Background Gut microbiota has been suggested to play a role in stroke patients. Nevertheless, little is known about gut microbiota and the clinical indexes in stroke patients. Methods Total of 30 cerebral ischemic stroke (CI) patients and 30 healthy control were enrolled in this study and the fecal gut microbiota was profiled via Illumina sequencing of the 16S rRNA V1-V2. The National Institutes of Health Stroke Scale (NIHSS) were used to quantify stroke severity and modified Rankin scale (mRS) to assess outcome for CI patients. The correlations between the clinical indexes and microbiota were evaluated. Results Though the microbial α-diversity and structure is similar between CI patients and healthy controls, the gut microbiota of CI patients had more short chain fatty acids producer including Odoribacter , Akkermansia, Ruminococcaceae_ UCG_005 and Victivallis . We also found that the special microbes were correlation with serum index, such as norank_O _ _Mollicutes_RF9 , Enterobacter , Ruminococcaceae _UCG-002 were negative correlation with LDL (r = − 0.401, P < 0.01), HDL (r = − 0.425, P < 0.01) and blood glucose (r = − 0.439, P < 0.001), while the HDL was significantly positive correlation with the genus Ruminococcus _1 (r = 0.443, P < 0.001). The Christensenellaceae _R-7_group and norank_f_ Ruminococcaceae was significantly positive correlation with NIHSS1M (r = 0.514, P < 0.05; r = 0.449, P < 0.05) and mRS (r = 0.471, P < 0.05, r = 0.503, P < 0.01), respectively. On the other hand, the genus Enterobacter was significantly negative correlation with NIHSS1M (r = 0.449, P < 0.05) and mRS (r = 0.503, P < 0.01). Conclusions This study suggests that CI patients showed significant dysbiosis of the gut microbiota with enriched short chain fatty acids producer, including Odoribacter , Akkermansia . This dysbiosis was correlation with the outcomes and deserves further study. Electronic supplementary material The online version of this article (10.1186/s12866-019-1552-1) contains supplementary material, which is available to authorized users.

This study suggested that LL-37 may play important role in the pathogenesis of COPD and may be a possible novel therapeutic target in COPD.

Wnt1, initially described as a modulator of embryonic development, has recently been discovered to exert cytoprotective effects in cellular models of several diseases, including Parkinson's disease (PD). We, therefore, examined the neuroprotective effects of exogenous Wnt1 on dopaminergic SH-SY5Y cells treated with 6-hydroxydopamine (6-OHDA). Here, we show that 10-500 μM 6-OHDA treatment decreased cell viability and increased lactate dehydrogenase (LDH) leakage. SH-SY5Y cells treated with 100 μM 6-OHDA for 24 h showed reduced Wnt/β-catenin activity, decreased mitochondrial transmembrane potential, elevated levels of reactive oxidative species (ROS) and phosphatidylserine (PS) extraversion, increased levels of Chop and Bip/GRP78 and reduced level of p-Akt (Ser473). In contrast, exogenous Wnt1 attenuated 6-OHDA-induced changes. These results suggest that activation of the Wnt/β-catenin pathway by exogenous Wnt1 protects against 6-OHDA-induced changes by restoring mitochondria and endoplasmic reticulum (ER) function.

Our conclusion suggests that hospital and organizational administrations should attach much importance to the moral distress experienced by clinical nurses in China. Further studies should focus on interventions about how to reduce the levels of the frequency and intensity of moral distress among clinical nurses.

Emerging evidence suggests that the process of small airway remodeling is mediated by profibrotic growth factors produced by epithelium, which are capable of activating the underlying mesenchymal cells with excessive collagen production. It has been demonstrated that human cathelicidin antimicrobial protein LL-37 is highly expressed in small airway epithelium from COPD patients. However, it is unknown whether the increased levels of LL-37 in epithelium are involved in the pathogenesis of small airway remodeling in COPD. In this study, we examined the expression of LL-37 in small airways from smokers with COPD and controls (non-smokers and smokers without COPD) by immunohistochemistry, and then the association between LL-37 expression in epithelium and the structural changes of small airway remodeling was analyzed. In vitro, the effect of CSE-induced epithelial secretion of LL-37 on collagen production in human lung fibroblasts (HFL-1 cell line) was studied in a co-culture system. Finally, the signaling pathways involved in the effect of LL-37 on fibroblast collagen production were evaluated. The results showed that LL-37 immunoreactivity in airway epithelium was significantly elevated in smokers with COPD compared with controls. In addition, the magnitude of LL-37 expression in epithelium was positively correlated with airway wall thickness and collagen deposition. In vitro, CSE-induced epithelial secretion of LL-37 promoted fibroblast collagen production. Finally, we showed that formyl peptide receptor-like 1 (FPRL1)-dependent extracellular signal-regulated kinase (ERK) signaling pathway was essential for LL-37-induced collagen production in HFL-1 cells. These results suggest that after cigarette smoke exposure, the increased levels of LL-37 in airway epithelium could stimulate collagen production in the underlying lung fibroblasts and may contribute to small airway remodeling in COPD.

Immune disorders may play an important role in the pathogenesis of Parkinson's disease (PD). Recently, polymorphisms in the HLA-DR region have been found to be associated with sporadic PD in European ancestry populations. However, polymorphisms in the HLA complex are highly variable with ethnic and geographic origin. To explore the relationships between polymorphisms of the HLA-DR region and sporadic PD in Chinese Han population, we genotyped 567 sporadic PD patients and 746 healthy controls in two independent series for the HLA-DRB1 locus with Polymerase chain reaction-sequence based typing(PCR-SBT). The χ2 test was used to evaluate the distribution of allele frequencies between the patients and healthy controls. The impact of HLA-DRB1 alleles on PD risk was estimated by unconditional logistic regression. We found a significant higher frequency of HLA-DRB1*0301 in sporadic PD patients than in healthy controls and a positive association, which was independent of onset age, between HLA-DRB1*0301 and PD risk. Conversely, a lower frequency of HLA-DRB1*0406 was found in sporadic PD patients than in healthy controls, with a negative association between HLA-DRB1*0406 and PD risk. Furthermore, a meta-analysis involving 195205 individuals was conducted to summarize the frequencies of these two alleles in populations from various ethnic regions, we found a higher frequency of HLA-DRB1*0301, but a lower frequency of HLA-DRB1*0406 in European ancestry populations than that in Asians, this was consistent with the higher prevalence of sporadic PD in European ancestry populations. Based on these results, we speculate that HLA-DRB1 alleles are associated with the susceptibility to sporadic PD in Chinese Han population, among them HLA-DRB1*0301 is a risk allele while the effect of HLA-DRB1*0406 deserves debate.

Background: Abnormal immune responses are involved in the development of Parkinson's disease (PD), and also affect peripheral blood lymphocytes. The profile of lymphocyte subsets in peripheral blood and whether it is relevant to the clinical features of PD patients remains controversial.Methods: To explore the role of peripheral blood lymphocytes (NK cells, B cells, CD3 + T cells, CD3 + CD4 + T cells and CD3 + CD8 + T cells) in the development of PD, a case-control study including 127 patients and 148 healthy controls was conducted, and peripheral blood lymphocyte subpopulations of participants were analysed by a FACSCalibur flow cytometer.Results: PD patients had a significantly higher percentage of NK cells and a lower percentage of CD3 + T cells and CD3 + CD4 + T cells than controls [16.4% (12.3%) vs. 12.6% (6.2%), 63.7% (14.2%) vs. 69.0% (6.6%), 33.1% (13.1%) vs. 38.9% (7.6%), P<0.05, respectively]. Through a binary logistic regression model adjusted for gender and age, we found that those who were outside of the reference range of peripheral blood lymphocytes (NK cell, B cell, CD3 + T cell and CD3 + CD4 + T cell) had an increased risk of PD [odds ratio (OR): 2.3, 5.1, 3.1 and 4.1, P<0.05, respectively]. Through a multivariable linear regression model adjusted for gender, age and levodopa equivalent daily dose, we found that deviation from the reference range of CD3 + CD8 + T cells (regression coefficient =3.474, P=0.015), course of disease (regression coefficient =0.411, P=0.004) and the Non-Motor Symptoms Scale (NMSS) scores (regression coefficient =0.553, P=5.92E−11) had a positive association with the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS)-III score (adjusted R 2 =0.364, F=13.004).Conclusions: Abnormal peripheral blood lymphocyte subpopulations have clinical relevance for PD.

Wu-tou decoction (WTD) is a classic traditional Chinese medicine formula and has been extensively used for the treatment of rheumatoid arthritis (RA). Previous reports indicate that WTD possesses anti-inflammatory and antinociceptive activities, and inhibits the development of arthritic joints and disease severity of collagen-induced arthritis (CIA) or adjuvant-induced rats; however, its action on angiogenesis of RA has not been clarified. This study aims to determine the anti-angiogenic activity of WTD in CIA rats and in various angiogenesis models. Our data showed that WTD (0.95, 1.9, and 3.8 g/kg) markedly reduced the immature blood vessels in synovial membrane tissues of inflamed joints from CIA rats. It also inhibited in vivo angiogenesis in chick embryo and VEGF-induced microvessel sprout formation ex vivo. Meanwhile, WTD suppressed VEGF-/MH7A-induced migration, invasion, adhesion, and tube formation of human umbilical vein endothelial cells (HUVECs). Moreover, WTD significantly reduced the expression of angiogenic activators, including vascular endothelial growth factor (VEGF), VEGFR2, interleukin (IL)-1β, IL-17, transforming growth factor-β, platelet-derived growth factor, placenta growth factor, angiopoietin (Ang) I and Ang II in synovium of CIA rats, and/or in HUVECs. More interestingly, WTD blocked the autophosphorylation of VEGF-induced VEGFR2 and consequently downregulated the signaling pathways of activated AKT, ERK1/2, JNK, and p38 in VEGF-induced HUVECs. These findings suggest for the first time that WTD possesses the anti-angiogenic effect in RA in vivo, ex vivo, and in vitro by interrupting the targeting of VEGFR2 activation.