SG and P-TDP-43 aggregates may be recapitulated in patient-derived neuronal and non-neuronal cells exposed to prolonged oxidative stress, which may be therefore exploited to study TDP-43 pathology and to develop individualized therapeutic strategies for ALS/FTD.Different methods have been proposed for the assessment of the nutritional status in frailty phenotypes. In the present narrative review article, we have summarized the number and specifications of nutritional items in existing frailty tools, in order to develop a possible means of assessment and operational definition of the nutritional frailty phenotype. In six different databases until December 2019, we searched for original articles regarding frailty tools (i.e., scales, indexes, scores, questionnaires, instruments, evaluations, screening, indicators), analyzing each tool regarding nutritional items. We identified 160 articles describing 71 frailty tools. Among the selected frailty tools, 54 were community-based (70 %), 17 hospital-based (22 %), 4 validated in long-term care institutions for older adults (LTCIOA) (5.1 %) and 2 validated in both community- and hospital-based settings, including LTCIOA (2.5 %). Fifty-two of these tools (73 %) included at least one nutritional item. Twenty-two (42 %) reported two or more nutritional items. The items were grouped in the following categories A) anthropometric measurements, B) laboratory measurements, and C) other nutritional-related measurements. Anthropometric measurements stood out compared to all other items. Nutritional items are included in the majority of frailty tools, strengthening the concept that they may have a direct implication on an increased risk of adverse health-related outcomes in frail subjects. This supports the development of the concept of nutritional frailty as an independent frailty phenotype. Subsequent steps will be to assess the contribution of each nutritional item to a possible operational definition of nutritional frailty and define the items that may best identify this new frailty phenotype.Diabetes is characterized by changed homeostasis of blood glucose levels, which is associated with various complications, including cardiomyopathy, atherosclerosis, endothelial dysfunction, nephropathy, retinopathy and neuropathy. In recent years, accumulative evidence has demonstrated that circular RNAs are identified as a novel type of noncoding RNAs (ncRNAs) involving in the regulation of various physiological processes and pathologic conditions. Specifically, the emergence of complications response to diabetes is finely controlled by a complex gene regulatory network in which circular RNAs play a critical role. Recently, circular RNAs are emerging as messengers that could influence cellular functions under diabetic conditions. Dysregulation of circular RNAs has been closely linked to the pathophysiology of diabetes-related complications. PCI-32765 In this review, we aimed to summarize the current progression and underlying mechanisms of circular RNA in the development of diabetes-related complications. We will also provide an overview of circular RNA-regulated cell communications in different types of cells that have been linked to diabetic complications. We anticipated that the completion of this review will provide potential clues for developing novel circular RNAs-based biomarkers or therapeutic targets for diabetes and its associated complications.Colorectal cancer (CRC) is one of the most common malignancies worldwide and a major cause of cancer-related deaths. Numerous studies have suggested that piwi-interacting RNAs (piRNAs), a new type of non-coding RNA (ncRNA), are closely related to the occurrence and development of cancer. piRNAs have been shown to regulate the occurrence of CRC by modulating multiple molecular signaling pathways. Here, the roles of piRNAs in CRC were reviewed to provide evidence for their potential as molecular targets for CRC.

The role of FoxP3, a master regulator of T regulatory cells, in allergic diseases such as asthma is of immense importance yet the effect of its gene variants on the disease predisposition is not fully understood. We studied the association of FoxP3 polymorphisms (-2383C/T and -3279C/A) in allergic asthma patients and their correlation with serum IL-4, IL-13, Total IgE, and Vitamin D levels.

In this study 350 individuals were enrolled, 150 allergic asthma patients and 200 healthy controls. SNP analyses were performed by RFLP. IL-4, IL-13 vitamin D and Total IgE were measured by ELISA.

The AA homozygous mutant of -3279C/A posed a three-fold risk [P<0.005; OR, 3.52] whereas the -2383C/T variants TT genotype carried a fourfold risk [P=0.002; OR, 4.04]. Haplotype analysis exhibited predisposition to allergic asthmawith CC/TT [P=0.01; OR 5.93 (95%CI)], AA/CC [P=0.01; OR 3.29] and AA/TT haplotypes [P=0; OR 11.86 (1.31-85.87)]. A negative correlation between IgE and Vitamin D was found [r=-0.30p-value 0.001] but a negative correlation betweenIgE and Vit D was established in the haplotype CC/TT [r=-0.45P=0.002] and CC/CT [r=-0.52P=0.04]. In allergic patients, the eosinophils count was high [p=0.003] and the mean levels of pro-inflammatory cytokines IL-4 and IL-13 were elevated [P<0.001] as well.

The study suggests SNP -3279 -AA genotype and, -2383-TT genotype in association with certain haplotypes pose a risk for allergy development. There was no correlation between different genotypes and serum levels of various cytokines.

The study suggests SNP -3279 -AA genotype and, -2383-TT genotype in association with certain haplotypes pose a risk for allergy development. There was no correlation between different genotypes and serum levels of various cytokines.Neuropathic pain is caused by damage or disease happened to somatosensory nerve system. Due to the high prevalence and inefficient clinic intervention, neuropathic pain has brought considerable burden for world health care system. It is urgent to find novel targets for neuropathic pain basic research and clinical management. In this study, we found that miR-22-3p was decreased in Chronic Constriction Injury （CCI）rats and involved in neuropathic pain progression. link2 Furthermore, it was found that ENO1 was a downstream target of miR-22-3p using bioinformatics analysis and luciferase reporter assays. MiR-22-3p downregulation promoted neuropathic pain via regulating inflammation factors expression by targeting ENO1. Then, we explored the upstream regulator of miR-22-3p using Miranda database. It was found that circular RNA ZNF609 sponged miR-22-3p by biotinylated RNA pull-down, AGO2-RIP, and luciferase reporter assays. Collectively, our study revealed that circZNF609 promoted inflammation factors expression to aggravate neuropathic pain progression via miR-22-3p/ENO1 axis in CCI rat models. Our study might provide a new direction for neuropathic pain basic research.The previous study indicated that transport stress resulted in oxidative damage and autophagy/mitophagy elevation, companied by NOX1 over- expression in the jejunal tissues of pigs. However, the transportation-related gene expression profile and NOX1 function in intestine remain to be explicated. In the current study, differentially expressed genes involved in PI3K-Akt and NF-κB pathways, oxidative stress and autophagy process have been identified in pig jejunal tissues after transcriptome analysis following transportation. The physiological functions of NOX1 down-regulation were explored against oxidative damage and excessive autophagy in porcine intestinal epithelial cells (IPEC-1) following NOX1 inhibitor ML171 and H2O2 treatments. NOX1 down-regulation could decrease the content of Malondialdehyde (MDA), Lactic dehydrogenase (LDH) activity and reactive oxygen species (ROS) level, and up-regulate superoxide dismutase (SOD) activity. Furthermore, mitochondrial membrane potential and content were restored, and the expressions of tight junction proteins (Claudin-1 and ZO-1) were also increased. Additionally, NOX1 inhibitior could down-regulate the expression of autophagy-associated proteins (ATG5, LC3, p62), accompanied by activating SIRT1/PGC-1α pathway. NOX1 down-regulation might alleviate oxidative stress-induced mitochondria damage and intestinal mucosal injury via modulating excessive autophagy and SIRT1/PGC-1α signaling pathway. The data will shed light on the molecular mechanism of NOX1 on intestine oxidative damage following pig transportation.

rs2274911 (Pro91Ser, G>A) is a missense mutation located on the second exon of the GPRC6A gene. Increasing evidence revealed a significant association between the A allele of rs2274911 and male diseases, such as oligospermia, cryptorchidism, and prostate tumor. However, the function of rs2274911 in healthy males is unclear.

A total of 1742 healthy men were selected from the Fangchenggang Area Male Health and Examination Survey (FAMHES). The association between rs2274911 and phenotype was evaluated. The cell characteristics of rs2274911 mutation (mu), wild-type GPRC6A (WT), and RFP control in human embryonic kidney (293T) and human prostate cancer (PC3) cells were analyzed. RNA sequencing was performed on PC3 cells.

E2 and PSA serum levels increased with the accumulation of the A allele (E2 G vs. A, -0.029 [-0.050, -0.008], P<0.01, P trend=0.027; PSA G vs. A, -0.040 [-0.079, 0.000], P<0.05, P trend=0.048). link3 rs2274911 enhanced the proliferation and invasion ability of PC3 or 293T cells and activated the ERK pathway. The genes were identified as rs2274911 mu-affected genes through RNA sequential analysis of rs2274911 mu, GPRC6A WT, and RFP control of PC3 cells. Most of these genes were related to cancer development processes, cAMP, and the ERK cell signaling pathway.

This project represents that rs2274911 is associated with E2 and PSA serum levels in Southern Chinese men. Rs2274991 mutation promotes 293T and PC3 cell proliferation in vitro. These results suggest that rs2274911 is a functional variant of GPRC6A.

This project represents that rs2274911 is associated with E2 and PSA serum levels in Southern Chinese men. Rs2274991 mutation promotes 293T and PC3 cell proliferation in vitro. These results suggest that rs2274911 is a functional variant of GPRC6A.CircRNAs are reported to exert a significant role in modulating genes in cancers, including osteosarcoma progression. Up to now, the function of circ_0010220 in osteosarcoma is still poorly known. The aim of our work was to figure out the potential mechanism of circ_0010220/miR-503-5p/CDCA4 axis in osteosarcoma progression. Firstly, quantitative RT-qPCR was utilized to measure the expression of circ_0010220 in osteosarcoma cells. Then, osteosarcoma cell proliferation, apoptosis, cell cycle, migration and invasion after loss of circ_0010220 were evaluated using CCK-8, flow cytometry, transwell migration, invasion and tumorigenesis experiments respectively. Circ_0010220 expression was markedly increased in osteosarcoma cells. Additionally, knockdown of circ_0010220 significantly depressed tumor growth. CCK-8 analysis indicated that down-regulation of circ_0010220 inhibited osteosarcoma cells proliferation. Flow cytometry assay showed that knockdown of circ_0010220 induced cell apoptosis and blocked cell cycle in the G1 phase.