Petersensong4294
Vitiligo can cause disfiguration, impair the social function of the patients and induce physiological burdens. However, limited research about the health-related quality of life has been conducted in vitiligo patients' sleeping conditions.
To evaluate the prevalence, severity, and risk factors of insomnia in vitiligo patients.
This case-control study was performed in March 2021. An online survey questionnaire including baseline information and the sleep-related instrument was sent to 762 vitiligo patients. The vitiligo-related evaluation was conducted by online video interview. According to whether having insomnia or not, patients were grouped and compared their clinical and demographic characteristics. The logistic regression model was conducted to analyze the risk factors for insomnia.
A total of 409 patients were included. About 49.9% of patients (204/409) experienced insomnia. About 55.9% (114/204) of the insomnia in vitiligo patients was adjustment sleep disorder caused by vitiligo. https://www.selleckchem.com/products/mv1035.html Development, is prevalent in vitiligo patients. Dermatologists should identify this condition carefully, especially humanistic factors in social life, and perform individualized "non-drug" treatment.Pruritus is the most burdensome and prevalent symptom in patients suffering from atopic dermatitis. Treating atopic itch has historically been a challenge due to multiple underlying mechanisms within its pathogenesis and an incomplete understanding of them. In recent years, our understanding of these mechanisms have increased tremendously and subsequently, new treatments have reached the market that target the pathophysiology of atopic itch from different angles. In addition, there are several promising new treatments currently in development and trials. In the current article, we discuss these currently available treatment options, their available evidence and efficacy, and highlight some of the more recent advancements in the field.
In the present study, we performed bioinformatics studies and in vitro functional assays to explore the underlying role of serpin family H member 1 (SERPINH1) in the diabetic retinopathy.
Common differentially expressed genes (DEGs) between diabetic retinal tissues and normal retinal tissues were analyzed using Gene Expression Omnibus (GEO) database. The proliferation and migration of human retinal endothelial cells (HRECs) was evaluated by MTS, EdU and wound healing assays, respectively; the miRNA and mRNAs expression levels of hub genes in HRECs were determined using quantitative real-time PCR (qRT-PCR). Protein levels were determined using a Western blot assay.
A total of 189 common DEGs were screened between two GEO datasets (GSE60436 and GSE94019), and ten potential hub genes that may link to the progression of diabetic retinopathy were detected. The qRT-PCR results showed that collagen, type I, alpha 1 (COL1A1), Collagen, type I, alpha 2 (COL1A2) and serpin family H member 1 (SERPINH1) mRNA expresssociated with diabetic retinopathy pathophysiology. Further mechanistic studies indicated that miR-29b/SERPINH1 signaling participated in high glucose-induced enhancement in the proliferation and migration of HRECs.
Guangdong, located in South China, is one of the areas heavily affected by HIV-1 in China. The transmission of HIV-1 among men who have sex with men (MSM) has gradually been increasing in Guangdong.
To investigate the characteristics of the HIV-1 drug resistance, and genetic transmission networks in MSM with antiretroviral therapy (ART) failure from 2014 to 2019 in Guangdong.
HIV-1
gene sequences were amplified. An online subtyping tool was used to determine the genotype, and a maximum likelihood phylogenetic tree was reconstructed to confirm the genotype results. The Stanford University HIV Drug Resistance Database was used to analyse the sequences of drug resistance mutations (DRMs) and drug resistance profiles. A pairwise Tamura-Nei 93 genetic distance-based method was used to analyse the genetic transmission networks.
Of 393 sequences isolated from HIV-infected MSM with ART failure, CRF01_AE (47.3%), CRF07_BC (21.4%) and CRF55_01B (21.4%) were the top three strains. 55.2% individuals harboured on network analysis revealed a complex transmission pattern, and more attention should be given to younger HIV-1-infected MSM with multiple links.
Accumulating evidence demonstrates that genetic susceptibility genes can be used as biomarkers to assess sepsis susceptibility, and genetic variation is associated with susceptibility and clinical outcomes in patients with sepsis and inflammatory disease. Although studies have shown that the lncRNA
is involved in inflammatory diseases, it remains unclear whether
gene polymorphisms are associated with susceptibility to inflammatory diseases, such as sepsis, in children.
We genotyped the rs6983267
polymorphism in 474 cases (pediatric sepsis) and 678 controls using TaqMan methods, and odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate the strength of associations.
Our results indicate that the rs6983267 T > G polymorphism is significantly associated with an increased risk of sepsis in children (TG and TT adjusted OR = 1.311, 95% CI = 1.016-1.743, GG and TT adjusted OR = 1.444, 95% CI = 1.025-2.034 dominant model GG/TG vs TT adjusted OR = 1.362, 95% CI = 1.055-1.756). Furthermore, the risk effect was more pronounced in children younger than 60 months who were male and who had sepsis.
We found that the
gene polymorphism rs6983267 T > G may be associated with an increased risk of pediatric sepsis in southern China. A larger multicenter study should be performed to confirm these results.
G may be associated with an increased risk of pediatric sepsis in southern China. A larger multicenter study should be performed to confirm these results.
Prostate cancer is the second leading cause of cancer death in men worldwide. Olaparib is clinically approved for the treatment prostate cancer, but cytotoxicity and off-target effects including DNA damage limit its clinical applications. In the current study, new strategies to improve the therapeutic efficacy of olaparib for the treatment of prostate cancer were investigated.
Two prostate cancer cell lines were exposed to the c-MET inhibitor PHA665752 and/or the PARP inhibitor olaparib. Cell counting kit-8, colony formation assays, and transwell assays were conducted to evaluate the cytotoxicity of olaparib alone or in combination with PHA665752 in prostate cancer cell lines. Western blotting, immunofluorescence staining, and the comet assay were used to assess the effects of PHA665752 on olaparib-induced DNA damage.
Combined inhibition of c-MET and PARP resulted in effective and synergistic blocking of the growth of prostate cancer cell lines. Invasion and migration were significantly suppressed when the agents were combined. Mechanistically, dual blocking of PARP and c-MET in prostate cancer cell lines was associated with an impaired DNA damage response. Interestingly, immunofluorescence staining analysis of RAD51 protein indicated that the c-MET inhibitor PHA665752 significantly impaired homologous repair via downregulated translocation of RAD51 into the nucleus in prostate cancer cells.
The combination of the c-MET inhibitor PHA665752 and the PARP inhibitor olaparib may be a promising therapeutic strategy in patients with prostate cancer.
The combination of the c-MET inhibitor PHA665752 and the PARP inhibitor olaparib may be a promising therapeutic strategy in patients with prostate cancer.
Glioblastoma multiforme (GBM) is the primary aggressive malignancy of the brain with poor outcome. Curcumin analogues are polyphenolic compounds as the bioactive substances extracted from turmeric. This study aims to investigate the anti-cancer effects of four curcumin analogues. Furthermore, the molecular mechanisms of dimethoxycurcumin in human gliomas were analyzed by Western blot.
Human LN229 and GBM8401 glioma cells were treated by four curcumin analogues with different number of methoxy groups. The cell viability, cell cycle, apoptosis, proliferation and ROS production of human gliomas were analyzed by flow cytometry. Moreover, the effects of four curcumin analogues on tumorigenesis of gliomas wereconducted by wound healing assay and colony formation assay. Furthermore, the molecular mechanisms of dimethoxycurcumin in human gliomas were analyzed by Western blot.
Our data showed that four different curcumin analogues including curcumin, bisdemethoxycurcumin, demethoxycurcumin, and dimethoxycurcumin promote sub-G1 phase, G2/M arrest, apoptosis, and ROS production in human glioma cells. Moreover, dimethoxycurcumin suppressed cell viability, migration, and colony formation, induction of sub-G1, G2/M arrest, apoptosis, and ROS production in glioma cells. Moreover, the mechanism of dimethoxycurcumin is ROS production to increase LC3B-II expression to induce autophagy. Furthermore, dimethoxycurcumin suppressed apoptotic marker, BCL-2 to promote apoptosis in LN229 and GBM8401 glioma cells.
Our study found that dimethoxycurcumin induced apoptosis, autophagy, ROS production and suppressed cell viability in human gliomas. Dimethoxycurcumin might be a potential therapeutic candidate in human glioma cells.
Our study found that dimethoxycurcumin induced apoptosis, autophagy, ROS production and suppressed cell viability in human gliomas. Dimethoxycurcumin might be a potential therapeutic candidate in human glioma cells.
Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related death worldwide with poor prognosis. Accumulating evidence indicates that miR-765 is an important regulator in the progression and prognosis of various cancers. In this study, the function in the progression and prognosis of NSCLC was investigated.
The expression of miR-765 in NSCLC was analyzed by qRT-PCR. The effect of miR-765 on cell proliferation, migration, and invasion of NSCLC was evaluated by CCK8 and Transwell assay. Kaplan-Meier analysis and Cox regression analysis were employed to assess the prognostic value of miR-765.
The results demonstrated the significant upregulation of miR-765 in NSCLC tissues and cell lines relative to normal tissues and cells. High miR-765 expression was significantly correlated with the TNM stage of patients. Patients with high miR-765 expression showed a poorer prognosis than that of patients with low miR-765 expression. Cox analysis indicated that miR-765 could be considered as an independent prognostic factor for NSCLC. Additionally, the upregulation of miR-765 was revealed to promote NSCLC cell proliferation, migration, and invasion by targeting BMP6.
The overexpression of miR-765 in NSCLC was associated with TNM stage and poor prognosis of patients. miR-765 served as a tumor promoter of NSCLC by regulating BMP6. These findings provide a potential biomarker and therapeutic target for the prognosis and treatment of NSCLC.
The overexpression of miR-765 in NSCLC was associated with TNM stage and poor prognosis of patients. miR-765 served as a tumor promoter of NSCLC by regulating BMP6. These findings provide a potential biomarker and therapeutic target for the prognosis and treatment of NSCLC.
