ObjectiveTo investigate the differential expression of integrin alpha-6（ITGA6） in abdominal wall endometriosis （AWE） tissues and its molecular mechanisms in regulating AWE. Methods36 AWE lesions were designated as the experimental group， while 36 cases of normal endometrial tissues served as the controls. Differential expression of ITGA6 between the two groups was assessed through immunohistochemical （IHC） staining. Human ITGA6 gene-specific interference sequences were designed， synthesized， and packaged into lentiviral vectors to establish the Ishikawa cell line with ITGA6-knockdown. Similarly， the ITGA6-overexpression cell line was constructed using the coding sequence （CDS） of the gene. Real-time PCR and Western blot were performed to detect changes in epithelial-mesenchymal transition（EMT）-related markers and angiogenesis-related indicators. Cell invasion and migration capabilities were assessed by Cell Scratch and Transwell assays. Furthermore， Western blot was conducted to profile PI3K/AKT pathway dynamics. ResultsEctopic endometrial tissues exhibited a marked increase in the number of ITGA6-positive cells and their expression intensity compared to eutopic endometrium （each P < 0.001）. Compared with the NC group， the ITGA6-knockdown group showed significantly reduced expression of N-cadherin， VEGF， and TGF-β1 （all P < 0.01）， while E-cadherin expression was markedly increased （P < 0.01）. Concomitantly， the invasion and migration capacities of ITGA6-low expression were significantly impaired （P < 0.001 for both）， accompanied by a marked reduction in AKT and phosphorylated AKT（p-AKT） levels （P < 0.001）. Conversely， overexpressing ITGA6 resulted in opposite effects. ConclusionITGA6 modulates EMT and angiogenesis in Ishikawa cells via the PI3K/AKT signaling pathway， thereby enhancing cell invasion and migration capabilities， which contributes to the pathogenesis of AWE.

Transfusion and Anemia Expertise Initiative-Control/Avoidance of Bleeding developed a strategy for platelet and plasma infusion management in critically ill children based on systematic reviews and consensus meetings of international multidisciplinary experts. One good practice statement and six expert consensus statements were proposed for plasma and platelet transfusions in critically ill children following severe trauma, traumatic brain injury, and/or intracranial hemorrhage. This article introduces the specific methods and basis for the formation of recommendations in this part of the guide.

To guide transfusion practice in critically ill children who often need plasma and platelet transfusions, the Transfusion and Anemia Expertise Initiative-Control/Avoidance of Bleeding (TAXI-CAB) developed Recommendations and Expert Consensus for Plasma and Platelet Transfusion Practice in Critically Ill Children. This guideline addresses 53 recommendations related to plasma and platelet transfusion in critically ill children with 8 kinds of diseases, laboratory testing, selection/treatment of plasma and platelet components, and research priorities. This paper introduces the specific methods and results of the recommendation formation of the guideline.

Purpose: There is still insufficient evidence for predicting stroke risk in patients with mild carotid atherosclerotic stenosis. This study aimed to explore the association between carotid intraplaque neovascularization (IPN) in mild stenosis and ischemic stroke, using contrast-enhanced ultrasound (CEUS) imaging. Methods: This retrospective observational study included 369 patients from July 2021 to March 2022. These patients were categorized as symptomatic or asymptomatic based on their recent history of ipsilateral ischemic stroke. Initial parameters of carotid plaques, such as IPN grading and contrast enhancement index, were assessed using B-mode ultrasonography and CEUS. The follow-up period lasted 12 months or until a newly-developed ischemic stroke occurred. Logistic regression models and Cox proportional-hazards regression models were employed to explore the associations between ultrasonic parameters and the incidence of recent and future ischemic strokes. Results: In patients with mild stenosis, both increasing age and grade 2 carotid IPN were significant predictors of recent primary ischemic stroke. Furthermore, grade 2 carotid IPN independently predicted future ischemic strokes in both symptomatic and asymptomatic patients. Conclusion This study demonstrated that carotid IPN as detected by CEUS imaging holds potential as a useful non-invasive biomarker for predicting recent and future ischemic strokes in patients with mild carotid stenosis.

Purpose: There is still insufficient evidence for predicting stroke risk in patients with mild carotid atherosclerotic stenosis. This study aimed to explore the association between carotid intraplaque neovascularization (IPN) in mild stenosis and ischemic stroke, using contrast-enhanced ultrasound (CEUS) imaging. Methods: This retrospective observational study included 369 patients from July 2021 to March 2022. These patients were categorized as symptomatic or asymptomatic based on their recent history of ipsilateral ischemic stroke. Initial parameters of carotid plaques, such as IPN grading and contrast enhancement index, were assessed using B-mode ultrasonography and CEUS. The follow-up period lasted 12 months or until a newly-developed ischemic stroke occurred. Logistic regression models and Cox proportional-hazards regression models were employed to explore the associations between ultrasonic parameters and the incidence of recent and future ischemic strokes. Results: In patients with mild stenosis, both increasing age and grade 2 carotid IPN were significant predictors of recent primary ischemic stroke. Furthermore, grade 2 carotid IPN independently predicted future ischemic strokes in both symptomatic and asymptomatic patients. Conclusion This study demonstrated that carotid IPN as detected by CEUS imaging holds potential as a useful non-invasive biomarker for predicting recent and future ischemic strokes in patients with mild carotid stenosis.

With the development of manned space technology,long-term space missions have gradually become a reality,but the problem of sleep disorders faced by astronauts has become increasingly prominent.The combined effects of microgravity,abnormal circadian rhythm,confined space pressure and psychological stress in space environment lead to the significant decline of sleep quality of astronauts,which is manifested as difficulty falling asleep,sleep fragmentation and reduction of deep sleep.Based on the theory of traditional Chinese medicine,this paper systematically analyzes the etiology and pathogenesis of astronaut sleep disorders,and reveals the unique advantages of transcutaneous electrical acupoint stimulation in space medicine,which provides a new idea for the construction of non-pharmacological sleep intervention system.Although there are technical difficulties,non-pharmacological therapy such as transcutaneous electrical acupoint stimulation is still a key breakthrough to solve sleep disorders in astronauts.It is expected to become an important part of space medicine and provide safe and efficient health protection for long-term space missions.

Objective To report the diagnosis,treatment,and verification process of a patient with sex development disorder whose chromosomal karyotype and genetic test results are inconsistent,and conduct a literature review to improve the understanding of the mosaic status of sexual development disorders.Methods A 14-year-old patient presented with primary amenorrhea on April 3,2020,at the First Affiliated Hospital of Hebei North University,exhibiting female sexual characteristics.The patient underwent ultrasonic/magnetic resonance imaging of gonads,assessment of gonadal axis function,chromosomal karyotype,and molecular genetic testing,as well as pelvic exploration,malignant gonads resection,and hormone replacement therapy,resulting in drug-induced menstruation.During the diagnosis and treatment,it was found that the patient's chromosomal karyotype analysis was inconsistent with the molecular genetic test results.Subsequently,samples from the three germ layer cells were taken,and fluorescence in situ hybridization(FISH)was used to detect the sex chromosomes in each germ layer cell.XY probes were used to label the gonadal pathological sections to explore the distribution differences of the Y chromosome in the gonads,and changes in anti-Müllerian hormone(AMH)levels before and after surgery were compared.Databases such as Wanfang and PubMed were searched to summarize relevant cohort study literature and understand the current status of research on this disease.Results The patient's body exhibited a significant differences between the 45,X and 46,XY cell lines in different germ layers and within the same layer tissues.The proportion of 45,X in buccal mucosal cells derived from the ectoderm was 30%(6/20),in peripheral blood lymphocytes derived from the mesoderm was 9.7%(11/114),and in bladder shed cells derived from endoderm was 20.4%(22/108).The gonadal pathological sections labeled with XY probes indicated a mosaic state with a reduced Y-chromosome;where the epididymal structure area had a 45,X cell line mosaic of 50.0%,and the malignant area had a normal"Y"content.After gonadal resection,AMH levels significantly dropped from 7.28 pmol/L to＜0.07 pmol/L.Literature review revealed that patients with 45,X/46,XY have a complex phenotype spectrum,most with features of Turner syndrome,and female phenotypes are at risk of gonadal tumors.Conclusions In the diagnosis of difficult cases of sex development disorders,when performing peripheral blood karyotype testing,the number of counted cells and analyzed cells should be increased as much as possible,and multi-germ layer cell sampling should be performed.Gonads with a high"Y"mosaic rate are more prone to malignancy in the abdominal cavity.Detecting AMH levels can distinguish cryptorchidism and anorchidism in sexual development disorders with Y chromosomes.

Objective To establish a stable,reliable,and clinically relevant porcine model of endotoxin-induced acute respiratory distress syndrome(ARDS).Methods Ten 8-month-old male Bama minipigs were deeply sedated,followed by invasive mechanical ventilation and electrocardiographic monitoring.Lipopolysaccharide(LPS)was intravenously pumped at 600 μg/(kg·h)for 3 hours,then maintained at 15 μg/(kg·h)thereafter.Dynamic monitoring was performed at five time points after LPS injection(LPS 0,1,3,5,and 8 h),including arterial blood gas analysis and chest computed tomography(CT)scans.Pathological examination of lung tissues obtained via bronchoscopic biopsy(HE staining and transmission electron microscopy)was conducted.These indicators were comprehensively used to evaluate the success of the animal model.Results At 5 hours after LPS administration,8 minipigs developed symptoms such as skin cyanosis,elevated body temperature,and respiratory distress.The oxygenation index decreased to<300 mmHg.Chest CT scans showed diffuse pulmonary infiltrates.Histopathology revealed alveolar edema and hyaline membrane formation.Transmission electron microscopy demonstrated disruption of pulmonary blood-air barrier,depletion of lamellar bodies in type Ⅱ pneumocytes,inflammatory cell infiltration,and exudation of plasma proteins and fibrin.Compared with LPS 0 h,at LPS 8 h,the oxygenation index and arterial blood pH were significantly decreased(P<0.001),while blood lactic acid and serum potassium were significantly increased(P<0.05);serum calcium and base excess were significantly decreased(P<0.05),and the lung injury score based on HE-stained lung sections was significantly increased(P<0.01).Conclusion The porcine ARDS model established by continuous LPS injection can dynamically simulate the pathophysiological characteristics and typical pathological manifestations of clinical septic ARDS,making it an effective tool to study the pathogenesis,prevention,and treatment strategies of septic ARDS.

Objective: To study the effects and potential mechanisms of the aquaporin 1(AQP1) inhibitor acetazolamide(AZ) on the proliferation, apoptosis, and inflammatory response of rheumatoid arthritis(RA) fibroblast-like synoviocytes(FLS). Methods: TNF-α-induced RA-FLS was served as in vitro RA model. MTT assay, IF staining, and EdU incorporation assay were applied to study AZ′s effects on RA-FLS proliferation. Hoechst staining, flow cytometry analysis of Annexin V-FITC/PI-stained cells, and mitochondrial membrane potential detection experiments were used to detect cell apoptosis. ELISA and quantitative real-time PCR methods were used to measure pro-inflammatory cytokine production. Cell autophagy was evaluated using IF staining and mCherry-GFP-LC3B puncta assay. Western blot was performed to detect the levels of autophagy, apoptosis, and proliferation-related proteins. Moreover, the role of autophagy inhibition in AZ′s effects on RA-FLS was examined by co-treating with the autophagy activator rapamycin(RAPA) or the autophagy inhibitor 3-methyladenine(3-MA). Results: AZ dose⁃dependently inhibited cell proliferation , promoted apoptosis , and reduced the production of pro⁃inflammatory cytokines in RA⁃FLS. Furthermore , AZ suppressed cytoprotective autophagy in these cells , as evidenced by decreased LC3B levels ( P < 0. 05 ) , increased p62 expression ( P < 0. 05 ) , and reduced autophagic flux ( P <0. 01) . Particularly , AZ ′s beneficial effects were reversed by RAPA⁃induced autophagy activation and enhanced by 3 ⁃MA⁃induced autophagy inhibition. Conclusion This study provides the first evidence that AZ hinders cytoprotective autophagy , thereby alleviating the hyperproliferation , apoptosis resistance , and aberrant inflammatory response of RA⁃FLS , revealing the core role of autophagy inhibition in AZ ′s anti⁃RA effects.