Aqua­trinitrato[2,4,6-tris­(pyridin-2-yl)-1,3,5-triazine]neodymium(III) dihydrate

In the title compound, [Nd(NO3)3(C18H12N6)(H2O)]·2H2O, the Nd3+ ion is in a distorted bicapped square-anti­prismatic geometry formed by three N atoms from the 2,4,6-tris­(pyridin-2-yl)-1,3,5-triazine (TPTZ) ligand, six O atoms from the three nitrate anions and one O atom from the aqua ligand. The mol­ecules are linked by O—H⋯O and O—H⋯N hydrogen bonds. Two types of π–π stacking inter­actions occur between the TPTZ ligands of adjacent complexes [centroid-to-centroid distances = 3.760 (4) and 3.870 (3) Å]

Bis(3,5-dimethyl­pyrazole)[N-salicyl­idene-β-alaninato(2–)]copper(II) dihydrate

In the title compound, [Cu(C10H10NO3)(C5H8N2)2]·2H2O, the CuII atom is coordinated by three N atoms and two O atoms in a distorted square-pyramidal geometry. The crystal packing is stabilized by inter­molecular O—H⋯O and N—H⋯O hydrogen bonds

Effect of mild moxibustion on intestinal microbiota and NLRP6 inflammasome signaling in rats with post-inflammatory irritable bowel syndrome

BACKGROUND: About one-third of refractory irritable bowel syndrome (IBS) cases are caused by gastrointestinal (GI) infection/inflammation, known as post-infectious/post-inflammatory IBS (PI-IBS). Although it is known that intestinal microbiota and host NOD-like receptor family pyrin domain containing 6 (NLRP6) inflammsome signaling are closely related to PI-IBS and moxibustion has a therapeutic effect on PI-IBS, whether moxibustion regulates the intestinal flora and host NLRP6 events in PI-IBS remains unclear. AIM: To examine the regulatory effect of moxibustion on intestinal microbiota and host NLRP6 inflammatory signaling in PI-IBS. METHODS: Sprague-Dawley rats were divided into a normal control group, a model control group, a mild moxibustion group, and a sham mild moxibustion group. PI-IBS rats in the mild moxibustion group were treated with moxibusiton at bilateral Tianshu (ST 25) and Zusanli (ST36) for 7 consecutive days for 10 min each time. The sham group rats were given the same treatment as the mild moxibustion group except the moxa stick was not ignited. Abdominal withdrawal reflex (AWR) score was measured to assess the visceral sensitivity, and colon histopathology and ultrastructure, colonic myeloperoxidase (MPO) activity, and serum C-reactive protein (CRP) level were measured to evaluate low-grade colonic inflammation in rats. The relative abundance of selected intestinal bacteria in rat feces was detected by 16S rDNA PCR and the NLRP6 inflammsome signaling in the colon was detected by immunofluorescence, qRT-PCR, and Western blot. RESULTS: The AWR score was significantly decreased and the low-grade intestinal inflammation reflected by serum CRP and colonic MPO levels was inhibited in the mild moxibustion group compared with the sham group. Mild moxibustion remarkably increased the relative DNA abundances of Lactobacillus, Bifidobacterium, and Faecalibacterium prausnitzii but decreased that of Escherichia coli in the gut of PI-IBS rats. Additionally, mild moxibustion induced mRNA and protein expression of intestine lectin 1 but inhibited the expression of IL-1β, IL-18, and resistance-like molecule β by promoting the NLRP6 and reducing the mRNA and protein expression of apoptosis-associated speck-like protein containing CARD (ASC) and cysteinyl-aspartate-specific proteinase 1 (Caspase-1). The relative DNA abundances of Lactobacillus, Bifidobacteria, Faecalibacterium prausnitzii, and Escherichia coli in each group were correlated with the mRNA and protein expression of NLRP6, ASC, and Caspase-1 in the colon. CONCLUSION: These findings indicated that mild moxibustion can relieve low-grade GI inflammation and alleviate visceral hypersensitivity in PI-IBS by regulating intestinal microbes and controlling NLRP6 inflammasome signaling

C-Reactive Protein and Risk of Parkinson's Disease: A Systematic Review and Meta-Analysis

Background: C-reactive protein (CRP) has been identified as a common inflammation-related cytokine. Although publications indicate that CRP is associated with the pathogenesis of neurological disorders and deemed to be a “risk factor” for Parkinson's disease (PD), the evidence exists still indefinitely. Here, we performed a systematic review with meta-analysis synthesizing all the eligible studies on serum, plasma, and cerebrospinal fluid (CSF) CRP levels and PD risk to investigate the potential relevance.Methods: A systematical search up to October 2018 was performed via PubMed, Embase, Science Direct, ISI Web of Science as well as three Chinese medical databases: China National Knowledge Infrastructure database (CNKI), VIP database and WanFang database. Risk was assessed by standardized mean difference (SMD) with 95% confidence interval (CI) to investigate the involvement of CRP levels in PD patients.Results: Twenty-three eligible case-control studies involving 4,598 individuals (2,646 PD patients and 1,932 healthy controls) were incorporated into this meta-analysis. Results have indicated significant increase of CRP levels in PD subjects when compared with control groups in serum (SMD = 1.115, 95% CI 0.619–1.61, P < 0.001), CSF (SMD = 1.127, 95% CI 0.133–2.120, P = 0.026) as well as whole blood (SMD = 1.071, 95% CI 0.715–1.426, P < 0.001).Conclusions: This meta-analysis revealed that PD is associated with an increase of CRP levels. CRP might be a risk factor for PD or PD leads to an inflammatory response

Experimental realization of Bloch oscillations in a parity-time synthetic silicon photonic lattice

As an important electron transportation phenomenon, Bloch oscillations have been extensively studied in condensed matter. Due to the similarity in wave properties between electrons and other quantum particles, Bloch oscillations have been observed in atom lattices, photonic lattices, and so on. One of the many distinct advantages for choosing these systems over the regular electronic systems is the versatility in engineering artificial potentials. Here by utilizing dissipative elements in a CMOS-compatible photonic platform to create a periodic complex potential and by exploiting the emerging concept of parity-time synthetic photonics, we experimentally realize spatial Bloch oscillations in a non-Hermitian photonic system on a chip level. Our demonstration may have significant impact in the field of quantum simulation by following the recent trend of moving complicated table-top quantum optics experiments onto the fully integrated CMOS-compatible silicon platform

A regulatory mutant on TRIM26 conferring the risk of nasopharyngeal carcinoma by inducing low immune response.

The major histocompatibility complex (MHC) is most closely associated with nasopharyngeal carcinoma (NPC), but the complexity of its genome structure has proven challenging for the discovery of causal MHC loci or genes. We conducted a targeted MHC sequencing in 40 Cantonese NPC patients followed by a two-stage replication in 1065 NPC cases and 2137 controls of Southern Chinese descendent. Quantitative RT-PCR analysis (qRT-PCR) was used to detect gene expression status in 108 NPC and 43 noncancerous nasopharyngeal (NP) samples. Luciferase reporter assay and chromatin immunoprecipitation (ChIP) were used to assess the transcription factor binding site. We discovered that a novel SNP rs117565607_A at TRIM26 displayed the strongest association (OR = 1.909, Pcombined = 2.750 × 10-19 ). We also observed that TRIM26 was significantly downregulated in NPC tissue samples with genotype AA/AT than TT. Immunohistochemistry (IHC) test also found the TRIM26 protein expression in NPC tissue samples with the genotype AA/AT was lower than TT. According to computational prediction, rs117565607 locus was a binding site for the transcription factor Yin Yang 1 (YY1). We observed that the luciferase activity of YY1 which is binding to the A allele of rs117565607 was suppressed. ChIP data showed that YY1 was binding with T not A allele. Significance analysis of microarray suggested that TRIM26 downregulation was related to low immune response in NPC. We have identified a novel gene TRIM26 and a novel SNP rs117565607_A associated with NPC risk by regulating transcriptional process and established a new functional link between TRIM26 downregulation and low immune response in NPC