Background Gestational weight gain is closely related to maternal and infant health outcomes. Pregnant women are simultaneously exposed to four metals—lithium (Li), vanadium (V), uranium (U), and bismuth (Bi)—through inhalation of fine particulate matter and consumption of contaminated food and water. Existing studies suggest that exposure to these metals may be associated with gestational weight gain. However, no study has yet explored the complex relationships between exposure to mixtures of these four metals and weight gain at different stages of pregnancy. Objective To investigate the associations between mixed exposure to Li, V, U, and Bi in early pregnancy and the average weekly gestational weight gain during both early pregnancy and mid-to-late pregnancy. Methods This prospective study recruited eligible women in early pregnancy from an obstetrics clinic of a tertiary hospital in Jinan, China, between September 2021 and July 2023. Pre-pregnancy weight, current weight (at 11⁺⁰ to 13⁺⁶ weeks of gestation), and spot urine samples (≥5.0 mL) were collected at enrollment. Urinary concentrations of Li, V, Bi, and U were determined using inductively coupled plasma mass spectrometry. Participants were followed up in late pregnancy (≥28 weeks of gestation) to collect information on physical activity via questionnaire; weight measurements at the last antenatal visit (35⁺⁰ to 37⁺⁶ weeks of gestation) were obtained from the hospital information system. After adjusting for covariates, multiple linear regression and generalized additive models were used to assess the associations of individual metals with weekly weight gain in early pregnancy and in mid-to-late pregnancy. Bayesian kernel machine regression (BKMR) and quantile-based g-computation (Qgcomp) were applied to evaluate the joint effects of the metal mixture exposure on weekly weight gain at the two gestational stages. Results A total of 313 pregnant women were included. The geometric means of urinary Li, V, U, and Bi concentrations were 37.07, 0.20, 0.06, and 0.04 μg·L⁻¹, respectively; after creatinine adjustment, the corresponding values were 46.82, 0.25, 0.07, and 0.05 μg·g⁻¹ (Cr). The mean weekly gestational weight gain was (0.19±0.25) kg in early pregnancy and (0.53 ± 0.18) kg in mid-to-late pregnancy. Both multiple linear regression and generalized additive models showed that urinary V concentration was positively associated with average weekly gestational weight gain in early pregnancy, while no significant associations were found for other metals or for gestational weight gain in mid-to-late pregnancy. In the BKMR model with early-pregnancy weight gain as the outcome, V had the strongest association [posterior inclusion probability (PIP)=0.773]. When other metals were fixed at their medians, V showed a positive non-linear association with the outcome. A significant single-metal effect of V and its interaction with Li were observed. Compared with the 50th percentile of the metal mixture, the average weekly weight gain in early pregnancy increased by 0.016 (95%CI: 0.003, 0.029) and 0.018 (95%CI: 0.001, 0.036) at the 60th and 65th percentiles, respectively; conversely, at the 25th percentile, it decreased by 0.026 (95%CI: 0.002, 0.050). Overall, the joint effect of the metal mixture on early- pregnancy weight gain showed an upward trend. In the BKMR model for mid-to-late pregnancy gestational weight gain, all PIPs were<0.5, and no significant single-metal effects, interactions, or joint effects were identified. Qgcomp results confirmed a positive association between the metal mixture and early-pregnancy weight gain (b=0.031, 95%CI: 0.010, 0.051; P<0.01), with V contributing the highest positive weight (0.71). No significant association was found for weight gain in mid-to-late pregnancy (b=0.007, P=0.339). Conclusion Higher levels of co-exposure to the Li, V, Bi, and U metal mixture during early pregnancy may be associated with increased average weekly weight gain in early pregnancy. Among these metals, V exhibits a predominant role and appears to interact with Li. No association is observed between early-pregnancy metal mixture exposure and average weekly gestational weight gain in mid-to-late pregnancy. These findings suggest that monitoring and managing metal exposure during early pregnancy may be crucial for the rational regulation of gestational weight gain.

ObjectiveTo establish a mouse model of hypoxic pulmonary hypertension (HPH) through intermittent hypoxia induction, and to develop a comprehensive and reliable evaluation system for the HPH model, thereby providing experimental evidence for mechanistic studies and translational applications related to this disease. MethodsTwenty-four male specific pathogen-free (SPF) BALB/c mice were randomly divided into a control group and a model group, with 12 mice per group. Mice in the model group were placed in a hypobaric oxygen chamber control system to establish the HPH model, whereas mice in the control group received no intervention. After 28 days of modeling, a comprehensive evaluation of the pathophysiological characteristics of both groups was performed using a general condition scoring scale, echocardiography, hemodynamic measurements, blood gas analysis, hematological tests, organ coefficient determination, histopathological examination, and enzyme-linked immunosorbent assay (ELISA). In addition, correlation analyses were conducted among echocardiographic parameters, the contents of endothelin‑1 (ET‑1) and N‑terminal pro‑B‑type natriuretic peptide (NT‑proBNP) in lung tissue, and other measured indices. ResultsWith prolonged modeling duration time, body weight, water intake, and activity level of mice in the model group were significantly decreased compared with the control group (P<0.05). Echocardiography showed that, compared with the control group, the model group exhibited increased right ventricular dimensions (P<0.01), right ventricular anterior wall thickening (P<0.01), and widened main pulmonary artery diameter (P<0.01), whereas the peak systolic velocity across the pulmonary valve, tricuspid annular plane systolic excursion, and peak systolic velocity of the tricuspid annulus were significantly decreased (P<0.001); tricuspid regurgitation was observed in some model animals. Hemodynamic results revealed that right ventricular systolic pressure was elevated in the model group compared with the control group (P<0.001). Blood gas analysis showed that pH, partial pressure of oxygen, oxygen saturation, actual bicarbonate, and total carbon dioxide were all decreased in the model group compared with the control group (P<0.01). Hematological indices demonstrated that lymphocyte counts (P<0.05) and reticulocyte counts (P<0.001) were decreased in the model group compared with the control group. Compared with the control group, the organ coefficients of heart and lung in the model group were significantly increased (P<0.05 and P<0.001). Pathological examination revealed that the right ventricular hypertrophy index was significantly increased in the model group (P<0.001), with varying degrees of damage to the right ventricle, pulmonary artery, and pulmonary vessels; both the pulmonary artery wall thickness percentage and the pulmonary wall area percentage were significantly elevated (P<0.001). ELISA results showed that the levels of ET‑1 and NT‑proBNP in lung tissues were significantly increased in the model group compared with the control group (P<0.05 and P<0.001, respectively). Correlation analysis indicated that some echocardiographic parameters were highly correlated with multiple indices in the development of HPH (P<0.05). ConclusionEchocardiography can accurately assess a series of hemodynamic changes in HPH, including right ventricular structural, functional impairment, and pulmonary hypertension. Laboratory tests not only help verify whether the model has been successfully established, but also provide deeper insights into the pathogenesis of HPH, evaluate the effects of interventions, and offer scientific evidence for clinical outcomes. Pathological examination can further confirm the alterations in pulmonary vascular remodeling and increased right heart load. This multimodal analysis provides a reliable animal model and evaluation paradigm for both basic and translational research on HPH, and is of great significance for exploring disease mechanisms and developing precision therapeutic strategies.

ObjectiveTo investigate the effects of Liuwei Dihuangwan on mammalian target of rapamycin （mTOR）-mediated synaptic plasticity in the prefrontal cortex-hippocampus circuit in the rat model of valproic acid （VPA）-induced autism spectrum disorder （ASD） and to explore its potential mechanism for reducing behavioral abnormalities in ASD rats. MethodsThirteen SD pregnant rats were randomized into the VPA group （10 rats） and the control group （3 rats）. On gestational day 13， the VPA group was intraperitoneally injected with VPA solution （600 mg·kg^-1）， while the control group was injected with an equal volume of normal saline. Male pups of 21 days old from both groups underwent behavioral tests to screen the ASD model rats （32 rats）. These rats were then randomly assigned to the model （distilled water）， vitamin D （1 480 U·kg^-1）， low-dose （0.75 g·kg^-1） Liuwei Dihuangwan， and high-dose （1.5 g·kg^-1） Liuwei Dihuangwan groups， and normal male pups were selected as the blank group （distilled water）， with 8 rats in each group. Each group was treated with the corresponding drug or an equal volume of distilled water via gavage daily. After drug administration， behavioral tests were conducted again， followed by anesthesia and tissue collection. Nissl staining was carried out to observe the morphological changes of neurons in the prefrontal cortex and hippocampus. Transmission electron microscopy was used to observe changes in hippocampal synaptic structure. Immunohistochemistry and Western blot were employed to determine the expression of mTOR， phosphatidylinositol 3-kinase （PI3K）， and protein kinase B （Akt） in the prefrontal cortex， as well as synaptophysin-1 （SYP-1）， postsynaptic density 95 （PSD95）， and N-methyl-D-aspartate receptors （NMDARs） in the hippocampus. ResultsCompared with the control group， the model group exhibited severe growth retardation and developmental deformities， with abnormal behavioral performance and pathological damage to neurons and synapses in the prefrontal cortex and hippocampus. Compared with the model group， all treatment groups showed reduced behavioral abnormalities and pathological damage to neurons and synapses in the prefrontal cortex and hippocampus， with the most significant effects in the high-dose Liuwei Dihuangwan group. Immunohistochemistry and Western blotting results showed that compared with the control group， the model group exhibited significantly increased protein levels and phosphorylation ratios of p-mTOR， p-Akt， and p-PI3K in the prefrontal cortex （P<0.05， P<0.01）， and decreased protein levels of SYP-1 and PSD95 and increased protein level of NMDARs in the hippocampus （P<0.01）. Compared with those in the model group， the protein levels of p-mTOR， p-Akt， and p-PI3K in the prefrontal cortex decreased in the vitamin D and high-dose Liuwei Dihuangwan groups （P<0.05）， and the p-mTOR/mTOR， p-Akt/Akt， and p-PI3K/PI3K ratios in the prefrontal cortex declined in the vitamin D group （P<0.05）. The high-dose Liuwei Dihuangwan group showed a reduction in p-PI3K/PI3K ratio （P<0.05）. The protein level of SYP-1 and PSD95 in the hippocampus increased in the vitamin D， low-dose Liuwei Dihuangwan， and high-dose Liuwei Dihuangwan groups （P<0.05， P<0.01）， while the protein level of NMDARs decreased in the vitamin D and high-dose Liuwei Dihuangwan groups （P<0.01）. ConclusionLiuwei Dihuangwan significantly reduces VPA-induced ASD-like behaviors and enhances the regeneration and repair of neurons in the prefrontal cortex and synaptic structures in the hippocampus by downregulating of PI3K/Akt/mTOR expression in the prefrontal cortex， upregulating SYP-1 and PSD95 expression in the hippocampus， and inhibiting NMDARs expression.

From July 22 to 24, 2026, the 2nd International Symposium on Environment and Reproductive Health and the 20th National Postgraduates Symposium on Environmental and Occupational Medicine were successfully held in Shanghai. The conference brought together experts, scholars, young researchers, and graduate students from Harvard University, National University of Singapore, Chinese University of Hong Kong, Peking University, Fudan University, Shanghai Jiao Tong University, and other domestic and foreign universities and scientific research institutions to carry out in-depth exchanges on cutting-edge issues such as environment and reproductive health, environmental exposure and health effects, occupational health, disease risks, and toxicological mechanisms. The conference featured a main hall, multiple sessions, an editorial board memebers & experts forum, excellent paper reports, a postgraduate parallel forum, and keynote presentations. This postgraduate symposium, themed "Research and practice: Healing the schism", attracted a total of 113 papers. This year marked the first time that the National Postgraduates Symposium on Environmental and Occupational Medicine was jointly held with an international academic conference. It further expanded the high-level platform for academic exchange and young talent cultivating, and promoted the deep integration of scientific research innovation, achievement dissemination, and public health practice.

Objective To observe the repair effect and mechanism of Danhuang Powder-containing serum on high glucose-induced vascular endothelial cell injury.Methods Danhuang Powder-containing serum was prepared.Human umbilical vein endothelial cells(HUVECs)were cultured to be divided into control group,recombinant human epidermal growth factor(called"growth factor"for short)group,Danhuang Powder group,high glucose group,high glucose+growth factor group,and high glucose+Danhuang Powder group.After corresponding intervention in each group for 48 hours,the cell ultrastructure and autophagy were observed under transmission electron microscope,apoptosis was detected by flow cytometry,and the protein expression levels of vascular endothelial growth factor(VEGF),epidermal growth factor(EGF)and basic fibroblast growth factor(bFGF)in the cells were detected by Western Blot.Results(1)The intra-mitochondrial ridges in the control group were clearly visible,autophagosomes and autolysosomes were fewer;mitochondria in the high glucose group were swollen and irregular,and appeared vacuolated;and the more typical autophagy-like structures were seen in the high glucose+Danhuang Powder group.(2)Compared with the high glucose group and high glucose+growth factor group,the apoptosis rate of cells in the high glucose+Danhuang Powder group was significantly decreased(P<0.05).(3)Compared with the high glucose group and the high glucose+growth factor group,the protein expression levels of VEGF,EGF and bFGF in the cells of the high glucose+Danhuang Powder group were significantly increased(P<0.05).Conclusion Danhuang Powder-containing serum can reduce the high glucose-induced damage in HUVEC cells,and its mechanism may be related to the activation of mitochondrial autophagy,and the inhibition of apoptosis,as well as the up-regulation of the expression of VEGF,EGF and bFGF.

Hepatocellular carcinoma(HCC)expresses abundant glycolytic enzymes and displays comprehensive glucose metabolism reprogramming.Aldolase A(ALDOA)plays a prominent role in glycolysis;however,little is known about its role in HCC development.In the present study,we aim to explore how ALDOA is involved in HCC proliferation.HCC proliferation was markedly suppressed both in vitro and in vivo following ALDOA knockout,which is consistent with ALDOA overexpression encouraging HCC prolifera-tion.Mechanistically,ALDOA knockout partially limits the glycolytic flux in HCC cells.Meanwhile,ALDOA translocated to nuclei and directly interacted with c-Jun to facilitate its Thr93 phosphorylation by P21-activated protein kinase;ALDOA knockout markedly diminished c-Jun Thr93 phosphorylation and then dampened c-Jun transcription function.A crucial site Y364 mutation in ALDOA disrupted its interaction with c-Jun,and Y364S ALDOA expression failed to rescue cell proliferation in ALDOA deletion cells.In HCC patients,the expression level of ALDOA was correlated with the phosphorylation level of c-Jun(Thr93)and poor prognosis.Remarkably,hepatic ALDOA was significantly upregulated in the promotion and progression stages of diethylnitrosamine-induced HCC models,and the knockdown of Aldoa strikingly decreased HCC development in vivo.Our study demonstrated that ALDOA is a vital driver for HCC development by activating c-Jun-mediated oncogene transcription,opening additional avenues for anti-cancer therapies.

Objective:To study the anti-inflammatory and protective effects of electroacupuncture on rats with cardiopulmo-nary resuscitation based on cholinergic anti-inflammatory pathway(CAP).Methods:Sixty male SD rats were randomly divided into sham operation group(Sham group),cardiopulmonary resuscitation group,electroacupuncture group,antagonist of α7-nicotinic ace-tylcholine receptor(α7nAChR)α Bungarus toxin group(αBGT group,1 μg/kg)and agonist of α7nAChR 3-(2,4-dimethoxybenzyli-dene)anabaseine(GTS-21)group(5 mg/kg),with 12 rats in each group.Model of cardiac arrest was established by inducing ventric-ular fibrillation in rats with percutaneous epicardial electrical stimulation,and routine resuscitation was performed,the defibrillation times,cardiopulmonary resuscitation duration and 72 h survival rate of rats in each group were observed and recorded.Neurological damage of rats in each group was scored(NDS score).Levels of inflammatory factors TNF-α,IL-1β and IL-6 in serum,heart,lung and brain of rats were measured by ELISA.HE staining was applied to evaluate the degree of tissue damage of heart,lung and brain tis-sues of rats in each group.Expressions of α7nAChR,NF-κB/MAPKs signal pathway related proteins in heart,lung and brain of rats in each group were detected by Western blot.Results:Compared with Sham group,the number of defibrillations,duration of cardiopul-monary resuscitation,NDS score,levels of TNF-α,IL-1β and IL-6 in serum,heart,lung and brain tissues,and NF-κB p65 protein in heart,lung and brain tissues in cardiopulmonary resuscitation group increased greatly(P<0.05),the 72 h survival rate,phosphory-lation levels of α7nAChR protein,ERK1/2,JNK and p38MAPK in heart,lung and brain tissues decreased greatly after restoration of spontaneous circulation(P<0.05),cells and neurons in the CA1 region of heart,lung and hippocampus were severely damaged.Com-pared with cardiopulmonary resuscitation group,change trend of relevant indicators in electroacupuncture group was opposite to the above,damage of cells and neurons in rat heart,lung and brain tissue was reduced(P<0.05).αBGT reduced the anti-inflammatory effect of electroacupuncture on cardiopulmonary resuscitation rats(P<0.05).GTS-21 enhanced the anti-inflammatory protection of electroacupuncture on cardiopulmonary resuscitation rats(P<0.05).Conclusion:Electroacupuncture has anti-inflammatory and pro-tective effects on cardiopulmonary resuscitation rats based on CAP,and NF-κB/MAPKs participate in α7nAChR mediated CAP.

Objective:To explore the characteristics of potential categories of chronic disease co-morbid patients' learned helplessness, and to analyze the differential characteristics of different categories of chronic disease co-morbid patients.Methods:Convenience sampling method was used to select patients with chronic disease co-morbidities who attended The NO.1 People's Hospital of Xiangyang, Hubei University of Medicine, from June to December 2023 as survey respondents. General information questionnaire, Learned Helplessness Scale, Health Questionnaire Somatic Symptom Cluster Scale, Kessler Psychological Distress Scale, and Comprehension Social Support Scale were used for the cross-sectional survey. The potential profile of learned helplessness, and the influencing factors of potential categories of learned helplessness was analyzed.Results:A total of 810 patients with chronic co-morbidities were investigated. There were 453 males and 357 females, aged (65.03±10.89) years old. The learned helplessness of these patients was categorized into three different potential categories, which were named as low-level learned helplessness group, medium-level learned helplessness group, high-level learned helplessness, accounting for 17.5% (142/810), 23.5% (190/810), and 59.0% (478/810), respectively. Compared with the low-level learned helplessness group, the probability of belonging to the medium-level learned helplessness group and high-level learned helplessness group was higher for patients with chronic co-morbidities with more severe physical symptoms ( OR=1.456, 1.391, both P<0.01). Compared with the low-level learned helplessness group, the probability of belonging to the medium-level learned helplessness group and high-level learned helplessness group was higher for patients with chronic co-morbidities with more severe the psychological distress ( OR=1.359, 1.917, both P<0.01). Compared with the low-level learned helplessness group, the probability of belonging to the medium-level learned helplessness group and high-level learned helplessness group was higher for patients with chronic co-morbidities with lower levels of social support ( OR=0.928, 0.874, both P<0.01). Compared with the low-level learned helplessness group, patients with a duration of illness >5 years were used as controls, patients with a duration of illness 2-5 years were more likely to belong to the medium-level learned helplessness group and high-level learned helplessness group ( OR=74.586, 62.620, both P<0.01). Compared with the low-level learned helplessness group, patients with neutral personalities were compared, patients with extroverted personalities had a lower probability of belonging to the medium-level learned helplessness group ( OR=0.105, P<0.05), while patients with introverted personalities had a lower probability of belonging to the medium-level learned helplessness group and high-level learned helplessness group ( OR=0.052, 0.046, both P<0.01). Conclusions:Patients with chronic disease co-morbidities have higher levels of learned helplessness during disease treatment and have more distinctive categorical characteristics. Healthcare professionals should adopt targeted nursing interventions according to different categories of chronic disease co-morbid patients to reduce the level of learned helplessness.

Objective:To explore the relationship between autistic trait and pain empathy among college students, as well as the mediating role of personal pain perception.Methods:From October to December 2023, a cross-sectional survey was conducted among 1 195 college students using the autism spectrum quotient, pain sensitivity questionnaire, fear of pain questionnaire, pain catastrophizing scale and empathy for pain scale.SPSS 27.0 software was used for descriptive statistics and correlation analysis.A structural equation model was constructed using Mplus 8.3 to examine the mediating effect of personal pain perception, which was composed of pain sensitivity, fear and catastrophizing cognition.Results:Autistic trait(22.00(18.00, 26.00))was significantly positively correlated with pain sensitivity (55.00(43.00, 70.00)), fair of pain (69.00(60.00, 78.00)), and pain catastrophizing cognition (16.00(8.00, 23.00)) ( r=0.112, 0.154, 0.204, all P<0.001).Autistic trait was also significantly positively correlated with affective distress(62.00(46.00, 80.00), r=0.162, P<0.001) and vicarious pain (14.00(8.00, 20.00), r=0.096, P<0.001) of pain empathy.Pain sensitivity, fear of pain and pain catastrophizing cognition were significantly positively correlated with affective distress( r=0.244, 0.332, 0.375, all P<0.001) and vicarious pain ( r=0.210, 0.232, 0.285, all P<0.001) of pain empathy.The effects of autistic trait on affective distress and vicarious pain dimensions of pain empathy were fully mediated by personal pain perception, with the mediating effects of 0.115( P<0.001, 95% CI=0.073-0.165) and 0.085( P<0.001, 95% CI=0.053-0.124). Conclusions:The autistic trait of college students can predict the affective distress and vicarious pain of pain empathy indirectly through personal pain perception.

Objective:To summarize the clinical characteristics, diagnostic and therapeutic approaches, and prognosis of posttransplant lymphoproliferative disease (PTLD) following kidney transplantation.Methods:A retrospective case series analysis was conducted on 7 PTLD patients after kidney transplantation treated in the Department of Transplant Oncology, Tianjin First Central Hospital between January 2018 and December 2023. Clinical features, laboratory findings, imaging and pathological characteristics, treatment modalities, and outcomes were analyzed.Results:Among 7 PTLD patients, there were 5 male and 2 females with a median age of 41 (17-65) years. The median time of onset after operation was 4 (0.5-11) years. Among them, 2 patients had early onset (<1 year post-transplantation) and 5 patients had late onset (>1 year). The clinical manifestations included abdominal mass in 4 cases, anemia in 4 cases, fever in 3 cases, lymphadenopathy in 4 cases, gastrointestinal bleeding in 1 case, abdominal pain in 2 cases, and intestinal obstruction in 2 cases. Pathological types included diffuse large B-cell lymphoma in 4 cases, Burkitt lymphoma in 1 case, marginal zone lymphoma in 1 case, and polymorphic PTLD in 1 case. Reducing the immunosuppressant level was the basal treatment plan, and rituximab, chemotherapy, surgery, radiotherapy and CD19-targeted chimeric antigen receptor therapy were given according to the pathological classification. Until the date of submission, 2 patients had died, 4 had a complete response, and 1 had a partial response. None of the patients had acute rejection, and 1 patient had chronic renal insufficiency.Conclusions:PTLD after kidney transplantation presents with nonspecific manifestations, necessitating prompt imaging and histopathological evaluation for definitive diagnosis. At the same time, a series of measures should be given to improve the prognosis, including discontinuous use of anti-metabolic drugs, dosage decline of calcitric phosphatase inhibitor by 50% or convert it to sirolimus treatment, and corresponding treatment according to the specific conditions of the recipient.