Reproductive toxicology最新文献

{"title":"The role of ATG7-mediated ferroptosis in formaldehyde-induced ovarian injury in rats.","authors":"Kun Mao, Hao-Zhe Yan, Jia-Qi Yang, Zi-Xin Yin, Xin-Qi Gao, Hao-Fu Liu, Heng Su, Yuan-Yuan Geng, Pan Ge, Dang-Xia Zhou","doi":"10.1016/j.reprotox.2025.108902","DOIUrl":"https://doi.org/10.1016/j.reprotox.2025.108902","url":null,"abstract":"<p><strong>Background: </strong>To investigate the mechanisms of toxicological damage of formaldehyde to the female reproductive system METHODS: A Mendelian randomization method was used to predict a causal relationship between ferroptosis genes and female infertility. Changes in the structure and function of rat ovaries were observed by HE staining and transmission electron microscopy. Combined with molecular experiments, we verified the alterations of GSH, iron ions, MDA levels, and the expression of ferroptosis genes.</p><p><strong>Results: </strong>Mendelian randomization suggested a significant causal relationship between ATG7 and female infertility. Animal experiments showed that formaldehyde caused abnormal follicular maturation and ovarian mitochondrial alterations. Meanwhile, formaldehyde induced elevated levels of iron ions and MDA and decreased GSH levels. Further detection by Western blotting and qRT-PCR revealed that the expression of the ferroptosis marker gene GPX4 decreased and ATG7 increased in the ovary after formaldehyde stimulation.</p><p><strong>Conclusions: </strong>Formaldehyde affected the structure and physiological function of rat ovary by activating the expression level of ATG7 and inhibiting the activity of GPX4, which caused iron overload and elevated levels of peroxides, leading to the occurrence of ferroptosis in ovarian tissue.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108902"},"PeriodicalIF":3.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143754355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uteroplacental adaptations to an altered gestational environment: Advances in clinical, animal model and in vitro studies.","authors":"Jayanth Ramadoss, Michael C Petriello, Madhu Chauhan","doi":"10.1016/j.reprotox.2025.108900","DOIUrl":"10.1016/j.reprotox.2025.108900","url":null,"abstract":"","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108900"},"PeriodicalIF":3.3,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TERT's protective effect on trophoblast cells: Reducing mitochondrial ROS","authors":"Zongyuan Tian,&nbsp;Xueran Wang,&nbsp;Yingyi Luan,&nbsp;Ruixia Liu","doi":"10.1016/j.reprotox.2025.108899","DOIUrl":"10.1016/j.reprotox.2025.108899","url":null,"abstract":"<div><h3>Objective</h3><div>The principal objective of this project is to elucidate the ameliorating function of telomerase reverse transcriptase (TERT) on placental trophoblast dysfunction and its associated mitochondrial dysfunction.</div></div><div><h3>Methods</h3><div>We utilised 50 μM hydrogen peroxide (H₂O₂) to induce an oxidative stress model in HTR-8/SVneo cells (NC group and OS group), subsequently establishing three experimental conditions via lentiviral transfection: untreated controls (Con group), TERT-overexpressing cells (OE group), and empty vector-transfected negative cells (Neg group). In order to explore the role of mitochondrial TERT, we employed the Src kinase familyinhibitor PP1 (4-Amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-<em>d</em>]pyrimidine), a cell-permeable small molecule specifically blocking the translocation of TERT in HTR-8/SVneo cells with overexpressed TERT. We established four experimental conditions: untreated overexpression group (OE group), H₂O₂-stimulated group (OS group), co-treatment group of H₂O₂ and PP1 (PP1 OS group), and PP1 treatment group alone (PP1 group). The expression and localization of TERT were analysed via qRT-PCR, immunofluorescence, and Western blotting. In addition, the cellular functions (viability, migration, invasion) were assessed using CCK-8, Calcein AM/PI staining, wound healing assay and Transwell assay. Mitochondrial integrity was thoroughly assessed using a mitochondrial membrane potential assay, an ATP content assay, a mtDNA copy number quantification and a mitochondrial morphology assay.</div></div><div><h3>Results</h3><div>The OE group demonstrated significantly reduced reactive oxygen species (ROS) levels compared to Con and Neg groups, accompanied by enhanced cellular viability and improved migratory and invasive capacities. Mitochondrial functional analyses revealed superior outcomes in the OE group, including stabilized mitochondrial membrane potential and ATP production, maintained mtDNA copy numbers, and preserved mitochondrial ultrastructure. Conversely, pharmacological inhibition with PP1 - a Src kinase family inhibitor that blocks TERT mitochondrial translocation - effectively abolished these protective effects. PP1-treated cells exhibited exacerbated oxidative stress, impaired cell viability, and diminished motility, confirming the essential role of mitochondrial-localized TERT in cellular homeostasis.</div></div><div><h3>Conclusions</h3><div>Elevated mitochondrial TERT levels were able to effectively mitigate the cellular functional damage induced by elevated ROS levels by maintaining mitochondrial stability. The above findings provide a theoretical basis for the development of intervention strategies for pregnancy-related disorders based on the regulation of mitochondrial TERT function.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"134 ","pages":"Article 108899"},"PeriodicalIF":3.3,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143696041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal exposure to phenanthrene impairs spermatogenesis and fertility by elevating apoptosis, altering gene expression, and disrupting steroidogenesis in adult male mice across two generations","authors":"Azar Afshar ,&nbsp;Hamid Nazarian ,&nbsp;Fatemeh Fadaefathabadi ,&nbsp;Reza Mastery-Farahani ,&nbsp;Fakhroddin Aghajanpour ,&nbsp;Reza Soltani ,&nbsp;Maryam Salimi ,&nbsp;Mohsen Nourozian ,&nbsp;Gholamreza Hassanzadeh","doi":"10.1016/j.reprotox.2025.108897","DOIUrl":"10.1016/j.reprotox.2025.108897","url":null,"abstract":"<div><h3>Background</h3><div>Phenanthrene, a polycyclic aromatic hydrocarbon, can enter the human body via various routes and affect reproductive health. Its low molecular weight enables its transfer from the mother to the fetus. However, comprehensive research on its effects on reproductive system development is lacking. This study aimed to examine the impacts of prenatal phenanthrene exposure on the reproductive systems of both the immediate offspring and their progeny.</div></div><div><h3>Methods</h3><div>Pregnant mice were divided into three groups: control, sham, and phenanthrene. From the detection of the vaginal plug until pregnancy day 18, mice in the phenanthrene group were administered phenanthrene solution (60 μg/kg), while sham mice received corn oil on alternate days. Following birth, male offspring were maintained without intervention until PND56. After puberty, a portion of these males were bred, while others were euthanized for histological and molecular analyses. The subsequent generation was born and developed under standard conditions without intervention, and underwent procedures similar to those of the first generation.</div></div><div><h3>Results</h3><div>The study revealed that exposure to phenanthrene during fetal development, across two consecutive generations, led to a reduction in the expression of genes associated with mitosis and meiosis, while simultaneously increasing the rate of cell death. Additionally, the research found that a decline in Leydig cells resulted in decreased serum testosterone levels, which subsequently led to diminished quality and quantity of sperm.</div></div><div><h3>Conclusion</h3><div>Prenatal phenanthrene exposure, by disrupting gene expression and steroidogenesis, causes impaired testicular tissue function, reduced spermatogenesis, and ultimately reduced male fertility rates in the F1 and F2.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"134 ","pages":"Article 108897"},"PeriodicalIF":3.3,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanisms associated with embryotoxic effects of heavy metals in the Sea Urchin","authors":"Carlos E. Escárcega-González ,&nbsp;Eduardo Hernández-Cuellar ,&nbsp;Fabián D. Ruiz Esparza-Juárez ,&nbsp;Jesús Chávez-Reyes","doi":"10.1016/j.reprotox.2025.108898","DOIUrl":"10.1016/j.reprotox.2025.108898","url":null,"abstract":"<div><div>The sea urchin embryo model has become a classic model for studying the harmful effects of heavy metals and the molecular responses associated with exposure to these pollutants. In this context, several biochemical pathways have been associated with exposure to heavy metals in sea urchin embryos, such as autophagy, apoptosis, oxidative stress, activation of heat shock proteins, and induction of metallothioneins. These biochemical pathways are activated or altered in embryos after exposure to heavy metals; therefore, this review provides a comprehensive literature exploration, summarizing the main biochemical changes observed in sea urchin embryos following exposure to certain heavy metals, such as cadmium, gadolinium, arsenic, manganese, zinc, mercury, copper, nickel, and lead.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"134 ","pages":"Article 108898"},"PeriodicalIF":3.3,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Use of the alternative test R-FETAX (Refined-Frog Embryo Teratogenicity Assay-Xenopus) to evaluate the Fetal Alcohol Spectrum Disorders (FASD)","authors":"M. Battistoni ,&nbsp;F. Di Renzo ,&nbsp;F. Metruccio ,&nbsp;R. Bacchetta ,&nbsp;E. Menegola","doi":"10.1016/j.reprotox.2025.108896","DOIUrl":"10.1016/j.reprotox.2025.108896","url":null,"abstract":"<div><div>Fetal Alcohol Spectrum Disorders (FASD) refer to a range of conditions in children caused by alcohol consumption during pregnancy, including morphological defects, developmental delays, and neurobehavioral impairments. Ethanol (EtOH) at high concentrations (1–3 % v/v) was shown to induce malformations and lethality in <em>Xenopus laevis</em> embryos exposed throughout the FETAX test (from the mid-blastula stage to the final pre-feeding larval stage). The aim of this work was to evaluate multiple morphological and neurobehavioral effects of EtOH exposure (0.1–3 % v/v) using the R-FETAX protocol. Embryos obtained through natural mating were exposed during specific developmental windows: the organogenetic period (sensitive to morphological abnormalities) and the neurodevelopmental window (sensitive to behavioral alterations). Additional groups were exposed either throughout the entire test duration (classical FETAX exposure) or for a brief 4-hour period before the end of the test (acute exposure). Lethality was monitored over the six-day test period. At the conclusion of the test, a functional deglutition test was performed, and external gross morphology as well as developmental delays (FETAX-score method) were assessed. Neurobehavioral swimming test was conducted only on tadpoles considered normal at gross morphological evaluation. Dose-response relationships were modeled using PROAST software to derive benchmark dose levels, with response set at levels used as points of departure for risk assessment. The findings demonstrated dose- and stage-specific effects that mimic FASD symptoms observed in humans. These results emphasize that no amount of alcohol exposure can be considered safe during development.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"134 ","pages":"Article 108896"},"PeriodicalIF":3.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143644161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zebrafish embryos as a teratogenicity screening tool to reduce potential birth defects","authors":"Zongyu Miao ,&nbsp;Jing Yang ,&nbsp;Lei Cai ,&nbsp;Zhenlie Huang ,&nbsp;Erping Yan ,&nbsp;Jinghui Peng ,&nbsp;Xueping Chen ,&nbsp;Jinping Cheng","doi":"10.1016/j.reprotox.2025.108895","DOIUrl":"10.1016/j.reprotox.2025.108895","url":null,"abstract":"<div><div>Teratogens play a crucial role in the development of birth defects, making effective screening vital for prevention and management. This study aimed to develop an optimized zebrafish embryo-based platform for teratogenicity screening and further evaluate its findings with established clinical and animal data. Zebrafish embryos [6–8 h post-fertilization (hpf)] were exposed to 19 different test solutions, including nine known teratogens and ten non-teratogens, in 96-well plates, and mortality and morphological abnormalities were assessed at 48, 72, and 96 hpf. The half-lethal concentration (LC₅₀) and half-effective concentration (EC₅₀) were calculated from the counts of dead and abnormal embryos, respectively. The teratogenicity index (TI), defined as LC₅₀/EC₅₀, was used to classify the chemicals. Of the tested compounds, eight were identified as teratogenic, nine as non-teratogenic, and two outliers due to solubility constraints in this assessment. Notably, extending the exposure duration to 96 hpf provided a more accurate assessment of teratogenicity compared to shorter exposures. Eight teratogenic substances exhibited a TI greater than 3, while (-)-thalidomide did not yield a definitive TI due to low solubility. Among the non-teratogenic chemicals, nine had a TI below 3, with ajmaline also lacking a precise TI due to solubility constraints. These findings suggest that using a 6–8 hpf to 96 hpf exposure window and establishing a TI threshold of 3 can facilitate reliable teratogenicity risk assessment. Furthermore, the phenotypes observed in zebrafish embryos were consistent with typical teratogenic malformations documented in clinical and animal studies. This study demonstrates that the refined zebrafish embryo teratogenicity testing method coupled with the TI, can be an effective tool for assessing teratogenic risk.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"134 ","pages":"Article 108895"},"PeriodicalIF":3.3,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143650101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bisphenol AF induces cell cycle arrest and apoptosis in TM3 Leydig cells via the p53 signaling pathway","authors":"Chenlu Li ,&nbsp;Haolong Luo ,&nbsp;Mengyuan Chen ,&nbsp;Fuxing Lin ,&nbsp;Xiangmei Ren ,&nbsp;Yefei Huang ,&nbsp;Li Zhou","doi":"10.1016/j.reprotox.2025.108882","DOIUrl":"10.1016/j.reprotox.2025.108882","url":null,"abstract":"<div><div>Bisphenol AF (BPAF), one of the most common bisphenol analogues, has been reported to exhibit higher estrogenic activity compared to bisphenol A (BPA) due to the presence of additional hydrophobic groups. To comprehensively understand the male reproductive toxicity of BPAF, TM3 Leydig cells were used to investigate the effects of BPAF on cell proliferation, apoptosis, and cell cycle arrest. The underlying mechanisms of cellular responses induced by BPAF were examined through analysis of target mRNA and protein expression. Results showed that BPAF treatment reduced cell viability and induced both G2/M cell cycle arrest and apoptosis in a time- and dose-dependent manner in TM3 Leydig cells. RNA sequencing analysis and experimental verification further revealed that the p53 signaling pathway was involved in BPAF-induced cytotoxicity. Furthermore, Pifithrin-α (PFT-α), a p53 inhibitor, attenuated BPAF-induced G2/M cell cycle arrest and apoptosis. These results demonstrate that the p53 signaling pathway mediates BPAF-induced cell cycle arrest and apoptosis in Leydig cells, providing mechanistic insights into BPAF’s toxicological effects on the male reproductive system.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"134 ","pages":"Article 108882"},"PeriodicalIF":3.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"1-(N-methyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal exposure induces testicular toxicity in male mice","authors":"Huage Liu","doi":"10.1016/j.reprotox.2025.108881","DOIUrl":"10.1016/j.reprotox.2025.108881","url":null,"abstract":"<div><div>Thirdhand smoke (THS), a residual cigarette smoke still remaining in indoor environment long after active smoking has ceased, has aroused more and more people’s attention on health. However, the impact of THS exposure on the male reproductive system, particularly in in-vivo study, remain unclear. Thus, this study aims to investigate the adverse effects of 1-(N-methyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal (NNA), a special component in THS, on testis. Herein, adult ICR mice were orally administered diluted dimethylsulfoxide (control), 0.075 μg/kg and 0.15 μg/kg NNA for 10 weeks. The findings revealed that NNA exposure, especially in 0.15 μg/kg dosage, significantly reduced the epithelium height and tubular area within the testis. Transcriptomic analysis indicated that NNA exposure interfered with the expression of genes associated with oxygen transport and oxygen binding processes, such as <em>Hbb-bs</em>, the downregulation of which also led to oxidative damage. Additionally, NNA exposure induced oxidative damage in testis by decreased levels of SOD and GSH enzymes, along with an increase in MDA level. In summary, our results demonstrate that NNA exposure causes impaired testicular structure and oxidative damage, indicating its testicular toxicity. This finding not only implies the detrimental effect of NNA on male reproduction, but also provides a fundamental basis for further research on the impact of THS exposure on male reproductive health.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"133 ","pages":"Article 108881"},"PeriodicalIF":3.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143561876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low-level exposure to environmental lithium element affects male reproductive outcomes: Results from the MARHCS cohort study in Chongqing, China and in vivo animal experiments","authors":"Lihong Wang ,&nbsp;Guanghui Zhang ,&nbsp;Xi Ling ,&nbsp;Mei Wan ,&nbsp;Qing Chen ,&nbsp;Lei Sun ,&nbsp;Huan Yang ,&nbsp;Tong Wang ,&nbsp;Jinyi Liu ,&nbsp;Jia Cao ,&nbsp;Lin Ao ,&nbsp;Peng Zou","doi":"10.1016/j.reprotox.2025.108875","DOIUrl":"10.1016/j.reprotox.2025.108875","url":null,"abstract":"<div><div>This study examined the effects of lithium exposure at environmental levels on semen quality and sex hormone levels. Questionnaires and biological samples were collected from 582 college students recruited in Chongqing, China. Sex hormones and semen parameters were measured by ELISA and CASA, respectively. Sperm telomere length and mitochondrial DNA copy number were determined using real-time Q-PCR. Lithium levels were quantified by ICP-MS. In addition, C57BL/6 mice were administered lithium chloride at doses within the range of environmental levels (LiCl; 0, 4.3, 12.8, and 38.4 mg/kg) for 35 days, and the expression of key proteins involved in testosterone synthesis was detected by western blot assay. In the population study, the median lithium levels in urine and seminal plasma were 18.80 and 5.38 μg/L, respectively. Each interquartile range increase of lithium levels in both urine and seminal plasma were associated with decreased serum testosterone (−2.47 %, 95 % CI: −4.52 %, −0.38 % for urine; −2.67 %, 95 % CI: −4.79 %, −0.50 % for seminal plasma) and progesterone (−6.38 %, 95 % CI: −11.09 %, −1.42 % for urine; −8.78 %, 95 % CI: −13.20 %, −4.04 % for seminal plasma). Mice treated with the highest LiCl dose (38.4 mg/kg) had significantly lower sperm motility, sperm concentration, and testosterone, progesterone, estradiol, and prolactin levels than mice in the control group (all <em>p</em> &lt; 0.05), and their Leydig cells showed marked mitochondrial vacuolation and swelling. These results support that environmental lithium exposure leads to decreased semen quality and testosterone by impairing Leydig cells.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"134 ","pages":"Article 108875"},"PeriodicalIF":3.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}