients with non-functioning endocrine pancreatic tumors had an elevated 18F-FDG uptake (SUVmax ?2.5). In addition, 18F-FDG PET/CT visualized 38 of 42 (90.5%) distant metastatic lesions. The 18F-FDG uptake had significant association with tumor size (P=0.012) and TNM stage (P=0.004). The application of 18F-FDG PET/CT has changed the management of 8 cases (8/31, 25.8%). In conclusion, 18F?FDG PET/CT plays an important role in detecting and staging non-functioning pancreatic neuroendocrine tumors.
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AMPK inhibits cardiac hypertrophy by promoting autophagy via mTORC1.
Arch. Biochem. Biophys.
PUBLISHED: 05-17-2014
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AMPK, a serine/threonine protein kinase, has proven to be an important positive regulator of autophagy, which is a key factor in the regulation of cardiac hypertrophy. Thus, we explored whether AMPK could inhibit cardiac hypertrophy by regulating autophagy. In pressure overload induced cardiac hypertrophy, decreased autophagy was detected. Administration of AMPK activators (AICAR and metformin) significantly blocked hypertrophy, accompanied by enhanced autophagy level in the hearts. Furthermore, AMPK activation resulted in enhanced autophagosome formation and unimpaired lysosomal function. In vitro studies demonstrated adenoviral overexpression of constitutively activated AMPK increased autophagy and blunted PE-induced cardiomyocyte hypertrophy. Additionally, we found AICAR reduced the phosphorylation of the mTORC1 downstream effectors 4EBP1 and p70S6K, but AKT, which is a downstream signal of mTORC2, was not affected. Furthermore, activation by AMPK failed to lead to an additive effect on autophagy induced by the mTORC1 inhibitor rapamycin, indicating AMPK activates autophagy through the inhibition of mTORC1 but not of mTORC2. This study proved that AMPK can inhibit cardiac hypertrophy by stimulating autophagy through mTORC1 signaling.
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[Clinical characteristics of 42 cases of malignant endometrial polyps].
Zhonghua Fu Chan Ke Za Zhi
PUBLISHED: 05-14-2014
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To investigate the clinicopathologic characteristics of premalignant and malignant endometrial polyps (EP) in premenopausal and postmenopausal women.
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Mutation of mouse Samd4 causes leanness, myopathy, uncoupled mitochondrial respiration, and dysregulated mTORC1 signaling.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 05-05-2014
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Sterile alpha motif domain containing protein 4 (Samd4) is an RNA binding protein that mediates translational repression. We identified a Samd4 missense mutation, designated supermodel, that caused leanness and kyphosis associated with myopathy and adipocyte defects in C57BL/6J mice. The supermodel mutation protected homozygous mice from high fat diet-induced obesity, likely by promoting enhanced energy expenditure through uncoupled mitochondrial respiration. Glucose tolerance was impaired due to diminished insulin release in homozygous mutant mice. The defects of metabolism in supermodel mice may be explained by dysregulated mechanistic target of rapamycin complex 1 (mTORC1) signaling, evidenced by hypophosphorylation of 4E-BP1 and S6 in muscle and adipose tissues of homozygous mice. Samd4 may interface with mTORC1 signaling through an interaction with 14-3-3 proteins and with Akt, which phosphorylates Samd4 in vitro.
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An Unusual Case of Systemic Inflammatory Myofibroblastic Tumor with Successful Treatment with ALK-Inhibitor.
Case Rep Pathol
PUBLISHED: 04-30-2014
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Systemic inflammatory myofibroblastic tumor is an exceedingly rare entity. A 45-year-old Hispanic female presented with a 6-month history of left-sided thigh pain, low back pain, and generalized weakness. PET/CT scan revealed abnormal activity in the liver, adrenal gland, and pancreas. MRI of the abdomen demonstrated two 6-7?cm masses in the liver. MRI of the lumbar spine demonstrated lesions in the L2 to L4 spinous processes, paraspinal muscles, and subcutaneous tissues, as well as an 8?mm enhancing intradural lesion at T11, all thought to be metastatic disease. A biopsy of the liver showed portal tract expansion by a spindle cell proliferation rich in inflammation. Tumor cells showed immunoreactivity for smooth muscle actin and anaplastic lymphoma kinase 1 (ALK1). Tissue from the L5 vertebra showed a process histologically identical to that seen in the liver. FISH analysis of these lesions demonstrated an ALK (2p23) gene rearrangement. The patient was successfully treated with an ALK-inhibitor, Crizotinib, and is now in complete remission. We present the first reported case, to our knowledge, of inflammatory myofibroblastic tumor with systemic manifestations and ALK translocation. This case is a prime example of how personalized medicine has vastly improved patient care through the use of molecular-targeted therapy.
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Cathepsin D Repairing Role in Photodamaged Skin Barrier.
Skin Pharmacol Physiol
PUBLISHED: 04-26-2014
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Backgrounds/Objectives: Cathepsin D plays an important part in maintaining a normal skin barrier. Our previous study found that cathepsin D decreased in chronic photodamaged skin. This study investigated the cathepsin D content change in the stratum corneum (SC) and the repairing role of cathepsin D in chronic photodamaged skin barrier via the application of cathepsin D gel. Methods: Cathepsin D gel (0.001%) was applied to chronic photodamaged (sun-exposed forearm) human skin on identical sites (1 cm²/area) twice daily for 2 weeks. At 30 min and at 1, 3, 7, and 14 days, skin hydration and transepidermal water loss (TEWL) average values were detected via noninvasive skin detection equipment. Cathepsin D and transglutaminase (TGase)-1 in the skin sublayers were separated and detected via tape stripping, ELISA and Western blot. Results: After 2 weeks of cathepsin D gel application, the skin moisture value increased from 86.8 ± 1.2 to 95.2 ± 2.7 (p < 0.05), while TEWL decreased from 17.88 ± 1.87 to 11.58 ± 2.14 (p < 0.05). Cathepsin D protein was detected in the upper epidermis (12.6 ± 2.6 ng/cm(2)), mid-epidermis (8.4 ± 0.8 ng/cm(2)) and deep epidermis (16.2 ± 2.6 ng/cm(2)) in the cathepsin D gel group compared to the control group (2.2 ± 0.7, 3.0 ± 1.1 and 3.85 ± 1.4 ng/cm(2), respectively; p < 0.05). TGase-1 enzyme expression was upregulated 2.54 ± 0.19 times in the matrix gel-treated skin. Conclusions: These data suggest that cathepsin D gel could increase the SC cathepsin D content and repair the epidermal barrier in chronic photodamaged skin. The mechanism might be related to increasing TGase-1 expression and activity. © 2014 S. Karger AG, Basel.
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Axl mediates tumor invasion and chemosensitivity through PI3K/Akt signaling pathway and is transcriptionally regulated by slug in breast carcinoma.
IUBMB Life
PUBLISHED: 04-17-2014
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The invasion and chemoresistance are crucial causes of morbidity and relapse for cancer patients. Axl is implicated in the modulation of cell invasion, cancer metastasis, and chemosensitivity in human breast carcinoma cell lines. Both breast cancer cell lines and tissues displayed increased expression of Axl, and it over expressed in highly metastatic breast cancer. The altered expression level of Axl was corresponding to the changed invasive phenotype and chemosensitivity of MDA-MB-231 cells both in vitro and in vivo. Further data indicated that experimental inhibition of Axl by RNAi assay inhibited phosphatidylinositol 3-kinase (PI3K)/Akt/GSK3? signaling pathway, resulted in the decrease of Slug expression, and further suppressed cell invasion properties and chemosensitivity. What is more, after the detection and statistics in human breast cancer specimens, we found the Axl expression was closely correlated with histological grade, lymph node metastasis, and clinical stage (P?
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The pattern of brain gray matter impairments in patients with subcortical vascular dementia.
J. Neurol. Sci.
PUBLISHED: 04-01-2014
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Though subcortical ischemic vascular dementia (SIVD) is known to initially affect subcortical regions, numerous brain imaging studies have also documented the widespread cortical alternations. Here we collected brain structural magnetic resonance imaging data from 34 SIVD patients and 35 healthy controls. Voxel-based morphometry (VBM), cortical thickness (and surface area) analysis and deep gray matter volume measurements were performed. VBM analysis showed gray matter volume reduction in lateral and medial temporal lobes, as well as orbitofrontal cortex in SIVD patients. The surface-based analyses revealed more subtle structural differences in the perisylvian area, medial temporal lobe, anterior and posterior cingulate, as well as prefrontal areas. Furthermore, analyses of deep gray matter demonstrated significant atrophy of the hippocampus, amygdala, nucleus accumbens and other nuclei. Finally, we found that thinning in the hippocampus and anterior cingulate cortex, as well as the volume decline in thalamus, caudate nucleus and amygdala was correlated with the cognitive impairment in patients. In conclusion, our study showed the structural abnormalities of the hippocampus and its associated outflow areas, as well as cortices implicated in cholinergic circuits in SIVD. These findings may bring new insights into the dysfunction of brain gray matter in SIVD.
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DCs sensitized with mPD-L1-Ig fusion protein improve the effect of heart transplantation in mice by promoting the generation of T-reg cells.
Cell. Immunol.
PUBLISHED: 03-20-2014
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To detect the effects of DCs sensitized by mPD-L1-Ig fusion protein in heart transplantation in mice as well as its mechanisms.
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Connective tissue growth factor and integrin ?v?6: A new pair of regulators critical for ductular reaction and biliary fibrosis.
Hepatology
PUBLISHED: 03-17-2014
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Connective tissue growth factor (CTGF) is a matricellular protein that mediates cell-matrix interaction through various subtypes of integrin receptors. This study investigated the role of CTGF and integrin ?v?6 in hepatic progenitor/oval cell activation, which often occurs in the form of ductular reactions (DRs) when hepatocyte proliferation is inhibited during severe liver injury. CTGF and integrin ?v?6 proteins were highly expressed in DRs of human cirrhotic livers and cholangiocarcinoma. Confocal microscopy analysis of livers from Ctgf promoter driven GFP reporter mice suggested that oval cells and cholangiocytes were the main sources of CTGF and integrin ?v?6 during liver injury induced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). Deletion of exon 4 of the Ctgf gene using tamoxifen inducible Cre-loxP system down-regulated integrin ?v?6 in DDC damaged livers of knockout mice. Ctgf deficiency or inhibition of integrin ?v?6 by administrating the neutralizing antibody 6.3G9 (10 mg/kg body weight) caused low levels of EpCAM and CK19 mRNAs. Also, there were smaller oval cell areas, fewer proliferating ductular epithelial cells, and lower cholestasis serum markers within two weeks after DDC treatment. Associated fibrosis was attenuated as indicated by reduced expression of fibrosis-related genes, smaller areas of ? smooth muscle actin staining and low collagen production based on hydroxyproline content and the Sirius red staining. Finally, integrin ?v?6 could bind to CTGF mediating oval cell adhesion to CTGF and fibronection substrata and promoting transforming growth factor (TGF)-?1 activation in vitro. Conclusions: CTGF and integrin ?v?6 regulate oval cell activation and fibrosis, probably through interacting with their common matrix and signal partners, fibronectin and TGF-?1. CTGF and integrin ?v?6 are potential therapeutic targets to control DRs and fibrosis in related liver disease. (Hepatology 2014).
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Phyllodes tumor of the breast: role of Axl and ST6GalNAcII in the development of mammary phyllodes tumors.
Tumour Biol.
PUBLISHED: 03-08-2014
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Phyllodes tumor exhibits an aggressive growth. The expression of many biological markers has been explored to discriminate between different grades of phyllodes tumor and to predict their behavior. The purpose of this study was to evaluate the implications of Axl and ST6GalNAcII in phyllodes tumors. Real-time PCR, Western blot, and immunohistochemical were used to analyze differential expression of ST6GalNAcII and Axl in phyllodes tumor (PT) cell lines and tissue specimens. RNAi assay, ECM invasion assay, and tumorigenicity assay were used to analyze the altered expression of ST6GalNAcII gene effects on the expression of Axl and invasive ability of phyllodes tumor cells in vitro and in vivo. Compared to benign tumors, borderline and malignant ones showed a remarkable increase in mRNA levels of Axl and ST6GalNAcII gene, and it was higher in malignant tumor cells than in borderline tumor cells. When ST6GalNAcII was silenced, compared to the control, the expression level of Axl was significantly reduced in malignant tumor cell transfectants and knockdown of ST6GalNAcII gene significantly inhibited invasive activity in malignant tumor cells. The high expression of ST6GalNAcII and Axl was significantly correlated with tumor grade and distance metastasis by immunohistochemical analysis. Axl and ST6GalNAcII expression increases with increasing tumor grade in mammary phyllodes tumors. ST6GalNAc II might be participated in the glycosylation of Axl, and this Axl glycosylation may mediate the tumorigenicity, invasion, and distant metastasis of PT cells.
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ISG12a mediates cell response to Newcastle disease viral infection.
Virology
PUBLISHED: 03-05-2014
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Newcastle disease virus (NDV) oncolysis is believed to be facilitated by a defective Type I interferon (IFN) response. We compared hepatocellular carcinoma (HCC)-derived cell lines and found that TRAIL-resistant cells were more susceptible to NDV oncolysis than were TRAIL-sensitive cells. In examining the IFN response, we found that basal expression of the IFN-stimulated gene (ISG)-12a was low in TRAIL-resistant but high in TRAIL-sensitive cells, and ISG12a over-expression or silencing enhanced or reduced their TRAIL sensitivities, respectively. Moreover, ISG12a over-expression in TRAIL-resistant cells decreased NDV replication but surprisingly increased oncolysis while ISG12a silencing had the opposite effect on TRAIL-sensitive cells. Finally, RIG-I and Noxa appear to also contribute to NDV oncolysis. Together, these results suggest that high basal ISG12a may inhibit NDV replication and oncolysis, while low basal ISG12a may allow sufficient NDV replication for induction of ISG12a, and other factors required for NDV oncolysis, with implications for future therapeutics.
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Hepatocyte Toll-like receptor 4 regulates obesity-induced inflammation and insulin resistance.
Nat Commun
PUBLISHED: 02-28-2014
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Chronic low-grade inflammation is a hallmark of obesity and thought to contribute to the development of obesity-related insulin resistance. Toll-like receptor 4 (Tlr4) is a key mediator of pro-inflammatory responses. Mice lacking Tlr4s are protected from diet-induced insulin resistance and inflammation; however, which Tlr4-expressing cells mediate this effect is unknown. Here we show that mice deficient in hepatocyte Tlr4 (Tlr4LKO) exhibit improved glucose tolerance, enhanced insulin sensitivity and ameliorated hepatic steatosis despite the development of obesity after a high-fat diet (HFD) challenge. Furthermore, Tlr4LKO mice have reduced macrophage content in white adipose tissue, as well as decreased tissue and circulating inflammatory markers. In contrast, the loss of Tlr4 activity in myeloid cells has little effect on insulin sensitivity. Collectively, these data indicate that the activation of Tlr4 on hepatocytes contributes to obesity-associated inflammation and insulin resistance, and suggest that targeting hepatocyte Tlr4 might be a useful therapeutic strategy for the treatment of type 2 diabetes.
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The UPF1 RNA surveillance gene is commonly mutated in pancreatic adenosquamous carcinoma.
Nat. Med.
PUBLISHED: 02-21-2014
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Pancreatic adenosquamous carcinoma (ASC) is an enigmatic and aggressive tumor that has a worse prognosis and higher metastatic potential than its adenocarcinoma counterpart. Here we report that ASC tumors frequently harbor somatically acquired mutations in the UPF1 gene, which encodes the core component of the nonsense-mediated RNA decay (NMD) pathway. These tumor-specific mutations alter UPF1 RNA splicing and perturb NMD, leading to upregulated levels of NMD substrate mRNAs. UPF1 mutations are, to our knowledge, the first known unique molecular signatures of pancreatic ASC.
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Stereoselectivity in bioaccumulation and excretion of epoxiconazole by mealworm beetle (Tenebrio molitor) larvae.
Ecotoxicol. Environ. Saf.
PUBLISHED: 02-08-2014
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Stereoselectivity in bioaccumulation and excretion of stereoisomers of epoxiconazole by mealworm beetle (Tenebrio molitor) larvae through dietary exposure was investigated. Liquid chromatography tandem mass spectrometry (HPLC-MS/MS) method that use a ChiralcelOD-3R[cellulosetris-Tris-(3, 5-dichlorophenyl-carbamate)] chromatography column was applied to carry out chiral separation of the stereoisomers. Wheat bran was spiked with racemic epoxiconazole at two dose levels of 20mg/kg and 2mg/kg (dry weight) to feed T. molitor larvae. The results showed that both the doses of epoxiconazole were taken up by Tenebrio molitor larvae rapidly at the initial stages. There was a significant trend of stereoselective bioaccumulation in the larvae with a preferential accumulation of (-)-epoxiconazole in the 20mg/kg dose. The stereoselectivity in bioaccumulation in the 2mg/kg dosage was not obvious compared to the 20mg/kg group. Results of excretion indicated an active excretion is an important pathway for the larvae to eliminate epoxiconazole which was a passive transport process with non stereoselectivity. The faster elimination might be the reason for the low accumulation of epoxiconazole, as measured by bioaccumulation factor (BAF).
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A preoperative serum signature of CEA(+) /CA125(+) /CA19-9???1000 U/mL indicates poor outcome to pancreatectomy for pancreatic cancer.
Int. J. Cancer
PUBLISHED: 02-05-2014
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Pancreatectomy is associated with significant morbidity and unpredictable outcome, with few diagnostic tools to determine, which patients gain the most benefit from this treatment, especially before the operation. This study aimed to define a preoperative signature panel of serum markers to indicate response to pancreatectomy for pancreatic cancer. Over 1000 patients with pancreatic cancer treated at two independent high-volume institutions were included in this study and were divided into three groups, including resected, locally advanced and metastatic. Eight serum tumor markers most commonly used in gastrointestinal cancers were analyzed for patient outcome. Preoperative CA19-9 independently indicated surgical response in pancreatic cancer. Patients with CA19-9 ?1000 U/mL generally had a poor surgical benefit. However, a subset of these patients still achieved a survival advantage when CA19-9 levels decreased postoperatively. CEA and CA125 in the presence of CA19-9 ?1000 U/mL could independently predict the non-decrease of CA19-9 postoperatively. The combination of the three markers was useful for predicting a worse surgical outcome with a median survival of 5.1 months vs. 23.0 months (p?
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Melatonin synergized with cyclosporine A improves cardiac allograft survival by suppressing inflammation and apoptosis.
Mol Med Rep
PUBLISHED: 02-05-2014
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Melatonin, a widespread physiological mediator, has been demonstrated to exhibit a dose?dependent immunoregulatory effect in vitro and in vivo, including mediating physiological circadian rhythms, neutralizing free radicals and exerting antisenescence actions. In the present study, the efficacy and mechanism of melatonin alone or in combination with cyclosporine (CsA) in prolonging heart transplantation survival was examined. Daily treatment with melatonin (200 mg/kg/day) through a gavage, significantly prolonged the survival of cardiac grafts (mean survival time, 13.4±2.4 days; n=7; P<0.0001) compared with the untreated controls (5.8±1.2 days; n=7). When CsA (5 mg/kg/day) was co?administered with melatonin (50 mg/kg/day), the survival rate improved (31.6±2.4 days; n=7; P<0.001), compared with that achieved by only 20 mg/kg/day CsA (22±2.8 days; n=7). As expected, melatonin significantly alleviated the inflammatory response and apoptosis as determined by TdT?mediated dUTP?biotin nick end labeling assay (P<0.05). Further analysis demonstrated that melatonin significantly reduced p65 activation and the release of inflammatory factors. Therefore, these findings indicate that melatonin in combination with CsA protected the cardiac allograft by inhibiting inflammation?induced apoptosis. These results provide evidence for a novel therapeutic approach for future immunosuppressive agents in organ transplantation.
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Arcuate AgRP neurons mediate orexigenic and glucoregulatory actions of ghrelin.
Mol Metab
PUBLISHED: 02-01-2014
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The hormone ghrelin stimulates eating and helps maintain blood glucose upon caloric restriction. While previous studies have demonstrated that hypothalamic arcuate AgRP neurons are targets of ghrelin, the overall relevance of ghrelin signaling within intact AgRP neurons is unclear. Here, we tested the functional significance of ghrelin action on AgRP neurons using a new, tamoxifen-inducible AgRP-CreER(T2) transgenic mouse model that allows spatiotemporally-controlled re-expression of physiological levels of ghrelin receptors (GHSRs) specifically in AgRP neurons of adult GHSR-null mice that otherwise lack GHSR expression. AgRP neuron-selective GHSR re-expression partially restored the orexigenic response to administered ghrelin and fully restored the lowered blood glucose levels observed upon caloric restriction. The normalizing glucoregulatory effect of AgRP neuron-selective GHSR expression was linked to glucagon rises and hepatic gluconeogenesis induction. Thus, our data indicate that GHSR-containing AgRP neurons are not solely responsible for ghrelin's orexigenic effects but are sufficient to mediate ghrelin's effects on glycemia.
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Human mesenchymal stromal cells attenuate graft-versus-host disease and maintain graft-versus-leukemia activity following experimental allogeneic bone marrow transplantation(1.)
Stem Cells
PUBLISHED: 01-27-2014
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We sought to define the effects and underlying mechanisms of human, marrow-derived mesenchymal stromal cells (hMSCs) on graft-versus-host disease (GvHD) and graft-versus-leukemia (GvL) activity. Irradiated B6D2F1 mice given C57BL/6 BM and splenic T-cells and treated with hMSCs had reduced systemic GvHD, donor T-cell expansion, and serum TNF? and IFN? levels. Bioluminescence imaging demonstrated that hMSCs redistributed from lungs to abdominal organs within 72h; and target tissues harvested from hMSC-treated alloBMT mice had less GvHD than untreated controls. Cryo-imaging more precisely revealed that hMSCs preferentially distributed to splenic marginal zones and regulated T-cell expansion in the white pulp. Importantly, hMSCs had no effect on in vitro cytotoxic T-cell activity and preserved potent GvL effects in vivo. Mixed leukocyte cultures containing hMSCs exhibited decreased T-cell proliferation, reduced TNF?, IFN?, and IL-10, but increased PGE2 levels. Indomethacin and E-prostanoid 2 (EP2) receptor antagonisms both reversed while EP2 agonism restored hMSC-mediated in vitro T-cell suppression, confirming the role for PGE2 . Furthermore, cyclo-oxygenase inhibition following alloBMT abrogated the protective effects of hMSCs. Together, our data show that hMSCs preserve GvL activity and attenuate GvHD and reveal that hMSC biodistribute to secondary lymphoid organs wherein they attenuate alloreactive T-cell proliferation likely through PGE2 induction. Stem Cells 2014.
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Upper airway cough syndrome in children and two inflammatory factors: TRPV1 and TGF-?2.
Int. J. Pediatr. Otorhinolaryngol.
PUBLISHED: 01-22-2014
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The aim of the study was to investigate upper airway cough syndrome (UACS) in children and to determine alternative methods to explore the relationships among TRPV1, TGF-?2, and UACS.
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Study on biodegradation of the second phase Mg17Al12 in Mg-Al-Zn alloys: in vitro experiment and thermodynamic calculation.
Mater Sci Eng C Mater Biol Appl
PUBLISHED: 01-14-2014
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The in vitro biodegradation behavior of Mg17Al12 as a second phase in Mg-Al-Zn alloys was investigated via electrochemical measurement and immersion test. The Hank's solutions with neutral and acidic pH values were adopted as electrolytes to simulate the in vivo environment during normal and inflammatory response process. Furthermore, the local orbital density functional theory approach was employed to study the thermodynamical stability of Mg17Al12 phase. All the results proved the occurrence of pitting corrosion process with crackings for Mg17Al12 phase in Hank's solution, but with a much lower degradation rate compared with both AZ31 alloy and pure magnesium. Furthermore, a preliminary explanation on the biodegradation behaviors of Mg17Al12 phase was proposed.
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Abnormal distribution of peripheral lymphocyte subsets induced by PDAC modulates overall survival.
Pancreatology
PUBLISHED: 01-12-2014
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The impairment of the immune system is prevalent in patients with malignancies, including pancreatic ductal adenocarcinoma (PDAC). The present study aimed to evaluate alternations of peripheral lymphocyte subsets in patients with PDAC, and also to assess the prognostic value of observed changes.
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Distinct Role of CD86 Polymorphisms (rs1129055, rs17281995) in Risk of Cancer: Evidence from a Meta-Analysis.
PLoS ONE
PUBLISHED: 01-01-2014
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Previous studies concerning the role of CD86 polymorphisms (rs1129055 and rs17281995) in cancer fail to provide compelling evidence. The aim of this study was to investigate the role of common polymorphisms in the risk of cancer by meta-analysis.
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Comparison of hybrid procedure and open surgical revascularization for multilevel infrainguinal arterial occlusive disease.
Clin Interv Aging
PUBLISHED: 01-01-2014
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To compare outcomes of hybrid (combined surgical and endovascular) procedures (HYBRID) with open surgical reconstructions (OPEN) in patients with multilevel infrainguinal artery occlusive diseases.
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Identification of rabbit annulus fibrosus-derived stem cells.
PLoS ONE
PUBLISHED: 01-01-2014
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Annulus fibrosus (AF) injuries can lead to substantial deterioration of intervertebral disc (IVD) which characterizes degenerative disc disease (DDD). However, treatments for AF repair/regeneration remain challenging due to the intrinsic heterogeneity of AF tissue at cellular, biochemical, and biomechanical levels. In this study, we isolated and characterized a sub-population of cells from rabbit AF tissue which formed colonies in vitro and could self-renew. These cells showed gene expression of typical surface antigen molecules characterizing mesenchymal stem cells (MSCs), including CD29, CD44, and CD166. Meanwhile, they did not express negative markers of MSCs such as CD4, CD8, and CD14. They also expressed Oct-4, nucleostemin, and SSEA-4 proteins. Upon induced differentiation they showed typical osteogenesis, chondrogenesis, and adipogenesis potential. Together, these AF-derived colony-forming cells possessed clonogenicity, self-renewal, and multi-potential differentiation capability, the three criteria characterizing MSCs. Such AF-derived stem cells may potentially be an ideal candidate for DDD treatments using cell therapies or tissue engineering approaches.
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Ultraviolet A-induced cathepsin K expression is mediated via MAPK/AP-1 pathway in human dermal fibroblasts.
PLoS ONE
PUBLISHED: 01-01-2014
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Cathepsin K (CatK), a cysteine protease with the potent elastolytic activity, plays a predominant role in intracellular elastin degradation in human dermal fibroblasts (HDFs), and contributes to solar elastosis. In previous studies, CatK expression was downregulated in photoaged skin and fibroblasts, but upregulated in acute UVA-irradiated skin and fibroblasts. The underlying mechanisms regulating UVA-induced CatK expression remain elusive.
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Particle swarm optimization with scale-free interactions.
PLoS ONE
PUBLISHED: 01-01-2014
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The particle swarm optimization (PSO) algorithm, in which individuals collaborate with their interacted neighbors like bird flocking to search for the optima, has been successfully applied in a wide range of fields pertaining to searching and convergence. Here we employ the scale-free network to represent the inter-individual interactions in the population, named SF-PSO. In contrast to the traditional PSO with fully-connected topology or regular topology, the scale-free topology used in SF-PSO incorporates the diversity of individuals in searching and information dissemination ability, leading to a quite different optimization process. Systematic results with respect to several standard test functions demonstrate that SF-PSO gives rise to a better balance between the convergence speed and the optimum quality, accounting for its much better performance than that of the traditional PSO algorithms. We further explore the dynamical searching process microscopically, finding that the cooperation of hub nodes and non-hub nodes play a crucial role in optimizing the convergence process. Our work may have implications in computational intelligence and complex networks.
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KAT5 silencing induces apoptosis of GBC-SD cells through p38MAPK-mediated upregulation of cleaved Casp9.
Int J Clin Exp Pathol
PUBLISHED: 01-01-2014
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The poor overall prognosis of Gallbladder carcinoma (GBC) patients and the limited therapeutic regimens for these patients demonstrates the need for better therapeutic modalities, while the growing evidences have indicated that those genes contributed to epigenetic regulation may serve as therapeutic targets. The function of histone acetylation on growth and survival of GBC cells remains unknown. In present study, an RNAi screening of 16 genes involving histone acetyltransferases (HATs) was applied to GBC-SD cells and we found that KAT5 knockdown specifically inhibits the proliferation of GBC-SD cells by casp9-mediated apoptosis. Microarray data analysis showed that KAT5 RNAi may result in cleaved casp9 upregulation through p38MAPK activation in GBC-SD cells. The mRNA expression level of KAT5 was significantly upregulated in GBC tissues than in the adjacent normal tissues. In consistence with the mRNA level, the protein expression of KAT5 was markedly increased in tissues from patients with poor prognosis than those with good prognosis. These findings strongly indicated that KAT5 was implicated in GBC tumorigenesis and that its expression level was associated with the prognosis. Our work may also provide a potential therapeutic target for treatment of GBC patients.
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Comparative study of root growth and sucrose-cleaving enzymes in metallicolous and non-metallicolous populations of Rumex dentatus under copper stress.
Ecotoxicol. Environ. Saf.
PUBLISHED: 12-25-2013
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Sucrose metabolism in roots of metallophytes is very important for root growth and maintenance of heavy metal tolerance. However, rare researches have been carried out on this topic so far. We tested here a hypothesis that roots of copper-tolerant plants should manifest higher activities of sucrose-cleaving enzymes than non-tolerant plants for maintaining root growth under Cu stress. Plants of two contrasting populations of metallophyte Rumex dentatus, one from an ancient Cu mine (MP) and the other from a non-mine site (NMP), were treated with Cu in controlled experiments. Cu treatment resulted in a higher root biomass and root/shoot biomass ratio in MP compared to NMP. More complicated root system architecture was showed in MP under Cu stress. Activities and transcript levels of acid invertase as well as contents of sucrose and reducing sugar in MP were elevated under Cu treatment, while activities of neutral/alkaline invertase and sucrose synthase showed no significant differences between two populations. The results indicate important roles of acid invertase in governing root growth under Cu stress.
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[Study on hydrogen autotrophic denitrification of bio-ceramic reactor].
Huan Jing Ke Xue
PUBLISHED: 12-25-2013
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Nitrate wastewater is processed in a bio-ceramic reactor based on hydrogen autotrophic denitrification. The implementation procedure of biological denitrification by hydrogen autotrophic denitrification was investigated. The effects of hydraulic retention time, influent nitrate load, influent pH, temperature and the amount of hydrogen were assessed throughout this trial. The results showed that the removal rate of NO-(3) -N was 94. 54% and 97. 47% when the hydraulic retention time was 24 h and 48 h, respectively. When the hydraulic retention time was in the range of 5-16 h, the removal rate gradually dropped with the shortening of the hydraulic retention time. When the influent NO-(3) -N concentration was low, with the increase in the influent NO-(3) -N concentration, the degradation rate also increased. The denitrification was inhibited when the NO-(3) -N concentration was higher than 110 mg.L-1. Neutral and alkaline environment was more suitable for the reactor. The reactor showed a wide range of temperature adaptation and the optimum temperature of the reactor was from 25 to 30 degrees C. When hydrogen was in short supply, the effect of denitrification was significantly reduced. These results indicated the specificity of hydrogen utilization by the denitrifying bacteria. The effluent nitrite nitrogen concentration was maintained at low levels during the operation.
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[Medical therapy of polyostotic fibrous dysplasia of the spinal column].
Beijing Da Xue Xue Bao
PUBLISHED: 12-18-2013
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To discuss treatments of spinal polyostotic fibrous dysplasia (PFD) and their clinical outcomes.
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Ligamentum teres hepatis patch enhances the healing of pancreatic fistula after distal pancreatectomy.
HBPD INT
PUBLISHED: 12-11-2013
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Pancreatic fistula is one of the most common complications after the distal pancreatectomy. Many methods have been tried to solve the problem, but no one is optimal, especially for the soft pancreatic stump cases. This study used ligamentum teres hepatis as a patch to cover the pancreatic stump. Between October 2010 and December 2012, seventy-seven patients who had undergone distal pancreatectomy with a soft pancreatic stump were divided into two groups: group A (n=39, patients received conventional ligated main pancreatic duct method) and group B (n=38, patients underwent a coverage procedure). Patients in group A had a longer recovery from postoperative pancreatic fistula than those in group B (16.4+/-3.5 vs 10.8+/-1.6 days, P<0.05). The coverage procedure with ligamentum teres hepatis is a safe, effective and convenient method for patients with a soft pancreas remnant during distal pancreatectomy.
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Excess LIGHT Contributes to Placental Impairment, Increased Secretion of Vasoactive Factors, Hypertension, and Proteinuria in Preeclampsia.
Hypertension
PUBLISHED: 12-09-2013
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Preeclampsia, a prevalent hypertensive disorder of pregnancy, is believed to be secondary to uteroplacental ischemia. Accumulating evidence indicates that hypoxia-independent mediators, including inflammatory cytokines and growth factors, are associated with preeclampsia, but it is unclear whether these signals directly contribute to placental damage and disease development in vivo. We report that LIGHT, a novel tumor necrosis factor superfamily member, is significantly elevated in the circulation and placentas of preeclamptic women compared with normotensive pregnant women. Injection of LIGHT into pregnant mice induced placental apoptosis, small fetuses, and key features of preeclampsia, hypertension and proteinuria. Mechanistically, using neutralizing antibodies specific for LIGHT receptors, we found that LIGHT receptors herpes virus entry mediator and lymphotoxin ? receptor are required for LIGHT-induced placental impairment, small fetuses, and preeclampsia features in pregnant mice. Accordingly, we further revealed that LIGHT functions through these 2 receptors to induce secretion of soluble fms-like tyrosine kinase-1 and endothelin-1, 2 well-accepted pathogenic factors in preeclampsia, and thereby plays an important role in hypertension and proteinuria in pregnant mice. Lastly, we extended our animal findings to human studies and demonstrated that activation of LIGHT receptors resulted in increased apoptosis and elevation of soluble fms-like tyrosine kinase-1 secretion in human placental villous explants. Overall, our human and mouse studies show that LIGHT signaling is a previously unrecognized pathway responsible for placental apoptosis, elevated secretion of vasoactive factors, and subsequent maternal features of preeclampsia, and reveal new therapeutic opportunities for the management of the disease.
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Capture, release and culture of circulating tumor cells from pancreatic cancer patients using an enhanced mixing chip.
Lab Chip
PUBLISHED: 11-13-2013
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Circulating tumor cells (CTCs) from peripheral blood hold important information for cancer diagnosis and disease monitoring. Analysis of this "liquid biopsy" holds the promise to usher in a new era of personalized therapeutic treatments and real-time monitoring for cancer patients. But the extreme rarity of CTCs in blood makes their isolation and characterization technologically challenging. This paper reports the development of a geometrically enhanced mixing (GEM) chip for high-efficiency and high-purity tumor cell capture. We also successfully demonstrated the release and culture of the captured tumor cells, as well as the isolation of CTCs from cancer patients. The high-performance microchip is based on geometrically optimized micromixer structures, which enhance the transverse flow and flow folding, maximizing the interaction between CTCs and antibody-coated surfaces. With the optimized channel geometry and flow rate, the capture efficiency reached >90% with a purity of >84% when capturing spiked tumor cells in buffer. The system was further validated by isolating a wide range of spiked tumor cells (50-50?000) in 1 mL of lysed blood and whole blood. With the combination of trypsinization and high flow rate washing, captured tumor cells were efficiently released. The released cells were viable and able to proliferate, and showed no difference compared with intact cells that were not subjected to the capture and release process. Furthermore, we applied the device for detecting CTCs from metastatic pancreatic cancer patients blood; and CTCs were found from 17 out of 18 samples (>94%). We also tested the potential utility of the device in monitoring the response to anti-cancer drug treatment in pancreatic cancer patients, and the CTC numbers correlated with the clinical computed tomograms (CT scans) of tumors. The presented technology shows great promise for accurate CTC enumeration, biological studies of CTCs and cancer metastasis, as well as for cancer diagnosis and treatment monitoring.
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Tissue Transglutaminase Contributes to the Pathogenesis of Preeclampsia and Stabilizes Placental Angiotensin Receptor Type 1 by Ubiquitination-Preventing Isopeptide Modification.
Hypertension
PUBLISHED: 11-04-2013
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Preeclampsia is a life-threatening pregnancy disorder that is widely thought to be triggered by impaired placental development. However, the placenta-related pathogenic factors are not fully identified, and their underlying mechanisms in disease development remain unclear. Here, we report that the protein level and enzyme activity of tissue transglutaminase (TG2 or tTG), the most ubiquitous member of a family of enzymes that conducts post-translational modification of proteins by forming ?-(?-glutamyl)-lysine isopeptide bonds, are significantly elevated in placentas of preeclamptic women. TG2 is localized in the placental syncytiotrophoblasts of patients with preeclampsia where it catalyzes the isopeptide modification of the angiotensin receptor type 1 (AT1). To determine the role of elevated TG2 in preeclampsia, we used a mouse model of preeclampsia based on injection of AT1-agonistic autoantibody. A pathogenic role for TG2 in preeclampsia is suggested by in vivo experiments in which cystamine, a potent transglutaminase inhibitor, or small interfering RNA-mediated TG2 knockdown significantly attenuated autoantibody-induced hypertension and proteinuria in pregnant mice. Cystamine treatment also prevented isopeptide modification of placental AT1 receptors in preeclamptic mice. Mechanistically, we revealed that AT1-agonistic autoantibody stimulation enhances the interaction between AT1 receptor and TG2 and results in increased AT1 receptor stabilization via transglutaminase-mediated isopeptide modification in trophoblasts. Mutagenesis studies further demonstrated that TG2-mediated isopeptide modification of AT1 receptors prevents ubiquitination-dependent receptor degradation. Taken together, our studies not only identify a novel pathogenic involvement of TG2 in preeclampsia but also suggest a previously unrecognized role of TG2 in the regulation of G protein-coupled receptor stabilization by inhibiting ubiquitination-dependent degradation.
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Expression Pattern of Class B Gene PAP3 in Flower Development of Pepper.
Int J Mol Sci
PUBLISHED: 10-30-2013
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Class B gene APETALA3 (AP3) plays a key role in the development of petals and stamens. Here, we investigated the expression pattern of PAP3 gene (genbank accession number: HM104635) in the buds of cytoplasmic male sterility line 121A and its near-isogenic restorer line 121C at four developmental stages and analyzed the possible association between Class B genes and cytoplasmic male sterility of pepper. Semi-quantitative PCR and quantitative real-time RT-PCR (qRT-PCR) as well as RNA in situ hybridization showed increased expression of PAP3 at late phase of anther development and its higher expression in restorer line compared with sterility line indicating PAP3s role at late developmental stage of anther and suppressed expression in sterility line. RNA in situ hybridization showed Class B gene features: high abundance in stamen and petal; lower expression in pistil; no expression in sepal. Results of transient expression in onion epidermal cells also showed PAP3 localized in the nucleus, which is consistent with the expression pattern of transcription factors of MADS-box gene family.
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Plexiform Fibromyxoma: Report of Two Pediatric Cases, Including the First Example in the Esophagus.
Pediatr. Dev. Pathol.
PUBLISHED: 10-25-2013
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Abstract Plexiform fibromyxoma is a distinctive mesenchymal neoplasm usually arising in the gastric antrum. We report two cases of this entity in pediatric patients, including the first case arising in the esophagus. The patients were a 16-year-old female who presented with chest pain and was found on CT scan to have a mid-esophageal mass at the level of the carina, and an 11-year-old female with a gastric mass. Both patients underwent surgical resection of their tumors, which histologically exhibited a plexiform growth pattern with multiple nodules in the muscularis propria and infiltrative borders. The nodules were composed of a rich myxoid stroma with bland uniform spindle cells, no mitoses or necrosis, and delicate blood vessels in the background. Immunohistochemical studies demonstrated the tumor cells were immunoreactive with smooth muscle actin, and negative with S-100, CD34, desmin, and c-kit. We report the first case of plexiform fibromyxoma originating in the esophagus, emphasize its occurrence in pediatric patients, and review the related literature.
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The critical role of Sestrin 1 in regulating the proliferation of cardiac fibroblasts.
Arch. Biochem. Biophys.
PUBLISHED: 10-10-2013
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The proliferation of cardiac fibroblasts is pivotal in the development of cardiac fibrosis. Sestrin 1, which functions as antioxidant, plays diverse roles in the regulation of proliferation and cellular injury that is induced by oxidative stress. However, little is known regarding the impact of Sestrin 1 on the proliferation of cardiac fibroblasts. In the present study, with knockdown of Sestrin 1 by siRNA, we surveyed the effect of Sestrin 1 on cardiac fibroblast proliferation. Downregulation of Sestrin 1 promotes Ang II-induced proliferation of cardiac fibroblasts, leading to increased DNA synthesis and collagen production. Moreover, in the absence of Ang II, a similar phenotype to the basal condition was detected with silencing of Sestrin 1. Further analysis of the pro-proliferating signals revealed that knockdown of Sestrin 1 significantly activated ERK1/2 and mTOR, meanwhile, downregulation of Sestrin 1 also enhanced the expression of collagen type I and CTGF, which play important role in the cardiac fibrosis. Consistent with the antioxidant property of Sestrin 1, we determined that the proliferation induced by silence of Sestrin 1 was accompanied by a remarkably enhanced production of reactive oxygen species (ROS). However, diminishing ROS by NAC, a potent antioxidant, could only partly repress the pro-proliferative effect of Sestrin 1-downregulation. Consequently, our study demonstrated that Sestrin 1 plays an important role in the proliferation of cardiac fibroblasts, and the effect could be partly mediated by decreased oxidative stress.
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Impact of delays on the synchronization transitions of modular neuronal networks with hybrid synapses.
Chaos
PUBLISHED: 10-05-2013
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The combined effects of the information transmission delay and the ratio of the electrical and chemical synapses on the synchronization transitions in the hybrid modular neuronal network are investigated in this paper. Numerical results show that the synchronization of neuron activities can be either promoted or destroyed as the information transmission delay increases, irrespective of the probability of electrical synapses in the hybrid-synaptic network. Interestingly, when the number of the electrical synapses exceeds a certain level, further increasing its proportion can obviously enhance the spatiotemporal synchronization transitions. Moreover, the coupling strength has a significant effect on the synchronization transition. The dominated type of the synapse always has a more profound effect on the emergency of the synchronous behaviors. Furthermore, the results of the modular neuronal network structures demonstrate that excessive partitioning of the modular network may result in the dramatic detriment of neuronal synchronization. Considering that information transmission delays are inevitable in intra- and inter-neuronal networks communication, the obtained results may have important implications for the exploration of the synchronization mechanism underlying several neural system diseases such as Parkinsons Disease.
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[Experimental treatment of pulmonary interstitial fibrosis with human umbilical cord blood mesenchymal stem cells].
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
PUBLISHED: 09-26-2013
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To investigate the therapeutic effect and possible action mechanism of human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) in the treatment of bleomycin-induced pulmonary fibrosis in rats.
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[Relationship of the elderly nutrition knowledge and their education level in Nanjing].
Wei Sheng Yan Jiu
PUBLISHED: 09-13-2013
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To study the relationship of the elderly nutrition knowledge, eating behavior and BMI status with their education level.
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Enantiomerization and Enantioselective Bioaccumulation of Benalaxyl in Tenebrio molitor Larvae from Wheat Bran.
J. Agric. Food Chem.
PUBLISHED: 09-13-2013
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The enantiomerization and enatioselecive bioaccumulation of benalaxyl by dietary exposure to Tenebrio molitor larvae under laboratory conditions were studied by HPLC-MS/MS. Exposure of enantiopure R-benalaxyl and S-benalaxyl in T. molitor larvae revealed significant enantiomerization with formation of the R enantiomers from the S enantiomers, and vice versa. Enantiomerization was not observed in wheat bran during the period of 21 days. For the bioaccumulation experiment, the enantiomer fraction in T. molitor larvae was maintained approximately at 0.6, whereas the enantiomer fraction in wheat bran was maintained at 0.5; in other words, the bioaccumulation of benalaxyl was enantioselective in T. molitor larvae. Mathematical models for a process of uptake, degradation, and enantiomerization were developed, and the rates of uptake, degradation, and enantiomerization of R-benealaxyl and S-benealaxyl were estimated, respectively. The results were that the rate of uptake of R-benalaxyl (kRa = 0.052 h(-1)) was slightly lower than that of S-benalaxyl (kSa = 0.061 h(-1)) from wheat bran; the rate of degradation of R-benalaxyl (kRd = 0.285 h(-1)) was higher than that of S-benalaxyl (kSd = 0.114 h(-1)); and the rate of enantiomerization of R-benalaxyl (kRS = 0.126 h(-1)) was higher than that of S-benalaxyl (kSR = 0.116 h(-1)). It was suggested that enantioselectivtiy was caused not only by actual degradation and metabolism but also by enantiomerization, which was an important process in the environmental fate and behavior of chiral pesticides.
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Fibrous dysplasia of the mobile spine: report of 8 cases and review of the literature.
Spine
PUBLISHED: 08-24-2013
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Eight cases of fibrous dysplasia (FD) of the mobile spine treated surgically at the same center were retrospectively reviewed.
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Serotonin 2C receptors in pro-opiomelanocortin neurons regulate energy and glucose homeostasis.
J. Clin. Invest.
PUBLISHED: 07-25-2013
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Energy and glucose homeostasis are regulated by central serotonin 2C receptors. These receptors are attractive pharmacological targets for the treatment of obesity; however, the identity of the serotonin 2C receptor-expressing neurons that mediate the effects of serotonin and serotonin 2C receptor agonists on energy and glucose homeostasis are unknown. Here, we show that mice lacking serotonin 2C receptors (Htr2c) specifically in pro-opiomelanocortin (POMC) neurons had normal body weight but developed glucoregulatory defects including hyperinsulinemia, hyperglucagonemia, hyperglycemia, and insulin resistance. Moreover, these mice did not show anorectic responses to serotonergic agents that suppress appetite and developed hyperphagia and obesity when they were fed a high-fat/high-sugar diet. A requirement of serotonin 2C receptors in POMC neurons for the maintenance of normal energy and glucose homeostasis was further demonstrated when Htr2c loss was induced in POMC neurons in adult mice using a tamoxifen-inducible POMC-cre system. These data demonstrate that serotonin 2C receptor-expressing POMC neurons are required to control energy and glucose homeostasis and implicate POMC neurons as the target for the effect of serotonin 2C receptor agonists on weight-loss induction and improved glycemic control.
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Alkaline pretreatment for enhancement of biogas production from banana stem and swine manure by anaerobic codigestion.
Bioresour. Technol.
PUBLISHED: 07-21-2013
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The objective of this research was to propose and investigate the availability of digested banana stem (BS) to produce biogas. Squeezed BS with less moisture content was used for biogas production through a combination of NaOH pretreatment, solid-state fermentation, and codigestion technologies. NaOH doses were optimized according to biogas fermentation performance, and the best dose was 6% (by weight) based on the total solid (TS) of BS. Under this condition, the lignin, cellulose, and hemicellulose contents decreased from 18.36%, 32.36% and 14.6% to 17.10%, 30.07%, and 10.65%, respectively, after pretreatment. After biogas digestion, TS and volatile solid (VS) reductions of the codigestion were 48.5% and 70.4%, respectively, and the biogas and methane yields based on VS loading were 357.9 and 232.4 mL/g, which were 12.1% and 21.4%, respectively, higher than the control. Results indicated that the proposed process could be an effective method for using BS to produce biogas.
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A new method of microskin autografting with a Vaseline-based moisture dressing on granulation tissue.
Burns
PUBLISHED: 07-03-2013
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In the conventional method of microskin autografting, aggressive early excision is adopted, followed by coverage with a microskin-allograft complex to close extensive burn wounds. However, early excision is always associated with a defect of viable tissue, resulting in massive blood loss and causing high risk to aged patients or those with other systemic diseases. We developed a new method in which an eschar thinning operation was first adopted, followed by raising granulation tissue and microskin autografting, which was covered by a Vaseline-based moisture dressing. A total of 52 patients were included in this study and randomly assigned to the control group (n=26) and the experimental group (n=26) for the conventional method and the new method, respectively. The re-epithelisation rate on the 21st day after autografting indicated that there was no significant difference between both groups. There was also no significant difference between the two groups when the re-epithelialisation rate was compared with the type of organisms cultured. However, the Vancouver Burn Skin Score (VBSS) results demonstrated a significant improvement of cosmetic appearance in the experimental group (score=2.1) as compared to the control group (score=3.9). The new method also showed other advantages, including less blood loss, shorter surgical duration and lower cost of surgery. From this prospective study, it can be concluded that the new method can be an alternative to the conventional microskin autografting procedure.
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