Background: High sensitivity C-reactive protein (hsCRP) predicts myocardial dysfunction after acute coronary syndromes. We aimed to study the association of hsCRP estimation at first acute myocardial infarction (AMI) with myocardial dysfunction and heart failure. Methods: This research was carried out at the Department of Physiology and Department of Emergency Medicine, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia. In this prospective study, 227 patients were studied. hsCRP levels were estimated when patients came to the emergency department at AMI, 7 days post AMI, and at 12 weeks of follow up after AMI. The outcome was change in myocardial functions, especially heart failure, 12 months after the attack. Results: Based on a cutoff mean value of hsCRP levels at admission (10.05±12.68 mg/L), patients were grouped into high and low C-reactive protein (CRP.) The ejection fraction was significantly lower at follow up in the high CRP group (37.29±12.97) compared to the low CRP group (43.85±11.77, p<0.0198). hsCRP had significant inverse correlation with left ventricular ejection fraction (r=-0.283, p<0.01). About 38.1% patients showed heart failure, with 23.6% in the high CRP group and 14.5% in the low CRP group (OR 2.4, p=0.028). Receiver operating characteristic curve analysis showed that CRP levels at AMI had a specificity of 79% and sensitivity of 83% to predict heart failure. Conclusion: A high hsCRP level measured at first AMI predicts myocardial dysfunction and heart failure. It is suggested that hsCRP plays an important role in the development of heart failure after myocardial infarction.

Nasopharyngeal carcinoma (NPC) is a malignant tumor that commonly occurs in southern China and Southeast Asia. Radiation therapy is the main treatment for patients with NPC, and the radioresistance of NPC is an unresolved clinical problem. This study focuses on the mechanism of NPC radioresistance and explores therapeutic targets and research directions for increasing the radiosensitivity of radioresistant cells.

Background: Previous research had shown that an imbalance in cell proliferation and apoptosis is a vital mechanism for tumorigenesis and cancer progression that may directly influence biological behaviors of cancer. microRNAs are associated with the occurrence and development of tumors. This study aimed to explore the influence of miR-937 on breast cancer regulation of APAF1 expression. Methods: Cancer Genome Altas microarray analysis (fold change > 2, p<0.05) was used to verify differentially expressed microRNAs and RT-qPCR was used to detect miR-937 mRNA level in breast cancer. Cell viability and proliferation were measured using CCK8 and colony formation assays, respectively, after the miR-937 mimics/inhibitors and their negative control were transfected into MCF7 cells. The variations in cell cycle and apoptosis were examined using flow cytometry. DAVID database was used to perform GO enrichment analysis. We use dual luciferase report system to detect the effect of miR-937 on the transcriptional activity of APAF1. APAF1 protein level was determined by Western blot assay. Results: miR-937 was up-regulated in breast cancer cell lines and high miR-937 expression is associated with a poorer survival rate in cancer patients. miR-937 overexpression promoted the viability, down-regulated the G1 phase ratios and increased the ability of colony formation in breast cancer cells. miR-937 inhibition inhibited the viability and the ability of colony formation, promoted the apoptosis and up-regulated the G1 phase ratios. Our results showed that miR-937 targeted bind to the APAF1-3'UTR. APAF1 overexpression inhibited the viability and the ability of colony formation, promoted the apoptosis and up-regulated the G1 phase ratios. After cells were co-transfection miR-937 mimics and APAF1, cell apoptosis level was increased. Conclusion: APAF1 up-regulation or APAF1 down-regulation in breast cancer may regulate cell proliferation and apoptosis.

Prevention of epithelial-mesenchymal transition (EMT) provides a novel treatment strategy for tumor metastasis. Our previous studies have shown that diallyl disulfide (DADS) inhibits Ras related C3 botulinum toxin substrate1 (Rac1) expression, being a potential agent that suppresses migration and invasion of colon cancer cells. The study provides information on the underlying mechanisms.

Colorectal cancer is a heterogeneous disease with complex genetic and epigenetic changes. LncRNA has recently been regarded as the biomarker in cancers. Novel biomarkers in colon cancer need to be identified.

Background: ASAP3 was first identified as a protein that promotes cell proliferation in hepatocellular carcinoma and later reported to be an Arf6-specific Arf GTPase-activating protein that regulates cell migration associated with cancer cell invasion. Materials and methods: Patients and tissue samples were from Hubei Cancer Hospital, human lung adenocarcinoma cell lines were obtained from the cell bank of the Chinese Academy of Science, nude mice (BALB/c nu/nu) were obtained from Shanghai SLAC Laboratory Animal Co. Ltd. Our methods contained immunohistochemistry, Western blotting, reverse-transcription polymerase chain reaction (RT-PCR), immunofluorescence staining, stable transfection of lung adenocarcinoma cells, chromatin immunoprecipitation (CHIP) and luciferase assay, wound healing and cell migration assay. Results: In this study, we show that ASAP3 overexpression promotes migration and invasiveness in human lung adenocarcinoma cells and accelerates tumor progression in a xenograft mouse model. In patient tumor samples, ASAP3 overexpression was significantly associated with lymph node metastasis and reduced overall survival. We also show that ASAP3 expression is induced under hypoxic conditions through hypoxia-inducible factor 1α (HIF-1α), which binds directly to HER1 or/and HER2 (hypoxia response element) in the ASAP3 promoter. ASAP3 overexpression counteracts the inhibition of lung adenocarcinoma progression caused by HIF-1α knockdown both in vitro and in vivo. Conclusion: Our results identify ASAP3 as a downstream target of HIF-1α that is critical for metastatic progression in lung adenocarcinoma.

IL-37 is a cytokine of IL-1 family that plays an important role in innate immunity and inflammation, and has been studied as a tumor suppressor in many cancers. However, it remains unclear whether IL-37 plays a regulatory role in tumor-infiltrating dendritic cells (DCs) in hepatocellular carcinoma (HCC).

Introduction: Cancer-related fatigue (CRF) is the most debilitating symptom with the greatest adverse side effect on quality of life. The etiology of this symptom is still not understood. The purpose of this study was to examine the relationship between mitochondrial gene expression, mitochondrial oxidative phosphorylation, electron transport chain complex activity, and fatigue in prostate cancer patients undergoing radiotherapy (XRT), compared to patients on active surveillance (AS). Methods: The study used a matched case-control and repeated-measures research design. Fatigue was measured using the revised Piper Fatigue Scale from 52 patients with prostate cancer. Mitochondrial oxidative phosphorylation, electron-transport chain enzymatic activity, and BCS1L gene expression were determined using patients' peripheral mononuclear cells. Data were collected at three time points and analyzed using repeated measures ANOVA. Results: The fatigue score was significantly different over time between patients undergoing XRT and AS (P<0.05). Patients undergoing XRT experienced significantly increased fatigue at day 21 and day 42 of XRT (P<0.01). Downregulated mitochondrial gene (BC1, ubiquinol-cytochrome c reductase, synthesis-like, BCS1L, P<0.05) expression, decreased OXPHOS-complex III oxidation (P<0.05), and reduced activity of complex III were observed over time in patients with XRT. Moreover, increased fatigue was significantly associated with downregulated BCS1L and decreased complex III oxidation in patients undergoing XRT. Conclusion: Our results suggest that BCS1L and complex III in mitochondrial mononuclear cells are potential biomarkers and feasible therapeutic targets for acute XRT-induced fatigue in this clinical population.

The published data indicate that the irradiation of the subventricular zone (SVZ) might play a role in the treatment of patients with glioblastoma (GBM). We aimed to determine whether radiation treatment doses (high vs low) applied to the SVZ can lead to an increase in progression free survival (PFS) and overall survival (OS).

Parquetina nigrescens (Pn) extract was evaluated for safety and antidiarrheal activity, formulated into stable suspensions, and characterized.

Stroke is one of the leading causes of morbidity, disability, and mortality in high-income countries. Early prehospital stroke recognition plays a fundamental role, because most clinical decisions should be made within the first hours after onset of symptoms. The Cincinnati Prehospital Stroke Scale (CPSS) is a validated screening tool whose utilization is suggested during triage. The aim of this study is to review the role of the CPSS by assessing its sensitivity and specificity in prehospital and hospital settings.

Protoparmeliopsis garovaglii is a widely distributed placodioid lichen, which develops a distinctly rosette thallus, composed of elongated and strongly inflated to sinuous-plicate lobes. The taxon is characterised by high morphological plasticity and varied composition of secondary metabolites. However, the epithet was never typified. As such, the identity of P. garovaglii, in its strict sense, was unknown for a long time. Our phylogenetic ITS rDNA analyses, including newly generated sequences, show that European (Austria, Poland), North American (USA) and South American (Bolivia, Peru) specimens of P. garovaglii are placed in a strongly supported monophyletic clade, sister to P. muralis. We provide the first molecular evidence of the occurrence of P. garovaglii in South America (Bolivia and Peru) and the second record in Central Europe (Poland) was also provided. Furthermore, we neotypify P. garovaglii and it is reported here for the first time from Poland.

MicroRNAs (miRNAs or miRs) serve crucial roles in the progression of osteoporosis. This study investigated the role and specific molecular mechanism of miR-135-5p in regulating osteoblast differentiation and calcification.

The completeness of septal myectomy (SM) is the key to surgery of hypertrophic obstructive cardiomyopathy (HOCM), but its planning is still based on echocardiographic findings. The need to perform radical SM requires the development of new cardio-visualisation techniques for monitoring myectomy quality.

Achyranthes bidentata is a herbal plant commonly used in the treatment of osteoporosis and bone nonunion with traditional Chinese medicine. Achyranthes bidentata alcohol is a major component extracted from Achyranthes bidentata, which has been proved to be able to exert a variety of pharmacological effects, such as anti-inflammation, antipyresis, anti-rheumatism, diuresis and anti-osteoporosis. Thirty male Sprague-Dawley rats aged 4 weeks were used in the experiment. All primary rat osteoblasts were cultured and amplified for further experiments. The osteoblasts were divided into six groups (5 rats in each group): the culture medium control group, the 25 µg/ml achyranthol group, the 50 µg/ml achyranthol group, the 100 µg/ml achyranthol group, 200 µg/ml achyranthol group, and the 25 µM PD98059+200 µg/ml achyranthol group. In this study, the effect of Achyranthes bidentata alcohol on the proliferation of osteoblasts was detected via methyl thiazolyl tetrazolium (MTT) assay. The effect of Achyranthes bidentata alcohol on the alkaline phosphatase (ALP) activity in osteoblasts was analyzed via ALP assay. The effect of Achyranthes bidentata alcohol on the expression of osteoblast marker gene, Runt-related transcription factor 2 (Runx2), was detected via reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry. Moreover, the phosphorylation or activation of extracellular signal-regulated kinase (ERK) in osteoblasts induced by Achyranthes bidentata alcohol was analyzed using western blotting. Achyranthes bidentata alcohol increased cell proliferation in a dose-dependent manner, increased the micro ribonucleic acid (miRNA) level in Runx2, enhanced the ALP activity in osteoblasts, and stimulated the activation of ERK (P<0.05). The expression of Runx2 with the inhibitor PD98059 was decreased significantly compared with that in the Achyranthes bidentata alcohol group (P<0.01). Immunohistochemical results manifested that the percentage of Runx2 positive cells in treated tissues was obviously higher than that in untreated tissues (P<0.01). Therefore, Achyranthes bidentata alcohol promotes the proliferation capacity of osteoblasts in a dose-dependent manner, enhances the expression of miRNA in Runx2, and stimulates the osteogenic differentiation of osteoblasts through activating the ERK signal transduction pathway.

Long intergenic non-coding RNA for kinase activation (LINK-A) long non-coding RNA (lncRNA) has been characterized in triple negative breast cancer, but its potential involvement in glioma has not been investigated. In the present study, serum levels of LINK-A lncRNA and survivin in patients with glioma and healthy controls were determined by RT-qPCR and ELISA, respectively. The diagnostic value of serum LINK-A lncRNA for glioma was evaluated by receiver operating characteristic (ROC) curve analysis. Potential correlations between serum levels of LINK-A lncRNA and survivin were analyzed by Pearson correlation coefficient. LINK-A lncRNA siRNA, LINK-A lncRNA-carrying expression vector and survivin-carrying expression vector were transfected into glioma cells, and the effects on LINK-A lncRNA expression, survivin expression and cell apoptosis were explored by RT-qPCR, western blot analysis and annexin V/propidium iodide staining. It was observed that the serum levels of LINK-A lncRNA and survivin were significantly higher in patients with glioma compared with healthy controls. Increased levels of LINK-A lncRNA distinguished glioma patients from healthy controls, based on ROC curve analysis. Serum levels of LINK-A lncRNA and survivin were positively correlated in glioma patients, but not in healthy controls. Overexpression of LINK-A lncRNA led to increased survivin protein expression, while survivin overexpression had no effect on LINK-A lncRNA expression. LINK-A lncRNA and survivin overexpression each reduced glioma cell apoptosis, but LINK-A lncRNA siRNA-mediated knockdown increased apoptosis. Survivin overexpression attenuated the inducing effects of LINK-A lncRNA knockdown on apoptosis. In conclusion, LINK-A lncRNA inhibited glioma cell apoptosis potentially by the upregulation of survivin. The present study revealed that LINK-A may serve as possible diagnostic marker for glioma.

The present study aimed to establish a microRNA (miRNA/miR) signature to predict the prognosis of patients with pancreatic cancer (PC) at the early stage and to investigate the involvement of competing endogenous RNAs (ceRNAs) in PC. Using mature miRNA expression profiles from The Cancer Genome Atlas, differentially expressed miRNAs in tissues derived from patients exhibiting early PC and tissues from healthy individuals were compared. The least absolute shrinkage and selection operator regression method was used to construct a miRNA-based signature for predicting prognosis. The miRNet tool, gene set enrichment analysis (GSEA) and the LncRNADisease database were utilized to explore the mechanistic involvement of ceRNAs. A total of seven downregulated miRNAs in PC (miR-424-5p, miR-139-5p, miR-5586-5p, miR-126-3p, miR-3613-5p, miR-454-3p and miR-1271-5p) were selected to generate a signature. Based on this seven-miRNA signature, it was possible to stratify patients with PC into low- and high-risk groups. The overall survival of the low-risk group was significantly longer than that of the high-risk group (P<0.001). The seven-miRNA signature was able to predict the 2-year-survival rate of patients with early PC with an area under the curve of 0.750. Furthermore, as opposed to routine clinicopathological features, this seven-miRNA signature was an independent prognostic factor according to multivariate Cox regression analysis. GSEA indicated that the extracellular matrix receptor interaction pathway and the transforming growth factor-β signaling pathway were enriched in the high-risk group. A ceRNA network of the seven-miR signature was constructed. In conclusion, the present study provided a seven-miRNA signature, according to which patients with early PC may be divided into high- and low-risk groups. The ceRNA network of the prognostic signature was preliminarily explored.

The objective of the present study was to evaluate whether an innovative quantitative ultrasound (QUS) technique, Radiofrequency Echographic Multi Spectromety, which combines B-mode ultrasound and radiofrequency signals, is reliable in typical Romanian patients compared to previous results obtained using dual-energy X-ray absorptiometry (DXA). The study prospectively included previously unscreened post-menopausal females with rheumatoid arthritis (RA) and age-matched healthy controls. Bone mineral density (BMD) measurements were performed with an EchoS machine (Echolight®), which combines B-mode ultrasound and radiofrequency signals. The study included 106 RA patients, with a median disease duration of 3.2 (0.5-22) years and 119 controls. RA patients had a significantly lower body weight, body mass index (BMI) and basal metabolic rate (BMR) than the controls, while the prevalence of obesity and body fat differed insignificantly. RA patients had a significantly lower spine and hip BMD, higher fracture risk and higher prevalence of osteoporosis. Compared to RA patients without osteoporosis, those with osteoporosis were significantly older and had a longer menopause duration, but they had a significantly lower BMI, body fat, BMR and prevalence of obesity. Among the controls and RA patients, the median spine and hip BMD became significantly higher as the BMI increased from underweight to obesity. In conclusion, osteoporosis is prevalent among RA patients, as a part of a complex transformation of body mass composition, involving BMI and fat mass. The novel QUS scanning technique was able to replicate the results of the established DXA measurement of BMD and is potentially suitable for screening wide populations for osteoporosis.

Previous studies examining whether autophagy has a protective or deleterious role during ischemia/reperfusion (I/R) injury have reported a varying role in different organs and remains a matter of debate. The aim of the current study was to explore the role of autophagy in hindlimb I/R injury in a murine model. An increase in apoptosis was observed in vitro, in C2C12 myoblast cells, following hypoxia/reoxygenation (H/R), while downregulation of autophagic flux was induced by chloroquine as compared with the vehicle group under hypoxia and H/R conditions. In vivo, an increase in severe damage of gastrocnemius muscles was observed in the I/R and ischemia groups compared with the control group, was more severe in the I/R group compared with the ischemia group. Electron microscopy revealed an increased number of autophagosomes in the ischemia group, whereas a reduced number was detected in the I/R group. Following administration of rapamycin, the infarct size ratio and cell apoptosis was significantly reduced, while the amount of autophagosomes significantly increased in the ischemic phase. In conclusion, autophagy is upregulated in the ischemia phase and downregulated in the reperfusion phase. Notably, upregulation of autophagy via rapamycin intervention during ischemia alleviated skeletal muscle damage, suggesting a potential protective role during hindlimb I/R injury.

The aim of the present study was to explore the association between apolipoprotein M (ApoM) and adiponectin, and the underlying mechanism, via observation of ApoM expression in an obese mouse model. For in vivo experiments, mice were randomly distributed into four groups: Control group, obese group, obese group treated with adiponectin, and normal group treated with adiponectin. Body weight, plasma adiponectin, blood glucose and fasting insulin were measured and visceral adipose tissue was weighed at the end of the experiment. ApoM and transcription factor forkhead box A2 (Foxa2) mRNA expression in the mouse liver was evaluated and the protein level of ApoM detected. For in vitro experiments, an insulin-resistant (IR) hepatic cell model was established by inducing the HepG2 cell line with a high concentration of insulin. Following treatment with adiponectin, changes in ApoM and Foxa2 mRNA expression and ApoM protein expression were evaluated in the control and IR HepG2 cells. Results demonstrated that compared with the control group, body weight, visceral adipose tissue weight, blood glucose, fasting insulin and insulin-resistance index (HOMA-IR) were significantly increased in the obese group, whilst plasma adiponectin, ApoM mRNA expression, Foxa2 mRNA expression and ApoM protein in the mouse liver were all significantly decreased. Following intervention with adiponectin in obese mice, blood glucose, insulin and HOMA-IR were significantly decreased, whilst plasma adiponectin, ApoM mRNA expression, Foxa2 mRNA expression and ApoM protein were all significantly increased. However, no significant difference was observed in visceral adipose tissue weight following the intervention of adiponectin in obese mice. In vitro, in the absence of intervention, ApoM and Foxa2 mRNA expression and ApoM protein expression were significantly lower in IR HepG2 cells compared with HepG2 cells. Following intervention with adiponectin on IR HepG2 cells, ApoM and Foxa2 mRNA expression and ApoM protein expression were significantly increased. However, the intervention did not have any effect on HepG2 cells. In conclusion, intervention with adiponectin elevated ApoM mRNA expression, potentially via relieving IR and upregulating Foxa2 mRNA expression.