Substrate-Induced Changes on the Optical Properties of Single-Layer WS2.

Among the most studied semiconducting transition metal dichalcogenides (TMDCs), WS2 showed several advantages in comparison to their counterparts, such as a higher quantum yield, which is an important feature for quantum emission and lasing purposes. We studied transferred monolayers of WS2 on a drilled Si3N4 substrate in order to have insights about on how such heterostructure behaves from the Raman and photoluminescence (PL) measurements point of view. Our experimental findings showed that the Si3N4 substrate influences the optical properties of single-layer WS2. Beyond that, seeking to shed light on the causes of the PL quenching observed experimentally, we developed density functional theory (DFT) based calculations to study the thermodynamic stability of the heterojunction through quantum molecular dynamics (QMD) simulations as well as the electronic alignment of the energy levels in both materials. Our analysis showed that along with strain, a charge transfer mechanism plays an important role for the PL decrease.

The inhibitory effect of LINC00261 upregulation on the pancreatic cancer EMT process is mediated by KLF13 via the mTOR signaling pathway.

PURPOSE: The long noncoding RNA LINC00261 was reported to be involved in carcinogenesis and has been validated as a tumor suppressor in pancreatic cancer (PC); however, how LINC00261 is regulated has not been fully examined. Here, we attempted to investigate the upstream and downstream targets of LINC00261 in PC. METHODS: LINC00261 expression in PC tissues was examined by the Gene Expression Omnibus (GEO) datasets and the Gene Expression Profiling Interactive Analysis (GEPIA) database. The quantitative reverse transcription polymerase chain reaction (qRT-PCR) assays were performed to detect the expression level of LINC00261 in PC cells. The location of LINC00261 in PC cells was identified by RNA fluorescence in situ hybridization (RNA-FISH). Cell Counting Kit-8 (CCK-8), cell apoptosis assay, transwell invasion and migration assays testified the critical role of LINC00261 in PC. The luciferase reporter assay was applied to confirm the binding of LINC00261 to its upstream transcription factor KLF13. The changes in LINC00261 related target protein levels were analyzed by Western blotting assay. RESULTS: LINC00261 was significantly lower in PC tissues and was mainly concentrated in the nucleus. Overexpression of LINC00261 inhibited the invasion and migration of PC cells. Mechanistically, transcription factor KLF13 was confirmed to inhibit the epithelial-mesenchymal transition (EMT) process of PC cells by promoting the transcription of LINC00261 and suppressing the expression of metastasis-associated proteins, such as matrix metalloproteinase MMP2 and vimentin, thus inhibiting the metastasis of PC. CONCLUSION: LINC00261 regulates PC cell metastasis through the "KLF13-LINC00261-mTOR-P70S6K1-S6" signaling pathway, which provides a significant set of potential PC therapeutic targets.

Cytomegalovirus infection as an underestimated trigger for checkpoint inhibitor-related pneumonitis in lung cancer: a retrospective study.

OBJECTIVES: Checkpoint inhibitor-related pneumonitis (CIP) is a rare but potentially fatal complication of immune checkpoint inhibitors (ICIs). At present, the mechanism of CIP is not completely clear. Cytomegalovirus (CMV) infection is widespread in the population. Chemotherapy and radiotherapy can lead to the reactivation of CMV. We aimed to investigate the association between CMV infection and CIP. MATERIALS AND METHODS: We retrospectively identified all lung cancer patients treated with ICIs at our institute from January 2016 to May 2020. The association between the development of CIP and CMV infection status was analyzed. RESULTS: Among 251 cases analyzed, 29 (11.6%) patients with CIP were identified, of whom 12 (4.78%) cases had grade 3-4 CIP. All 12 patients with grade 3-4 pneumonitis were CMV-IgG-positive, indicating a previous CMV infection. Except for one CMV-DNA-positive patient, the other patients were CMV-DNA-negative. All but one patient was CMV pp65 antigen-positive, indicating an early reactivation of the virus. The histological features of CMV pneumonia were not found in all available lung tissues, including lung transplantation pathology in one patient and lung biopsies in three patients. Except for one patient who received delayed antiviral therapy, the symptoms improved after glucocorticoid combined with antiviral therapy. CONCLUSIONS: The use of ICIs can restore the immune function and cause an immune response to CMV antigen while the infection is still latent. Our study suggests that CIP may be an immune reconstitution syndrome associated with CMV infection. CMV infection may represent a potentially important trigger for CIP. Patients with severe CIP should be vigilant against CMV infection. The early use of glucocorticoid combined with antiviral therapy is pivotal to good prognosis.

A signature of 14 immune-related gene pairs predicts overall survival in gastric cancer.

OBJECTIVE: Increasing evidence demonstrates that immune signature plays an important role in the prognosis of gastric cancer (GC). We aimed to develop and validate a robust immune-related gene pair (IRGP) signature for predicting the prognosis of GC patients. METHODS: RNA-Seq data and corresponding clinical information of GC cohort were downloaded from the TCGA (The Cancer Genome Atlas Program) data portal. GSE84437 and GSE15459 microarray datasets were included as independent external cohorts. Least absolute shrinkage and selection operator (LASSO) regression analysis was used to build the best prognostic signature. All patients were classified into the high immune-risk and low immune-risk groups via the optimal cut-off of the signature scores determined by time-dependent receiver-operating characteristic (ROC) curve analysis. The prognostic role of the signature was measured by a log-rank test and a Cox proportional hazard regression model. RESULTS: 14 immune gene pairs consisting of 25 unique genes were identified to construct the immune prognostic signature. High immune-risk groups showed poor prognosis in the TCGA datasets and GSE84437 datasets as well as in the GSE15459 datasets (all P < 0.001). The 14-IRGP signature was an independent prognostic factor of GC after adjusting for other clinical factors (P < 0.05). Functional analysis revealed that DNA integrity checkpoint, DNA replication, T-cell receptor signaling pathway, and B-cell receptor signaling pathway were enriched in the low immune-risk groups. B cells naive and Monocytes were significantly higher in the high-risk group, and B-cell memory and T-cell CD4 memory activated were significantly higher in the low-risk group. The prognostic signature based on IRGP reflected infiltration by several types of immune cells. CONCLUSION: The novel proposed clinical-immune signature is a promising biomarker for prediction overall survival in patients with GC and providing new insights into the treatment strategies.

The efficacy and safety of immunotherapy targeting the PD-1 pathway for advanced urothelial carcinoma: a meta-analysis of published clinical trials.

INTRODUCTION: Urothelial carcinoma (UC) is an aggressive malignancy and has a poor prognosis in the metastatic state. Treatment of UC remains a challenge, and as a first-line regimen for advanced UC, standard platinum-based chemotherapy is unfit for many patients due to numerous comorbidities and poor performance status. Recently, five immune checkpoint inhibitors have been approved for the treatment of patients with advanced UC who were ineligible for platinum-based regimens or suffered tumor progression in post-platinum setting. However, not long ago, the U.S. Food and Drug Administration restricted the use of two common immune checkpoint blockades, atezolizumab and pembrolizumab, due to uncertain survival benefit as mono-therapy. In this scenario, we reviewed rapidly surfacing clinical trials to assess the efficacy and safety of immunotherapy targeting the PD-1 pathway for advanced UC. METHODS: A comprehensive search was conducted in PubMed, EMBASE and Cochrane Library for all clinical trials where the efficacy and safety were reported. Our primary outcome was efficacy evaluated by objective response rate (ORR), 1-year overall survival (OS) rate and 1-year progression-free survival (PFS) rate, and second outcome was safety assessed by any grade and grade 3-4 treatment-related adverse events (TRAEs). We chose percentages with 95% confidence intervals (CI) as the evaluation indexes and used a random-effects model to account for heterogeneity. RESULTS: We included 14 clinical trials with 2674 total patients in this meta-analysis. After removing unqualified studies on the basis of sensitivity analyses, 13 studies were pooled to evaluate the overall ORR, 8 studies for the 1-year OS rate and 6 studies for the 1-year PFS rate. The pooled data of ORR, 1-year OS rate, and 1-year PFS rate were 0.20 (95% CI 0.18-0.22, I2 = 38.4%, P = 0.078), 0.50 (95% CI 0.46-0.53, I2 = 30.3%, P = 0.186), and 0.17 (95% CI 0.14-0.20, I2 = 0.0%, P = 0.668), respectively. Similarly, 13 trials were utilized to compute the pooled rate of any-grade TRAEs. The pooled estimation of any-grade was 0.65 (95% CI 0.63-0.67, I2 = 1.7%, P = 0.429). The pooled rate of grade 3-4 TRAEs subgroups with Atezolizumab, Pembrolizumab, Durvalumab, Nivolumab and Avelumab were 0.11 (95% CI 0.06-0.15, I2 = 83.5%, P = 0.000), 0.15 (95% CI 0.13-0.18, I2 = 0.0%, P = 0.971), 0.06 (95% CI 0.03-0.09, I2 = 0.0%, P = 0.566), 0.19 (95% CI 0.15-0.23, I2 = 0.0%, P = 0.480) and 0.08 (95% CI 0.05-0.11, I2 = 0.0%, P = 0.702), respectively. CONCLUSION: This study showed that the immunotherapy targeting the PD-1 pathway had durable efficacy and acceptable safety in patients with advanced UC. The comprehensive role of immune checkpoint inhibitors in comparison to other treatments needs further confirmation basing on RCTs.

Association of NF-κB1 gene polymorphisms with coronary artery disease in a Han Chinese population.

Nuclear factor (NF)-κB is a transcription factor that controls cell proliferation, differentiation, and immunity. Activated NF-κB1 is associated with the pathogenesis of coronary artery disease (CAD) and genetic polymorphisms in NF-κB1 have a plausible role in modulating the risk of CAD. To identify markers that contribute to the genetic susceptibility to CAD, we examined the potential association between CAD and single nucleotide polymorphisms (SNPs; rs28362491, rs230531, rs230528, rs1005819, rs4648055, rs3774964, and rs3774968) in the NF-κB1 gene using SNaPshot SNP genotyping assay. Participants included 361 patients with CAD and 385 healthy controls. The genotype and allele frequencies of the rs28362491 (promoter region) polymorphism in the CAD patients were significantly different from those in the healthy controls. The frequency of the D allele was significantly higher in CAD patients than in the healthy controls (P = 0.005 after Bonferroni correction). Strong linkage disequilibrium was observed in one block (D' > 0.9). Haplotype analysis revealed that haplotypes in block 1 of the NF-κB1 gene did not display a risk or protective effect (P > 0.05). These data suggest that NF-κB1 gene polymorphisms confer susceptibility to CAD and also support the notion that dysfunction of NF-κB1 is involved in the pathophysiological process of CAD.

Association between interleukin-17A polymorphism and coronary artery disease susceptibility in the Chinese Han population.

Coronary artery disease (CAD) is a major global health problem. In China, the incidence of CAD and the rate of mortality arising from it have increased every year. Interleukin-17A (IL-17A) is a proinflammatory cytokine produced by activated T cells, and it may be involved in the development of CAD. Genetic polymorphisms in functional regions of the IL17A gene have a plausible role in modulating the risk of CAD. To evaluate the role of IL17A polymorphisms as a risk factor for CAD, we performed a detailed analysis of possible functional single nucleotide polymorphisms (SNPs) in regulatory regions of IL17A. This study examined the potential association between CAD and five SNPs (rs8193037, rs8193036, rs3819024, rs2275913, and rs3748067) of the IL17A gene. The allelic or genotypic frequencies of the rs8193037 (promoter region) and rs8193036 (promoter region) polymorphisms in CAD were significantly different from those in healthy controls. The CAD subjects had a significantly lower frequency of the A allele of rs8193037 (P = 0.009, OR = 1.772, 95%CI = 1.146- 2.742) and the T allele of rs8193036 (P = 0.010, OR = 1.754, 95%CI = 1.139-2.701). Strong linkage disequilibrium was observed in one block (D' > 0.9). Significantly fewer T-G-G-A haplotypes (P = 0.045) were found in CAD subjects in block 1. These data suggest that IL17A gene polymorphisms confer susceptibility to CAD, and support the notion that dysfunction of IL-17A is involved in the pathophysiological process of CAD.

Multiple sequence alignment based on combining genetic algorithm with chaotic sequences.

In bioinformatics, sequence alignment is one of the most common problems. Multiple sequence alignment is an NP (nondeterministic polynomial time) problem, which requires further study and exploration. The chaos optimization algorithm is a type of chaos theory, and a procedure for combining the genetic algorithm (GA), which uses ergodicity, and inherent randomness of chaotic iteration. It is an efficient method to solve the basic premature phenomenon of the GA. Applying the Logistic map to the GA and using chaotic sequences to carry out the chaotic perturbation can improve the convergence of the basic GA. In addition, the random tournament selection and optimal preservation strategy are used in the GA. Experimental evidence indicates good results for this process.

Construction of a protein-protein interaction network of Wilms' tumor and pathway prediction of molecular complexes.

Wilms' tumor (WT), or nephroblastoma, is the most common malignant renal cancer that affects the pediatric population. Great progress has been achieved in the treatment of WT, but it cannot be cured at present. Nonetheless, a protein-protein interaction network of WT should provide some new ideas and methods. The purpose of this study was to analyze the protein-protein interaction network of WT. We screened the confirmed disease-related genes using the Online Mendelian Inheritance in Man database, created a protein-protein interaction network based on biological function in the Cytoscape software, and detected molecular complexes and relevant pathways that may be included in the network. The results showed that the protein-protein interaction network of WT contains 654 nodes, 1544 edges, and 5 molecular complexes. Among them, complex 1 is predicted to be related to the Jak-STAT signaling pathway, regulation of hematopoiesis by cytokines, cytokine-cytokine receptor interaction, cytokine and inflammatory responses, and hematopoietic cell lineage pathways. Molecular complex 4 shows a correlation of WT with colorectal cancer and the ErbB signaling pathway. The proposed method can provide the bioinformatic foundation for further elucidation of the mechanisms of WT development.

Meta-analysis of the IL-10 promoter polymorphisms and pediatric asthma susceptibility.

The results of previous epidemiological studies exploring the relationship between interleukin-10 (IL-10) promoter polymorphisms and susceptibility to pediatric asthma are not consistent. Therefore, we have performed a systematic review and meta-analysis to provide a more convincing conclusion. Odds ratios (OR) with their 95% confidence intervals (CIs) were used to evaluate the strength of association between the IL-10 promoter polymorphisms and susceptibility to pediatric asthma. Publication bias was examined by Begg's funnel plots and the Egger test. A detailed literature search based on stringent parameters yielded sixteen relevant studies, comprising 2494 cases and 2160 controls. The overall population showed no significant association between the IL-10 -1082G/A polymorphism and pediatric asthma risk in any of the genetic models (dominant model: OR = 1.583, 95%CI = 0.614-4.076, P = 0.342; allelic model: OR = 1.214, 95%CI = 0.748-1.971, P = 0.433; additive model: OR = 2.240, 95%CI = 0.950-5.277, P = 0.065; recessive model: OR = 1.435, 95%CI = 0.659-3.128, P = 0.363). Subgroup analyses revealed a significant association between different ethnicity and atopic status subgroups. However, there was no evidence of a significant association between the other two polymorphisms (-819C/ T and -592C/A) and pediatric asthma in our study. No significant publication bias was observed in this meta-analysis. The results of this study indicate that the IL-10 -1082G/A polymorphism might be a risk factor for asthma in children. However, because of the small sample size included in the subgroup analyses, the results should be interpreted with caution.

CAMK4 gene variation is associated with hypertension in a Uygur population.

Considering that calcium/calmodulin-dependent kinase 4 (CAMK4) plays a pivotal role in blood pressure regulation, we investigated the association between a CAMK4 polymorphism (rs10491334) and hypertension in the Han, Kazak, and Uygur ethnic groups. We studied 1224 patients with hypertension and 967 normotensive controls classified into three ethnic groups (Han, Kazak, and Uygur). The rs10491334 polymorphism was genotyped using a TaqMan® 5'-nuclease assay. In the Uygur group, the T-allele frequency in patients with hypertension was twice that of the controls (12.5 vs 6.38%), and T-allele carriers had a significantly increased risk of hypertension compared with non-carriers (odds ratio = 2.200; 95% confidence interval = 1.473-3.285, P < 0.001). However, no significant correlation was found in the Han and Kazak groups. The T-allele of rs10491334 in CAMK4 was associated with hypertension in the Uygur group.

Construction of polycythemia vera protein interaction network and prediction of related biological functions.

Here, polycythemia vera (PV)-related genes were screened by the Online Mendelian Inheritance in Man (OMIM), and literature pertaining to the identified genes was extracted and a protein-protein interaction network was constructed using various Cytoscape plugins. Various molecular complexes were detected using the Clustervize plugin and a gene ontology-enrichment analysis of the biological pathways, molecular functions, and cellular components of the selected molecular complexes were identified using the BiNGo plugin. Fifty-four PV-related genes were identified in OMIM. The protein-protein interaction network contains 5 molecular complexes with correlation integral values >4. These complexes regulated various biological processes (peptide tyrosinase acidification, cell metabolism, and macromolecular biosynthesis), molecular functions (kinase activity, receptor binding, and cytokine activity), and the cellular components were mainly concentrated in the nucleus, intracellular membrane-bounded organelles, and extracellular region. These complexes were associated with the JAK-STAT signal transduction pathway, neurotrophic factor signaling pathway, and Wnt signaling pathway, which were correlated with chronic myeloid leukemia and acute myeloid leukemia.

Galantamine protects against lipopolysaccharide-induced acute lung injury in rats.

Lipopolysaccharide (LPS)-induced endotoxemia triggers the secretion of proinflammatory cytokines and can cause acute lung injury (ALI). The high mobility group box 1 (HMGB1) protein plays an important role as a late mediator of sepsis and ALI. Galantamine (GAL) is a central acetylcholinesterase inhibitor that inhibits the expression of HMGB1. This study evaluated the effects of GAL by measuring levels of inflammatory mediators and observing histopathological features associated with LPS-induced ALI. Sixty 8-10 week old male Sprague-Dawley rats (200-240 g) were randomized into three groups as follows: control group, LPS group (7.5 mg/kg LPS), and LPS+GAL group (5 mg/kg GAL before LPS administration). Histopathological examination of lung specimens obtained 12 h after LPS administration was performed to analyze changes in wet-to-dry (W/D) weight ratio, myeloperoxidase (MPO) activity, and HMGB1 expression level. Additionally, plasma concentrations of tumor necrosis factor-α, interleukin-6, and HMGB1 were measured using an enzyme-linked immunosorbent assay at 0 (baseline), 3, 6, 9, and 12 h after LPS administration. Mortality in the three groups was recorded at 72 h. LPS-induced ALI was characterized by distortion of pulmonary architecture and elevation of MPO activity, W/D weight ratio, and levels of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-6, and HMGB1. Pretreatment with GAL significantly reduced the LPS-induced lung pathological changes, W/D weight ratio, levels of pro-inflammatory cytokines and MPO activity (ANOVA). Moreover, GAL treatment significantly decreased the mortality rate (ANOVA). In conclusion, we demonstrated that GAL exerted a protective effect on LPS-induced ALI in rats.

Novel polymorphic microsatellite markers for Bellamya and their application in population genetics of three species.

Bellamya is a widely distributed freshwater snail genus in China; however, its genetic diversity is completely unknown. Sixty-five novel microsatellite loci were isolated and characterized from a microsatellite-enriched library of Bellamya aeruginosa genomic DNA. Most of the 65 loci were successfully amplified. We found high polymorphic information content values for these loci, ranging from 0.235 to 0.892. There were 3 to 12 alleles per locus, and the HE and HO varied from 0.425 to 0.953 and 0.026 to 1.000, respectively. Fifteen loci deviated significantly from Hardy-Weinberg equilibrium after Bonferroni's correction. All 65 SSR markers were tested in an additional five Bellamya species, and 96.9% of the 325 locus/taxon combinations tested resulted in cross-species amplification. Seven polymorphic microsatellite markers were randomly selected for comparison among nine populations of three species. All populations had moderate to high genetic diversity. In genetic distance-based cluster analysis, the populations of B. aeruginosa and B. dispiralis formed species-based clusters, whereas populations of B. angularia did not. The three examined Bellamya species could be differentiated using SSR markers. These microsatellite loci should be useful for genetic diversity analysis, analysis of phylogenetic relationship, and species delimitation of Bellamya.

Construction of gene/protein interaction networks for primary myelofibrosis and KEGG pathway-enrichment analysis of molecular compounds.

The objective of this study was the development of a gene/protein interaction network for primary myelofibrosis based on gene expression, and the enrichment analysis of KEGG pathways underlying the molecular complexes in this network. To achieve this, genes involved in primary myelofibrosis were selected from the OMIM database. A gene/protein interaction network for primary myelofibrosis was obtained through Cytoscape with the literature mining performed using the Agilent Literature Search plugin. The molecular complexes in the network were detected by ClusterViz plugin and KEGG pathway enrichment of molecular complexes was performed using DAVID online. We found 75 genes associated with primary myelofibrosis in the OMIM database. The gene/protein interaction network of primary myelofibrosis contained 608 nodes, 2086 edges, and 4 molecular complexes with a correlation integral value greater than 4. Molecular complexes involved in KEGG pathways are related to cytokine regulation, immune function regulation, ECM-receptor interaction, focal adhesion, actin cytoskeleton regulation, cell adhesion molecules, and other biological behavior of tumors, which can provide a reliable direction for the treatment of primary myelofibrosis and the bioinformatic foundation for further understanding the molecular mechanisms of this disease.

Overexpression of EsMcsu1 from the halophytic plant Eutrema salsugineum promotes abscisic acid biosynthesis and increases drought resistance in alfalfa (Medicago sativa L.).

The stress phytohormone abscisic acid (ABA) plays pivotal roles in plants' adaptive responses to adverse environments. Molybdenum cofactor sulfurases influence aldehyde oxidase activity and ABA biosynthesis. In this study, we isolated a novel EsMcsu1 gene encoding a molybdenum cofactor sulfurase from Eutrema salsugineum. EsMcus1 transcriptional patterns varied between organs, and its expression was significantly upregulated by abiotic stress or ABA treatment. Alfalfa plants that overexpressed EsMcsu1 had a higher ABA content than wild-type (WT) plants under drought stress conditions. Furthermore, levels of reactive oxygen species (ROS), ion leakage, and malondialdehyde were lower in the transgenic plants than in the WT plants after drought treatment, suggesting that the transgenic plants experienced less ROS-mediated damage. However, the expression of several stress-responsive genes, antioxidant enzyme activity, and osmolyte (proline and total soluble sugar) levels in the transgenic plants were higher than those in the WT plants after drought treatment. Therefore, EsMcsu1 overexpression improved drought tolerance in alfalfa plants by activating a series of ABA-mediated stress responses.

Analysis of the gene-protein interaction network in glioma.

Glioma is the most aggressive type of brain tumor. Great progress has been achieved in glioma treatment, but the protein-protein interaction networks underlining glioma are poorly understood. We identified the protein-protein interaction network for glioma based on gene expression and predicted biological pathways underlying the molecular complexes in the network. Genes involved in glioma were selected from the Online Mendelian Inheritance in Man (OMIM) database. A literature search was performed using the Agilent Literature Search plugin, and Cytoscape was used to establish a protein-protein interaction network. The molecular complexes in the network were detected using the Clusterviz plugin, and pathway enrichment of molecular complexes was performed using DAVID online. There were 378 glioma genes in the OMIM database. The protein-protein interaction network in glioma contained 1814 nodes, 6471 edges, and 8 molecular complexes. There were 17 pathways (false discovery rate <1), which were related to cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway, chemokine signaling pathway, oocyte meiosis, progesterone-mediated oocyte maturation, transmembrane transport of small molecules, metabolism of amino acids, and notch signaling pathway, among others. Our results provide a bioinformatic foundation for further studies of the mechanisms of glioma.

Treating congenital megacolon by transplanting GDNF and GFRα-1 double genetically modified rat bone marrow mesenchymal stem cells.

We studied the survival and gene expression of glial cell line-derived neurotrophic factor (GDNF) and GDNF receptor α-1 (GFRα-1) double-genetically modified rat bone marrow mesenchymal stem cells (BMSCs) transplanted into the intestinal walls of the rat models with congenital megacolon and determine the feasibility of treatment by transplantation of double-genetically modified rat BMSCs. The rat colorectal intestinal wall nerve plexus was treated with the cationic surface active agent benzalkonium chloride to establish an experimental megacolon model. The rat target genes GDNF and GFRα-1 were extracted and ligated into pEGFP-N1. Eukaryotic fluorescent expression vectors carrying the GDNF and GFRα-1 genes were transfected into BMSCs by in vitro culture. We treated congenital megacolon by transplanting double-genetically modified rat bone marrow mesenchymal stem cells. The pEGFP-EGFP-GDNF-GFRα-1 double-gene co-expressing the eukaryotic expression plasmid vector was successfully established. Protein gene protein 9.5 and vasoactive intestinal peptide-positive ganglion cells showed no positive expression in the phosphate-buffered saline transplantation group based on an immunofluorescence test at 1, 2, and 4 weeks after transplantation of BMSCs. Additionally, compared with the phosphate-buffered saline transplantation group, the expression of rearranged during transfection, GDNF, and GFRα-1 mRNA in the stem cell transplantation group increased gradually. The double-genetically modified BMSCs colonized and survived in the intestinal wall of the experimental megacolon rat model and expressed related genes, partially recovering the colonic neuromuscular regulatory functions and thus providing an experimental basis for treating congenital megacolon by cellular transplantation.

Comparison of high-intensity focused ultrasound therapy under nasal endoscopy guidance versus first-line drug treatment in patients with persistent allergic rhinitis.

The aim of this study was to determine whether high-intensity focused ultrasound (HIFU) therapy under nasal endoscopy guidance could provide better efficacy and safety in patients with persistent allergic rhinitis (PAR) than the first-line drugs recommended by the World Health Organization. A total of 120 adult patients with PAR were randomly divided into 2 groups (N = 60 each). One group underwent HIFU therapy under nasal endoscopy guidance using an ultrasound rhinitis therapeutic machine. The other group served as the control group and was treated with corticosteroid nasal spray and oral cetirizine hydrochloride. All patients underwent follow-up treatment for 1 year, after which the efficacy and safety were evaluated. There was no significant difference between the two groups (P > 0.05) in the total effective rate. Moreover, no complications such as nasal adhesion, septal perforation, mucosal atrophy, and hyposmia were observed, indicating that HIFU was as effective as the first-line drug treatments recommended by the World Health Organization for symptom relief in PAR patients. The treatment efficacy, repeatability, safety, economical aspects, ease of performance, and few complications of HIFU therapy strongly suggest that HIFU should be routinely incorporated into clinical practice.

Effect of Rhizoma paridis total saponins on apoptosis of colorectal cancer cells and imbalance of the JAK/STAT3 molecular pathway induced by IL-6 suppression.

We observed the influence of different concentrations of Rhizoma paridis total saponins (RPTS) on the apoptosis of colorectal cancer cells and explored the internal mechanism involved. We determined whether RPTS influences the interleukin-6 (IL-6)/Janus kinase (JAK)-signal transducer and activator of transcription-3 (STAT3) apoptosis molecular pathway and looked for colon cancer-related signal transduction pathways or targets inducing apoptosis. We also cultured SW480 colorectal cancer cells using different concentrations of RPTS (10, 20, 40, and 80 µg/ mL), and observed the effect of RPTS on SW480 cell morphology under a fluorescence inverted microscope. We detected serum IL-6 using the polymerase chain reaction and the expression of JAK-STAT3 protein by western blot. After treating SW480 with RPTS and Hoechst 33258 dyeing, we found that the typical apoptosis morphology had changed. Secretion of IL-6 in the serum decreased significantly (P < 0.05), and STAT3 levels were reduced. RPTS can significantly promote apoptosis in SW480 colorectal cancer cells. The mechanism may be that it suppresses the secretion of IL-6 and inhibits the IL-6/JAK-STAT3 protein signaling pathway.