Background: A simple superoposterior approach to thoracic transforaminal epidural injections (TFEIs) under ultrasonographic guidance was proposed to reduce zoster-associated pain (ZAP) involving multiple thoracic nerves and the likelihood of transitioning to postherpetic neuralgia (PHN). Methods: Patients were prospectively enrolled. Primary endpoints were the burden of illness (BOI) scores and epidural contrast spread. Secondary endpoints included number of needle insertion attempts, sensory blockade, hemodynamic changes, procedure time, radiation dose, adverse events, rescue analgesics, PHN incidence and EuroQoL 5-Dimension scores. Results: Thirty-five injections were performed in 27 patients. Median levels of cephalad-caudad epidural contrast spread were 3, 4, and 5 ml following injections of 2, 3, and 4 ml. Dorsal epidural spread was observed at levels 3, 4, and 5, whereas concurrent ventral spread was observed at levels 2, 3, and 4. BOI scores at 30–180 days significantly decreased (mean difference: −25.3, 95% CI [−57.4 to 6.6], P = 0.005), accounting for reduced rescue analgesic requirements and PHN occurrence and improved EuroQoL 5-Dimension scores. Median sensory blockade at 5 min post-procedure was at level 2, 3, and 4 after 2, 3, and 4 ml of therapeutic injectate. No significant hemodynamic changes were noted at 15 min post-injection. No serious adverse events were observed. Conclusions Spread of thoracic epidural contrast to all involved nerves was confirmed using this novel technique. Simplified needle placement reduced the technical difficulty and risk of complications. It might be a promising alternative approach for ZAP.

Sj?gren's syndrome(SS)is one of the common rheumatic diseases in clinical practice.Modern medicine commonly uses drugs such as artificial tears,saliva,glucocorticoids,immunosuppressants,and biologics to control the condition.Clinical practice has shown that in addition to modern medical basic treatment,the use of traditional Chinese medicine(TCM)can help improve the clinical efficacy of SS.According to the symptoms and signs of Sj?gren's syndrome in TCM,it is classified as"dryness and obstruction",and the core pathogenesis of the disease is spleen deficiency and deficiency of body fluids.Subsequently,toxic and pathogenic factors gather,leading to the decline of internal organs.The initial causes are spleen damage,unstable barrier,and invasion of pathogenic factors.The core link is spleen dysfunction,insufficient body fluid,and dryness arising from it.Spleen deficiency generates evil,obstruction of qi,and lack of body fluids are the root causes of illness.The main treatment method is the"spleen strengthening method",which treats spleen deficiency,dampness and stagnation,and the body fluid is not distributed.The treatment focuses on strengthening the spleen and qi,supplementing the lungs and generating fluids.Spleen deficiency leads to loss of vitality,blood stasis obstructs blood vessels,and the treatment is to strengthen the spleen,soothe the liver,remove blood stasis,and unblock the orifices.The spleen yang is not vigorous,and qi transformation is impaired.The treatment is to invigorate the spleen and warm the stomach,promote yang circulation,and promote diuresis.

Objective To investigate the risk factor for adverse events(AEs)after non-sedated esophagogastroduodenoscopy(EGD).Methods The data on clinical manifestations,adverse events after non-sedated EGD and common risk factors were collected and retrospectively analyzed with statistical methods in patients who underwent non-sedated EGD from May 2018 to June 2019.These patients were divided into AEs group and non-AEs group.Results Of 2 384 patients,57.67%(1 375/2 384)presented with nausea,12.79%(305/2 384)vomiting,and 5.79%(138/2 384)presented with pharyngalgia.Multivariate Logistic regression analysis was performed.Advanced age(≥65 years old)(OR=0.683,95%CI:0.506-0.921)was protective factors for nausea after non-sedated EGD.Hypertension(OR=1.361,95%CI:1.026-1.806),overweight(OR=1.399,95%CI:1.154-1.695),obesity(OR=2.594,95%CI:1.760-3.823)and inspection duration>15 min(OR=3.107,95%CI:2.296-4.206)were independent risk factors for nausea after non-sedated EGD.Advanced age(OR=0.393,95%CI:0.221-0.699)and imported equipment(OR=0.697,95%CI:0.546-0.890)were protective factors for vomiting after non-sedated EGD.Moreover,inspection duration>15 min(OR=1.641,95%CI:1.008-2.699)was independent risk factors for vomiting after non-sedated EGD.There was no difference in success rate of non-sedated EGD between two groups(P<0.05).Conclusion Hypertension,overweight and obesity were independent risk factors for nausea after non-sedated EGD.The advanced age and imported equipment were protective factors for vomiting after non-sedated EGD.In addition,inspection duration over 15 min is a risk factor for AEs such as nausea and vomiting after nonsedative EGD.Whether AEs occurred or not is non-related to success rate of non-sedated EGD.

Gastric cancer is a common clinical tumor,and its incidence and mortality rates rank among the top of malignant tumors.Helicobacter pylori(Hp)is an important carcinogenic factor for gastric cancer.Studies have found that in addition to Hp,other microorganisms in the stomach also play a key role in the progression of gastric cancer.The composition and diversity of the gastric microbiota vary significantly under different gastric disease conditions,which may affect the progression of gastric cancer.Hp can induce gastric epithelial inflammation and oxidative stress through various virulence factors,thereby promoting the occurrence of gastric cancer.Non-Hp microorganisms can be involved in the process of gastric cancer through pathways such as metabolic changes and immune regulation.In recent years,with the development of high-throughput sequencing technology,the complexity of gastric microbiota has gradually been revealed,which provides new insights for the early warning and intervention of gastric cancer.This article comprehensively review the role of gastric microbiota in the progression of gastric cancer.

OBJECTIVE To evaluate the efficacy and safety of letermovir in preventing cytomegalovirus(CMV)infection after allogeneic hematopoietic stem cell transplantation(allo-HSCT).METHODS A retrospective cohort study was conducted,enrolling patients who underwent allo-HSCT at the Department of Hematology,Shanghai General Hospital Affiliated to Shanghai Jiao Tong University School of Medicine,from August 30,2022,to February 21,2024.Patients who initiated letermovir prophylaxis within 28 days post-transplantation were assigned to the experimental group(99 cases),while those who did not initiate letermovir within this period were assigned to the control group(18 cases).The incidence and clinical characteristics of CMV infection(including the number of CMV infection cases,the number of cases progressing to CMV disease,recurrent CMV disease,onset time of CMV infection,and treatment duration),immune function recovery within 120 days post-transplantation,and the occurrence of transplantation-related complications(including CD4+and CD8+T-cell recovery,Epstein-Barr virus infection,acute graft-versus-host disease,human herpesvirus 6 infection,and posttransplant lymphoproliferative disorders)and adverse events were recorded.Univariate and multivariate Cox regression analyses were performed to identify factors influencing CMV infection.RESULTS A total of 117 patients were included,among whom 15 developed CMV infection,5 progressed to CMV disease,and 2 experienced recurrent CMV disease.The CMV infection rate in the experimental group was significantly lower than that in the control group(P＜0.001),and the onset time of CMV infection was significantly delayed(P=0.014).The proportion of patients with CD4+T-cell counts≥200 cells/μL in the experimental group was significantly lower than that in the control group(P=0.022).During the follow-up period,elevated creatinine levels were observed in 1 patient,and nausea and vomiting were observed in 2 patients.Multivariate Cox regression analysis revealed that the use of high-dose corticosteroids was a risk factor for CMV infection(HR=6.230,95%CI of 1.255-30.926,P=0.025),while initiating letermovir within 28 days post-transplantation was a protective factor(HR=0.125,95%CI of 0.045-0.348,P＜0.001).CONCLUSIONS Early initiation of letermovir after allo-HSCT significantly reduces the CMV infection rate and delays the onset of infection,with favorable short-term safety.

Objective:To analyze relevant factors influencing severe acute radiation enteritis (SARE) during total neoadjuvant therapy (TNT) for locally advanced rectal cancer (LARC). To identify specific prediction indicators of the occurrence and progression of radiation enteritis by investigating the effect relationships between radiation enteritis and multidimensional factors.Methods:A total of 92 patients with rectal adenocarcinoma who received total neoadjuvant therapy at the First Affiliated Hospital of Soochow University from January 2020 to September 2023 were enrolled in this study. Their relevant information was collected, encompassing clinical nutritional indicators, dynamic changes in hematological parameters, systemic inflammatory indicators, and the occurrence of adverse reactions. Then, risk factors associated with radiation enteritis were determined using logistic regression analysis. Based on independent risk factors, a nomogram model for risk prediction was constructed.Results:Univariate analysis revealed significant correlations of the SARE occurrence with certain nutritional indicators, local tumor measurement data, and laboratory parameters. Multivariate regression analysis further identified the independent risk factors for SARE occurrence, including albumin reduction >26.5% before vs. after treatment ( OR = 5.010, 95% CI: 1.766-14.154, P = 0.010), rectual tenesmus rating of Grade 1-3 ( OR = 3.639, 95% CI: 1.425-9.300, P = 0.024), and elevated disease activity index (DAI) score ( OR ≈ 7.683 per 1-point increase, 95% CI: 1.105-53.410, P = 0.039). The prediction model constructed based on these factors demonstrated high prediction efficiency (AUC = 0.841; 95% CI: 0.749-0.934). Conclusions:The nomogram model constructed using albumin reduction, rectal tenesmus rating, and DAI score can provide accurate, simple, and low-cost risk prediction of radiation enteritis during TNT for LARC patients. This model facilitates the early clinical identification of high-risk patients, providing a basis for implementing personalized adjustments to radiotherapy regimens and enhancing nutritional interventions.

Sj?gren's syndrome(SS)is one of the common rheumatic diseases in clinical practice.Modern medicine commonly uses drugs such as artificial tears,saliva,glucocorticoids,immunosuppressants,and biologics to control the condition.Clinical practice has shown that in addition to modern medical basic treatment,the use of traditional Chinese medicine(TCM)can help improve the clinical efficacy of SS.According to the symptoms and signs of Sj?gren's syndrome in TCM,it is classified as"dryness and obstruction",and the core pathogenesis of the disease is spleen deficiency and deficiency of body fluids.Subsequently,toxic and pathogenic factors gather,leading to the decline of internal organs.The initial causes are spleen damage,unstable barrier,and invasion of pathogenic factors.The core link is spleen dysfunction,insufficient body fluid,and dryness arising from it.Spleen deficiency generates evil,obstruction of qi,and lack of body fluids are the root causes of illness.The main treatment method is the"spleen strengthening method",which treats spleen deficiency,dampness and stagnation,and the body fluid is not distributed.The treatment focuses on strengthening the spleen and qi,supplementing the lungs and generating fluids.Spleen deficiency leads to loss of vitality,blood stasis obstructs blood vessels,and the treatment is to strengthen the spleen,soothe the liver,remove blood stasis,and unblock the orifices.The spleen yang is not vigorous,and qi transformation is impaired.The treatment is to invigorate the spleen and warm the stomach,promote yang circulation,and promote diuresis.

Background and Aims:Chronic skin ulcers are a significant disease affecting patients'daily lives and psychological well-being.Abnormalities in the cells and extracellular matrix within the tissue may disrupt the balance of the microenvironment,hindering the normal skin repair process and leading to delayed healing of the ulcer.There is currently a lack of research on the mechanisms underlying the development of chronic ulcers and their diagnostic biomarkers.Single-cell sequencing,a newly developed high-throughput sequencing method in recent years,uses gene sequencing at the single-cell resolution to precisely reveal disease mechanisms and has been applied in various diseases.This study used single-cell transcriptome sequencing(scRNA-Seq)to investigate the cellular heterogeneity in chronic skin ulcer tissue to elucidate the potential molecular mechanisms behind delayed healing and provide new insights for clinical treatment.Methods:The scRNA-Seq technology was used to compare the differences in cell subpopulations and gene expression between chronic ulcer tissue and normal skin tissue.Single cells were sorted using a microfluidic platform,and cDNA libraries were constructed for subsequent differential gene analysis and functional enrichment analysis.Results:scRNA-Seq analysis revealed significant immune-metabolic remodeling features in chronic ulcer tissue:the number of B cells,monocytes,and macrophages in ulcer tissue increased by 2.1 to 3.5 times compared to the normal tissue control.This was accompanied by widespread activation of collagen synthesis genes(COL1A1/COL3A1)and synergistic suppression of immune regulators(e.g.,granzyme family GZMA/GZMB/H).Cross-cell subpopulation functional network analysis showed that hypoxia response mediated by the HIF-1 signaling pathway and PI3K/Akt pathway abnormalities formed a positive feedback loop,exacerbating the imbalance in the secretion of inflammatory factors(CXCL3/8,TGFBI)and compensatory upregulation of mitochondrial oxidative phosphorylation.Conclusion:Chronic skin ulcers exhibit significant differences in cellular heterogeneity and gene expression,suggesting that chronic ulcers are not simply tissue defects but a complex pathological process dominated by chronic inflammation and immune dysregulation.The coordinated dysregulation of multiple cell subpopulations in the ulcer microenvironment,along with persistent inflammatory responses and metabolic abnormalities,is interconnected through the HIF-1/TNF/MAPK pathway network.Downregulation of granzyme gene family members and abnormal histone modifications may contribute to immune clearance defects,providing a theoretical basis for developing novel therapies targeting epigenetic regulation or mitochondrial function.

Background and Aims:Chronic skin ulcers are a significant disease affecting patients'daily lives and psychological well-being.Abnormalities in the cells and extracellular matrix within the tissue may disrupt the balance of the microenvironment,hindering the normal skin repair process and leading to delayed healing of the ulcer.There is currently a lack of research on the mechanisms underlying the development of chronic ulcers and their diagnostic biomarkers.Single-cell sequencing,a newly developed high-throughput sequencing method in recent years,uses gene sequencing at the single-cell resolution to precisely reveal disease mechanisms and has been applied in various diseases.This study used single-cell transcriptome sequencing(scRNA-Seq)to investigate the cellular heterogeneity in chronic skin ulcer tissue to elucidate the potential molecular mechanisms behind delayed healing and provide new insights for clinical treatment.Methods:The scRNA-Seq technology was used to compare the differences in cell subpopulations and gene expression between chronic ulcer tissue and normal skin tissue.Single cells were sorted using a microfluidic platform,and cDNA libraries were constructed for subsequent differential gene analysis and functional enrichment analysis.Results:scRNA-Seq analysis revealed significant immune-metabolic remodeling features in chronic ulcer tissue:the number of B cells,monocytes,and macrophages in ulcer tissue increased by 2.1 to 3.5 times compared to the normal tissue control.This was accompanied by widespread activation of collagen synthesis genes(COL1A1/COL3A1)and synergistic suppression of immune regulators(e.g.,granzyme family GZMA/GZMB/H).Cross-cell subpopulation functional network analysis showed that hypoxia response mediated by the HIF-1 signaling pathway and PI3K/Akt pathway abnormalities formed a positive feedback loop,exacerbating the imbalance in the secretion of inflammatory factors(CXCL3/8,TGFBI)and compensatory upregulation of mitochondrial oxidative phosphorylation.Conclusion:Chronic skin ulcers exhibit significant differences in cellular heterogeneity and gene expression,suggesting that chronic ulcers are not simply tissue defects but a complex pathological process dominated by chronic inflammation and immune dysregulation.The coordinated dysregulation of multiple cell subpopulations in the ulcer microenvironment,along with persistent inflammatory responses and metabolic abnormalities,is interconnected through the HIF-1/TNF/MAPK pathway network.Downregulation of granzyme gene family members and abnormal histone modifications may contribute to immune clearance defects,providing a theoretical basis for developing novel therapies targeting epigenetic regulation or mitochondrial function.

ObjectiveTo explore the effects of different dosage forms of Kaixinsan （KXS） on the morphology and function of mitochondria in rat models of Alzheimer's disease （AD） and potential mechanisms of action. MethodsMale SD rats were randomly assigned to a sham group， model group， treatment groups receiving KXS decoction， powders， and granules （3.08 g·kg^-1）， as well as donepezil group （0.51×10^-3 g·kg^-1）， with 10 rats in each group. AD model was created using intracerebroventricular injection of streptozocin （STZ）. After 30 days of administration， behavioral assessments were conducted， and mitochondrial morphology was observed using transmission electron microscopy. Mitochondrial respiratory chain complex content was measured via enzyme-linked immunosorbent assay （ELISA）. Changes in mitochondrial membrane potential were measured via JC-1 staining， and superoxide dismutase （SOD） activity and reactive oxygen species （ROS） levels were measured via biochemical assays. The mRNA expression of adenosine 5'-monophosphate-activated protein kinase （AMPK）， peroxisome proliferator-activated receptor gamma coactivator-1α （PGC-1α）， and silent information regulator 3 （SIRT3） was detected by real-time fluorescent quantitative polymerase chain reaction （Real-time PCR）， and Western blot was used to examine the protein expression levels of optic atrophy protein1 （OPA1）， mitochondrial fission protein 1 （FIS1）， AMPK， p-AMPK， PGC-1α， and SIRT3. ResultsCompared with the sham group， rats in the model group had significantly lower recognition index， spontaneous alternation rate， escape latency， number of platform crossings， time spent in the target quadrant， and percentage of distance traveled in the target quadrant distance （P<0.05， P<0.01）. Significant mitochondrial damage was observed in the hippocampal tissue， with a marked decrease in mitochondrial respiratory chain complex content （P<0.01） and reduced mitochondrial membrane potential （P<0.05）. Additionally， the SOD activity was reduced， while ROS levels were elevated （P<0.01）. The mRNA expression of PGC-1α and SIRT3 was significantly downregulated （P<0.01）， along with decreased protein expression levels of OPA1， p-AMPK/AMPK， PGC-1α， and SIRT3， whereas FIS1 protein expression was significantly upregulated （P<0.05， P<0.01）. Compared with the model group， rats in KXS-treated groups （various dosage forms） showed significant improvement in behavioral indexes （P<0.05， P<0.01）， reduced hippocampal mitochondrial damage， and more organized mitochondrial cristae. Mitochondrial respiratory chain complex content was significantly increased （P<0.05， P<0.01）， and mitochondrial membrane potentials were elevated （P<0.05）. SOD activity was elevated， and ROS levels were significantly reduced （P<0.05， P<0.01）. Furthermore， the mRNA expression of PGC-1α and SIRT3 was upregulated， with increased protein levels of OPA1， p-AMPK/AMPK， PGC-1α， and SIRT3， while FIS1 protein expression levels were significantly reduced （P<0.05， P<0.01）. Across the KXS-treated groups， the granule group showed a higher spontaneous alternation rate than the decoction and powder groups （P<0.05）. ConclusionKXS decoction， powders， and granules can improve the learning and memory ability of rats， with granules being the most effective. The mechanism of action may involve activation of the AMPK/PGC-1α/SIRT3 signaling pathway， improvement of the mitochondrial function， and subsequent amelioration of the brain energy metabolism disorders.