Objective To understand the current situation and influencing factors of work-related musculoskeletal disorders (WMSDs) in medical staff in Beijing City. Methods A total of 2 687 medical staff were selected as the research subjects using the multi-stage sampling method. The current situation of WMSDs and occupational stress, anxiety symptoms, depressive symptoms, and insomnia symptoms were investigated using the Musculoskeletal Disorders Questionnaire, the Core Occupational Stress Scale, the Generalized Anxiety Disorder Scale, the Patient Health Questionnaire Depression Scale, and the Self-Sleep Management Questionnaire. The Max-Min Hill-Climbing algorithm was used to construct a Bayesian network model to analyze the influencing factors and internal relationships of WMSDs and to conduct reasoning and prediction of the model. Results The prevalence of WMSDs among the research subjects was 88.9%. Binary logistic regression analysis was used to identify age, educational level, personal monthly income, anxiety symptoms, depressive symptoms, insomnia symptoms, prolonged forward-head desk work, and prolonged static posture work to construct the Bayesian network model. The model consisted of nine nodes and eleven directed edges. Prolonged static posture work, prolonged forward-head desk work, and anxiety symptoms were directly related to WMSDs. Age and educational level were indirectly related to WMSDs through their influence on prolonged forward-head desk work. Depression symptoms were indirectly associated with WMSDs through their influence on anxiety symptoms. The model's prediction accuracy was 90.5%. Conclusion The prevalence of WMSDs among medical staff in Beijing City is relatively high. Prolonged static posture work, prolonged forward-head desk work, and anxiety symptoms may directly increase the risk of developing WMSDs.

Objective::To analyze fetal renal abnormality genetic features and the prenatal characteristics of the 17q12 microdeletion syndrome.Methods::This prospective cohort study examined prenatal ultrasound findings of renal abnormalities in pregnant women who underwent single nucleotide polymorphism (SNP) array or copy number variation sequencing (CNV-seq) testing on amniotic fluid or fetal tissue at Tianjin Central Obstetrics and Gynecology Hospital between January 2016 and August 2022. The study cohort comprised women with advanced maternal age, fetal ultrasound anomalies, high-risk non-invasive prenatal testing results, or suspected 17q12 microdeletion syndrome. Comprehensive clinical data, including maternal age, detailed ultrasound findings, and pregnancy outcomes, were systematically collected. SNP-array analysis was conducted using an Affymetrix CytoScan 750 K Array Chip to identify CNVs and loss of heterozygosity, while CNV-seq was performed on the Illumina HiSeq 2000 platform. Detected variants were classified according to the American College of Medical Genetics and Genomics guidelines. Statistical analyses were performed using SPSS version 27.0.Results::Abnormal renal development was identified in 141 patients, among whom 26 exhibited hyperechogenic kidneys (HCK). Of these, 12 cases were associated with 17q12 microdeletion syndrome, while the remaining 14 were linked to other chromosomal abnormalities. When excluding patients with HCK, those diagnosed with polycystic kidney disease demonstrated a higher prevalence of chromosomal abnormalities compared to those with multicystic dysplastic kidney and renal dysplasia. Although isolated conditions such as horseshoe kidney, hydronephrosis, ectopic kidney, and unilateral kidney typically presented with normal chromosomal findings, the incidence of chromosomal abnormalities increased when these conditions coexisted with other anomalies. A detailed analysis of the correlation between 17q12 microdeletion syndrome and HCK revealed that 12 out of the 14 patients diagnosed with 17q12 microdeletion syndrome exhibited HCK. Genetic testing confirmed the syndrome in seven patients, with five cases attributed to novel mutations and two cases resulting from inherited mutations.Conclusion::Fetal HCK was closely associated with the 17q12 microdeletion syndrome, and polycystic kidney disease showed a higher rate of chromosomal abnormalities. Chromosome test results were mostly normal in patients with other renal abnormalities, such as kidney dysplasia, horseshoe kidneys, hydronephrosis, kidney deficiency, and ectopic kidneys. Prenatal diagnosis is recommended, especially in cases of non-isolated fetal renal abnormalities. This study provides strong evidence supporting a link between fetal renal abnormalities and genetic syndromes.

Objective::To analyze fetal renal abnormality genetic features and the prenatal characteristics of the 17q12 microdeletion syndrome.Methods::This prospective cohort study examined prenatal ultrasound findings of renal abnormalities in pregnant women who underwent single nucleotide polymorphism (SNP) array or copy number variation sequencing (CNV-seq) testing on amniotic fluid or fetal tissue at Tianjin Central Obstetrics and Gynecology Hospital between January 2016 and August 2022. The study cohort comprised women with advanced maternal age, fetal ultrasound anomalies, high-risk non-invasive prenatal testing results, or suspected 17q12 microdeletion syndrome. Comprehensive clinical data, including maternal age, detailed ultrasound findings, and pregnancy outcomes, were systematically collected. SNP-array analysis was conducted using an Affymetrix CytoScan 750 K Array Chip to identify CNVs and loss of heterozygosity, while CNV-seq was performed on the Illumina HiSeq 2000 platform. Detected variants were classified according to the American College of Medical Genetics and Genomics guidelines. Statistical analyses were performed using SPSS version 27.0.Results::Abnormal renal development was identified in 141 patients, among whom 26 exhibited hyperechogenic kidneys (HCK). Of these, 12 cases were associated with 17q12 microdeletion syndrome, while the remaining 14 were linked to other chromosomal abnormalities. When excluding patients with HCK, those diagnosed with polycystic kidney disease demonstrated a higher prevalence of chromosomal abnormalities compared to those with multicystic dysplastic kidney and renal dysplasia. Although isolated conditions such as horseshoe kidney, hydronephrosis, ectopic kidney, and unilateral kidney typically presented with normal chromosomal findings, the incidence of chromosomal abnormalities increased when these conditions coexisted with other anomalies. A detailed analysis of the correlation between 17q12 microdeletion syndrome and HCK revealed that 12 out of the 14 patients diagnosed with 17q12 microdeletion syndrome exhibited HCK. Genetic testing confirmed the syndrome in seven patients, with five cases attributed to novel mutations and two cases resulting from inherited mutations.Conclusion::Fetal HCK was closely associated with the 17q12 microdeletion syndrome, and polycystic kidney disease showed a higher rate of chromosomal abnormalities. Chromosome test results were mostly normal in patients with other renal abnormalities, such as kidney dysplasia, horseshoe kidneys, hydronephrosis, kidney deficiency, and ectopic kidneys. Prenatal diagnosis is recommended, especially in cases of non-isolated fetal renal abnormalities. This study provides strong evidence supporting a link between fetal renal abnormalities and genetic syndromes.

Objective:To discuss the damage effect of vesicular stomatitis virus(VSV)on the vascular endothelial(VE)barrier,and to clarify its mechanism.Methods:The canine kidney cells were used to amplify VSV.The half tissue culture infective dose(TCID50)of VSV was determined using mouse brain endothelial tumor bEnd.3 cells,and subsequent experiment was conducted using 300 times the TCID50.The bEnd.3 cells were divided into infection 0 h group,infection 4 h group,infection 8 h group,and infection 12 h group for VE barrier damage experiments due to VSV infection.The bEnd.3 cells were also divided into control group,infection group,and correction group for experiments to inhibit the VSV replication and restore the VE barrier.The bEnd.3 cells were inoculated into Transwell chambers to construct an in vitro VE barrier model.Cell voltage resistance meter was used to detect the transepithelial resistance(TER)in various groups after the bEnd.3 cells were infected with VSV at different time points;fluorescein isothiocyanate-dextran leakage assay was used to detect the permeability coefficients of the cells in various groups;immunofluorescence staining was used to observe the localization changes of VE-cadherin,β-catenin,and phosphorylated β-catenin(p-β-catenin)in cytoskeleton and adherens junctions(AJs)of the bEnd.3 cells after VSV infection;real-time fluorescence quantitative PCR(RT-qPCR)method was used to detect the expression levels of Wnt and β-catenin mRNA in the cells in various groups;Western blotting method was used to detect the expression levels of Wnt,β-catenin,and p-β-catenin proteins in the cells in various groups.Results:The TCID50 of VSV was 10-4.5·100 μL-1.TheTranswell chamber experiment results showed that compared with infection 0 h group,the TERs in the cells in the other groups were significantly decreased(P＜0.05),and the permeability coefficients were significantly increased(P＜0.05).The immunofluorescence staining results showed that compared with control group,the cytoskeleton of the bEnd.3 cells in infection group was disordered,the cell gaps was increased,the linear index of AJs was significantly decreased(P＜0.05),and β-catenin and p-β-catenin translocated from the cell membrane to the perinuclear area.The RT-qPCR results showed that compared with infection 0 h group,the expression levels of Wnt mRNA in the cells in the other groups were significantly decreased(P＜0.05),while the expression levels of β-catenin mRNA showed no statistically significant difference(P＞0.05).The Western blotting results showed that compared with infection 0 h group,the expression levels of Wnt protein in the cells in the other groups were significantly decreased(P＜0.05),the expression levels of β-catenin showed no statistically significant differences(P＞0.05),and the expression levels of p-β-catenin were significantly increased(P＜0.05).After inhibiting the VSV replication and correcting the low density lipoprotein receptor(LDLR)abnormalities,the Transwell chamber experiment results showed that compared with infection group,the TER in the cells in correction group was significantly increased(P＜0.05),and the permeability coefficient was significantly decreased(P＜0.05).The immunofluorescence staining results showed that compared with infection group,the gaps in the cells in correction group were reduced,and the perinuclear aggregation of β-catenin and p-β-catenin in the cells was restrained.The RT-qPCR results showed that compared with infection group,the expression level of Wnt mRNA in the cells in correction group was significantly increased(P＜0.05).The Western blotting results showed that compared with infection group,the expression level of Wnt protein in the cells in correction group was significantly increased(P＜0.05),the expression level of β-catenin showed no statistically significant difference(P＞0.05),and the expression level of p-P-catenin was significantly decreased(P＜0.05).Conclusion:VSV infection can cause the LDLR inactivation,reduce the expression level of Wnt protein,increase the phosphorylation level of β-catenin and cause its internalization,disrupt the stability of AJs,and ultimately lead to VE barrier damage.

Objective:To investigate the clinical manifestations, imaging features and prognosis of posterior reversible encephalopathy syndrome with spinal cord involvement (PRES-SCI).Methods:The clinical data of 1 patient with PRES-SCI admitted to the Department of Neurology of the First Affiliated Hospital of Zhengzhou University in November 2021 were analyzed, and the data of 38 patients with PRES-SCI reported in domestic and foreign databases and this patient were collected for pooled analysis.Results:The main clinical manifestations of 39 PRES-SCI patients (including this patient) included headache (79.5%, 31/39), visual disturbance (79.5%, 31/39), vomiting (46.2%, 18/39), disturbance of consciousness (38.5%, 15/39), limb weakness (28.2%, 11/39) and seizure (23.1%, 9/39). There were up to 97.4% (38/39) of patients who had significantly elevated blood pressure. The imaging feature was long-segment spinal cord lesion involving central gray matter. Approximately 89.7% (35/39) of the spinal cord lesions originated from the junction of the medulla oblongata and the cervical spinal cord. The median number of abnormal spinal cord segments corresponding to the vertebral body was 9 (the shortest was 4 and the longest was the entire spinal cord). Thirty-eight patients had brain lesions, and the most frequently involved sites were medulla oblongata (82.1%, 32/39), occipital lobe (46.2%, 18/39), pons (43.6%, 17/39), parietal lobe (41.0%, 16/39), and cerebellum (38.5%, 15/39). Among 38 patients completing the follow-up, 31 patients (81.6%) were clinically recovered.Conclusions:Posterior reversible encephalopathy syndrome could involve the spinal cord. For patients with long-segment spinal cord lesions and significantly increased blood pressure or other risk factors, PRES-SCI should be considered. Timely identification and treatment could make most patients recovery.

In 2019, preterm births (PTB) accounted for approximately 0.66 million deaths globally. PTB is also associated with a significantly higher risk of mortality and long-term complications for newborns. Long-term studies associated several factors, including disruption of immune tolerance and inflammation, with PTB. However, the pathogenesis of PTB remains unclear. Gonadal steroid hormones are critical for pregnancy maintenance and regulation of immune and inflammatory responses. However, it is not clear how unbalanced gonadal steroid hormones, such as imbalanced estrogen/androgen or estrogen/progesterone contribute to PTB. In this review, we discuss how gonadal steroid hormones mediate dysfunction in immune tolerance and inflammatory responses, which are known to promote the occurrence of PTB, and provide insight into PTB prediction.

Steroid hormones, including progestagens, estrogens, androgens, corticosteroids, and their precursor cholesterol, perform essential functions in the successful establishment and maintenance of pregnancy and normal fetal development. As the core endocrine organ at the prenatal stage, the human placenta is involved in the biosynthesis, metabolism, and delivery of steroid hormones. Steroidogenic pathways are tightly regulated by placenta-intrinsic cytochrome P450 and hydroxysteroid dehydrogenase. However, the relationship between placental steroidogenic enzyme expression and adverse pregnancy outcomes is controversial. In this review, we summarize the possible upstream regulatory mechanisms of placental steroidogenic enzymes in physiologic and pathophysiologic states. We also describe the human placental barrier model and examine the potential of single-cell sequencing for evaluating the primary functions and cellular origin of steroidogenic enzymes. Finally, we examine the existing evidence for the association between placental steroidogenic enzyme dysregulation and adverse pregnancy outcomes.

In 2019, preterm births (PTB) accounted for approximately 0.66 million deaths globally. PTB is also associated with a significantly higher risk of mortality and long-term complications for newborns. Long-term studies associated several factors, including disruption of immune tolerance and inflammation, with PTB. However, the pathogenesis of PTB remains unclear. Gonadal steroid hormones are critical for pregnancy maintenance and regulation of immune and inflammatory responses. However, it is not clear how unbalanced gonadal steroid hormones, such as imbalanced estrogen/androgen or estrogen/progesterone contribute to PTB. In this review, we discuss how gonadal steroid hormones mediate dysfunction in immune tolerance and inflammatory responses, which are known to promote the occurrence of PTB, and provide insight into PTB prediction.

Steroid hormones, including progestagens, estrogens, androgens, corticosteroids, and their precursor cholesterol, perform essential functions in the successful establishment and maintenance of pregnancy and normal fetal development. As the core endocrine organ at the prenatal stage, the human placenta is involved in the biosynthesis, metabolism, and delivery of steroid hormones. Steroidogenic pathways are tightly regulated by placenta-intrinsic cytochrome P450 and hydroxysteroid dehydrogenase. However, the relationship between placental steroidogenic enzyme expression and adverse pregnancy outcomes is controversial. In this review, we summarize the possible upstream regulatory mechanisms of placental steroidogenic enzymes in physiologic and pathophysiologic states. We also describe the human placental barrier model and examine the potential of single-cell sequencing for evaluating the primary functions and cellular origin of steroidogenic enzymes. Finally, we examine the existing evidence for the association between placental steroidogenic enzyme dysregulation and adverse pregnancy outcomes.

Objective:Utilizing multi-criterion optimization (MCO) technology to improve plan design quality based on knowledge-based planning (KBP) model.Methods:Fifty-five patients with nasopharyngeal carcinoma (NPC) who had completed radiotherapy were selected, and fixed-field intensity-modulated radiotherapy (IMRT) technology was used in each case. Among them, 40 cases were randomly selected as training set 1. Then, IMRT plans in training set 1 were preprocessed by MCO technology to construct a new training set 2. With the initial training set 1 and the processed training set 2 as training samples, the traditional KBP model and the MCO-KBP model refined by MCO technology were trained, respectively. Among the remaining 15 cases, 5 cases were randomly selected as the validation set, and the remaining 10 cases were used as the test set. After verification, the test set was used to statistically analyze the plan quality of the initial manual plan and the automatic plan generated by the traditional KBP model and the MCO-KBP model.Results:The target dose (D 95%) of plans generated by the traditional KBP model and the MCO-KBP model met the clinical requirements. Conformity index (CI) and homogeneity index (HI) were almost the same ( P>0.05), and the doses of organ at risk (OAR) of the automatic plans generated by the MCO-KBP model were lower than those of the traditional KBP model. For example, compared with the traditional KBP model, the average D max of the brainstem in the automatic plans generated by the MCO-KBP model was lower by 2.13 Gy, the average D mean of the left parotid gland was lower by 1.39 Gy, the average D mean of the right parotid gland was lower by 1.59 Gy, and the average D max of the left optic nerve was lower by 1.42 Gy, the average D max of the right optic nerve was lower by 1.16 Gy, and the average D max of the pituitary gland was lower by 1.88 Gy. All of the above-mentioned dosimetry indexes were statistically significant. Conclusion:Compared with the traditional KBP model, the IMRT plans designed by the refined MCO-KBP model have obvious advantages in the protection of OAR, which proves the feasibility of utilizing MCO technology to improve the plan design quality of the KBP model.