ABSTRACT Background: While sarcopenia is an important clinical finding in individuals diagnosed with chronic heart failure (CHF), efforts to identify a reliable biomarker capable of predicting the overall muscular and functional decline in CHF patients have been unsuccessful to date. Objectives: The objectives of this study were to study the diagnostic utility of MicroRNA (miRNA)-1-3p as a predictor of sarcopenia status in individuals diagnosed with CHF. Methods: In total, 80 individuals with heart failure exhibiting a left ventricular ejection fraction < 50% were enrolled in this study. All patients were analyzed to assess miR-1-3p expression levels, with body composition being evaluated through dual-energy X-ray absorptiometry and sarcopenia being defined based on the sum of appendicular lean muscle mass (ALM) divided by height in meters squared and handgrip strength (HGS). In addition, the activation of the Akt/mTOR signaling pathway was evaluated in these individuals. Results: In total, 40 of the enrolled patients (50%) exhibited sarcopenia. Sarcopenic patients presented with increased miR-1-3p expression levels as compared to non-sarcopenic individuals (1.69 ± 0.132 vs. 1.22 ± 0.106; p < 0.05). With respect to sarcopenic indices, appendicular skeletal mass index was most strongly correlated with miR-1-3p expression, which was also strongly correlated with HGS. High levels of Akt/mTOR signaling pathway components were expressed in sarcopenic individuals, highlighting a significant relationship between miR-1-3p activity and signaling through this pathway. Moreover, miR-1-3p was identified as a specific marker for sarcopenia in individuals with CHF. Conclusion: These results suggest that circulating miR-1-3p levels are related to Akt/mTOR pathway activation and can offer valuable insight into the overall physical capacity and muscular integrity of CHF patients as a predictor of sarcopenia.

Abstract A summarized physicochemical profile of nine multifloral honeys produced by Apis cerana cerana Fabricius in Qiongzhong region located in Hainan province was exhibited, regarding pH (3.72-4.02), moisture (19.20-22.53%), fructose (34.40-38.70 g 100 g-1), glucose (31.60-35.05 g 100 g-1), sucrose (less than 3%), color (31.00-80.00 mm Pfund), ash content (0.17-0.45 g 100 g-1), soluble solid (75.87-79.10 ◦Brix), and electrical conductivity (343.67-678.33 μS cm-1). Potassium showed the highest concentration, followed by calcium. Manganese, boron, iron, aluminium, and zinc were the main micro-elements while cadmium and hydrargyrum were not detected in all honey samples. The antiradical activity was shown to be significantly negative correlated with total phenolic content (TPC) (r2 = −0.756) and total flavonoid content (TFC) (r2 = −0.477). Among all tested honey samples, sample A exhibited the highest levels of TPC (45.46 mg GAE 100 g-1), TFC (10.02 mg RE 100 g-1), and antiradical activity (DPPH IC50 = 2.63 mg mL-1). Our results will be useful in determining to set the standard for A. cerana cerana honey.

Abstract microRNA (miRNA) had been found played an important role in occurrence and development of acute myocardial infarction (AMI) disease. In this paper, we found that the circulating miR-223-3p in AMI patients was significantly higher than that in unstable angina (UA) patients and healthy people. Univariate and logistic regression analysis showed the circulating miR-223-3p was a protective factor in the occurrence of AMI. We also found that the circulating miR-223-3p was negatively correlated with the serum CK-MB, cTnI, AST, LDH, TNF-α, IL-6, IL-1β and IL-8. The luciferase reporter gene system confirmed that miR-223-3p targeted inhibition of NLRP3 expression in THP-1 and human peripheral blood mononuclear cell (PBMC), and miR-223-3p was negatively correlated with the expression of NLRP3 in the PBMC of AMI patients. In PBMC of healthy people, miR-146a-mimic could increase the expression of NLRP3, but decreased the level of TNF-α secretion. Moreover, H2C9 cells apoptosis by TNF-α in a dose-dependent. In conclusion, these results suggested that miR-223-3p suppressed inflammation to protect cardiomyocytes by targeting NLRP3 in AMI patients.

Abstract Background: Multiple sclerosis (MS) is a central nervous system disease with a high disability rate. Modern molecular biology techniques have identified a number of key genes and diagnostic markers to MS, but the etiology and pathogenesis of MS remain unknown. Results: In this study, the integration of three peripheral blood mononuclear cell (PBMC) microarray datasets and one peripheral blood T cells microarray dataset allowed comprehensive network and pathway analyses of the biological functions of MS-related genes. Differential expression analysis identified 78 significantly aberrantly expressed genes in MS, and further functional enrichment analysis showed that these genes were associated with innate immune response-activating signal transduction (p = 0.0017), neutrophil mediated immunity (p = 0.002), positive regulation of innate immune response (p = 0.004), IL-17 signaling pathway (p < 0.035) and other immune-related signaling pathways. In addition, a network of MS-specific protein–protein interactions (PPI) was constructed based on differential genes. Subsequent analysis of network topology properties identified the up-regulated CXCR4, ITGAM, ACTB, RHOA, RPS27A, UBA52, and RPL8 genes as the hub genes of the network, and they were also potential biomarkers of MS through Rap1 signaling pathway or leukocyte transendothelial migration. RT-qPCR results demonstrated that CXCR4 was obviously up-regulated, while ACTB, RHOA, and ITGAM were down-regulated in MS patient PBMC in comparison with normal samples. Finally, support vector machine was employed to establish a diagnostic model of MS with a high prediction performance in internal and external datasets (mean AUC = 0.97) and in different chip platform datasets (AUC = (0.93). Conclusion: This study provides new understanding for the etiology/pathogenesis of MS, facilitating an early identification and prediction of MS.

Abstract The effects of deformation on transformation kinetics during continuous cooling and microstructure evolution of a medium carbon high strength steel were investigated by metallographic method, dilatometry and X-ray diffraction etc. The results show that ausforming accelerated the ferrite and martensite transformation, but significantly retarded the bainite transformation. In addition, the amount of retained austenite decreased first and then increased, while the carbon content in retained austenite increased with the accumulation of strain. The change trend of the average dislocation density in martensite with strain showed the opposite trend as that of the amount of retained austenite. Moreover, the martensite laths were refined by ausforming. The work provides the theoretical reference for the design of parameters of thermalmechanical controlled process (TMCP) in the production of medium-carbon high strength steels.

Abstract Background Osteoporosis (OP) is common in patients with chronic obstructive pulmonary disease (COPD). The relationship between OP and COPD has been primarily studied in male patients, and few reports are available in postmenopausal women. Objective The purpose of this study was to investigate the association between bone mineral density (BMD) and COPD in postmenopausal women. Methods This cross-sectional study included 133 clinically stable female ex-smokers with confirmed COPD, and 31 age-matched “ex-smoker” female controls. We analyzed groups according to their airway obstruction category. BMD was measured on dual-energy X-ray absorptiometry images of the left femoral neck. Results Patients with COPD had lower T-scores and higher prevalence of osteopenia/OP than the control group. In the COPD group, the airway obstruction category was significantly associated with the T-score after adjustment for confounders. Multivariate logistic regression analysis showed COPD was an independent marker for increased risk of osteopenia/OP in postmenopausal women. Conclusions COPD and airway obstruction category were strongly related to BMD. Postmenopausal women with COPD, especially those with severe airway obstruction, had a higher prevalence rate and a higher risk of osteopenia and OP than female controls without COPD.

Abstract Background: Studies have shown that cancer susceptibility candidate 11 (CASC11), a newly discovered long non-coding RNA (lncRNA), was aberrantly overexpressed in hepatic carcinoma, gastric cancer and colorectal cancer. However, its effects on cervical cancer has been kept unknown up to now. The present study was aimed to investigate the relationship between lncRNA CASC11 and cervical cancer and further explore the mechanism of CASC11 effect on cervical cancer progression. Materials: Quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of CASC11 in cancerous and adjacent normal tissues of patients with cervical cancer as well as in cell lines. The proliferation, migration, invasion and apoptosis were assayed after transfecting the cell with si-CASC11 or pcDNA3.1-CASC11. TOP/FOP-Flash luciferase reporter assay and western blot were used to analysis the activation of Wnt/β-catenin signaling pathway. Si-CASC11-transfected HeLa cells were subcutaneously inoculated into male athymic (nude) mice to investigate the effect of CASC11 on the tumor formation. Results: We discovered that CASC11, the expression of which was positively associated with the tumor size and the FIGO staging and negatively related to the patients' survival rate, was up-regulated in the cervical cancer tissues and cell lines. Silencing CASC11 inhibited the proliferation, migration as well as invasion and promoted the cell apoptosis. Conversely, overexpression of CASC11 facilitated the cancer cell's proliferation, migration and invasion ability and suppressed the apoptosis. Further study showed that CASC11 promoted the migration and invasion of cervical cancer cells by activating Wnt/β-catenin signaling pathway and silencing CASC11 inhibited the tumor growth in vivo. Conclusion: Our study demonstrated that CASC11 promoted the cervical cancer progression by activating Wnt/β-catenin signaling pathway for the first time, which provides a new target or a potential diagnostic biomarker of the treatment for cervical cancer.

The present study aimed to identify microRNAs (miRNAs) that are involved in neuropathic pain and predict their corresponding roles in the pathogenesis and development process of neuropathic pain. The rat model of neuropathic pain caused by spared nerve injury (SNI) was established in Sprague-Dawley male rats, followed by small RNA sequencing of the L3–L6 dorsal root ganglion. Real-time PCR was performed to validate the differently expressed miRNAs. Functional verification was performed by intrathecally injecting the animals with miRNA agomir. A total of 72 differentially expressed miRNAs were identified in the SNI rats, including 33 upregulated and 39 downregulated miRNAs. The results of qPCR further verified the expression levels of rno-miR-6215 (P=0.015), rno-miR-1224 (P=0.030), rno-miR-1249 (P=0.038), and rno-miR-488-3p (P=0.048), which were all significantly downregulated in the SNI rats compared to the control ones. The majority of differentially expressed miRNAs were associated with phosphorylation, intracellular signal transduction, and cell death. Target prediction, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses suggested that these differentially expressed miRNAs targeted genes that are related to axon guidance, focal adhesion, and Ras and Wnt signaling pathways. Moreover, miR-1224 agomir significantly alleviated SNI-induced neuropathic pain. The current findings provide new insights into the role of miRNAs in the pathogenesis of neuropathic pain.

OBJECTIVES: Esophageal leiomyoma is the most common benign tumor of the esophagus, and it originates from mesenchymal tissue. This study analyzed the clinicopathological characteristics of esophageal leiomyoma and aimed to evaluate the role of endoscopic ultrasonography in the diagnosis and treatment selection for these lesions. METHODS: Two hundred and twenty-five patients who had suspected esophageal leiomyomas in endoscopic ultrasonography were enrolled at the Endoscopy Center of The First Affiliated Hospital, Zhejiang University from January 1st, 2009 to May 31th, 2015. The main outcomes included the demographic and morphological characteristics, symptoms, comparisons of diagnosis and treatment methods, adverse events, and prognosis. RESULTS: One hundred and sixty-seven patients were diagnosed as having an esophageal leiomyoma by pathological examination. The mean patient age was 50.57±9.983 years. In total, 62.9% of the lesions originated from the muscularis mucosa, and the others originated from the muscularis propria. The median distance to the incisors was 30±12 cm. The median diameter was 0.72±0.99 cm. As determined by endoscopic ultrasonography, most existing leiomyomas were homogeneous, endophytic, and spherical. The leiomyomas from the muscularis mucosa were smaller than those from the muscularis propria and much closer to the incisors (p<0.05). SMA (smooth muscle antibody) (97.2%) and desmin (94.5%) were positive in the majority of patients. In terms of treatments, patients preferred endoscopic therapies, which led to less adverse events (e.g., intraoperative bleeding, local infection, pleural effusion) than surgical operations (p<0.05). The superficial leiomyomas presented less adverse events and better recovery (p<0.05) than deep leiomyomas. CONCLUSION: Endoscopic ultrasonography has demonstrated high accuracy in the diagnosis of esophageal leiomyomas and provides great support in selecting treatments; however, EUS cannot completely avoid misdiagnosis, so combining it with other examinations may be a good strategy to solve this problem.

Background: Transforming growth factor-ß receptor II (TGFBR2) is a key component of TGF-ß signaling pathway. TGFBR2 can be detected in the generation of heart. The mouse embryos of TGFBR2 gene knockout exhibited congenital heart defects. Methods: We conducted a case-control study to investigate the association between TGFBR2 gene polymorphisms and congenital heart defects in Han Chinese population. 125 patients with congenital heart defects and 615 unrelated controls were recruited. Two tagging single nucleotide polymorphisms (tagSNPs) in 5’ upstream of TGFBR2 gene (rs6785358, -3779A/G; rs764522, -1444C/ G) were selected and genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) assay. Results: A significant difference was seen in the distribution of genotypes between patients with congenital heart defects and controls for SNP rs6785358 (P=0.043). For SNP rs6785358 the carrier of the G allele (AG/GG genotype) showed a significantly higher risk of congenital heart defects compared with AA homozygotes (OR=1.545, 95% CI: 1.013-2.356). Further analysis by sex stratification indicated that individuals carrying G allele (AG/GG genotype) for SNP rs6785358 have a higher susceptibility to congenital heart defects (OR=2.088, 95%CI: 1.123-3.883, P=0.019) in males, but not females (OR=1.195, 95%CI: 0.666-2.146, P=0.55). No statistical significance was detected in the distribution of genotypes and allele frequencies for SNP rs764522 between patients and controls. Conclusion: Our result suggested that SNP rs6785358 of TGFBR2 gene was associated with increased risk of congenital heart defects in Han Chinese men and further research would be warranted.

Antecedentes: Factor de crecimiento transformante ß receptor II (TGFBR2) es un componente clave de la via de señalización de TGF-ß. TGFBR2 puede ser detectado en la generación de corazón. Los embriones de ratón de TGFBR2 gene knockout mostraron defectos congénitos del corazón. Métodos: Hemos realizado un estudio de casos y controles para investigar la asociación entre polimorfismos del gen TGFBR2 y defectos congénitos del corazón en la población china han. 125 pacientes con defectos congénitos del corazón y 615 unrelated controles fueron reclutados. Marcado de dos polimorfismos de nucleótido único (tagsnps) en 5 ‘aguas arriba del gen TGFBR2 (rs6785358, - 3779a / g; rs764522, - 1444c / g) fueron seleccionados y genotipados por reacción en cadena de la polimerasa (PCR) - polimorfismos de longitud de fragmentos de restricción (RFLP) de ensayo. Resultados: Se observó una diferencia significativa en la distribución de genotipos entre pacientes con defectos congénitos del corazón y controles para SNP rs6785358 (P = 0043). La SNP rs6785358 el porteador del alelo G (AG / GG genotipo) mostraron un importante crecimiento y mayor riesgo de defectos congénitos del corazón en comparación con AA homocigotos (OR = 1.545, IC del 95%: 1.013-2.356). Más análisis por sexo estratificación indicó que los individuos con alelo G (AG / GG genotipo) para SNP rs6785358 tienen una mayor susceptibilidad a defectos congénitos del corazón (OR = 2.088, IC del 95%: 1.123-3.883, p = 0.019) en machos, pero no en las mujeres (OR = 1.195, IC del 95%: 0.666-2.146, p = 0.55). No hay significación estadística fue detectado en la distribución de los genotipos y frecuencias de alelos de SNP rs764522 entre pacientes y controles. Conclusión: Nuestros resultados sugieren que el SNP rs6785358 de gen TGFBR2 se asoció con un mayor riesgo de defectos congénitos del corazón en los chinos han hombres y más investigación estaría justificada.

Background In recent years, nickel (Ni) has been widely applied in industrial and agricultural production and has become a kind of environmental pollution. In this study, the effect of nickel chloride (NiCl2) with different concentrations on Arabidopsis genomic stability and DNA methylation has been demonstrated. The nucleolus variation and 18S rDNA methylation after NiCl2 treatment have been analyzed. Results The results are as follows: (1) The NiCl2 could result in heritable genomic methylation variations. The genomic DNA methylation variations have been detected by methylation-sensitive amplified polymorphism (MSAP) molecular markers, and the result showed that after NiCl2 treatment, there was methylation variation in T0 generation seedlings, and partial site changes maintained in T1 generation, which suggested that the effects of NiCl2 on DNA methylation could be heritable in offspring. (2) NiCl2 brought deformity and damage to nucleolar structure in Arabidopsis root tip cells, and the damage was positively correlated with the NiCl2 concentration. 3. In the nucleolus, there was an increased cytosine methylation in 18S rDNA. The plant nucleolus variation and 18S rDNA methylation may be used as an examination indicator for Ni pollution in soil or plant. Conclusions NiCl2 application caused variation of DNA methylation of the Arabidopsis genomic and offspring's. NiCl2 also resulted in nucleolar injury and deformity of root tip cells. The methylation rate of 18S rDNA also changed by adding NiCl2.

OBJECTIVE: To estimate influenza-associated mortality in urban China. METHODS: Influenza-associated excess mortality for the period 2003-2008 was estimated in three cities in temperate northern China and five cities in the subtropical south of the country. The estimates were derived from models based on negative binomial regressions, vital statistics and the results of weekly influenza virus surveillance. FINDINGS: Annual influenza-associated excess mortality, for all causes, was 18.0 (range: 10.9-32.7) deaths per 100000 population in the northern cities and 11.3 (range: 7.3-17.8) deaths per 100000 in the southern cities. Excess mortality for respiratory and circulatory disease was 12.4 (range: 7.4-22.2) and 8.8 (range: 5.5-13.6) deaths per 100000 people in the northern and southern cities, respectively. Most (86%) deaths occurred among people aged >65 years. Influenza-associated excess mortality was higher in B-virus-dominant seasons than in seasons when A(H3N2) or A(H1N1) predominated, and more than half of all influenza-associated mortality was associated with influenza B virus. CONCLUSION: Between 2003 and 2008, seasonal influenza, particularly that caused by the influenza B virus, was associated with substantial mortality in three cities in the temperate north of China and five cities in the subtropical south of the country.

OBJETIVO: Calcular la mortalidad asociada a la gripe en la China urbana. MÉTODOS: Se calculó el exceso de mortalidad asociado a la gripe durante el periodo comprendido entre 2003 y 2008 en tres ciudades del norte de China con clima templado y en cinco ciudades del sur del país con clima subtropical. Los cálculos se obtuvieron de modelos basados en regresiones binomiales negativas, estadísticas vitales y de los resultados de la vigilancia semanal del virus de la gripe. RESULTADOS: El exceso de mortalidad anual asociado a la gripe, por todas las causas, fue de 18,0 (rango: 10,9-32,7) muertes por cada 100000 habitantes en las ciudades del norte y de 11,3 (rango: 7,3-17,8) muertes por cada 100000 habitantes en las ciudades del sur. La mayor parte de este exceso de mortalidad - 12,4 (rango: 7,4-22,2) y 8,8 (rango: 5,5-13,6) muertes por cada 100000 habitantes en las ciudades del norte y del sur, respectivamente - se atribuyeron a una enfermedad respiratoria y/o circulatoria. La mayoría de las muertes (el 86%) ocurrió en personas con una edad >65 años. El exceso de mortalidad asociado a la gripe fue superior en épocas con un virus B dominante que en épocas en las que predominaron los virus A(H3N2) o A(H1N1). Más de la mitad de la mortalidad total asociada a la gripe se asoció al virus B de la gripe. CONCLUSIÓN: Entre 2003 y 2008, la gripe estacional, particularmente la causada por el virus B de la gripe, estuvo asociada a la mortalidad sustancial en tres ciudades de China con clima templado y en cinco ciudades del sur del país con clima subtropical.

OBJECTIF: Estimer la mortalité associée à la grippe en Chine urbaine. MÉTHODES: La mortalité excessive associée à la grippe pour la période 2003-2008 a été évaluée dans trois villes de la zone tempérée du nord de la Chine et dans cinq villes de la zone subtropicale du pays. Les estimations ont été établies sur des modèles basés sur des régressions binomiales négatives, des statistiques vitales et les résultats de la surveillance hebdomadaire de la grippe. RÉSULTATS: La mortalité annuelle excessive associée à la grippe, dans tous les cas, a été de 18 (plage: 10,9-32,7) décès pour une population de 100 000 personnes dans les villes du nord et de 11,3 (plage: 7,3-17,8) décès pour une population de 100 000 personnes dans les villes du sud. La plus grande partie de cette mortalité excessive - respectivement 12,4 (plage: 7,4-22,2) et 8,8 (plage: 5,5-13,6) décès pour une population de 100 000 personnes dans les villes du nord et du sud - a été attribuée à des maladies respiratoires et/ou circulatoires. La plupart des décès (86%) sont survenus chez des personnes de >65 ans. La mortalité excessive associée à la grippe a été plus élevée lors des saisons où prédominait le virus B plutôt que lors de celles où prédominaient les virus A(H3N2) ou A(H1N1) et plus de la moitié de l'ensemble de la mortalité associée à la grippe a été associée au virus B de la grippe. CONCLUSION: De 2003 à 2008, la grippe saisonnière, surtout celle provoquée par le virus B, a été associée à une mortalité substantielle dans trois villes du nord tempéré de Chine et dans cinq villes du sud subtropical du pays.

A pot experiment was conducted to evaluate the effect of nitrogen (N) fertilizer and maize straw incorporation on the accumulation of NH4+-15N and N0(3)--15N in soil inorganic N pool among three consecutive cropping cycles, aimed to search for an effective N management practice to decrease superfluous accumulation of soil inorganic N and fertilizer N losses. The results showed that the amounts of soil NH4+-15N, N0(3)-15N and inorganic 15N, and their percent to applied 15N-labeled fertilizer declined significantly with sampling time (p ≤ 0.001).Compared to low N application rate (44.64 mg N kg-1 soil), high N application rate (89.28 mg N kg-1 soil) enhanced significantly the amounts of soil NH4+-15N, N0(3)--15N and inorganic 15N by 238.6%, 132.9% and 197.3%, respectively (p ≤ 0.001). In contrast, maize straw addition declined significantly the amounts of soil NH4+-15N and inorganic 15N by 21.4% and 16.1% compared to without maize straw (p ≤ 0.001). The results suggested that a combined application of chemical fertilizer and maize straw with a wide C/N ratio is an important means for reducing the superfluous accumulation of fertilizer N as soil inorganic N to subsequently lower its loss.