Research progress on the mechanism of exosome-mediated virus infection.

Exosomes are extracelluar vesicles that facilitate intercellular communication and are pivotal in post-transcriptional regulation within cellular gene regulatory networks, impacting pathogen dynamics. These vesicles serve as crucial regulators of immune responses, mediating cellular interactions and enabling the introduction of viral pathogenic regions into host cells. Exosomes released from virus-infected cells harbor diverse microRNAs (miRNAs), which can be transferred to recipient cells, thereby modulating virus infection. This transfer is a critical element in the molecular interplay mediated by exosomes. Additionally, the endosomal sorting complex required for transport (ESCRT) within exosomes plays a vital role in virus infection, with ESCRT components binding to viral proteins to facilitate virus budding. This review elucidates the roles of exosomes and their constituents in the invasion of host cells by viruses, aiming to shed new light on the regulation of viral transmission via exosomes.

Associations between back pain incidence, and physical activity and sedentary behaviours: A prospective cohort study with data from over 365,000 participants.

OBJECTIVE: To examine the associations between (i) various types of physical activity and the risk of back pain incidence, and (ii) the influence of substituting sedentary behaviours with physical activities on back pain incidence. DESIGN: A prospective cohort study. METHODS: We analyzed UK Biobank data collected from 365,307 participants who were free of back pain at baseline. The exposures were total, light, moderate and vigorous physical activity, and sedentary behaviours. The outcome was back pain incidence. The main statistical models were the Cox proportional hazard model and the isotemporal substitution model. RESULTS: In the follow-up time (median, 12.97 years; inter-quartile range, 12.10-13.71), 25,189 individuals developed back pain. The associations between all types of physical activity and incident back pain were significantly non-linear (p < 0.001) among the general population and other subgroups. High physical activity was associated with a decreased risk of back pain compared with no physical activity. The lowest risk occurred in the 1801-2400 MET-min/week subgroup of total physical activity (HR 0.64, 95% CI 0.59-0.69), approximately consisting of 1200, 600, and 600 MET-min/week of light, moderate and vigorous physical activity, respectively. Extremely high vigorous physical activity was related to high risk, specifically in males (HR 1.13, 95% CI 1.02-1.25). Replacing 1 hour/day of sedentary behaviours with an equal time of physical activity reduced the risk of incident back pain by 2%-8% (p < 0.05). CONCLUSION: Physical activity was related to a reduced risk of back pain incidence (except over-high vigorous physical activity). Substituting sedentary behaviours with physical activities reduced the risk of future back pain.

Efficacy and safety of antibiotics for treatment of leptospirosis: a systematic review and network meta-analysis.

BACKGROUND: Leptospirosis, an important zoonotic bacterial disease, commonly affects resource-poor populations and results in significant morbidity and mortality worldwide. The value of antibiotics in leptospirosis remains unclear, as evidenced by the conflicting opinions published. METHODS: We conducted a search in the PubMed, Web of Science, and Cochrane Library databases for studies. These studies included clinical trials and retrospective studies that evaluated the efficacy or safety of antibiotics for leptospirosis treatment. The primary outcomes assessed were defervescence time, mortality rate, and hospital stays. Subgroup analyses were performed based on whether there were cases involving children and whether there were cases of severe jaundice. Safety was defined as the prevalence of adverse events associated with the use of antibiotics. p scores were utilized to rank the efficacy of the antibiotics. RESULTS: There are included 9 randomized controlled trials (RCTs), 1 control trial (CT), and 3 retrospective studies (RS) involving 920 patients and 8 antibiotics. Six antibiotics resulted in significantly shorter defervescence times compared to the control, namely cefotaxime (MD, - 1.88; 95% CI = - 2.60 to - 1.15), azithromycin (MD, - 1.74; 95% CI = - 2.52 to - 0.95), doxycycline (MD, - 1.53; 95% CI = - 2.05 to - 1.00), ceftriaxone (MD, - 1.22; 95% CI = - 1.89 to - 0.55), penicillin (MD, - 1.22; 95% CI = - 1.80 to - 0.64), and penicillin or ampicillin (MD, - 0.08; 95% CI = - 1.01 to - 0.59). The antibiotics were not effective in reducing the mortality and hospital stays. Common adverse reactions to antibiotics included Jarisch-Herxheimer reaction, rash, headache, and digestive reactions (nausea, vomiting, diarrhea, abdominal pain, and others). CONCLUSIONS: Findings recommend that leptospirosis patients be treated with antibiotics, which significantly reduced the leptospirosis defervescence time. Cephalosporins, doxycycline, and penicillin are suggested, and azithromycin may be a suitable alternative for drug-resistant cases. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42022354938.

Fenofibrate alleviates NAFLD by enhancing the PPARα/PGC-1α signaling pathway coupling mitochondrial function.

BACKGROUND: To comprehend the influences of fenofibrate on hepatic lipid accumulation and mitochondrial function-related signaling pathways in mice with non-alcoholic fatty liver disease (NAFLD) secondary to high-fat diets together with free fatty acids-influenced HepG2 cells model. MATERIALS AND METHODS: A random allocation of male 6-week C57BL/6J mice into three groups was done, including controls, model (14 weeks of a high-fat diet), and fenofibrate [similar to the model one with administered 0.04 g/(kg.d) fenofibrate by gavage at 11 weeks for 4 weeks] groups, which contained 10 mice each. This study verified NAFLD pathogenesis via mitochondrial functions in hepatic pathological abnormalities, liver index and weight, body weight, serum biochemical indexes, oxidative stress indicators, mitochondrial function indexes, and related signaling pathways. The effect of fenofibrate intervention was investigated in NAFLD model mice. In vitro, four groups based on HepG2 cells were generated, including controls, the FFA model (1.5 mmol/L FFA incubation for 24 h), LV-PGC-1α intervention (similar to the FFA model one after PPARGC1A lentivirus transfection), and LV control intervention (similar to the FFA model one after negative control lentivirus transfection) groups. The study investigated the mechanism of PGC-1α related to lipid decomposition and mitochondrial biosynthesis by Oil red O staining, colorimetry and western blot. RESULTS: In vivo experiments, a high-fat diet achieved remarkable changes regarding liver weight, liver index, serum biochemical indicators, oxidative stress indicators, liver pathological changes, mitochondrial function indicators, and body weight of the NAFLD model mice while fenofibrate improved the objective indicators. In the HepG2 cells model, the lipid accumulation increased significantly within the FFA model group, together with aggravated hepatocytic damage and boosted oxidative stress levels. Moreover, FFA induced excessive mitosis into fragmented in mitochondrial morphology, ATP content in cells decreased, mtDNA replication fold decreased, the expression of lipid decomposition protein PPARα reduced, mitochondrial biosynthesis related protein PGC-1α, NRF-1 and TFAM decreased. PGC-1α overexpression inhibited lipid deposition by improving mitochondrial biosynthesis and lipid decomposition. CONCLUSION: Fenofibrate up-regulated PPARα/PGC-1α signaling pathway, promoted mitochondrial ß-oxidation, reduced oxidative stress damage and lipid accumulation of liver. PGC-1α overexpression enhanced mitochondrial biosynthesis and ATP production, and reduced HepG2 intracellular accumulation of lipids and oxidative stress.

[Effect and mechanism of Zexie Decoction in promoting white adipose tissue browning/brown adipose tissue activation based on GLP-1R/cAMP/PKA/CREB pathway].

This study investigated the mechanism of Zexie Decoction(ZXD) in promoting white adipose tissue browning/brown adipose tissue activation based on the GLP-1R/cAMP/PKA/CREB pathway. A hyperlipidemia model was induced by a western diet(WD) in mice, and the mice were divided into a control group, a model group(WD), and low-, medium-, and high-dose ZXD groups. An adipogenesis model was induced in 3T3-L1 cells in vitro, and with forskolin(FSK) used as a positive control, low-, medium-, and high-dose ZXD groups were set up. Immunohistochemistry and immunofluorescence results showed that compared with the WD group, ZXD promoted the expression of UCP1 in white and brown adipose tissues, and also upregulated UCP1, CPT1ß, PPARα, and other genes in the cells. Western blot analysis showed a dose-dependent increase in the protein expression of PGC-1α, UCP1, and PPARα with ZXD treatment, indicating that ZXD could promote the white adipose tissue browning/brown adipose tissue activation. Hematoxylin-eosin(HE) staining results showed that after ZXD treatment, white and brown adipocytes were significantly reduced in size, and the mRNA expression of ATGL, HSL, MGL, and PLIN1 was significantly upregulated as compared with the results in the WD group. Oil red O staining and biochemical assays indicated that ZXD improved lipid accumulation and promoted lipolysis. Immunohistochemistry and immunofluorescence staining for p-CREB revealed that ZXD reversed the decreased expression of p-CREB caused by WD. In vitro intervention with ZXD increased the protein expression of CREB, p-CREB, and p-PKA substrate, and increased the mRNA level of CREB. ELISA detected an increase in intracellular cAMP concentration with ZXD treatment. Molecular docking analysis showed that multiple active components in Alismatis Rhizoma and Atractylodis Macrocephalae Rhizoma could form stable hydrogen bond interactions with GLP-1R. In conclusion, ZXD promotes white adipose tissue browning/brown adipose tissue activation both in vivo and in vitro, and its mechanism of action may be related to the GLP-1R/cAMP/PKA/CREB pathway.

Surface Roughness-Induced Changes in Important Physical Features of CoFeSm Thin Films on Glass Substrates during Annealing.

Co60Fe20Sm20 thin films were deposited onto glass substrates in a high vacuum setting. The films varied in thickness from 10 to 50 nm and underwent annealing processes at different temperatures: room temperature (RT), 100, 200, and 300 °C. Our analysis encompassed structural, magnetic, electrical, nanomechanical, adhesive, and optical properties in relation to film thickness and annealing temperature. X-ray diffraction (XRD) analysis did not reveal characteristic peaks in Co60Fe20Sm20 thin films due to insufficient growth-driving forces. Electrical measurements indicated reduced resistivity and sheet resistance with increasing film thickness and higher annealing temperatures, owing to hindered current-carrier transport resulting from the amorphous structure. Atomic force microscope (AFM) analysis showed a decrease in surface roughness with increased thickness and annealing temperature. The low-frequency alternating current magnetic susceptibility (χac) values increased with film thickness and annealing temperature. Nanoindentation analysis demonstrated reduced film hardness and Young's modulus with thicker films. Contact angle measurements suggested a hydrophilic film. Surface energy increased with greater film thickness, particularly in annealed films, indicating a decrease in contact angle contributing to this increase. Transmittance measurements have revealed intensified absorption and reduced transmittance with thicker films. In summary, the surface roughness of CoFeSm films at different annealing temperatures significantly influenced their magnetic, electrical, adhesive, and optical properties. A smoother surface reduced the pinning effect on the domain walls, enhancing the χac value. Additionally, diminished surface roughness led to a lower contact angle and higher surface energy. Additionally, smoother surfaces exhibited higher carrier conductivity, resulting in reduced electrical resistance. The optical transparency decreased due to the smoother surface of Co60Fe20Sm20 films.

Long-term survival and risk analysis of thoracic endovascular aortic repair for type B aortic dissection.

To explore the safety and efficacy of thoracic endovascular aortic repair (TEVAR) in the treatment of patients with type B aortic dissection, and to evaluate the risk factors for long-term mortality. Our study retrospectively evaluated 729 patients with type B aortic dissection, who were divided into the thoracic endovascular aortic repair group and the optimal medical treatment group according to their treatment. In-hospital mortality, death within 30 days, and aortic-related mortality were lower in the thoracic endovascular aortic repair group than in the optimal medical treatment group (p < 0.05). The cumulative overall survival rates for the thoracic endovascular aortic repair group at 1 year, 5 years, and 10 years were 92.5%, 84.1%, and 73.5%, respectively. The Cox analysis found that TEVAR was beneficial in reducing mortality and that a vertical length of the dissection exceeding 150 mm was a risk factor for mortality.

Epigenetic signature discriminates lymphatic metastasis in BRAF wild-type thyroid carcinoma: methylation role of GRIK2.

Aim: Conservative treatment approaches for thyroid carcinoma (TC) patients with wild-type B-type Raf kinase (BRAF) pose risks of long-term recurrence. The association of DNA methylation with TC metastasis is unclear. Patients & methods: Here we analyzed data from 179 BRAF wild-type TC patients in the The Cancer Genome Atlas database, identifying significant metastasis-associated CpGs. A logistic regression model was developed and validated for discriminating lymphatic metastasis in BRAF wild-type TC. Results: The model showed high accuracy (AUC: 0.924 training set; 0.812 and 0.773 external cohorts). TAGLN, MRPL4, CLDN10 and GRIK2 emerged as diagnostic markers. GRIK2, downregulated due to promoter hypermethylation, acted as a TC suppressor. Conclusion: Our 5-CpG epigenetic signature effectively discriminates lymphatic metastasis in BRAF wild-type TC, highlighting GRIK2's tumor-suppressive role influenced by promoter hypermethylation.

Acidosis promotes the metastatic colonization of lung cancer via remodeling of the extracellular matrix and vasculogenic mimicry.

Acidosis is a hallmark of the tumor microenvironment caused by the metabolic switch from glucose oxidative phosphorylation to glycolysis. It has been associated with tumor growth and progression; however, the precise mechanism governing how acidosis promotes metastatic dissemination has yet to be elucidated. In the present study, a long­term acidosis model was established using patient­derived lung cancer cells, to identify critical components of metastatic colonization via transcriptome profiling combined with both in vitro and in vivo functional assays, and association analysis using clinical samples. Xenograft inoculates of 1 or 10 acidotic cells mimicking circulating tumor cell clusters were shown to exhibit increased tumor incidence compared with their physiological pH counterparts. Transcriptomics revealed that profound remodeling of the extracellular matrix (ECM) occurred in the acidotic cells, including upregulation of the integrin subunit α­4 (ITGA4) gene. In clinical lung cancer, ITGA4 expression was found to be upregulated in primary tumors with metastatic capability, and this trait was retained in the corresponding secondary tumors. Expression of ITGA4 was markedly upregulated around the vasculogenic mimicry structures of the acidotic tumors, while acidotic cells exhibited a higher ability of vasculogenic mimicry in vitro. Acidosis was also found to induce the enrichment of side population cells, suggesting an enhanced resistance to noxious attacks of the tumor microenvironment. Taken together, these results demonstrated that acidosis actively contributed to tumor metastatic colonization, and novel mechanistic insights into the therapeutic management and prognosis of lung cancer were discussed.

Extracellular Vesicles for Muscle Atrophy Treatment.

Skeletal muscle atrophy is a progressive chronic disease associated with various conditions, such as aging, cancer, and muscular dystrophy. Interleukin-6 (IL-6) is highly correlated with or plays a crucial role in inducing skeletal muscle atrophy. Extracellular vehicles (EVs), including exosomes, mediate cell-cell communication, and alterations in the genetic material contained in EVs during muscle atrophy may impair muscle cell signaling. Transplantation of muscle progenitor cell-derived EVs (MPC-EVs) is a promising approach for treating muscle diseases such as Duchenne muscular dystrophy (DMD). Moreover, stem cell-derived EVs with modification of microRNAs (e.g., miR-26 and miR-29) have been reported to attenuate muscle atrophy. Unbiased RNA-Seq analysis suggests that MPC-EVs may exert an inhibitory effect on IL-6 pathway. Here, we review the latest advances concerning the mechanisms of stem cell/progenitor cell-derived EVs in alleviating muscle atrophy, including anti-inflammatory and anti-fibrotic effects. We also discuss the clinical application of EVs in the treatment of muscle atrophy.

Efficacy and safety of acupoint application in the treatment of ulcerative colitis: A systematic review and meta-analysis.

BACKGROUND: The efficacy of acupoint application in the treatment of ulcerative colitis (UC) is still controversial. The purpose of this study is to systematically evaluate the clinical efficacy and safety of acupoint application in the treatment of ulcerative colitis. METHODS: The databases of China National Knowledge Infrastructure (CNKI), Chinese Biology Medicine (CBM), VIP, Wanfang, Embase, PubMed, the Cochrane Library and Web of Science were searched. The time limit was from the establishment of the database to July 2022. The published randomized controlled trials of acupoint application in the treatment of UC were analyzed by meta-analysis and trial sequential analysis. RESULTS: A total of 13 studies were included, with a total sample size of 878 cases. Compared with conventional western medicine, acupoint application can effectively improve the effective rates of clinical comprehensive (risk ratio [RR] 1.13, 95% confidence interval [CI] 1.06-1.20, P = .0003), syndrome (RR 1.13, 95% CI 1.03-1.24, P = .009), and interleukin-4 (IL-4) (mean differences 2.62, 95% CI 1.96-3.28, P < .00001) in the treatment of UC, and reduce interferon-γ (mean differences -5.38, 95% CI -6.81 to -3.94, P < .00001). The effective rates of colonoscopy (RR 0.94, 95% CI 0.84-1.05, P = .25), pathological examination (RR 1.04, 95% CI 0.90-1.20, P = .60) and rate of adverse reaction (RR 0.55, 95% CI 0.25-1.21, P = .14) were the same. Trial sequential analysis indicated that the benefits of effective rates of clinical comprehensive and syndrome, IL-4, and interferon-γ were conclusive. Harbord regression showed no publication bias (P = .98). The evaluation of evidence quality suggested that the evidence quality of effective rates of clinical comprehensive and syndrome was moderate and the evidence quality of other indicators was low or very low. CONCLUSION: Acupoint application is a safe and effective method for the treatment of UC, and has the prospect of clinical application.

miR-30e-5p-mediated FOXD1 promotes cell proliferation by blocking cellular senescence and apoptosis through p21/CDK2/Rb signaling in head and neck carcinoma.

Forkhead box D1 (FOXD1) belongs to the FOX protein family, which has been found to function as a oncogene in multiple cancer types, but its role in head and neck squamous cell carcinoma (HNSCC) requires further investigation. Our research aimed to investigate the function of FOXD1 in HNSCC. Bioinformatics analysis indicated that mRNA level of FOXD1 was highly expressed in HNSCC tissues, and over-expressed FOXD1 was related to poor prognosis. Moreover, FOXD1 knockdown increased the ratio of senescent cells but decreased the proliferation ability, while FOXD1 overexpression obtained the opposite results. In vitro experiments revealed that FOXD1 bound to the p21 promoter and inhibited its transcription, which blocked the cyclin dependent kinase 2 (CDK2)/retinoblastoma (Rb) signaling pathway, thus preventing senescence and accelerating proliferation of tumor cells. CDK2 inhibitor could reverse the process to some extent. Further research has shown that miR-3oe-5p serves as a tumor suppressant by repressing the translation of FOXD1 through combining with the 3'-untranslated region (UTR). Thus, FOXD1 resists cellular senescence and facilitates HNSCC cell proliferation by affecting the expression of p21/CDK2/Rb signaling, suggesting that FOXD1 may be a potential curative target for HNSCC.

Pediatric restrictive cardiomyopathy: a case report.

Restrictive cardiomyopathy (RCM) is a rare childhood cardiomyopathy that is a challenging diagnostic problem for clinicians. We describe a case of an 8-year-old girl with a 2-year history of shortness of breath on exertion. Electrocardiogram and echocardiography showed biatrial enlargement, while cardiac magnetic resonance showed biatrial dilation and normal pericardial thickness. Left and right heart catheterization revealed a left ventricular (LV) end-diastolic pressure (EDP) of 20 mmHg, right ventricular (RV) EDP of 13 mmHg, and pulmonary arterial systolic pressure of 51 mmHg. LV and RV pressure traces showed that LV and RV pressures moved concordantly with respiration, and that the systolic area index was 0.98. Cardiac catheterization data were therefore supportive of RCM. Next-generation sequencing identified a heterozygous variant of the troponin I gene (TNNI3; c.574C>T). Combining these findings led to a diagnosis of RCM. The patient's parents chose conservative treatment, but at the 12-month follow-up she died of worsening heart failure and cerebral infarction. This case emphasizes the need for cardiac catheterization and genetic testing in RCM, and suggests that anticoagulants should be recommended to reduce the risk of thromboembolic events.

COTE-1 promotes the proliferation and invasion of small cell lung cancer by regulating autophagy activity via the AMPK/mTOR signaling pathway.

BACKGROUND: COTE-1 has been found to promote the proliferation and invasion of non-small cell lung cancer. However, the mechanism of COTE-1 in SCLC is still unclear. Exploring the role of COTE-1 in SCLC is expected to provide a potential target for the prognosis and treatment of SCLC. METHODS: The expression of COTE-1 and ki-67 was detected by immunohistochemical staining. PCR detected COTE-1 expression level. Cell proliferation activity was detected by CCK8 assay. A wound healing test detected cell migrative ability. Transwell invasion assay detected cell invasive ability. The numbers of autophagosomes were observed by transmission electron microscopy. WB detected the expression levels of autophagy-related proteins and AMPK/mTOR pathway-related proteins. The effect of COTE-1 expression level on the proliferation of SCLC tumor tissues was investigated by establishing a mouse SCLC xenograft tumor model. RESULTS: The expression of COTE-1 in SCLC tissues and cells was higher than that in normal tissues and cells. In SCLC cells with high COTE-1 expression, the expression level of autophagy proteins was notably increased, the number of intracellular autophagosomes increased, and the proliferative activity, migration and invasion abilities were enhanced. COTE-1 promotes autophagy, proliferation, and invasion of SCLC cells under nutrient deprivation by activating the AMPK/mTOR signaling pathway. Activation of autophagy by COTE-1 promotes the proliferation and development of xenograft tumors in a mouse model of SCLC. CONCLUSION: COTE-1 promotes the proliferation, migration and invasion of small cell lung cancer by mediating autophagy based on the AMPK/mTOR pathway.

Factors affecting distal false lumen enlargement after thoracic endovascular aortic repair for type B aortic dissection.

Objective: To investigate the factors influencing distal false lumen enlargement after thoracic endovascular aortic repair (TEVAR) for type B aortic dissection. Materials and methods: Data were collected on patients with type B aortic dissection who underwent TEVAR from January 2008 to August 2022. Patients were divided into a distal aortic segmental enlargement (DSAE) group and a non-DSAE group based on whether the distal false lumen was dilated more than 5 mm on computed tomographic angiography (CTA) images. To analyze the independent influences on distal false lumen dilatation after TEVAR, the variables with a P value < 0.05 during univariate analysis were included in the binary logistic regression analysis model. Results: A total of 335 patients were included in this study, with 85 in the DSAE group and 250 in the non-DSAE group. The mean age was 52.40 ± 11.34 years, 289 (86.27%) were male patients, and the median follow-up time was 6.41 (11.99-29.99) months. There were significant differences in Marfan syndrome, chronic obstructive pulmonary disease (COPD), and follow-up time between the two groups. In terms of morphology, there were statistically significant differences in the number of tears, the size of the primary tear, and the length of dissection between the two groups. Binary logistic regression analysis indicated that Marfan syndrome, COPD, and the primary tear size were associated with distal false lumen dilatation. Conclusions: Marfan syndrome, COPD, and the primary tear size influence distal aortic segmental enlargement after TEVAR in type B aortic dissection patients.

Effect and mechanisms of exercise for complex regional pain syndrome.

Complex regional pain syndrome characterized by severe pain and dysfunction seriously affects patients' quality of life. Exercise therapy is gaining attention because it can effectively relieve pain and improve physical function. Based on the previous studies, this article summarized the effectiveness and underlying mechanisms of exercise interventions for complex regional pain syndrome, and described the gradual multistage exercise program. Exercises suitable for patients with complex regional pain syndrome mainly include graded motor imagery, mirror therapy, progressive stress loading training, and progressive aerobic training. In general, exercise training for patients with complex regional pain syndrome not only alleviates pain but also improves physical function and positive mental status. The underlying mechanisms of exercise interventions for complex regional pain syndrome include the remodeling of abnormal central and peripheral nervous system, the regulation of vasodilation and adrenaline levels, the release of endogenous opioids, and the increased anti-inflammatory cytokines. This article provided a clear explanation and summary of the research on exercise for complex regional pain syndrome. In the future, more high-quality studies with sufficient sample sizes may provide more exercise regimens and better evidence of efficacy.

Analysis of influencing factors and a predictive model of small airway dysfunction in adults.

BACKGROUND: Small airway dysfunction (SAD) is a widespread but less typical clinical manifestation of respiratory dysfunction. In lung diseases, SAD can have a higher-than-expected impact on lung function. The aim of this study was to explore risk factors for SAD and to establish a predictive model. METHODS: We included 1233 patients in the pulmonary function room of TangDu Hospital from June 2021 to December 2021. We divided the subjects into a small airway disorder group and a non-small airway disorder group, and all participants completed a questionnaire. We performed univariate and multivariate analyses to identify the risk factors for SAD. Multivariate logistic regression was performed to construct the nomogram. The performance of the nomogram was assessed and validated by the Area under roc curve (AUC), calibration curves, and Decision curve analysis (DCA). RESULTS: One. The risk factors for small airway disorder were advanced age (OR = 7.772,95% CI 2.284-26.443), female sex (OR = 1.545,95% CI 1.103-2.164), family history of respiratory disease (OR = 1.508,95% CI 1.069-2.126), history of occupational dust exposure (OR = 1.723,95% CI 1.177-2.521), history of smoking (OR = 1.732,95% CI 1.231-2.436), history of pet exposure (OR = 1.499,95% CI 1.065-2.110), exposure to O3 (OR = 1.008,95% CI 1.003-1.013), chronic bronchitis (OR = 1.947,95% CI 1.376-2.753), emphysema (OR = 2.190,95% CI 1.355-3.539) and asthma (OR = 7.287,95% CI 3.546-14.973). 2. The AUCs of the nomogram were 0.691 in the training set and 0.716 in the validation set. Both nomograms demonstrated favourable clinical consistency. 3.There was a dose‒response relationship between cigarette smoking and SAD; however, quitting smoking did not reduce the risk of SAD. CONCLUSION: Small airway disorders are associated with age, sex, family history of respiratory disease, occupational dust exposure, smoking history, history of pet exposure, exposure to O3, chronic bronchitis, emphysema, and asthma. The nomogram based on the above results can effectively used in the preliminary risk prediction.

Acupuncture alleviates acute peritonitis: A case report.

Many inflammatory and infectious entities can affect the peritoneum acutely, and patients with peritonitis often have painful expressions. Abdominal pain can be aggravated by coughing, breathing, and turning the body. Here we report the case of an 88-year-old patient with acute gastrointestinal perforation. The patient has been experiencing pain in the right lower abdomen, presenting persistent colic. The X-ray of abdomen and abdominal computed tomography showed perforation of digestive tract. In addition to the use of anti-infection and stomach protection agents, we use different analgesic injections, but the effect on reducing the pain was not obvious. After acupuncture treatment, the patient quickly relieved the pain of acute peritonitis in 1 minute. However, to our knowledge, there is few literature showing that acupuncture relieves preoperative opioid-induced hyperalgesia in patients with acute peritonitis. Based on this case, we suggest acupuncture as an option in the management of relieving the pain of acute peritonitis when opioid therapy is ineffective.

Analysis of T1-T2 stage oropharyngeal squamous cell carcinoma treated with transoral robotic surgery.

Objective: Transoral robotic surgery (TORS) has become an effective treatment for early-stage oropharyngeal squamous cell carcinomas (OPSCCs). We aimed to analyze the clinical safety and efficacy of TORS for human papilloma virus (HPV)-positive and HPV-negative OPSCC in China. Methods: Patients with OPSCC of pT1-T2 stage who underwent TORS from March 2017 to December 2021 were analyzed. Results: A total of 83 patients (HPV-positive, n = 25; HPV-negative, n = 58) were included. The median age of the patients was 57.0 years and 71 were men. The majority of primary tumor sites were palatine tonsils (52, 62.7%) and base of tongues (20, 24.1%). Three patients have a positive margin. A total of 12 (14.5%) patients received tracheotomies, the average duration of tracheostomy tube use was 9.4 days, and nasogastric tube was 14.5 days. No patient had a long-term tracheotomy. The 3-year overall survival (OS), disease-free survival (DFS), and recurrence-free survival (RFS) for all 83 patients were 89.5%, 80.1%, and 83.3%, respectively. The OS at 3 years between the HPV-positive group and HPV-negative group were 100% versus 84.3% (P = .07), while the DFS and RFS between two groups also showed no significant difference. Among multivariate cox regression analysis of all potential risk factors, smoking was the significant risk factors for disease recurrence (P < .05). Conclusion: Transoral robotic surgery achieved encouraging oncologic outcomes and safety in T1-T2 stage OPSCC treatment, regardless of HPV status. Level of Evidence: 4.