Critically ill patients often experience significant skeletal muscle wasting due to prolonged bed rest, metabolic disorders, inflammatory responses and malnutrition, which affects the patient's mobility and may also lead to increased mortality. Timely and accurate assessment of muscle status is important for optimizing treatment strategies and improving patient prognosis. There are various limitations in the current methods of assessing muscle mass, and muscle ultrasound, as a noninvasive, convenient, low-cost and suitable technique for bedside monitoring, has received increasing attention for its application in muscle assessment of critically ill patients. However, there are still a number of challenges in its practical application, such as the lack of uniform standards for the measurement method, the high dependence on the operation, and the reproducibility of the data that needs to be optimized, and so on. The aim of this article is to systematize the research progress of muscle ultrasound in muscle assessment of critically ill patients, and to discuss the advantages and limitations of its clinical application, in order to provide a scientific basis for future research and clinical practice.
Humans ; Critical Illness ; Ultrasonography ; Muscle, Skeletal/diagnostic imaging*

In recent years, with the continuous advancement of related research, the clinical value of clot waveform analysis (CWA) in the diagnosis and management of thrombotic diseases has become increasingly prominent. As a dynamic coagulation monitoring technology based on optical principles, CWA overcomes the limitations of traditional coagulation tests (e.g., APTT, PT), which rely on single time-point parameters, in identifying hypercoagulable states, predicting thrombotic risk, and monitoring anticoagulant efficacy. By analyzing the kinetic profiles of the coagulation cascade, CWA provides multidimensional insights. This article elucidates the theoretical basis and principles of CWA, systematically reviews its applications in arterial/venous thrombosis, other hypercoagulability-related disorders, and anticoagulation therapy monitoring, and synthesizes recent advances of CWA for thrombotic diseases. Specifically, multiple studies demonstrate that CWA-APTT parameters (e.g., peak height Min1, Min2, Delta) can sensitively detect hypercoagulability. Combining CWA with the Padua score significantly enhances the predictive power for venous thromboembolism (VTE) risk assessment. CWA shows clinical utility in evaluating hypercoagulability in patients with acute myocardial infarction (AMI) and acute cerebral infarction (ACI), where parameters such as Min1, Min2, and Max2 exhibit greater sensitivity than conventional APTT. These metrics may predict AMI complications and guide clinical management. Additionally, CWA demonstrates value in diverse scenarios including pregnancy, inflammation-associated hypercoagulability (e.g., COVID-19, Kawasaki disease), and rare thrombotic conditions (e.g., chronic spontaneous urticaria). Beyond diagnostic and risk-stratification advantages, CWA serves as a novel tool for personalized anticoagulation monitoring. Its derivative technology, clot-fibrinolysis waveform analysis (CFWA), extends applications to fibrinolysis assessment—aiding in identifying coagulation status in deep vein thrombosis (DVT) patients, tracking coagulation/fibrinolysis dynamics in COVID-19, and evaluating efficacy of anticoagulant/antifibrinolytic therapies. Nevertheless, despite its unique strengths, challenges such as device dependency, insufficient standardization, and heterogeneity in parameter interpretation hinder widespread clinical adoption, necessitating further investigation. Future directions include establishing multidimensional thrombotic risk assessment systems integrating CWA and developing AI-powered automated CWA analysis platforms to enhance clinical accessibility.

Objective To systematically evaluate the risk prediction models for anastomotic leakage (AL) in patients with esophageal cancer after surgery. Methods A computer-based search of PubMed, EMbase, Web of Science, Cochrane Library, Chinese Medical Journal Full-text Database, VIP, Wanfang, SinoMed and CNKI was conducted to collect studies on postoperative AL risk prediction model for esophageal cancer from their inception to October 1st, 2023. PROBAST tool was employed to evaluate the bias risk and applicability of the model, and Stata 15 software was utilized for meta-analysis. Results A total of 19 literatures were included covering 25 AL risk prediction models and 7373 patients. The area under the receiver operating characteristic curve (AUC) was 0.670-0.960. Among them, 23 prediction models had a good prediction performance (AUC>0.7); 13 models were tested for calibration of the model; 1 model was externally validated, and 10 models were internally validated. Meta-analysis showed that hypoproteinemia (OR=9.362), postoperative pulmonary complications (OR=7.427), poor incision healing (OR=5.330), anastomosis type (OR=2.965), preoperative history of thoracoabdominal surgery (OR=3.181), preoperative diabetes mellitus (OR=2.445), preoperative cardiovascular disease (OR=3.260), preoperative neoadjuvant therapy (OR=2.977), preoperative respiratory disease (OR=4.744), surgery method (OR=4.312), American Society of Anesthesiologists score (OR=2.424) were predictors for AL after esophageal cancer surgery. Conclusion At present, the prediction model of AL risk in patients with esophageal cancer after surgery is in the development stage, and the overall research quality needs to be improved.

Objective To investigate the correlation between skeletal muscle mass index(ASMI)and islet β cell reserve function in patients with newly diagnosed type 2 diabetes mellitus(T2DM).Methods A total of 100 patients with newly diagnosed T2DM were included in this study.All the patients were admitted to the Department of Endocrinology in the First People's Hospital of Yinchuan between June 2022 and November 2023.They were divided into two groups according to their skeletal muscle mass index(ASMI):patients with T2DM accompanied by sarcopenia(Sar,n=50)group,and patients with simple T2DM(T2DM,n=50)group.Additionally,a control(NC)group consisting of 50 healthy participants was selected.Fasting C-peptide levels,liver and kidney function,blood lipid profiles,and other indicators were assessed in all the individuals.The correlation between ASMI and other indicators was analyzed,and the influencing factors for ASMI and T2DM combined with sarcopenia were analyzed respectively.Results The levels of HbA1c,FPG,and TG were higher,while FC-P and Scr levels were lower in the T2DM group and Sar group compared with the NC group(P<0.05).FPG was higher,while ASMI,FC-P,BMI were lower in the Sar group than in the T2DM group(P<0.05).Spearman correlation analysis revealed a negative correlation between ASMI and FPG and HbA1c(P<0.05),whereas a positive correlation was observed with BMI,ALT,Scr,SUA and FC-P(P<0.05).Multiple linear regression analysis indicated that BMI,HbA1c and FC-P were influencing factors for ASMI(P<0.05).Furthermore,logistic regression analysis demonstrated that BMI,HbA1c,FC-P were influencing factors for T2DM with sarcopenia(P<0.05).Conclusions The level of ASMI may be related to the reserve function of islet β cells.

Aim To investigate whether adipose differentiation-related proteins promote macrophage lipid accu-mulation by upregulating acyl-CoA synthetase long-chain family member 3(ACSL3)expression through PI3K/Akt.Methods The experiments were divided into 24 h group,different PLIN2 expression groups,HA-PLIN2+SC97 group and HA-PLIN2+LY294002 group.Western blot was used to detect the protein expression of PLIN2,Akt,p-Akt and ACSL3 in cells,RT-qPCR was used to detect the mRNA level of PLIN2 in cells,and oil red O was used to observe the degree of lipid accumulation in cells.Results The protein expression levels of Akt,p-Akt and ACSL3 in macrophages overex-pressing PLIN2 were significantly increased(P＜0.05),and p-Akt nuclear translocation was increased,with fluorescence labeling of PLIN2 and Akt overlapping.After adding the PI3K/Akt agonist SC97 to macrophages overexpressing PLIN2,the expression level of ACSL3 significantly increased(P＜0.05),and the degree of intracellular lipid accumulation in-creased;After adding the PI3K/Akt inhibitor LY294002 to macrophages overexpressing PLIN2,the expression level of AC-SL3 significantly decreased(P＜0.05),and the degree of intracellular lipid accumulation decreased.Conclusion PLIN2 upregulates ACSL3 expression through PI3K/Akt,thereby promoting macrophage lipid accumulation.

Aim To investigate whether adipose differentiation-related proteins promote macrophage lipid accu-mulation by upregulating acyl-CoA synthetase long-chain family member 3(ACSL3)expression through PI3K/Akt.Methods The experiments were divided into 24 h group,different PLIN2 expression groups,HA-PLIN2+SC97 group and HA-PLIN2+LY294002 group.Western blot was used to detect the protein expression of PLIN2,Akt,p-Akt and ACSL3 in cells,RT-qPCR was used to detect the mRNA level of PLIN2 in cells,and oil red O was used to observe the degree of lipid accumulation in cells.Results The protein expression levels of Akt,p-Akt and ACSL3 in macrophages overex-pressing PLIN2 were significantly increased(P＜0.05),and p-Akt nuclear translocation was increased,with fluorescence labeling of PLIN2 and Akt overlapping.After adding the PI3K/Akt agonist SC97 to macrophages overexpressing PLIN2,the expression level of ACSL3 significantly increased(P＜0.05),and the degree of intracellular lipid accumulation in-creased;After adding the PI3K/Akt inhibitor LY294002 to macrophages overexpressing PLIN2,the expression level of AC-SL3 significantly decreased(P＜0.05),and the degree of intracellular lipid accumulation decreased.Conclusion PLIN2 upregulates ACSL3 expression through PI3K/Akt,thereby promoting macrophage lipid accumulation.

Objective To investigate the correlation between skeletal muscle mass index(ASMI)and islet β cell reserve function in patients with newly diagnosed type 2 diabetes mellitus(T2DM).Methods A total of 100 patients with newly diagnosed T2DM were included in this study.All the patients were admitted to the Department of Endocrinology in the First People's Hospital of Yinchuan between June 2022 and November 2023.They were divided into two groups according to their skeletal muscle mass index(ASMI):patients with T2DM accompanied by sarcopenia(Sar,n=50)group,and patients with simple T2DM(T2DM,n=50)group.Additionally,a control(NC)group consisting of 50 healthy participants was selected.Fasting C-peptide levels,liver and kidney function,blood lipid profiles,and other indicators were assessed in all the individuals.The correlation between ASMI and other indicators was analyzed,and the influencing factors for ASMI and T2DM combined with sarcopenia were analyzed respectively.Results The levels of HbA1c,FPG,and TG were higher,while FC-P and Scr levels were lower in the T2DM group and Sar group compared with the NC group(P<0.05).FPG was higher,while ASMI,FC-P,BMI were lower in the Sar group than in the T2DM group(P<0.05).Spearman correlation analysis revealed a negative correlation between ASMI and FPG and HbA1c(P<0.05),whereas a positive correlation was observed with BMI,ALT,Scr,SUA and FC-P(P<0.05).Multiple linear regression analysis indicated that BMI,HbA1c and FC-P were influencing factors for ASMI(P<0.05).Furthermore,logistic regression analysis demonstrated that BMI,HbA1c,FC-P were influencing factors for T2DM with sarcopenia(P<0.05).Conclusions The level of ASMI may be related to the reserve function of islet β cells.

OBJECTIVE: To analysis clinical phenotype and potential genetic cause of a family affected with hereditary coagulation factor Ⅻ deficiency. METHODS: The prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FIB), D-Dimer (D-D), coagulation factor Ⅻ activity (FⅫ:C) and coagulation factor Ⅻ antigen (FⅫ:Ag) were determined for phenotype diagnosis of the proband and his family members(3 generations and 5 people). Targeted capture and whole exome sequencing were performed in peripheral blood sample of the proband. Possible disease-causing mutations of F12 gene were obtained and further confirmed by Sanger sequencing. The corresponding mutation sites of the family members were analyzed afterwards. The online bioinformatics software AutoPVS1 and Mutation Taster was used to predict the effects of mutation sites on protein function. RESULTS: The APTT of the proband was significantly prolonged, reaching 180.9s. FⅫ:C and FⅫ:Ag of the proband was significantly reduced to 0.8% and 4.17%, respectively. The results of whole exome sequencing displayed that there were compound heterozygous mutations in F12 gene of the proband, including the c.1261G＞T heterozygous nonsense mutation in exon 11 (causing p.Glu421*) and the c.251dupG heterozygous frameshift mutation in exon 4 (causing p.Trp85Metfs*53). Both mutations are loss of function mutations with very strong pathogenicity, leading to premature termination of the protein. AutoPVS1 and Mutation Taster software predicted both mutations as pathogenic mutations. The results of Sanger sequencing revealed that c.1261G＞T heterozygous mutation of the proband was inherited from his mother, for which his brother and his daughter were c.1261G＞T heterozygous carriers. Genotype-phenotype cosegregation was observed in this family. CONCLUSION The c.1261G＞T heterozygous nonsense mutation in exon 11 and the c.251dupG heterozygous frameshift mutation in exon 4 of the F12 gene probably account for coagulation factor Ⅻ deficiency in this family. This study reports two novel pathogenic F12 mutations for the first time worldwide.
Blood Coagulation Disorders ; Codon, Nonsense ; Factor XII/genetics* ; Female ; Heterozygote ; Humans ; Male ; Mutation ; Pedigree

ObjectiveTo investigate effect of conducting training of autism spectrum disorder （ASD） early screening skill on improving the ability to early identify ASD of medical staffs in primary care hospitals. MethodsIn September 2021， the training of ASD early screening skills was carried out for medical staffs from 20 primary care hospitals in Chengdu. After training， the training effect was evaluated. The numbers of referrals from primary care hospitals to superior hospitals， confirmed ASD as well as their average diagnostic age of children with ASD before and after training were used as evaluation indicators. ResultsAfter training， the number of children with suspected ASD referred by primary care hospitals was more than that before training ［（16.65±11.60） vs. （3.40±2.23）， t=5.431， P<0.01］， the number of children diagnosed with ASD was more than that before training［（6.85±4.93） vs. （2.45±1.67）， t=4.171， P<0.01］， and the differences were statistically significant. As for the diagnosed age of ASD children， after training， the average age was lower than that before training ［（34.95±11.67） vs. （42.2±14.64）， t=-2.553， P=0.019］. ConclusionTraining of ASD early screening skills for medical staffs in primary care hospitals may help to improve their ability to early screening ASD children.

OBJECTIVE To provide a reference for the safety of guselkumab in clinical use. METHODS The reporting odds ratio and the Bayesian confidence propagation neural network were used to mine the data of adverse drug events （ADE） related to guselkumab in FAERS database from the fourth quarter of 2017 to the second quarter of 2022. RESULTS & CONCLUSIONS A total of 29 951 ADE reports related to guselkumab were screened， involving 197 （3 871 cases） ADE signals and 21 system organs. The major ADE signals of guselkumab manifested as infectious and invasive diseases， systemic disease and various reactions at the site of administration， and skin and subcutaneous tissue　diseases， which were basically consistent with the instructions. The new ADE signals were found， such as neoplasm of orbit， gallbladder adenocarcinoma， sweat gland disorder， decreased blood uric acid， eyelid retraction， angioimmunoblastic T-cell lymphoma， nonalcoholic fatty liver disease， hyperplastic cholecystopathy， tracheomalacia， inner ear disorder， etc. And the severe ADE signals included severe infections in various parts of the body， liver and gallbladder diseases， tumor， etc.