Work-related musculoskeletal disorders (WMSDs) represent a significant occupational health challenge among healthcare professionals globally, posing substantial threats to physical and mental well-being as well as work sustainability. Adopting preventive behaviors—including ergonomic postural adjustments, optimized work-rest scheduling, proper use of protective and assistive equipment, and regular physical activity—is essential for mitigating the risk of WMSDs. Guided by the social ecological model, the review synthesized current evidence on the determinants of WMSDs preventive behaviors across four levels: intrapersonal characteristics, work environment conditions, interpersonal support, and policy/institutional factors. The findings suggest that higher educational attainment, favorable health-related behavioral patterns, optimized ergonomic work environments, adoption of supportive collaborative systems, strong organizational support, as well as policy safeguards facilitate preventive behavior adoption. Conversely, limited prevention-related knowledge, low risk perception, insufficient physical activity, excessive workload, lack of appropriate protective equipment, inadequate ergonomic training, a prevailing culture of presenteeism, and inadequate policy implementation constitute significant barriers. Multi-dimensional intervention strategies targeting these determinants are warranted to enhance preventive behaviors, reduce the risk of WMSDs, and strengthen occupational health protection for healthcare professionals.

BACKGROUND:A large number of articles have reported the effect and mechanism of platelet-rich plasma and hydrogel in the treatment of spinal cord injury,but few articles have summarized their treatment strategies for spinal cord injury. OBJECTIVE:To summarize the pathological process of spinal cord injury and the strategies of repairing spinal cord injury with platelet-rich plasma and hydrogel alone and in combination. METHODS:PubMed and CNKI databases were searched for articles published from inception to March 2024 by computer.The Chinese search terms were"spinal cord injury,platelet-rich plasma,hydrogel."The English search terms were"spinal cord injury,spinal cord,platelet-rich plasma,hydrogel,angiogenesis,neuralgia,combination therapy."Articles were screened according to inclusion and exclusion criteria,and 128 articles were finally included for review and analysis. RESULTS AND CONCLUSION:(1)The classification of platelet-rich plasma is complex and diverse,and the effects of platelet-rich plasma in the repair treatment of spinal cord injury are various,but they all show certain positive effects,that is,they can promote axon regeneration,stimulate angiogenesis,and treat neuropathic pain and so on.(2)The effect of platelet-rich plasma is mainly due to the growth factors contained in platelet-rich plasma.(3)There are many types of hydrogels,which mainly play the role of filling,simulating extracellular matrix,carrying drugs and biological products,and carrying cells as scaffolds in the repair treatment of spinal cord injury.(4)Compared with single therapy,combination therapy of platelet-rich plasma and hydrogel can promote nerve regeneration and spinal cord function recovery more effectively.

Iron overload is strongly associated with heart disease. Ferroptosis is a new form of regulated cell death indicated in cardiac ischemia-reperfusion (I/R) injury. However, the specific molecular mechanism of myocardial injury caused by iron overload in the heart is still unclear, and the involvement of ferroptosis in iron overload-induced myocardial injury is not fully understood. In this study, we observed that ferroptosis participated in developing of iron overload and I/R-induced cardiomyopathy. Mechanistically, we discovered that Parkin inhibited iron overload-induced ferroptosis in cardiomyocytes by promoting the ubiquitination of long-chain acyl-CoA synthetase 4 (ACSL4), a crucial protein involved in ferroptosis-related lipid metabolism pathways. Additionally, we identified p53 as a transcription factor that transcriptionally suppressed Parkin expression in iron-overloaded cardiomyocytes, thereby regulating iron overload-induced ferroptosis. In animal studies, cardiac-specific Parkin knockout mice (Myh6-CreER ^T2 /Parkin ^fl/fl ) fed a high-iron diet presented more severe myocardial damage, and the high iron levels exacerbated myocardial I/R injury. However, the ferroptosis inhibitor Fer-1 significantly suppressed iron overload-induced ferroptosis and myocardial I/R injury. Moreover, Parkin effectively protected against impaired mitochondrial function and prevented iron overload-induced mitochondrial lipid peroxidation. These findings unveil a novel regulatory pathway involving p53-Parkin-ACSL4 in heart disease by inhibiting of ferroptosis.

Background: s/Aims: Sarcomatoid hepatocellular carcinoma (HCC) is a rare histological subtype of HCC characterized by extremely poor prognosis; however, its molecular characterization has not been elucidated. Methods: In this study, we conducted an integrated multiomics study of whole-exome sequencing, RNA-seq, spatial transcriptome, and immunohistochemical analyses of 28 paired sarcomatoid tumor components and conventional HCC components from 10 patients with sarcomatoid HCC, in order to identify frequently altered genes, infer the tumor subclonal architectures, track the genomic evolution, and delineate the transcriptional characteristics of sarcomatoid HCCs. Results: Our results showed that the sarcomatoid HCCs had poor prognosis. The sarcomatoid tumor components and the conventional HCC components were derived from common ancestors, mostly accessing similar mutational processes. Clonal phylogenies demonstrated branched tumor evolution during sarcomatoid HCC development and progression. TP53 mutation commonly occurred at tumor initiation, whereas ARID2 mutation often occurred later. Transcriptome analyses revealed the epithelial–mesenchymal transition (EMT) and hypoxic phenotype in sarcomatoid tumor components, which were confirmed by immunohistochemical staining. Moreover, we identified ARID2 mutations in 70% (7/10) of patients with sarcomatoid HCC but only 1–5% of patients with non-sarcomatoid HCC. Biofunctional investigations revealed that inactivating mutation of ARID2 contributes to HCC growth and metastasis and induces EMT in a hypoxic microenvironment. Conclusions We offer a comprehensive description of the molecular basis for sarcomatoid HCC, and identify genomic alteration (ARID2 mutation) together with the tumor microenvironment (hypoxic microenvironment), that may contribute to the formation of the sarcomatoid tumor component through EMT, leading to sarcomatoid HCC development and progression.

The plants of the genus Caragana Fabr. are desert plants of the Leguminosae family, which are widely used in traditional ethnomedicine, with the effects of nourishing Yin and nourishing blood, dispelling wind and removing dampness, clearing heat and detoxifying toxins. The anti-inflammatory effect of Caragana Fabr. has attracted much attention, the research on the related mechanism has made some progress, but it lacks systematic collation. By summarising the anti-inflammatory effects of the active ingredients of Caragana Fabr., the authors found that they have good anti-inflammatory activities on different inflammatory cell models in vitro, and have good improvement effects on rheumatoid arthritis, colitis, complex nephritis, and acute lung injury and other disease models. The anti-inflammatory effects of the active components of this genus mainly include the reduction of the levels of a variety of pro-inflammatory factors, and the signalling pathways involved mainly include TLR4/NF-κB, TLR4/MAPK, TLR4/NF-κB/IRF3, JAK/STAT-1, ERK/STAT-1 and so on. Therefore, the paper mainly reviews the research progress on the anti-inflammatory effects and mechanisms of the Caragana Fabr. plants and their active components according to disease types, with a view to providing reference for the in-depth study of their anti-inflammatory activities and the development of new products with related functions.

Patients with advanced pregnancy complicated by acute ST-segment elevation myocardial infarction are relatively rare both domestically and internationally,and there are currently no relevant guidelines to guide clinical treatment.In this case,a 39-year-old pregnant woman was admitted to the hospital with sudden chest pain,and the electrocardiogram showed extensive anterior ST-segment elevation myocardial infarction.Coronary angiography showed subtotal subtotal occlusion of the proximal left anterior descending artery.Reperfusion and revascularization were given,and the blood flow grade of the trial of thrombolytic in myocardial infarction was restored.Complete intravascular ultrasonography to determine the cause of occlusion due to spontaneous hematoma of the left anterior descending artery.After the operation,a reasonable antiplatelet and anticoagulant treatment regimen was selected according to the coronary artery lesion,and the pregnancy was terminated at the appropriate time,and 1 live male baby was successfully delivered.Maternal and fetal health was followed up after 1、3 and 6 months.Through the experience and summary of the treatment process,combined with the literature,the pathogenesis of this disease is discussed,and the strategy of revascularization,the selection of antithrombotic drugs and the timing of pregnancy termination are discussed in depth for clinical reference.

This paper reported a type 1 diabetes patient who had severe diabetic nephropathy, retinopathy, hypertension, and hypothyroidism before pregnancy. The patient's blood glucose control was poor before pregnancy, and the complications were not properly treated. This was an unintended pregnancy, with a pre-pregnancy glycated hemoglobin A1c of 7.8% and early pregnancy urine protein of 3.81-4.53 g/24 h. Considering the patient's poor blood glucose control before pregnancy and the lack of proper treatment for multiple complications including nephropathy, a multidisciplinary consultation at an external hospital recommended termination of the pregnancy. However, the patient was determined to continue the pregnancy and was referred to Peking University First Hospital. Through strict blood glucose control, monitoring and evaluation of complications, and comprehensive management, the patient's blood glucose and blood pressure were well controlled during pregnancy. Regular monitoring of urine protein, renal function, and ocular fundus was conducted. At 31 weeks and 4 days of gestation, the patient's 24-hour urine protein significantly increased. After promoting fetal lung maturity, a cesarean section was performed at 34 weeks and 1 day of gestation, resulting in a successful delivery with good maternal and neonatal outcomes. At the 42-day postpartum follow-up, the patient's blood glucose and blood pressure were stable, urine protein returned to pre-pregnancy levels, and the infant was in good general condition.

Objective:To summarize the clinical and genetic features of neuroinflammation, autoinflammation, splenomegaly and anemia (NASA) syndrome and investigate the pathogenic mechanism.Methods:The clinical data of 2 patients diagnosed with NASA syndrome at Department of Pediatrics, Peking Union Medical College Hospital were retrospectively analyzed. Variants were identified by gene panel sequencing and confirmed by Sanger sequencing. The function of IRAK4 gene variants was studied in vitro.Results:Among the 2 patients, case 1 was an 8-year-old girl and case 2 was a 10-year-old boy. Both patients presented in early childhood with anemia and hepatosplenomegaly. Case 1 was also experienced recurrent seizures. Laboratory examinations showed elevated inflammatory markers and neuroimaging revealed bilateral basal ganglia calcification. In case 2, anemia and inflammation markers were well controlled after treatment with tocilizumab, while case 1 succumbed to recurrent seizures. Genetic tests verified compound heterozygous variants in IRAK4 gene: case 1 carries a nonsense variant c.592G>T (p.G198X) and a missense variant c.248A>C (p.D83A), which were respectively from the parents; case 2 carries a c.831+3A>G variant and a frameshift variant c.540delT (p.F180Lfs*26), and the former was inherited from the father and the latter from the mother. The reverse transcription and Sanger sequencing results confirmed that c.831+3A>G variant led to exon 7 skipping. In vitro studies indicated that c.592G>T, c.540delT and c.831+3A>G variants resulted in truncated interleukin-1 receptor-associated kinase-4 (IRAK4) protein while c.248A>C do not cause changes in IRAK4 protein expression level and protein length.Conclusions:NASA syndrome should be considered in children with early-onset anemia, hepatosplenomegaly, recurrent seizures, elevated inflammatory markers and intracranial calcification. IRAK4 gene variants may lead to impaired anti-inflammatory function of IRAK4 protein, contributing to the autoinflammatory phenotype.

Objective:To investigate the clinical characteristics of urea cycle disorder (UCD), the efficacy and safety of glyceryl phenylbutyrate (GPB) therapy in pediatric patients with UCD.Methods:This study was a retrospective, single-arm, multicenter clinical study. The clinical data of 20 pediatric patients with UCD who received GPB treatment at 9 hospitals nationwide between December 2021 and August 2024 were collected. The clinical manifestations, laboratory results, and molecular genetic characteristics were analyzed, ammonia levels and other laboratory results were evaluated pre-post GPB therapy by paired t-tests or Wilcoxon tests. Results:Among the 20 pediatric patients with UCD, there were 8 males and 12 females, and the onset age was 2.8 (1.4, 5.7) years. The ammonia levels were 174 (125, 342) μmol/L at first onset. The symptoms included vomiting in 6 cases, drowsiness in 5 cases, epilepsy in 5 cases, developmental delay in 5 cases, psychiatric and behavioral abnormalities in 3 cases, and lethargy in 1 case, and 18 cases exhibited abnormal liver function. Twenty cases included 6 UCD subtypes, with 11 cases being ornithine transcarbamylase deficiency. A total of 27 variants were identified, 11 (41%) of which were novel. The age of patients who began GPB therapy was 4.0 (1.5, 6.6) years. Ten cases stopped GPB after 4.2 (3.4, 5.3) months, with 4 patients undergoing liver transplantation and 6 discontinuing for financial reasons. The remaining ten patients continued GPB therapy for 11.6 (8.6, 14.0) months. The duration of GPB treatment was 6.0 (4.2, 12.3) months, at the final visit, the levels of ammonia, platelets and aspartate aminotransferase were lower compared to those of pre-treatment (all P<0.05). The serum albumin level was higher than that of pre-treatment ( P=0.016). Two patients suffered only one episode of acute hyperammonaemia, with ammonia levels of 232 and 141 μmol/L, respectively. Nine cases experienced adverse effects potentially related to GPB, decreased appetite in 6 cases, vomiting in 3 cases, abnormal skin oil odor in 2 cases, somnolence, fatigue and diarrhea each in 1 case, with symptoms improved within 6 (3, 10) days. Conclusions:UCD primarily manifests with neurological and gastrointestinal symptoms, and early diagnosis of UCD could be achieved through the analysis of ammonia. GPB may effectively reduce ammonia levels in UCD pediatric patients, with favorable safety and tolerability.