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.

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.

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.

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.

AIM:This study aims to investigate the effects of baicalin on the hypoxia-inducible factor-1α(HIF-1α)/solute carrier family 7 member 11(SLC7A11)/glutathione peroxidase 4(GPX4)axis and the ferroptosis induced by oxidized low-density lipoprotein(ox-LDL)in RAW264.7 macrophage-derived foam cells.METHODS:RAW264.7 cells were categorized into five groups:control,ox-LDL,baicalin+ox-LDL,ferrostatin-1(Fer-1;ferroptosis inhibitor)+ox-LDL,and baicalin+Fer-1+ox-LDL.To induce foam cell formation,RAW264.7 macrophages were exposed to 100 μg/mL ox-LDL for 24 h.Oil red O staining was employed to visualize lipid droplet formation in each group.The ultrastructure of the mitochondria was examined using transmission electron microscopy.Fluorescence microscopy was utilized to assess the fluorescence intensity of intracellular reactive oxygen species(ROS),lipid peroxides,and Fe2+.A colorimetric assay facilitated the measurement of malondialdehyde(MDA)and glutathione(GSH)levels.Additionally,Western blot analy-sis was conducted to quantify protein levels of HIF-1α,SLC7A11,and GPX4.RESULTS:The model group exhibited foam cell formation,abundant lipid droplets,significant swelling of mitochondrial structures,and observable shortening or disappearance of cristae.There was a marked increase in intracellular fluorescence intensity of ROS,lipid peroxides,and Fe2+,alongside elevated MDA levels and decreased GSH levels.HIF-1α protein expression was significantly increased,while SLC7A11 and GPX4 protein expressions were notably decreased(P<0.05).In comparison to the model group,both the baicalin+ox-LDL and Fer-1+ox-LDL groups demonstrated a significant reduction in lipid droplets,improved mitochon-drial structures,decreased fluorescence intensity of ROS,lipid peroxides,and Fe2+,as well as lower MDA levels and higher GSH levels.Additionally,HIF-1α expression significantly decreased,while SLC7A11 and GPX4 expressions sig-nificantly increased(P<0.05).Furthermore,the baicalin+Fer-1+ox-LDL group showed a more pronounced reduction in lipid droplets,near-normal mitochondrial structures,lower fluorescence intensity of ROS,lipid peroxides,and Fe2+,de-creased MDA levels,and increased GSH levels compared to the baicalin+ox-LDL group;HIF-1α,SLC7A11,and GPX4 protein expressions were also significantly reduced(P<0.05).CONCLUSION:Baicalin modulates the HIF-1α/SLC7A11/GPX4 axis,thereby inhibiting ox-LDL-induced ferroptosis in macrophage-derived foam cells.

Objective To design an 8-channel gene analyzer to take the place of the widely used gene analyzer with problems in inconvenient consumable replacement and short storage time of electrophoresis polymer.Methods The 8-channel gene analyzer had its mechanical components composed of an automatic sample loading table,a polymer injection module,a high-voltage temperature control module,an optical module and an integrated U box,its electrical control system made up of a host computer(an embedded computer)and three slave computers(a sampling control board,a polymer injection control board and a high-voltage temperature control board).The automatic sample loading table involved in four motors and transmission systems for x,y,z directions and optical alignment,the transmission systems adopted mainly belt drive mode and the optical alignment motor had its threads with an anti-backlash structure;the polymer injuection module was manipulated by the polymer injection control board,and the polymer block was made of highly transparent acrylic material;the high-voltage temperature control module realized the regulation of electrophoresis voltage and the detection of electrophoresis current by the low-ripple precision high-voltage power supply,and controlled the temperature of the heating furnace by the proportional-integral-differential(PID)algorithm;the optical module consisted of an excitation module and a light-receiving module,which had the base of the reflector made of low expansion coefficient alloy material;the integrated U box had the electrophoresis polymer,capillary array,polymer block and anode buffer in a plastic housing;the host computer had the data acquisition software programmed with C# and C++,and the slave computers were controlled by STM32 SCM.Results The 8-channel gene analyzer had no significant differences with the widely used ABI3500 gene analyzer in resolution,precision accuracy and clinical results.Conclusion The 8-channel gene analyzer gains advantages in consumable replacement and storage time of electrophoresis polymer,and can meet the requirements for gene sequencing.[Chinese Medical Equipment Journal,2025,46(2):24-30]

Objective:To evaluate the prevalence, potential risk factors, and correlation between coronary and peripheral microvascular dysfunction in heart failure with non-reduced ejection fraction (nHFrEF) patients.Methods:This was a prospective registry study. nHFrEF patients admitted to Zhongshan Hospital affiliated with Fudan University from December 2021 to December 2023 were enrolled. According to coronary flow reserve (CFR) or reactive congestion index (RHI), enrolled patients were divided into coronary microvascular endothelial dysfunction (CMD) group (CFR<2.5) and no CMD group (CFR≥2.5) or peripheral microvascular endothelial dysfunction (MED) group (RHI<1.67) and no MED group (RHI≥1.67). Patients′ general information, laboratory and auxiliary examination data were collected. Univariate and multivariate logistic regression were used to analyze the influencing factors of CMD and MED in nHFrEF patients, and Spearman correlation analysis was used to evaluate the correlation between MED and CMD.Results:A total of 142 nHFrEF patients were enrolled, aged 69.0 (59.0, 74.0) years, with a male proportion of 66.9% (95/142). The grouping results were as follows: (1) According to CFR, there were 73 cases in the CMD group and 69 cases in the no CMD group; (2) According to RHI, there were 57 cases in the MED group and 85 cases in the no MED group. The prevalence of CMD and MED in this study was 51.4% (73/142) and 40.1% (57/142), respectively. Univariate logistic regression analysis showed that increased heart rate, chronic kidney disease, atrial fibrillation, elevated N-terminal pro-B type natriuretic peptide levels, and increased urinary albumin/creatinine ratio were risk factors for CMD, while increased RHI was a protective factor for CMD; Atrial fibrillation is a risk factor for MED, while increased CFR is a protective factor for MED. Incorporating clinically significant variables from univariate analysis into multivariate analysis, the results showed that increased heart rate and elevated RHI remained risk and protective factors for CMD, respectively; increased CFR remains a protective factor for MED. Spearman correlation analysis showed that CFR was negatively correlated with lg urinary albumin/creatinine ratio, lg cardiac troponin T, lg N-terminal pro-B type natriuretic peptide, and heart rate; RHI is positively correlated with CFR.Conclusions:The prevalence of CMD and MED in nHFrEF patients is high, and the two have a certain positive correlation. Increased heart rate and RHI are risk and protective factors for CMD, respectively, while increased CFR is a protective factor for MED. MED may be a potential therapeutic target for nHFrEF patients.

Objective:To evaluate the feasibility of using the domestic ArcherQA system for fast and simplified independent verification of CyberKnife (CK) stereotactic radiotherapy (SRT) plans.Methods:SRT plans of 57 patients treated with CK at Tianjin Medical University Cancer Institute and Hospital from August 2021 to August 2022 were retrospectively analyzed, including 15 intracranial, 30 pulmonary, and 12 abdominal tumors cases. Point-dose and planar-dose verifications were performed using an ionization chamber and radiochromic films embedded in a homogeneous phantom, and the results were compared with those calculated by the treatment planning system (TPS). The localization CT images and corresponding SRT plans were imported into the ArcherQA system for independent dose verification and analysis. The correlation between ArcherQA results and phantom measurements was analyzed, with comparisons of target mean dose differences and γ pass rates.Results:Phantom measurement results showed, the measured point-dose differences for intracranial, lung, and abdominal plans were -0.94% ± 3.22%, 1.92% ± 2.05%, and 2.12% ± 0.77%, respectively. The mean dose differences in target dose calculation between ArcherQA and TPS: intracranial in the gross tumor volume (GTV) regions were 0.34% ± 2.21%, lung tumor GTV were -2.47% ± 2.46%, and abdominal tumor GTV were 0.80% ± 2.61%, respectively. Among them, the abdominal GTV region showed the highest correlation between ArcherQA and measured results ( r=0.78). The average two-dimensional γ pass rates (2 mm/2%, threshold=10%) measured using phantom films were 95.92% ± 2.35% for intracranial, 95.70% ± 2.74% for lung, and 96.74% ± 3.41% for abdominal tumors plans, respectively. The three-dimensional ArcherQA results showed comparable γ pass rates (1 mm/2%, threshold=10%) for lung and abdominal GTV and PTV regions, with similar medians and data dispersion to film measurements. Conclusions:The ArcherQA system enables rapid and efficient independent dose verification of CK SRT plans without the need for additional hardware. The verification results show good correlation with phantom measurements, supporting its potential as an auxiliary quality assurance tool in clinical CK SRT implementation.

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.