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Globally methane (CH4) emissions from ruminant livestock account for 29% of total CH4 emissions. Inherited variation about CH4 emissions of different animal species might provide new opportunity for manipulating CH4 production. Six rumen-simulating fermenters (Rusitec) were set up for this study lasting for 16 d. The diet consisted of forage to concentrate ratio of 50:50 with barley straw as the forage. Treated vessels were supplied with rumen fluid from yak or cattle (3 vessels per animal species). Microbial growth was measured using 15N as a marker. The microbial community structure from liquid- and solid-fraction of each vessel was determined based on the 16S rRNA genes targeting both bacteria and archaea with MiSeq platform. CH4 yield was lower when the inoculum used from yak than that from cattle (0.26 and 0.33 mmol CH4/g dry matter intake, respectively). Lower H2 production was observed in Rusitec fermenters with rumen fluid from yak compare with that from cattle (0.28 and 0.86 mmol/d, respectively). The apparent digestibility of neutral detergent fiber, the isovalerate percentage with respect to the total amount of volatile fatty acids, the hydrogen recovery, and the proportion of liquid-associated microbial nitrogen derived from ammonia-nitrogen were higher in Rusitec fermenters incubated with rumen fluid from cattle than that from yak. The relative abundances of methanogens were no difference between two animal species. We hypothesize that more H2 production contributes to the higher methane emissions in cattle compare with yak. [ABSTRACT FROM AUTHOR]

Increasing clinical lines of evidence have shown the coinfection/superinfection of porcine circovirus type 2 (PCV2) and classical swine fever virus (CSFV). Here, we investigated whether PCV2 and CSFV could infect the same cell productively by constructing an in vitro coinfection model. Our results indicated that PCV2-free PK15 cells but not ST cells were more sensitive to PCV2, and the PK15 cell line could stably harbor replicating CSFV (PK15-CSFV cells) with a high infection rate. Confocal and super-resolution microscopic analysis showed that PCV2 and CSFV colocalized in the same PK15-CSFV cell, and the CSFV E2 protein translocated from the cytoplasm to the nucleus in PK15-CSFV cells infected with PCV2. Moreover, PCV2-CSFV dual-positive cells increased gradually in PK15-CSFV cells in a PCV2 dose-dependent manner. In PK15-CSFV cells, PCV2 replicated well, and the production of PCV2 progeny was not influenced by CSFV infection. However, CSFV reproduction decreased in a PCV2 dose-dependent manner. In addition, cellular apoptosis was not strengthened in PK15-CSFV cells infected with PCV2 in comparison with PCV2-infected PK15 cells. Moreover, using this coinfection model we further demonstrated PCV2-induced apoptosis might contribute to the impairment of CSFV HCLV strain replication in coinfected cells. Taken together, our results demonstrate for the first time the coinfection/superinfection of PCV2 and CSFV within the same cell, providing an in vitro model to facilitate further investigation of the underlying mechanism of CSFV and PCV2 coinfection. [ABSTRACT FROM AUTHOR]

It has been hypothesized that the cytosolic esterase-induced fluorescence intensity (CEIFI) from carboxy dimethyl fluorescein diacetate (CMFDA) in platelets may related to platelet functions. In the present study, we measured the change of CEIFI in platelets during storage, and examined the correlations of CEIFI with the in vitro functionality of stored platelets, including the ADP-induced aggregation activity, hypotonic shock response, expression of CD62P as well as platelet apoptosis. The CEIFI of fresh platelets, when tested at 10 μM CMFDA, the mean fluorescence intensity index (MFI) was 305.9 ± 49.9 (N = 80). After 1-day storage, it was 203.8 ± 34.4, the CEIFI of the stored platelets started to decline significantly, and reduced to 112.7 ±27.7 after 7-day storage. The change in CEIFI is highly correlated to all four functional parameters measured, with the correlation coefficients being 0.9813, 0.9848, -0.9945 and -0.9847 for the ADP-induced aggregation activity, hypotonic shock response (HSR), expression of CD62P and platelet apoptosis respectively. The above results show that the CEIFI measurement of platelets represents well the viability and functional state of in vitro stored platelets. This may be used as a convenient new method for quality evaluation for stored platelets if this result can be further validated by the following clinical trials. [ABSTRACT FROM AUTHOR]

Purpose: Recently, genetic polymorphism (rs3803662C>T) in TOX3 was reported to induce the risk of breast cancer. In this study, we hypothesized that rs3803662 could influence gastric cancer survival outcomes. Methods: With multiplex SNaPshot method, we genotyped TOX3 rs3803662 in 880 gastric patients with surgical resection. The association between genotype and survival outcomes was performed by the Kaplan-Meier method, Cox regression analysis models and the log-rank test. Results: There was no association in the analyses of rs3803662 and survival of gastric cancer. However, the stratified analysis by histology showed that rs3803662 CT/TT genotype was associated with a significantly better survival for diffuse-type gastric cancer (log-rank p = 0.030, hazard ratio [HR]  = 0.67, 95% confidence interval [CI]  = 0.46–0.96), than the CC genotype. In addition, this favorable effect was especially obvious among gastric cancer patients with tumor size >5 cm, T3 and T4 depth of invasion, lymph node metastasis, no drinking, no distant metastasis, no chemotherapy and gastric cardia cancer. Conclusions: TOX3 rs3803662 might play an important role in the prognostic outcome and treatment of gastric cancer, especially perhaps further help in explaining the reduced risk of death associated with diffuse-type gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Myelin transcription factor 1 (MYT1) and its homologue MYT1-like (MYT1L) are the two main members of MYT/NZF family transcription factors, which are highly related, share a high degree of identity and show similar regulatory functions in neural development. There are evidences from several cytology experiments showing that MYT1 is associated with carcinoma. Methodology/Principal Findings: In the present study, we genotyped 944 surgically resected gastric cancer patients by the SNaPshot method to explore the association of MYT1L rs17039396 polymorphism with survival of gastric cancer in a Chinese population. We found that cardia cancer patients carrying MYT1L rs17039396 GG genotype survived for a significantly shorter time than those carrying the GA genotype. This significance was enhanced in the dominant model (GG vs. GA/AA, log-rank P = 0.001), suggesting a potential protect role of the variant A allele. Multivariate Cox regression analyses showed that the AG/GG genotypes were associated with a significantly decreased risk of death from gastric cancer (adjusted hazard ratio (HR) = 0.57, 95% confidence interval (CI) = 0.40–0.81). Stratification analyses further showed that such protective effect was statistically significant in subgroups of patients with tumor size ≤5 cm (adjusted HR = 0.34, 95%CI = 0.19–0.64), well-moderate gastric cancer (adjusted HR = 0.59, 95%CI = 0.35–0.98), no lymph-node metastasis (adjusted HR = 0.49, 95%CI = 0.31–0.76), no distant metastasis (adjusted HR = 0.59, 95%CI = 0.41–0.84). Conclusions/Significance: In conclusion, these data represents the first demonstration that MYT1L rs17039396 variants could indentified as a favorable prognostic indicator for gastric cancer, particularly among the cardia gastric cancer. Further validation in other larger studies with different ethnic populations and functional evaluations are needed. [ABSTRACT FROM AUTHOR]

Objective: To investigate the association of SOX2 expression in tumor with clinicopathological features and survival of non-small-cell lung carcinoma (NSCLC) patients. Methods: Publications assessing the clinicopathological characteristics and prognostic significance of SOX2 in NSCLC were identified up to May 2013. A meta-analysis of eligible studies was performed using standard statistical methods to clarify the association between SOX2 expression and these clinical parameters. Results: A total of eight studies met the inclusion criteria. Analysis of these data showed that SOX2 expression was positively associated with squamous histology, (pooled OR = 5.26, 95% CI: 1.08–25.6, P = 0.040). Simultaneously, we also found that SOX2 expression was positively associated with overall survival (pooled HR = 0.65, 95% CI: 0.47–0.89, P = 0.007, random-effect). Conclusions: SOX2 expression in tumor is a candidate positive prognostic biomarker for NSCLC patients. [ABSTRACT FROM AUTHOR]

Background: The IL-4, IL-4 receptor (IL4R), and IL-13 genes are crucial immune factors and may influence the course of various diseases. In the present study, we investigated the association between the potential functional polymorphisms in IL-4, IL-4R, and IL-13 and coal workers' pneumoconiosis (CWP) risk in a Chinese population. Methods: Six polymorphisms (C-590T in IL-4, Ile50Val, Ser478Pro, and Gln551Arg in IL-4R, C-1055T and Arg130Gln in IL-13) were genotyped and analyzed in a case-control study of 556 CWP and 541 control subjects. Results: Our results revealed that the IL-4 CT/CC genotypes were associated with a significantly decreased risk of CWP (odds ratio (OR) = 0.74, 95% confidence interval (CI) = 0.58-0.95), compared with the TT genotype, particularly among subgroups of age ,65 years (OR = 0.68, 95%CI = 0.46-0.99) and dust exposure years $26 years (OR = 0.69, 95%CI = 0.50-0.94). Moreover, the polymorphism was significantly associated with risk of CWP patients with stage I. In addition, a combined effect was observed in a dose-dependent manner with increasing numbers of risk variant alleles (Ptrend = 0.023), and individuals with 11-12 risk alleles had a 47% higher risk of CWP than those with 0-8 risk alleles (OR = 1.47, 95% CI = 1.05- 2.05). Conclusions: Our results suggest that the IL-4 C-590T polymorphism is involved in the etiology of CWP and susceptibility to this disease. Larger studies are warranted to validate our findings. [ABSTRACT FROM AUTHOR]

Expression of p53 appears to be correlated to prognosis in patients with malignancy, but its role in gastric carcinoma has remained controversial. Recently we reported that JWA, an ADP-ribosylation-like factor 6 interacting protein 5 (ARL6ip5), was both prognostic for overall survival and predictive for platinum-based treatment of gastric cancer. In this study, we aimed to investigate p53 expression as a prognostic and predictive marker in resectable gastric cancer, alone and in combination with JWA. Expression of p53 was examined in three large patient cohorts (total n=1155) of gastric cancer. High expression of p53 was significantly correlated with unfavorable clinicopathologic parameters and decreased overall patient survival. Furthermore, patients with high p53 expression in tumors acquired remarkable survival benefit from adjuvant first-line platinum-based-chemotherapy. The synergy between p53 and JWA in predicting patient outcome was demonstrated, while no significantly elevated predictive value concerning chemotherapy was observed. Thus, p53 expression is a potent prognostic and predictive factor for resectable gastric cancer with adjuvant platinum-based chemotherapy. A combined effect of p53 with JWA as efficient prognostic indicators was found for the first time.

Our previous studies indicated that JWA plays an important role in DNA damage repair, cell migration, and regulation of MAPKs. In this study, we investigated the role of JWA in chemical carcinogenesis using conditional JWA knockout (JWA(Δ2/Δ2)) mice and two-stage model of skin carcinogenesis. Our results indicated that JWA(Δ2/Δ2) mice were resistant to the development of skin papillomas initiated by 7, 12-dimethylbenz(a)anthracene (DMBA) followed by promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA). In JWA(Δ2/Δ2) mice, the induction of papilloma was delayed, and the tumor number and size were reduced. In primary keratinocytes from JWA(Δ2/Δ2) mice, DMBA exposure induced more intensive DNA damage, while TPA-promoted cell proliferation was reduced. The further mechanistic studies showed that JWA deficiency blocked TPA-induced activation of MAPKs and its downstream transcription factor Elk1 both in vitro and in vivo. JWA(Δ2/Δ2) mice are resistance to tumorigenesis induced by DMBA/TPA probably through inhibition of transcription factor Elk1 via MAPKs. These results highlight the importance of JWA in skin homeostasis and in the process of skin tumor development.

Background: Arsenic is well-established as a human carcinogen, but the molecular mechanisms leading to arsenic-induced carcinogenesis are complex and elusive. It is not been determined if the epithelial-mesenchymal transition (EMT) and stem cell-like properties contribute in causing to carcinogen-induced malignant transformation and subsequent tumor formation., Methods: To investigate the molecular mechanisms underlying EMT and the emergence of cancer stem cell-like properties during neoplastic transformation of human bronchial epithelial (HBE) cells induced by chronic exposure to arsenite. HBE cells were continuously exposed to arsenite. Spheroid formation assays and analyses of side populations (SPs) were performed to confirm that arsenite induces the acquired EMT and cancer stem cell-like phenotype. Treated HBE cells were molecularly characterized by RT-PCR, Western blots, immunofluorescence, Southwestern assays, reporter assays, and chromatin immunoprecipitation., Results: With chronic exposure to arsenite, HBE cells undergo an EMT and then acquire a malignant cancer stem cell-like phenotype. Twist1 and Bmi1 are involved in arsenite-induced EMT. The process is directly regulated by HIF-2α. The self-renewal genes, Oct4, Bmi1, and ALDH1, are necessary for arsenite-mediated maintenance of stem cells., Conclusions: EMT, regulated by HIF-2α, and the development of a cancer stem cell-like phenotype are associated with arsenite-induced transformation of HBE cells.