Mapping research trends regarding the mechanism of dysphagia from 1993 to 2023: a bibliometrics study and visualization analysis.

As a common consequence of various neurogenic disorders, dysphagia has a significant impact on the quality of life for patients. To promote the development the field of swallowing, it will be helpful to clarify the pathological and therapeutic mechanisms of dysphagia. Through visual analysis of related papers from 1993 to 2023 in the Web of Science Core Collection (WoSCC) database, the research status and development trend of the pathogenesis of dysphagia were discussed. The co-occurrence study was finished using CiteSpace 6.2 R4 software, including keywords, countries, institutions, and authors. Finally, 1,184 studies satisfied the inclusion requirements. The findings of the visualization analysis suggested that aspiration and gastroesophageal reflux disease would be the areas of greatest interest for researchers studying the mechanism of dysphagia. As for the latest occurred research trends, fMRI, signals and machine learning emerging into the field of view of researchers. Based on an analysis of country co-occurrence, United States, Japan and China rank the top three, in terms of the number of publications on dysphagia. University System of Ohio is the organization that has published the most amount of articles regarding the mechanism of dysphagia. Other highly published schools in the top three include State University System of Florida and Northwestern University. For the prolific authors, German, Rebecca Z published the most articles at present, whose own research team working closely together. Several closely cooperating research teams have been formed at present, including the teams centered around German, Rebecca Z, Warnecke, Tobias and Hamdy Shaheen. This study intuitively analyzed the current research status of the mechanism of dysphagia, provided researchers with research hotspots in this field.

Proteomic profiling of laser capture microdissection kidneys from diabetic nephropathy patients.

Diabetic nephropathy (DN) remains the primary cause of end-stage renal disease (ESRD), warranting equal attention and separate analysis of glomerular, tubular, and interstitial lesions in its diagnosis and intervention. This study aims to identify the specific proteomics characteristics of DN, and assess changes in the biological processes associated with DN. 5 patients with DN and 5 healthy kidney transplant donor control individuals were selected for analysis. The proteomic characteristics of glomeruli, renal tubules, and renal interstitial tissue obtained through laser capture microscopy (LCM) were studied using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Significantly, the expression of multiple heat shock proteins (HSPs), tubulins, and heterogeneous nuclear ribonucleoproteins (hnRNPs) in glomeruli and tubules was significantly reduced. Differentially expressed proteins (DEPs) in the glomerulus showed significant enrichment in pathways related to cell junctions and cell movement, including the regulation of actin cytoskeleton and tight junction. DEPs in renal tubules were significantly enriched in glucose metabolism-related pathways, such as glucose metabolism, glycolysis/gluconeogenesis, and the citric acid cycle. Moreover, the glycolysis/gluconeogenesis pathway was a co-enrichment pathway in both DN glomeruli and tubules. Notably, ACTB emerged as the most crucial protein in the protein-protein interaction (PPI) analysis of DEPs in both glomeruli and renal tubules. In this study, we delve into the unique proteomic characteristics of each sub-region of renal tissue. This enhances our understanding of the potential pathophysiological changes in DN, particularly the potential involvement of glycolysis metabolic disorder, glomerular cytoskeleton and cell junctions. These insights are crucial for further research into the identification of disease biomarkers and the pathogenesis of DN.

Screening for optimal parameters for modified pharyngeal electrical stimulation for the treatment of dysphagia after stroke in rats.

Pharyngeal electrical stimulation (PES), a novel noninvasive peripheral nerve stimulation technique, can effectively improve neurogenic dysphagia and increase the safety and effectiveness of swallowing in the clinic. However, the lack of animal models for dysphagia has limited the mechanistic research on PES, which affects its wide application. Therefore, determining optimal parameters for PES in rats is needed to enable mechanistic studies. Modified PES (mPES), which has different waves and pulse widths from PES, was used; in previous studies mPES was found to have a neurological mechanism like that of PES. A poststroke dysphagia (PSD) model was established, and rats with dysphagia were grouped into three different intensities (0.1 mA, 0.5 mA, and 1 mA) for the selection of optimal intensity and three different frequencies (1 Hz, 2 Hz, and 5 Hz) for the selection of optimal frequency based on a stimulation duration of 10 min in the clinic. A Videofluroscopic Swallow Screen (VFSS) was used to assess swallowing function in rats before and after mPES treatment. The results showed that the 1 mA group had better swallowing function (p < 0.05) than the model group. Compared with the model group, the 1 Hz and 5 Hz groups had the same improvement in swallowing function (p < 0.05). However, the increase in excitatory signals in the sensorimotor cortex was more pronounced in the 5 Hz group than in the other frequency stimulation groups (p < 0.05). Combining the clinical findings with the above results, we concluded that the optimal stimulation parameter for mPES in rats is "frequency: 5 Hz, current intensity: 1 mA for 10 min/day", which provides a basis for future basic experimental studies of mPES in animals.

A genomic instability-associated lncRNA signature for predicting prognosis and biomarkers in lung adenocarcinoma.

Genomic instability (GI) was associated with tumorigenesis. However, GI-related lncRNA signature (GILncSig) in lung adenocarcinoma (LUAD) is still unknown. In this study, the lncRNA expression data, somatic mutation information and clinical survival information of LUAD were downloaded from The Cancer Genome Atlas (TCGA) and performed differential analysis. Functional and prognosis analysis revealed that multiple GI-related pathways were enriched. By using univariate and multivariate Cox regression analysis, 5 GI-associated lncRNAs (AC012085.2, FAM83A-AS1, MIR223HG, MIR193BHG, LINC01116) were identified and used to construct a GILncSig model. Mutation burden analysis indicated that the high-risk GI group had much higher somatic mutation count and the risk score constructed by the 5 GI-associated lncRNAs was an independent predictor for overall survival (OS) (P < 0.05). Overall, our study provides valuable insights into the involvement of GI-associated lncRNAs in LUAD and highlights their potential as therapeutic targets.

Single-cell RNA sequencing reveals the gene expression profile and cellular communication in human fetal heart development.

The heart is the central organ of the circulatory system, and its proper development is vital to maintain human life. As fetal heart development is complex and poorly understood, we use single-cell RNA sequencing to profile the gene expression landscapes of human fetal hearts from the four-time points: 8, 10, 11, 17 gestational weeks (GW8, GW10, GW11, GW17), and identified 11 major types of cells: erythroid cells, fibroblasts, heart endothelial cells, ventricular cardiomyocytes, atrial cardiomyocytes, macrophage, DCs, smooth muscle, pericytes, neural cells, schwann cells. In addition, we identified a series of differentially expressed genes and signaling pathways in each cell type between different gestational weeks. Notably, we found that ANNEXIN, MIF, PTN, GRN signalling pathways were simple and fewer intercellular connections in GW8, however, they were significantly more complex and had more intercellular communication in GW10, GW11, and GW17. Notably, the interaction strength of OSM signalling pathways was gradually decreased during this period of time (from GW8 to GW17). Together, in this study, we presented a comprehensive and clear description of the differentiation processes of all the main cell types in the human fetal hearts, which may provide information and reference data for heart regeneration and heart disease treatment.

A Reference Profile of N-Glycosylation for Human Kidney and the Identification of Cell-Cell Interactions between Parietal Epithelial Cells and Capillary Endothelial Cells by Single-Cell Glycosylation-Sequencing.

BACKGROUND: N-glycosylation is one of the most common posttranslational modifications in humans, and these alterations are associated with kidney diseases. METHODS: A novel technological approach, single-cell N-acetyllactosamine sequencing (scLacNAc-seq), was applied to simultaneously detect N-glycosylation expression and the transcriptome at single-cell resolution in three human kidney tissues from zero-time biopsy. Cell clusters, glycation abundance in each cell cluster, functional enrichment analysis, cell-cell crosstalk, and pseudotime analysis were applied. RESULTS: Using scLacNAc-seq, 24,247 cells and 22 cell clusters were identified, and N-glycan abundance in each cell was obtained. Transcriptome analysis revealed a close connection between capillary endothelial cells (CapECs) and parietal epithelial cells (PECs). PECs and CapECs communicate with each other through several pairs of ligand receptors (e.g., TGFB1-EGFR, GRN-EGFR, TIMP1-FGFR2, VEGFB-FLT1, ANGPT2-TEK, and GRN-TNFRSF1A). Finally, a regulatory network of cell-cell crosstalk between PECs and CapECs was constructed, which is involved in cell development. CONCLUSIONS: We here, for the first time, constructed the glycosylation profile of 22 cell clusters in the human kidney from zero-time biopsy. Moreover, cell-cell communication between PECs and CapECs through the ligand-receptor system may play a crucial regulatory role in cell proliferation.

Integrating analysis of mRNA expression profiles indicates Sgk1 as a key mediator in muscle-brain crosstalk during resistance exercise.

Abundant evidence has shown the protective effect of aerobic exercise on central neuronal system, however, research about resistance exercise remains limited. To evaluate the effect and potential molecular mechanisms of resistance exercise in improving cognition and mental health, three-month-old male C57BL/6J mice underwent resistance training for five weeks. Body parameters, cognitive performance and synaptic plasticity were then assessed. In both groups, total RNA from the frontal cortex, hippocampus and gastrocnemius was isolated and sequenced, GO term and KEGG analysis were performed to identify molecular mechanisms. The results from RNA sequencing were then verified by RT-PCR. Our data found that mice in training group showed reduced anxiety-like behavior and better spatial memory. Accordingly, resistance exercise specifically increased the number of thin spines without affecting the number of other kind of spines. mRNA sequence analysis showed that resistance exercise induced differential expression of hundreds of genes in the above three tissues. KEGG analysis indicated the FoxO signaling pathway the most significant changed pathway throughout the brain and muscle. GO terms analysis showed that Sgk1 was enriched in the three key cognition related BP, including long-term memory, learning or memory and memory, and the expression level of Sgk1 was positive related with cognitive performance in the water maze. In conclusion, resistance exercise improved the mental health, cognition and synaptic plasticity of mice. Integrating analysis of mRNA expression profiles in frontal cortex, hippocampus and muscle reveals Sgk1 as the key mediator in brain-muscle crosstalk.

NAC1 transcriptional activation of LDHA induces hepatitis B virus immune evasion leading to cirrhosis and hepatocellular carcinoma development.

Our study aimed to elucidate the molecular mechanisms underlying NAC1 (nucleus accumbens associated 1) transcriptional regulation of LDHA and its role in HBV immune evasion, thus contributing to the development of cirrhosis and hepatocellular carcinoma (HCC). Utilizing public datasets, we performed differential gene expression and weighted gene co-expression network analysis (WGCNA) on HBV-induced cirrhosis/HCC data. We identified candidate genes by intersecting differentially expressed genes with co-expression modules. We validated these genes using the TCGA database, conducting survival analysis to pinpoint key genes affecting HBV-HCC prognosis. We also employed the TIMER database for immune cell infiltration data and analyzed correlations with identified key genes to uncover potential immune escape pathways. In vitro, we investigated the impact of NAC1 and LDHA on immune cell apoptosis and HBV immune evasion. In vivo, we confirmed these findings using an HBV-induced cirrhosis model. Bioinformatics analysis revealed 676 genes influenced by HBV infection, with 475 genes showing differential expression in HBV-HCC. NAC1 emerged as a key gene, potentially mediating HBV immune escape through LDHA transcriptional regulation. Experimental data demonstrated that NAC1 transcriptionally activates LDHA, promoting immune cell apoptosis and HBV immune evasion. Animal studies confirmed these findings, linking NAC1-mediated LDHA activation to cirrhosis and HCC development. NAC1, highly expressed in HBV-infected liver cells, likely drives HBV immune escape by activating LDHA expression, inhibiting CD8 + T cells, and promoting cirrhosis and HCC development.

Multi-omics data-based analysis characterizes molecular alterations of the vesicle genes in human colorectal cancer.

The role of vesicular genes in the development of colorectal cancer (CRC) is crucial. Analyzing alterations in these genes at multi-omics can aid in understanding the molecular pathways behind colorectal carcinogenesis and identifying potential treatment targets. However, studies on the overall alteration of vesicular genes in CRC are still lacking. In this study, we aimed to investigate the relationship between vesicle genetic alterations and CRC progression. To achieve this, we analyzed molecular alterations in CRC vesicle genes at eight levels, including mRNA, protein, and epigenetic levels. Additionally, we examined CRC overall survival-related genes that were obtained from a public database. Our analysis of chromatin structural variants, DNA methylation, chromatin accessibility, and proteins (including phosphorylation, ubiquitination, and malonylation), along with RNA-seq data from the TCGA database, revealed multiple levels of alterations in CRC vesicle genes in the collected tissue samples. We progressively examined the alterations of vesicle genes in mRNA and protein levels in CRC and discovered the hub genes. Further investigation identified the probable essential transcription factors. This study contributes to a thorough knowledge of the connection between vesicle gene alterations at multiple levels and the development of CRC and offers a theoretical framework for the identification of novel treatment targets.

Photochemical evolution of the molecular composition of dissolved organic carbon and dissolved brown carbon from wood smoldering.

Recently, extreme wildfires occur frequently around the world and emit substantial brown carbon (BrC) into the atmosphere, whereas the molecular compositions and photochemical evolution of BrC remain poorly understood. In this work, primary smoke aerosols were generated from wood smoldering, and secondary smoke aerosols were formed by the OH radical photooxidation in an oxidation flow reactor, where both primary and secondary smoke samples were collected on filters. After solvent extraction of filter samples, the molecular composition of dissolved organic carbon (DOC) was determined by Fourier transform ion cyclotron resonance mass spectrometry (FTICR MS). The molecular composition of dissolved BrC was obtained based on the constraints of DOC formulae. The proportion of dissolved BrC fractions accounted for approximately 1/3-1/2 molecular formulae of DOC. The molecular characteristics of dissolved BrC showed higher levels of carbon oxidation state, double bond equivalents, and modified aromaticity index than those of DOC, indicating that dissolved BrC fractions were a class of organic structures with relatively higher oxidation state, unsaturated and aromatic degree in DOC fractions. The comparative analysis suggested that aliphatic and olefinic structures dominated DOC fractions (contributing to 70.1%-76.9%), while olefinic, aromatic, and condensed aromatic structures dominated dissolved BrC fractions (contributing to 97.5%-99.9%). It is worth noting that dissolved BrC fractions only contained carboxylic-rich alicyclic molecules (CRAMs)-like structures, unsaturated hydrocarbons, aromatic structures, and highly oxygenated compounds. CRAMs-like structures were the most abundant species in both DOC and dissolved BrC fractions. Nevertheless, the specific molecular characteristics for DOC and dissolved BrC fractions varied with subgroups after aging. The results highlight the similarities and differences in the molecular compositions and characteristics of DOC and dissolved BrC fractions with aging. This work will provide insights into understanding the molecular composition of DOC and dissolved BrC in smoke.

Comprehensive assessment of HF-rTMS treatment mechanism for post-stroke dysphagia in rats by integration of fecal metabolomics and 16S rRNA sequencing.

Background: The mechanism by which high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) improves swallowing function by regulating intestinal flora remains unexplored. We aimed to evaluate this using fecal metabolomics and 16S rRNA sequencing. Methods: A Post-stroke dysphagia (PSD) rat model was established by middle cerebral artery occlusion. The magnetic stimulation group received HF-rTMS from the 7th day post-operation up to 14th day post-surgery. Swallowing function was assessed using a videofluoroscopic swallowing study (VFSS). Hematoxylin-eosin (H&E) staining was used to assess histopathological changes in the intestinal tissue. Intestinal flora levels were evaluated by sequencing the 16S rRNA V3-V4 region. Metabolite changes within the intestinal flora were evaluated by fecal metabolomics using liquid chromatography-tandem mass spectrometry. Results: VFSS showed that the bolus area and pharyngeal bolus speed were significantly decreased in PSD rats, while the bolus area increased and pharyngeal transit time decreased after HF-rTMS administration (p < 0.05). In the PSD groups, H&E staining revealed damaged surface epithelial cells and disrupted cryptal glands, whereas HF-rTMS reinforced the integrity of the intestinal epithelial cells. 16S rRNA sequencing indicated that PSD can disturb the intestinal flora and its associated metabolites, whereas HF-rTMS can significantly regulate the composition of the intestinal microflora. Firmicutes and Lactobacillus abundances were lower in the PSD group than in the baseline group at the phylum and genus levels, respectively; however, both increased after HF-rTMS administration. Levels of ceramides (Cer), free fatty acids (FA), phosphatidylethanolamine (PE), triacylglycerol (TAG), and sulfoquinovosyl diacylglycerol were increased in the PSD group. The Cer, FA, and DG levels decreased after HF-rTMS treatment, whereas the TAG levels increased. Peptococcaceae was negatively correlated with Cer, Streptococcus was negatively correlated with DG, and Acutalibacter was positively correlated with FA and Cer. However, these changes were effectively restored by HF-rTMS, resulting in recovery from dysphagia. Conclusion: These findings suggest a synergistic role for the gut microbiota and fecal metabolites in the development of PSD and the therapeutic mechanisms underlying HF-rTMS.

A causal relationship between panic disorder and risk of alzheimer disease: a two-sample mendelian randomization analysis.

BACKGROUND: Observational studies have suggested a link between panic disorder (PD) and Alzheimer disease (AD). This study aimed to identify the underlying association of PD with the risk of AD using Mendelian randomization. METHODS: Genetic instrumental variables (IVs) were retrieved in the genome-wide association study between PD and AD. Then, five different models, namely inverse variance weighting (IVW), weighted median, weighted mode, MR-Egger and MR-robust adjusted profile scores (MR-RAPS), were used for MR Analysis. Finally, the heterogeneity and pleiotropy of identified IVs were verified by multiple sensitivity tests. RESULTS: The Cochran's Q test based on MR Egger and IVW showed that no evidence of heterogeneity was found in the effects of instrumental variables, so a fixed-effect model was used. IVW analysis (OR 1.000479, 95% CI [1.000147056, 1.000811539], p = 0.005) indicated that PD was associated with an increased risk of AD, and a causal association existed between them. Meanwhile, weighted median (OR 1.000513373, 95% CI [1.000052145, 1.000974814], p = 0.029) and MR-RAPS (OR 1.000510118, 95% CI [1.000148046, 1.00087232], p = 0.006) also showed the similar findings. In addition, extensive sensitivity analyses confirmed the robustness and accuracy of these results. CONCLUSION: This investigation provides evidence of a potential causal relationship between PD and the increased risk of AD. Based on our MR results, when diagnosing and treating patients with PD, clinicians should pay more attention to their AD-related symptoms to choose therapeutic measures or minimize comorbidities. Furthermore, the development of drugs that improve both PD and AD may better treat patients with these comorbidities.

Investigating the causal associations between five anthropometric indicators and nonalcoholic fatty liver disease: Mendelian randomization study.

BACKGROUND: Although the etiology of nonalcoholic fatty liver disease (NAFLD) has not been thoroughly understood, the emerging roles of anthropometric indicators in assessing and predicting the risk of NAFLD have been highlighted by accumulating evidence. AIM: To evaluate the causal relationships between five anthropometric indicators and NAFLD employing Mendelian randomization (MR) design. METHODS: The Anthropometric Consortium provided genetic exposure data for five anthropometric indicators, including hip circumference (HC), waist circumference (WC), waist-to-hip ratio (WHR), body mass index (BMI), and body fat percentage (BF). Genetic outcome data for NAFLD were obtained from the United Kingdom Biobank and FinnGen Consortium. Genome-wide significant single nucleotide polymorphisms were chosen as instrumental variables. Univariable MR (UVMR) and multivariable MR (MVMR) designs with analytical approaches, including inverse variance weighted (IVW), MR-Egger, weighted median (WM), and weighted mode methods, were used to assess the causal relationships between anthropometric indicators and NAFLD. RESULTS: Causal relationships were revealed by UVMR, indicating that a higher risk of NAFLD was associated with a per-unit increase in WC [IVW: odds ratio (OR) = 2.67, 95%CI: 1.42-5.02, P = 2.25 × 10-3], and BF was causally associated with an increased risk of NAFLD (WM: OR = 2.23, 95%CI: 1.07-4.66, P = 0.033). The presence of causal effects of WC on the decreased risk of NAFLD was supported by MVMR after adjusting for BMI and smoking. However, no causal association between BF and NAFLD was observed. In addition, other causal relationships of HC, WHR (BMI adjusted), and BMI with the risk of NAFLD were not retained after FDR correction. CONCLUSION: This study establishes a causal relationship, indicating that an increase in WC is associated with a higher risk of NAFLD. This demonstrates that a suitable decrease in WC is advantageous for preventing NAFLD.

SMG9 is a novel prognostic-related biomarker in glioma correlating with ferroptosis and immune infiltrates.

Background: Glioma is the most frequent type of malignancy that may damage the brain with high morbidity and mortality rates and patients' prognoses are still dismal. Ferroptosis, a newly uncovered mode of programmed cell death, may be triggered to destroy glioma cells. Nevertheless, the significance of ferroptosis-related genes (FRGs) in predicting prognosis in glioma individuals is still a mystery. Methods: The CGGA (The Chinese Glioma Atlas), GEO (Gene Expression Omnibus), and TCGA (The Cancer Genome Atlas) databases were all searched to obtain the glioma expression dataset. First, TCGA was searched to identify differentially expressed genes (DEGs). This was followed by a machine learning algorithm-based screening of the glioma's most relevant genes. Additionally, these genes were subjected to Gene Ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) functional enrichment analyses. The chosen biological markers were then submitted to single-cell, immune function, and gene set enrichment analysis (GSEA). In addition, we performed functional enrichment and Mfuzz expression profile clustering on the most promising biological markers to delve deeper into their regulatory mechanisms and assess their clinical diagnostic capacities. Results: We identified 4444 DEGs via differential analysis and 564 FRGs from the FerrDb database. The two were subjected to intersection analysis, which led to the discovery of 143 overlapping genes. After that, glioma biological markers were identified in fourteen genes by the use of machine learning methods. In terms of its use for clinical diagnosis, SMG9 stands out as the most significant among these biomarkers. Conclusion: In light of these findings, the identification of SMG9 as a new biological marker has the potential to provide information on the mechanism of action and the effect of the immune milieu in glioma. The promise of SMG9 in glioma prognosis prediction warrants more study.

Modified Approach for Extraperitoneal Colostomy Creation in Laparoscopic Abdominoperineal Resection.

BACKGROUND: Parastomal hernia is a major long-term complication after abdominoperineal resection. Extraperitoneal colostomy has been proposed as an effective step for parastomal hernia prevention, but it has not been widely used as it is technically demanding and time-consuming. We proposed a modified approach for extraperitoneal colostomy creation by entering the extraperitoneal space through the arcuate line of the posterior rectus sheath. OBJECTIVE: To evaluate the safety, difficulty, and efficacy of long-term parastomal hernia prevention of the modified approach for extraperitoneal colostomy creation compared with the conventional transperitoneal colostomy approach. DESIGN: This was a retrospective evaluation of a surgical and video database. SETTINGS: This was a single-institution retrospective study. PATIENTS: Clinical data of 74 patients who underwent laparoscopic abdominoperineal resection surgery from January 2019 to January 2020 in the Department of General Surgery, Qilu Hospital of Shandong University, were retrospectively reviewed. MAIN OUTCOME MEASURES: Baseline characteristics, time required for colostomy creation (from skin incision to colostomy maturation), perioperative complications, and long-term colostomy-related complications were compared. RESULTS: Baseline characteristics did not differ between the 2 approaches. The BMI level ranged from 19.5 to 29.4 for patients undergoing extraperitoneal approach. Time required for colostomy creation median [interquartile range], (22 [21-25] minutes for extraperitoneal vs 23 [21-25] minutes for transperitoneal, p = 0.861) were comparable between the 2 approaches. The cumulative incidence of parastomal hernia was significantly greater with transperitoneal colostomy than extraperitoneal colostomy at 2 and 3 years postoperatively (16.2% vs 0%, p = 0.025, and 21.6% vs 0%, p = 0.005). The remaining perioperative complications and long-term colostomy-related complications did not differ between the 2 approaches. LIMITATIONS: This study is limited by its retrospective design and small sample size. CONCLUSIONS: The modified approach for extraperitoneal colostomy creation is safe, technically simple, and effective for long-term parastomal hernia prevention in patients with a BMI of 19.5 to 29.4.

Risk factors for anastomotic leak and postoperative morbidity after right hemicolectomy for colon cancer: results from a prospective, multi-centre, snapshot study in China.

BACKGROUND: Right hemicolectomy is the standard treatment for right-sided colon cancer. There is variation in the technical aspects of performing right hemicolectomy as well as in short-term outcomes. It is therefore necessary to explore best clinical practice following right hemicolectomy in expert centres. METHODS: This snapshot study of right hemicolectomy for colon cancer in China was a prospective, multicentre cohort study in which 52 tertiary hospitals participated. Eligible patients with stage I-III right-sided colon cancer who underwent elective right hemicolectomy were consecutively enrolled in all centres over 10 months. The primary endpoint was the incidence of postoperative 30-day anastomotic leak. RESULTS: Of the 1854 patients, 89.9 per cent underwent laparoscopic surgery and 52.3 per cent underwent D3 lymph node dissection. The overall 30-day morbidity and mortality were 11.7 and 0.2 per cent, respectively. The 30-day anastomotic leak rate was 1.4 per cent. In multivariate analysis, ASA grade > II (P < 0.001), intraoperative blood loss > 50 ml (P = 0.044) and D3 lymph node dissection (P = 0.008) were identified as independent risk factors for postoperative morbidity. Extracorporeal side-to-side anastomosis (P = 0.031), intraoperative blood loss > 50 ml (P = 0.004) and neoadjuvant chemotherapy (P = 0.004) were identified as independent risk factors for anastomotic leak. CONCLUSION: In high-volume expert centres in China, laparoscopic resection with D3 lymph node dissection was performed in most patients with right-sided colon cancer, and overall postoperative morbidity and mortality was low. Further studies are needed to explore the optimal technique for right hemicolectomy in order to improve outcomes further.

Participation of the nucleus tractus solitarius in the therapeutic effect of electroacupuncture on post-stroke dysphagia through the primary motor cortex.

BACKGROUND: Post-stroke dysphagia (PSD), a common and serious disease, affects the quality of life of many patients and their families. Electroacupuncture (EA) has been commonly used effectively in the treatment of PSD, but the therapeutic mechanism is still under exploration at present. We aim to investigate the effect of the nucleus tractus solitarus (NTS) on the treatment of PSD by EA at Lianquan (CV23) through the primary motor cortex (M1). METHODS: C57 male mice were used to construct a PSD mouse model using photothrombotic technique, and the swallowing function was evaluated by electromyography (EMG) recording. C-Fos-positive neurons and types of neurons in the NTS were detected by immunofluorescence. Optogenetics and chemical genetics were used to regulate the NTS, and the firing rate of neurons was recorded via multichannel recording. RESULTS: The results showed that most of the activated neurons in the NTS were excitatory neurons, and multichannel recording indicated that the activity levels of both pyramidal neurons and interneurons in the NTS were regulated by M1. This process was involved in the EA treatment. Furthermore, while chemogenetic inhibition of the NTS reduced the EMG signal associated with the swallowing response induced by activation of M1 in PSD mice, EA rescued this signal. CONCLUSION: Overall, the NTS was shown to participate in the regulation of PSD by EA at CV23 through M1.

Molecular dynamics simulation of the interaction between monofluoronitrobenzene and Ti electrode.

In the process of degradation of aqueous fluoro-nitrobenzene (FNB) solution by titanium (Ti) electrode, the interaction between aqueous FNB solution and Ti electrode has an important impact on the performance and catalytic performance of electrode materials. The interaction involves complex physical, chemical and physical chemical processes, however, the mechanism of action is still unclear. In this study, Materials Studio software was used to design and construct molecular models of the interactions between aqueous FNB (p-, m-, o-FNB) solutions and Ti electrode, and molecular dynamics (MD) simulation was carried out in the absence of applied electric field and external electric field of 0.02 V/Å, respectively. Density functional theory (DFT) method was used to calculate the frontier molecular orbitals of three FNB molecules. Based on the calculation and analysis of the interaction energy (ΔE), diffusion coefficient (D) and radial distribution function (RDF), the interaction mechanism was discussed. It provides a theoretical basis for further research and development of Ti electrode degradation of fluorine compounds. The results showed that the order of ΔE between the three different aqueous FNB solutions and Ti surface is m-FNB > p-FNB > o-FNB when there is no external electric field. Under electric field of 0.02 V/Å, the order is p-FNB > m-FNB > o-FNB. The substitution position of F has an important effect on the HOMO of the nitro group and the LUMO of C-H in the three FNB molecules, and also affects the chemical reaction activity. In the model system, the diffusivity of different FNB solutions with electric field is less than that without electric field. The presence of an external electric field makes the diffusion of water and FNB molecules more orderly. The analysis results of RDF show that the bonding interactions between different FNB molecules and Ti surface is not much different before 3.5 Å, and all of them are weak. At about 8 Å, FNB molecule forms a non-bond with Ti electrode. ΔE, D and RDF of the model system can be changed by applying a certain external electric field, and the results are in better agreement with the experimental results.

Qualitative Proteome-wide Lysine Crotonylation Profiling Reveals Protein Modification Alteration in the Leukocyte Extravasation Pathway in Systemic Lupus Erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is a severe systemic autoimmune disease with multiple manifestations. Lysine crotonylation (Kcr) is a newly discovered posttranslational modification epigenetic pattern that may affect gene expression and is linked to diseases causally. METHODS: We collected blood samples from 11 SLE individuals and 36 healthy subjects. Then, we used highly sensitive liquid chromatography-mass spectrometry technology to carry out proteomics and quantitative crotonylome analysis of SLE peripheral blood mononuclear cells in this investigation, which indicated the unique etiology of SLE. Finally, we verified the expression of critical protein in the leukocyte extravasation pathway by online database analysis and Western blot. RESULTS: There were 618 differentially expressed proteins (DEPs), and 612 crotonylated lysine sites for 272 differentially modified proteins (DMPs) found. These DEPs and DMPs are primarily enriched in the leukocyte extravasation signaling pathway, such as MMP8, MMP9, and ITGAM. CONCLUSIONS: This is the first study of crotonylated modification proteomics in SLE. The leukocyte extravasation signaling pathway had a considerable concentration of DEPs and DMPs, indicating that this pathway may be involved in the pathogenic development of SLE.

Systematic proteomics profiling of lysine crotonylation of the lung at Pseudoglandular and Canalicular phases in human fetus.

Lung tissue is an important organ of the fetus, and genomic research on its development has improved our understanding of the biology of this tissue. However, the proteomic research of developing fetal lung tissue is still very scarce. We conducted comprehensive analysis of two developmental stages of fetal lung tissue of proteomics. It showed the developmental characteristics of lung tissue, such as the down-regulation of metabolism-related protein expression, the up-regulation of cell cycle-related proteins, and the regulation in proteins and pathways related to lung development. In addition, we also discovered some key core proteins related to lung development, and provided some key crotonylation modification sites that regulation during lung tissue development. Our comprehensive analysis of lung proteomics can provide a more comprehensive understanding of the developmental status of lung tissue, and provide a certain reference for future research and epigenetics of lung tissue.