Purpose: The genomic characteristics of uterine sarcomas have not been fully elucidated. This study aimed to explore the genomic landscape of the uterine sarcomas (USs). Materials and Methods: Comprehensive genomic analysis through RNA-sequencing was conducted. Gene fusion, differentially expressed genes (DEGs), signaling pathway enrichment, immune cell infiltration, and prognosis were analyzed. A deep learning model was constructed to predict the survival of US patients. Results: A total of 71 US samples were examined, including 47 endometrial stromal sarcomas (ESS), 18 uterine leiomyosarcomas (uLMS), three adenosarcomas, two carcinosarcomas, and one uterine tumor resembling an ovarian sex-cord tumor. ESS (including high-grade ESS [HGESS] and low-grade ESS [LGESS]) and uLMS showed distinct gene fusion signatures; a novel gene fusion site, MRPS18A–PDC-AS1 could be a potential diagnostic marker for the pathology differential diagnosis of uLMS and ESS; 797 and 477 uterine sarcoma DEGs (uDEGs) were identified in the ESS vs. uLMS and HGESS vs. LGESS groups, respectively. The uDEGs were enriched in multiple pathways. Fifteen genes including LAMB4 were confirmed with prognostic value in USs; immune infiltration analysis revealed the prognositic value of myeloid dendritic cells, plasmacytoid dendritic cells, natural killer cells, macrophage M1, monocytes and hematopoietic stem cells in USs; the deep learning model named Max-Mean Non-Local multi-instance learning (MMN-MIL) showed satisfactory performance in predicting the survival of US patients, with the area under the receiver operating curve curve reached 0.909 and accuracy achieved 0.804. Conclusion USs harbored distinct gene fusion characteristics and gene expression features between HGESS, LGESS, and uLMS. The MMN-MIL model could effectively predict the survival of US patients.

Purpose: The genomic characteristics of uterine sarcomas have not been fully elucidated. This study aimed to explore the genomic landscape of the uterine sarcomas (USs). Materials and Methods: Comprehensive genomic analysis through RNA-sequencing was conducted. Gene fusion, differentially expressed genes (DEGs), signaling pathway enrichment, immune cell infiltration, and prognosis were analyzed. A deep learning model was constructed to predict the survival of US patients. Results: A total of 71 US samples were examined, including 47 endometrial stromal sarcomas (ESS), 18 uterine leiomyosarcomas (uLMS), three adenosarcomas, two carcinosarcomas, and one uterine tumor resembling an ovarian sex-cord tumor. ESS (including high-grade ESS [HGESS] and low-grade ESS [LGESS]) and uLMS showed distinct gene fusion signatures; a novel gene fusion site, MRPS18A–PDC-AS1 could be a potential diagnostic marker for the pathology differential diagnosis of uLMS and ESS; 797 and 477 uterine sarcoma DEGs (uDEGs) were identified in the ESS vs. uLMS and HGESS vs. LGESS groups, respectively. The uDEGs were enriched in multiple pathways. Fifteen genes including LAMB4 were confirmed with prognostic value in USs; immune infiltration analysis revealed the prognositic value of myeloid dendritic cells, plasmacytoid dendritic cells, natural killer cells, macrophage M1, monocytes and hematopoietic stem cells in USs; the deep learning model named Max-Mean Non-Local multi-instance learning (MMN-MIL) showed satisfactory performance in predicting the survival of US patients, with the area under the receiver operating curve curve reached 0.909 and accuracy achieved 0.804. Conclusion USs harbored distinct gene fusion characteristics and gene expression features between HGESS, LGESS, and uLMS. The MMN-MIL model could effectively predict the survival of US patients.

Purpose: The genomic characteristics of uterine sarcomas have not been fully elucidated. This study aimed to explore the genomic landscape of the uterine sarcomas (USs). Materials and Methods: Comprehensive genomic analysis through RNA-sequencing was conducted. Gene fusion, differentially expressed genes (DEGs), signaling pathway enrichment, immune cell infiltration, and prognosis were analyzed. A deep learning model was constructed to predict the survival of US patients. Results: A total of 71 US samples were examined, including 47 endometrial stromal sarcomas (ESS), 18 uterine leiomyosarcomas (uLMS), three adenosarcomas, two carcinosarcomas, and one uterine tumor resembling an ovarian sex-cord tumor. ESS (including high-grade ESS [HGESS] and low-grade ESS [LGESS]) and uLMS showed distinct gene fusion signatures; a novel gene fusion site, MRPS18A–PDC-AS1 could be a potential diagnostic marker for the pathology differential diagnosis of uLMS and ESS; 797 and 477 uterine sarcoma DEGs (uDEGs) were identified in the ESS vs. uLMS and HGESS vs. LGESS groups, respectively. The uDEGs were enriched in multiple pathways. Fifteen genes including LAMB4 were confirmed with prognostic value in USs; immune infiltration analysis revealed the prognositic value of myeloid dendritic cells, plasmacytoid dendritic cells, natural killer cells, macrophage M1, monocytes and hematopoietic stem cells in USs; the deep learning model named Max-Mean Non-Local multi-instance learning (MMN-MIL) showed satisfactory performance in predicting the survival of US patients, with the area under the receiver operating curve curve reached 0.909 and accuracy achieved 0.804. Conclusion USs harbored distinct gene fusion characteristics and gene expression features between HGESS, LGESS, and uLMS. The MMN-MIL model could effectively predict the survival of US patients.

Objective:To investigate the effects and underlying mechanisms of the hypoxia-inducible factor-1α (HIF-1α) agonist Roxadustat in alleviating pulmonary ischemia-reperfusion injury (IRI) in mice.Method:This study consisted of both in vivo and in vitro experiments. Thirty-six male C57/BL6 mice (6~8 weeks old) were used. In the animal experiments, 20 mice underwent left pulmonary artery ligation to establish the IRI model and were divided into reperfusion groups of 0, 1, 2, or 4 hours (IR-0/1/2/4 h, n=4 each), with a sham group ( n=4) as control. Temporal and spatial changes in pulmonary HIF-1α expression were analyzed. Another 16 mice were randomized into four groups: sham ( n=4), I/R+vehicle (DMSO, n=4), and I/R+Roxadustat treatment at 25 mg/kg or 50 mg/kg (I/R+ROX-LD, I/R+ROX-HD, n=4 each). Roxadustat or DMSO was administered intraperitoneally once daily for 5 days before surgery. Lung injury, inflammation, and endothelial apoptosis were subsequently assessed. In the cell experiments, human umbilical vein endothelial cell (HUVEC) was subjected to hypoxia-reoxygenation (H/R) to determine the time course of HIF-1α expression. Cells pretreated with Roxadustat (25 μmol) were then exposed to H/R, and HIF-1α expression and apoptosis were analyzed. To verify the role of HIF-1α, siRNA knockdown of HIF-1α mRNA was performed before Roxadustat pretreatment and H/R exposure. Result:In vivo, pulmonary HIF-1α mRNA expression increased progressively after reperfusion, while protein expression peaked early and subsequently declined ( P<0.05). Immunofluorescence staining revealed HIF-1α predominantly localized to pulmonary endothelial cells following I/R. Compared with the I/R+DMSO group, Roxadustat (both doses) upregulated HIF-1α expression in lung tissue. In vitro, HIF-1α mRNA expression increased continuously after H/R, while protein levels first rose and then decreased ( P<0.05). Roxadustat pretreatment upregulated Bcl-2 and downregulated Bax and cleaved caspase-3 compared with the H/R group ( P<0.05). HIF-1α knockdown reversed these effects, resulting in decreased Bcl-2 and increased Bax and cleaved caspase-3 expression relative to the Roxadustat-treated group. Conclusion:The HIF-1α agonist Roxadustat inhibits vascular endothelial apoptosis, alleviates endothelial injury, reduces inflammatory cell infiltration in lung tissue, and lowers inflammatory responses in mice with pulmonary ischemia-reperfusion injury.

Objective:To investigate the effects and underlying mechanisms of the hypoxia-inducible factor-1α (HIF-1α) agonist Roxadustat in alleviating pulmonary ischemia-reperfusion injury (IRI) in mice.Method:This study consisted of both in vivo and in vitro experiments. Thirty-six male C57/BL6 mice (6~8 weeks old) were used. In the animal experiments, 20 mice underwent left pulmonary artery ligation to establish the IRI model and were divided into reperfusion groups of 0, 1, 2, or 4 hours (IR-0/1/2/4 h, n=4 each), with a sham group ( n=4) as control. Temporal and spatial changes in pulmonary HIF-1α expression were analyzed. Another 16 mice were randomized into four groups: sham ( n=4), I/R+vehicle (DMSO, n=4), and I/R+Roxadustat treatment at 25 mg/kg or 50 mg/kg (I/R+ROX-LD, I/R+ROX-HD, n=4 each). Roxadustat or DMSO was administered intraperitoneally once daily for 5 days before surgery. Lung injury, inflammation, and endothelial apoptosis were subsequently assessed. In the cell experiments, human umbilical vein endothelial cell (HUVEC) was subjected to hypoxia-reoxygenation (H/R) to determine the time course of HIF-1α expression. Cells pretreated with Roxadustat (25 μmol) were then exposed to H/R, and HIF-1α expression and apoptosis were analyzed. To verify the role of HIF-1α, siRNA knockdown of HIF-1α mRNA was performed before Roxadustat pretreatment and H/R exposure. Result:In vivo, pulmonary HIF-1α mRNA expression increased progressively after reperfusion, while protein expression peaked early and subsequently declined ( P<0.05). Immunofluorescence staining revealed HIF-1α predominantly localized to pulmonary endothelial cells following I/R. Compared with the I/R+DMSO group, Roxadustat (both doses) upregulated HIF-1α expression in lung tissue. In vitro, HIF-1α mRNA expression increased continuously after H/R, while protein levels first rose and then decreased ( P<0.05). Roxadustat pretreatment upregulated Bcl-2 and downregulated Bax and cleaved caspase-3 compared with the H/R group ( P<0.05). HIF-1α knockdown reversed these effects, resulting in decreased Bcl-2 and increased Bax and cleaved caspase-3 expression relative to the Roxadustat-treated group. Conclusion:The HIF-1α agonist Roxadustat inhibits vascular endothelial apoptosis, alleviates endothelial injury, reduces inflammatory cell infiltration in lung tissue, and lowers inflammatory responses in mice with pulmonary ischemia-reperfusion injury.

Objective To investigate the changes of serum cardiac-specific troponin I (cTnI) level in patients after lung transplantation. Methods Clinical data of patients undergoing lung transplantation in our hospital from December 2016 to December 2022 were retrospectively analyzed. The relationship between postoperative serum cTnI level and clinical characteristics were explored. Results Finally 20 patients were collected, including 15 males and 5 females with an average age of (51.65±12.79) years. The serum cTnI level was significantly increased after lung transplantation. The serum cTnI reached the highest level on the first day after transplantation, and significantly decreased from the third day after transplantation. The serum cTnI levels in patients with obstructive pulmonary disease and bilateral lung transplantation were significantly higher than those in patients with restrictive pulmonary disease and unilateral lung transplantation on the day after surgery and on the first day after transplantation. Conclusion Transient myocardial injury can occur after lung transplantation, which is characterized by an abnormal increase in serum cTnI level.

Objective:To analyze the status and its influencing factors of job burnout among female workers of labor-intensive enterprises.Methods:A total of 750 female workers from 5 labor-intensive enterprises in Guangdong Province were selected as the study subjects by random cluster sampling method in August, 2019. 665 valid questionnaires were collected, and the effective recovery rate was 88.67%. The Maslach Burnout Inventory-General Survey was used to assess job burnout and its influencing factors were analyzed.Results:Among 665 female workers, 429 (64.51%) found to have different levels of burnout, among which 380 (57.14%) were mild to moderate burnout and 49 (7.37%) were severe burnout. The comprehensive scores of job burnout in different age, marital status, current post working age, working time per week, personal monthly income, working system and occupational stress groups were statistically significant ( P<0.01) . There were significant differences in the score of emotional exhaustion in different age, marital status, current working age, working time per week, personal monthly income and occupational stress groups ( P<0.05) . There were significant differences in the dimensions of depersonalization in different age, weekly work time, personal monthly income, working system and occupational stress groups ( P<0.05) . There were significant differences in the dimensions of low individual achievement in different education levels, weekly work time, working system and occupational stress groups ( P<0.05) . Conclusion:The female workers of labor-intensive enterprises are generally have mild to moderate job burnout. The main influencing factors of job burnout are weekly work time and occupational stress.

Objective:To analyze the status and its influencing factors of job burnout among female workers of labor-intensive enterprises.Methods:A total of 750 female workers from 5 labor-intensive enterprises in Guangdong Province were selected as the study subjects by random cluster sampling method in August, 2019. 665 valid questionnaires were collected, and the effective recovery rate was 88.67%. The Maslach Burnout Inventory-General Survey was used to assess job burnout and its influencing factors were analyzed.Results:Among 665 female workers, 429 (64.51%) found to have different levels of burnout, among which 380 (57.14%) were mild to moderate burnout and 49 (7.37%) were severe burnout. The comprehensive scores of job burnout in different age, marital status, current post working age, working time per week, personal monthly income, working system and occupational stress groups were statistically significant ( P<0.01) . There were significant differences in the score of emotional exhaustion in different age, marital status, current working age, working time per week, personal monthly income and occupational stress groups ( P<0.05) . There were significant differences in the dimensions of depersonalization in different age, weekly work time, personal monthly income, working system and occupational stress groups ( P<0.05) . There were significant differences in the dimensions of low individual achievement in different education levels, weekly work time, working system and occupational stress groups ( P<0.05) . Conclusion:The female workers of labor-intensive enterprises are generally have mild to moderate job burnout. The main influencing factors of job burnout are weekly work time and occupational stress.

Cancer is the most cause death of among adolescents and young adults (AYAs).Psychological distress caused by cancer affects AYAs' effective coping abilities of disease,physical symptoms and treatment.This paper mainly introduces the related concepts,screening tools and intervention progress of psychological distress of AYAs cancer patients to deepen the understanding of these among clinical professionals and provide reference for implement effective interventions to patients.

Objective To evaluate the clinical curative effect of ulinastatin combined with CRRT in the treatment of multiple organ dysfunction syndrome(MODS).Methods Sixty eight patients with MODS who were admitted to ICU from July 2013 to July 2015 were randomly divided into three groups:control group,CRRT group,combined group;Patients' APACHE Ⅱ,SOFA scores level of inflammatory markers were recorded before treatment and after treatment of 72 hours and 7 days.The mortality of the three groups in ICU were compared.Results After 72 hours and a week of treatment,the level of IL-10,IL-6,TNF-α,WBC、PCT、CRP in CRRT group and combined group were significantly better than that of control group(P＜0.05),and combined group were significantly better than that of CRRT group.Compared with the control group,the oxygen index,lactic acid,ALT significantly im proved in CRRT group and combined group were better than control group,after 72 hours and a week of treatment(P＜0.05),and the cornbined group was the most obvious.After a week of treatment,the mortality rate of CRRT group and combined group was significantly better than the control group (P＜0.05),while there was no statistical differences between CRRT group and combined group(P＞0.05).Conclusion Ulinastatin combined with CRRT is an effective method for the treatment of MODS.