Room-Temperature High-Performance Thermoelectric Bi0.6 Sb0.4 Te: Elimination of Detrimental Band Inversion in BiTe.

Room-temperature thermoelectric materials are the key to miniaturizing refrigeration equipment and have great scientific and social implications, yet their application is hindered by their extreme scarcity. BiTe exhibiting strong spin-orbit coupling peaks ZT at 600 K. Herein, we discover the synergy effect of Sb doping in BiTe that eliminates the detrimental band inversion and leads to an overlap of conduction band (CB) and valence band that significantly increases the S from 33 to 124 µV K-1 . In addition, this effect enhances the µ from 58 to 92 cm2  V-1 s-1 owing to the sharp increase in the CB slope along the Γ-A in the first Brillouin zone. Furthermore, Sb doping increases the anharmonicity, shortens the phonon lifetime and lowers κlat . Finally, Se/Sb codoping further optimizes the ZT to 0.6 at 300 K, suggesting that Bi0.6 Sb0.4 Te1-y Sey is a potential room-temperature TE material.

Activated leukocyte cell adhesion molecule regulates the interaction between pancreatic cancer cells and stellate cells.

Activated leukocyte cell adhesion molecule (ALCAM/CD166) is a transmembrane glycoprotein that is involved in tumor progression and metastasis. In the present study, the expression and functional role of ALCAM in pancreatic cancer cells and pancreatic stellate cells (PSCs) was investigated. Tissue specimens were obtained from patients with pancreatic ductal adenocarcinoma (n=56) or chronic pancreatitis (CP; n=10), who underwent pancreatic resection, and from normal pancreatic tissue samples (n=10). Immunohistochemistry was used to analyze the localization and expression of ALCAM in pancreatic tissues. Subsequently, reverse transcription­quantitative polymerase chain reaction and immunoblotting were applied to assess the expression of ALCAM in pancreatic cancer Panc­1 and T3M4 cells, as well as in PSCs. An enzyme­linked immunosorbent assay was used to measure ALCAM levels in cell culture medium stimulated by hypoxia, tumor necrosis factor (TNF)­α and transforming growth factor­ß. Silencing of ALCAM was performed using ALCAM small interfering (si)RNA and immunocytochemistry was used to analyze the inhibition efficiency. An invasion assay and a cell interaction assay were performed to assess the invasive ability and co­cultured adhesive potential of Panc­1 and T3M4 cells, as well as PSCs. Histologically, ALCAM expression was generally weak or absent in pancreatic cancer cells, but was markedly upregulated in PSCs in pancreatic cancer tissues. ALCAM was highly expressed in PSCs from CP tissues and PSCs surrounding pancreatic intraepithelial neoplasias, as well as in pancreatic cancer cells. ALCAM mRNA was highly expressed in PSCs, with a low to moderate expression in T3M4 and Panc­1 cells. Similar to the mRNA expression, immunoblotting demonstrated that ALCAM protein levels were high in PSCs and T3M4 cells, but low in Panc­1 cells. The expression of TNF­α increased, while hypoxia decreased the secretion of ALCAM in pancreatic cancer Panc­1 and T3M4 cells, and also in PSCs. Silencing of ALCAM by siRNA revealed no significant alteration in the invasion of pancreatic cancer cells, however, it inhibited the invasive ability of PSCs, and decreased the interaction between Panc­1 cells and PSCs. In conclusion, ALCAM is upregulated in PSCs of pancreatic cancer tissues, suggesting a potential role of ALCAM in regulating pancreatic cancer cell­PSC interactions.

Clinicopathological and prognostic significance of programmed cell death ligand 1 (PD-L1) expression in patients with esophageal squamous cell carcinoma: a meta-analysis.

BACKGROUND: The clinicopathological and prognostic significance of programmed cell death ligand 1 (PD-L1) expression in patients with esophageal squamous cell carcinoma (ESCC) remains controversial. To investigate this question, we conducted a meta-analysis. METHODS: A comprehensive literature search of electronic databases (up to July 10, 2016) was performed for relevant studies using multiple search strategies. Correlation between PD-L1 expression and clinicopathological features/overall survival (OS) was analyzed. RESULTS: A total of 1,350 ESCC patients from eight studies were included. The pooled odds ratios (ORs) indicated that none of the clinicopathological characteristics was correlated with PD-L1 expression, including gender [OR =0.84; 95% confidence interval (CI): 0.59-1.18; P=0.31], histological differentiation (OR =1.33; 95% CI: 0.95-1.85; P=0.09), tumor depth (OR =0.66; 95% CI: 0.33-1.35; P=0.26), status of lymph node metastasis (OR =0.67; 95% CI: 0.30-1.52; P=0.34), distal metastasis (OR =0.66; 95% CI: 0.40-1.09; P=0.10) and tumor node metastasis (TNM) stage (OR =0.93; 95% CI: 0.49-1.75; P=0.82). The combined hazard ratio (HR) for OS showed a trend that overexpression of PD-L1 might be associated with the survival outcome of ESCC, though the difference was not statistically significant (HR =1.65; 95% CI 0.95-2.85; P=0.07). CONCLUSIONS: Based on the published studies, PD-L1 overexpression in ESCC was not associated with common clinicopathological characteristics. PD-L1 might be a poor prognostic biomarker for ESCC. Further large-scale research should be performed to reveal the precise clinicopathological and prognostic significance of PD-L1 in ESCC by unified testing standard.

Rare case of upper gastrointestinal bleeding in achalasia.

Achalasia is a prototypic esophageal motility disorder with complications including aspiration-pneumonia, esophagitis, esophageal-tracheal fistula, spontaneous rupture of the esophagus, and squamous cell carcinoma. However, achalasia is rarely associated with esophageal stones and ulcer formation that lead to upper gastrointestinal bleeding. Here, we report the case of a 61-year-old woman who was admitted to our department after vomiting blood for six hours. Physical examination revealed that the patient had severe anemia and mild palpitation in the upper abdomen. CT revealed lower esophageal dilatation and esophageal wall thickening, and an emergency upper endoscopy showed that the esophagus was substantially expanded by a dark round stone, with multiple ulcers on the esophageal wall and a slit in the cardiac mucosa with a large clot attached. The patient's history included ingestion of 1 kg hawthorn three days prior. The acute upper gastrointestinal bleeding was caused by Mallory-Weiss syndrome associated with achalasia and an esophageal stone. For patients with achalasia, preventing excessive ingestion of tannins is crucial to avoid complications such as bleeding and rupture.

Crohn Disease of the Vulva without Gastrointestinal Manifestations in a 16-Year-Old Girl.

BACKGROUND: Crohn disease of the vulva is a rare disease that is difficult to diagnose. There are limited reports describing treatment of this condition. OBJECTIVE: To describe the diagnosis and treatment of a 16-year-old girl with Crohn disease of the vulva, without onset of intestinal symptoms. METHODS: Crohn disease was diagnosed by histopathology. The patient was treated with corticosteroids and followed for 1 year. RESULTS: After the final diagnosis, cutaneous lesions responded rapidly to corticosteroid treatment, which was gradually stopped after 6 months. The disease was well controlled at the 1-year follow-up. CONCLUSION: Crohn disease of the vulva can develop alone without the onset of intestinal symptoms. Diagnosis relies on special pathologic findings. Corticosteroid treatment is effective for this condition.

Participation of microbiota in the development of gastric cancer.

There are a large number of bacteria inhabiting the human body, which provide benefits for the health. Alterations of microbiota participate in the pathogenesis of diseases. The gastric microbiota consists of bacteria from seven to eleven phyla, predominantly Proteobacteria, Firmicutes, Bacteroidetes, Actinobacteria and Fusobacteria. Intrusion by Helicobacter pylori (H. pylori) does not remarkably interrupt the composition and structure of the gastric microbiota. Absence of bacterial commensal from the stomach delays the onset of H. pylori-induced gastric cancer, while presence of artificial microbiota accelerates the carcinogenesis. Altered gastric microbiota may increase the production of N-nitroso compounds, promoting the development of gastric cancer. Further investigation of the carcinogenic mechanisms of microbiota would benefit for the prevention and management of gastric cancer.

Relatedness of Helicobacter pylori populations to gastric carcinogenesis.

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that infects half of the human population. The infection is associated with chronic inflammation of the gastric mucosa and peptic ulcers. It is also a major risk factor for gastric cancer. Phylogenetic analysis of global strains reveals there are seven populations of H. pylori, including hpAfrica1, hpAfrica2, hpEastAsia, hpEurope, hpNEAfrica, hpAsia2 and hpSahul. These populations are consistent with their geographical origins, and possibly result from geographical separation of the bacterium leading to reduced bacterial recombination in some populations. For each population, H. pylori has evolved to possess genomic contents distinguishable from others. The hpEurope population is distinct in that it has the largest genome of 1.65 mbp on average, and the highest number of coding sequences. This confers its competitive advantage over other populations but at the cost of a lower infection rate. The large genomic size could be a cause of the frequent occurrence of the deletion of the cag pathogenicity island in H. pylori strains from hpEurope. The incidence of gastric cancer varies among different geographical regions. This can be attributed in part to different rates of infection of H. pylori. Recent studies found that different populations of H. pylori vary in their carcinogenic potential and contribute to the variation in incidence of gastric cancer among geographical regions. This could be related to the ancestral origin of H. pylori. Further studies are indicated to investigate the bacterial factors contributing to differential virulence and their influence on the clinical features in infected individuals.

Specific HLA-DQB1 alleles associated with risk for development of hepatocellular carcinoma: a meta-analysis.

AIM: To evaluate the association of human leukocyte antigen (HLA)-DQB1 alleles with hepatocellular carcinoma (HCC) through meta-analysis of published data. METHODS: Case-control studies on HLA-DQB1 allele association with HCC published up to January 2010 were included in the analyses. The odds ratios (ORs) of HLA-DQB1 allele distributions in HCC patients were analyzed and compared with healthy controls. The meta-analysis software REVMAN 5.0 was applied for investigating heterogeneity among individual studies and for summarizing all the studies. A meta-analysis was performed using fixed-effect or random-effect methods, depending on the absence or presence of significant heterogeneity. Seven case-control studies containing 398 cases and 594 controls were included in the final analysis. RESULTS: Among the five family alleles, two (DQB1*02 and DQB1*03) were found to be significantly associated with the risk of HCC. The combined OR for the association of DQB1*02 and DQB1*03 allele with the risk for HCC was 1.78 (95% CI: 1.05-3.03, P = 0.03) and 0.65 (95% CI: 0.48-0.89, P = 0.007), respectively. Among the 13 specific alleles, two (DQB1*0502 and DQB1*0602) were significantly associated with risk of HCC. The combined OR for the association of DQB1*0502 and DQB1*0602 allele with the risk for HCC was 1.82 (95% CI: 1.14-2.92, P = 0.01) and 0.58 (95% CI: 0.36-0.95, P = 0.03), respectively. No significant association was established for other HLA-DQB1 family alleles and specific alleles. CONCLUSION: Our results support the hypothesis that specific HLA-DQB1 allele families and alleles might influence the susceptibility or resistance to HCC, although it needs further investigations.

Performance of the aspartate aminotransferase-to-platelet ratio index for the staging of hepatitis C-related fibrosis: an updated meta-analysis.

UNLABELLED: The aspartate aminotransferase-to-platelet ratio index (APRI), a tool with limited expense and widespread availability, is a promising noninvasive alternative to liver biopsy for detecting hepatic fibrosis. The objective of this study was to update the 2007 meta-analysis to systematically assess the accuracy of APRI in predicting significant fibrosis, severe fibrosis, and cirrhosis stage in hepatitis C virus (HCV) monoinfected and HCV / human immunodeficiency virus (HIV) coinfected individuals. Studies comparing APRI versus biopsy in HCV patients were identified via a thorough literature search. Areas under summary receiver operating characteristic curves (AUROC), sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were used to examine the APRI accuracy for the diagnosis of significant fibrosis, severe fibrosis, and cirrhosis. Heterogeneity was explored using meta-regression. Twenty-one additional studies were eligible for the update and, in total, 40 studies were included in this review (n = 8,739). The summary AUROC of the APRI for the diagnosis of significant fibrosis, severe fibrosis, and cirrhosis were 0.77, 0.80, and 0.83, respectively. For significant fibrosis, an APRI threshold of 0.7 was 77% sensitive and 72% specific. For severe fibrosis, a threshold of 1.0 was 61% sensitive and 64% specific. For cirrhosis, a threshold of 1.0 was 76% sensitive and 72% specific. Moreover, we found that the APRI was less accurate for the identification of significant fibrosis, severe fibrosis, and cirrhosis in HIV/HCV coinfected patients. CONCLUSION: Our large meta-analysis suggests that APRI can identify hepatitis C-related fibrosis with a moderate degree of accuracy. Application of this index may decrease the need for staging liver biopsy specimens among chronic hepatitis C patients.

Association between HLA-DRB1 alleles polymorphism and hepatocellular carcinoma: a meta-analysis.

BACKGROUND: HLA-DRB1 allele polymorphisms have been reported to be associated with hepatocellular carcinoma susceptibility, but the results of these previous studies have been inconsistent. The purpose of the present study was to explore whether specific HLA-DRB1 alleles (DRB1*07, DRB1*12, DRB1*15) confer susceptibility to hepatocellular carcinoma. METHODS: Case-control studies on HLA-DRB1 alleles association with HCC were searched up to January 2010 through a systematic review of the literature. The odds ratios (ORs) of HLA-DRB1 allele distributions in patients with hepatocellular carcinoma were analyzed against healthy controls. The meta-analysis software REVMAN 5.0 was applied for investigating heterogeneity among individual studies and for summarizing all the studies. Meta-analysis was performed using fixed-effect or random-effect methods, depending on absence or presence of significant heterogeneity. RESULTS: Eight case-control studies were included in the final analysis. Among the 3 HLA-DRB1 alleles studied, DRB1*07 and DRB1*12 were significantly associated with the risk of HCC in the whole populations (OR = 1.65, 95% CI: 1.08-2.51, P = 0.02 and OR = 1.59, 95% CI: 1.09-2.32, P = 0.02, respectively). No significant association was established for DRB1*15 allele with HCC in the whole populations. Subgroup analysis by ethnicity showed that DRB1*07, DRB1*12 and DRB1*15 alleles significantly increased the risk of hepatocellular carcinoma in Asians (OR = 2.10, 95% CI: 1.06-4.14, P = 0.03; OR = 1.73, 95% CI: 1.17-2.57, P = 0.006 and OR = 2.88, 95%CI: 1.77-4.69, P <0.001, respectively). CONCLUSION: These results support the hypothesis that specific HLA-DRB1 alleles might influence the susceptibility of hepatocellular carcinoma. Large, multi-ethnic confirmatory and well designed studies are needed to determine the host genetic determinants of hepatocellular carcinoma.