Toxicology and Industrial Health最新文献

{"title":"The history of the Toxicology Roundtable-75 years of scientific discussion.","authors":"David G Serota, Christopher N Papagiannis","doi":"10.1177/07482337261461349","DOIUrl":"10.1177/07482337261461349","url":null,"abstract":"","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"329-340"},"PeriodicalIF":1.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148303252","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":"Humanin improved the rotenone-induced reactive oxygen species formation in PC12 cells by modulating the SIRT3/Nrf2/HO-1 signaling pathway.","authors":"Yaohui Shan, Xu Liu, Wei Ge, Qifu Zhang, Sai Yan","doi":"10.1177/07482337261445494","DOIUrl":"10.1177/07482337261445494","url":null,"abstract":"<p><p>ObjectiveMitochondrial dysfunction is the key factor in rotenone-induced neurotoxicity in dopaminergic neurons. This study aimed to investigate the role and potential mechanism of the mitochondrial DNA encoded peptide Humanin (HN) in alleviating rotenone-induced neurotoxicity.MethodsRotenone was added to the cultured PC12 cells to induce neurotoxicity. PC12 cells were preincubated with HN, which has a protective effect. Cell counting kit-8 (CCK-8) was used to evaluate PC12 cell viability. Flow cytometry to detect the content of reactive oxygen species (ROS) in PC12 cells. Western blot analysis was used to detect the expression of superoxide dismutase 2 (SOD2), acetylated SOD (Ac-SOD), sirtuin 3 (SIRT3), nuclear factor erythroid 2-related factor 2 (Nrf2), heme-oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase 1 (NQO1). The corresponding kits were used to measure the NAD+/NADH ratio and SOD content separately.ResultsHN pretreatment significantly increased PC12 cell survival, reduced ROS formation, and increased the NAD⁺/NADH ratio. It also increased the expression of SIRT3, Nrf2, HO-1, and NQO1 proteins and decreased the expression of Ac-SOD protein under rotenone exposure. At the same time, it also activated the Nrf2/HO-1 signaling pathway, which depends on HN-mediated SIRT3 activation.ConclusionThese results suggest that HN plays a protective role in rotenone-induced neurotoxicity by suppressing oxidative stress and activating the antioxidant response via the Nrf2/HO-1 pathway, which is regulated by SIRT3 in PC12 cells.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"275-283"},"PeriodicalIF":1.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147781995","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":"Dibromoacetonitrile mediated depression-like behavior in mice and induced HT22 cytotoxicity through the MKP-1/P38 MAPK signaling pathway and the antagonistic effect of N-acetylcysteine.","authors":"Cong Qi, Xinwei Xu, Lan Zhang, Jiahui Gao, Guosheng Shan, Guangqiao Liang, Yang Ye, Fang Li","doi":"10.1177/07482337261453434","DOIUrl":"10.1177/07482337261453434","url":null,"abstract":"<p><p>Environmental pollutants are an important cause of depression. Dibromoacetonitrile (DBAN) is a disinfection by-product, which is neurotoxic and induces oxidative stress. This study aimed to elucidate whether and how DBAN provoked depression-like behavior. Mitogen-activated protein kinase phosphatase-1 (MKP-1) and P38 mitogen-activated protein kinase (MAPK) are key factors in depression. In mice, 8-week gavage with 20 mg/kg DBAN caused depressive symptoms, serotonin (5-HT) loss, hippocampal neuronal damage, and elevated MKP-1/P38 MAPK signaling; 80 mg/kg proved lethal. DBAN disturbed the intestinal flora of mice. Depression-related bacteria <i>Firmicutes</i> increased. <i>Bacteroidota</i> showed a decreasing trend, and the relative abundance of <i>Bifidobacterium</i> also showed a decreasing trend. Co-treatment with antioxidant N-acetylcysteine (NAC, 150 mg/kg) prevented mortality, restored 5-HT and norepinephrine, normalized MKP-1/P38 phosphorylation, and alleviated behavioral deficits. 10 μM DBAN raised reactive oxygen species (ROS), upregulated MKP-1, increased the phosphorylation levels of P38 and c-Jun amino-terminal kinase (JNK), and decreased the phosphorylation levels of the extracellular signal-regulated kinase (ERK1/2) in HT22 cells. Following HT22 cell MKP-1 knockdown and DBAN exposure, HT22 cells exhibited decreased MKP-1 expression along with decreased P38 and JNK phosphorylation levels. Still, the levels of ERK1/2 phosphorylation were not significantly affected. NAC exerts a prophylactic protective effect against these adverse outcomes.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"284-302"},"PeriodicalIF":1.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148035211","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":"Perfluorooctane sulfonate (PFOS) increases metastatic potential of thyroid cancer cells in correlation with activation of multiple invasion-related signaling proteins.","authors":"Phichamon Phetchahwang, N Monique Paricharttanakul, Kriengsak Lirdprapamongkol, Jisnuson Svasti","doi":"10.1177/07482337261461640","DOIUrl":"10.1177/07482337261461640","url":null,"abstract":"<p><p>Perfluorooctane sulfonate (PFOS) is a man-made chemical widely used in many products and acts as an endocrine-disrupting chemical (EDC). PFOS has spread to the environment through industrial manufacturing processes and disposal of PFOS-containing products. There is growing evidence that environmental pollutants may have promoting effects on cancer cell aggressiveness, rapid growth, and metastasis. Thyroid cancer is an endocrine-related cancer that can respond to EDCs. This study aimed to explore the effect of PFOS on the growth and metastatic potential (invasion capability) of FTC-133 human thyroid cancer cells. PFOS exposure for 72 h (1 pM to 10 µM) did not stimulate growth of FTC-133 cells. However, PFOS exposure at low concentration (1 nM) enhanced invasion capability of the cells, with no correlation to the expression level of estrogen receptors. FTC-133 cells exposed to 1 nM PFOS displayed increasing phosphorylation of multiple invasion-related signaling proteins, including Akt, ERK, and EphA2. Our study revealed that PFOS at low concentration may influence thyroid cancer progression by increasing the metastatic potential of cancer cells.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"320-327"},"PeriodicalIF":1.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148266069","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":"Biological and computational evidence of dinotefuran-DNA interactions: A combined <i>in</i> <i>vitro</i> and <i>in</i> <i>silico</i> study.","authors":"Mazlume Piril Coskun, Ayla Celik, Hakan Arslan","doi":"10.1177/07482337261453776","DOIUrl":"10.1177/07482337261453776","url":null,"abstract":"<p><p>The potential of the neonicotinoid insecticide dinotefuran to induce oxidative DNA damage was evaluated in human peripheral blood lymphocyte cultures at three concentrations (0.05, 0.15, and 0.30 µg/mL) using the single-cell gel electrophoresis assay (COMET). Its ability to interact with DNA was further examined through molecular docking analysis. The comet assay results revealed statistically significant increases (<i>p</i> < 0.001) in both the genetic damage index (GDI) and the percentage of heavily damaged cells (DCP) at all tested concentrations compared with the negative control. DNA damage within individual cells caused by genotoxic agents can thus be effectively detected using the comet assay, as demonstrated in our study. Additionally, the optimized molecular structure, total energy, molecular orbital energies, molecular electrostatic potential (MEP) maps, and global reactivity parameters of dinotefuran were obtained using the DFT/B3LYP/6-311G(d,p) method. The fully optimized energy was predicted, and geometric parameters were compared with available single-crystal structure data. Computational studies employing density functional theory (DFT) and MEP analyses provided detailed insights into the geometric and electronic characteristics of dinotefuran, suggesting that the compound possesses significant chemical reactivity and potential for biological activity upon interaction with DNA. Molecular docking studies with the B-DNA dodecamer (PDB ID: 1BNA) yielded a minimum binding energy of -6.24 kcal/mol. Dinotefuran was found to form four conventional hydrogen bonds, two carbon-hydrogen bonds, and one π-donor hydrogen bond with DNA, primarily involving guanosine, cytosine, and thymidine bases. These interactions are consistent with the experimental evidence of genetic-oxidative DNA damage, indicating that dinotefuran can establish strong molecular interactions with DNA.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"303-319"},"PeriodicalIF":1.6,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148144817","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":"Subchronic γ-hexachlorocyclohexane exposure is associated with altered TLR4-linked pulmonary immune responses following endotoxin challenge: Insights from a two-hit mouse model.","authors":"Anita Tewari, Deepali Kalambhe, R S Sethi","doi":"10.1177/07482337261453446","DOIUrl":"10.1177/07482337261453446","url":null,"abstract":"<p><p>γ-Hexachlorocyclohexane (γ-HCH) is a persistent organochlorine pesticide widely used in agriculture and public health. While its neurotoxicity in humans and animals is well documented, its toxic effects on non-target organs, particularly the lungs, remain poorly understood. In the general population, diet is the primary route of γ-HCH exposure; however, the long-term effects of dietary exposure on pulmonary immunity remain poorly understood. This study employed a two-hit murine model to determine whether prolonged oral exposure of γ-HCH alters pulmonary immune responses to a secondary inflammatory challenge. Swiss albino male mice were administered γ-HCH orally (0.12 mg/kg body weight) for 60 or 90 days, followed by an acute intranasal lipopolysaccharide (LPS) challenge at the respective terminal time points. Systemic and local inflammatory responses were assessed by quantifying cytokine levels (IL-1β and TNFα) in serum and bronchoalveolar lavage fluid using ELISA. Lung tissues were assessed for TLR4 and TNFα expression by immunohistochemistry and examined ultrastructurally by transmission electron microscopy. Subchronic γ-HCH exposure led to a significant increase in IL-1β and TNFα levels, accompanied by robust expression of these markers in pneumocytes, alveolar epithelial cells, and vascular endothelium. Upon LPS challenge, γ-HCH-treated mice showed exacerbated pulmonary inflammation with histopathological changes. Interestingly, the inflammatory response in γ-HCH + LPS groups was not consistently greater than that in the LPS-only group; in some cases, cytokine levels were moderately reduced. These findings suggest that subchronic dietary γ-HCH exposure primes the immune system and alters pulmonary inflammatory responsiveness to a subsequent endotoxin challenge. This pattern is consistent with immune modulation rather than amplified protective immunity. While the observed responses are associated with activation of innate immune signaling pathways, including TLR4-linked mechanisms, further functional studies are required to establish causal relationships. Overall, this study underscores the importance of cumulative and sequential environmental exposures when assessing immunotoxic potential of persistent organic pollutants.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"258-273"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148035252","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":"Knockout of <i>histone deacetylase</i> 6 exacerbates PM_2.5-induced pulmonary injury by affecting renin-angiotensin system balance in mice.","authors":"Yang Zhang, Lifang Jin, Caixia Fan, Guoquan Fu, Huarong Huang, Junyan Yan","doi":"10.1177/07482337261444574","DOIUrl":"10.1177/07482337261444574","url":null,"abstract":"<p><p>Fine particulate matter (PM_2.5) deposition in the lungs can induce pulmonary injury. Histone deacetylase 6 (HDAC6), a critical member of the histone deacetylase family, plays a key role in regulating lung diseases. In this study, we explored the mechanism of HDAC6 in PM_2.5 (10 mg/kg)-induced pulmonary injury using an <i>HDAC6</i> knockout (KO) mouse model, employing immunohistochemical, western blot, and transcriptome analyses. Results indicated that <i>HDAC6</i> KO exacerbated PM_2.5-induced epithelial barrier dysfunction by altering the expression of zonula occludens-1 (ZO-1) and zonula occludens-2 (ZO-2). Moreover, <i>HDAC6</i> KO increased the susceptibility of lung tissue to PM_2.5 by inhibiting E-cadherin expression and promoting N-cadherin expression. Transcriptome analysis of PM_2.5-treated lungs in the <i>HDAC6</i> KO group revealed significant alterations in the renin-angiotensin system (RAS). The expression levels of RAS components, including angiotensin-converting enzyme II (ACE2), angiotensin II (Ang II), renin, and Agtrl1b, were quantified. Notably, both PM_2.5 and <i>HDAC6</i> KO disrupted RAS balance. The PM_2.5-treated <i>HDAC6</i> KO group exhibited a pronounced reduction in ACE2 and elevation in Ang II, suggesting increased susceptibility to PM_2.5. These results indicate that <i>HDAC6</i> KO exacerbates PM_2.5-induced pulmonary injury by affecting RAS balance. This study provides a theoretical foundation for understanding the role of HDAC<i>6</i> in PM_2.5-induced pulmonary injury.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"245-257"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782014","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":"Integrative computational elucidation of molecular mechanisms and multi-target interactions in paraquat-induced pulmonary fibrosis.","authors":"Guiyan Du, Shengyao Tang, Tian Shi, Guosheng Liu, Xia Huang, Jian Chang","doi":"10.1177/07482337261442635","DOIUrl":"10.1177/07482337261442635","url":null,"abstract":"<p><p>Paraquat (PQ), a widely used herbicide, induces severe pulmonary fibrosis through complex mechanisms that are not fully understood. This study employed an integrated computational approach combining network toxicology, molecular docking, dynamics simulations, and AlphaFold2-based protein design to systematically investigate PQ-induced pulmonary fibrotic processes. We identified 111 common targets from pulmonary fibrosis and PQ toxicity databases, among which AKT1, IL6, TP53, and CASP3 were recognized as core targets. Functional enrichment analyses revealed significant involvement of oxidative stress, inflammatory response, and apoptotic pathways. Molecular docking demonstrated strong binding affinity between PQ and key targets (docking scores < -5 kcal/mol), while molecular dynamics simulations confirmed stable interactions with favorable binding energies (< -12 kcal/mol). Furthermore, AlphaFold2 predicted three novel proteins exhibiting even higher binding affinity to PQ than natural targets. These findings reveal that PQ might promote pulmonary fibrosis by stably binding to core proteins and activating critical pathological pathways, providing valuable insights for developing targeted biomarkers and therapeutic strategies against PQ-induced lung injury.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"233-244"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676972","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":"The effect of occupational lead toxicity on testosterone secretion and the L-arginine nitric oxide pathway.","authors":"Lütfiye Tutkun, Servet Birgin İritaş, Murat Büyükşekerci, Vugar Ali Türksoy, Deniz Özkan Vardar, Özgür Öztan, Serdar Deniz, Zübeyir Dedeoğlu, Engin Tutkun","doi":"10.1177/07482337261441688","DOIUrl":"10.1177/07482337261441688","url":null,"abstract":"<p><p>Endocrine-disrupting chemicals (EDCs), including heavy metals such as lead (Pb), interfere with hormonal homeostasis, particularly in the hypothalamic-pituitary-gonadal (HPG) axis. Occupational lead exposure is linked to male reproductive dysfunction and cardiovascular risk via oxidative stress and endothelial impairment. This study investigated the effects of chronic lead exposure on testosterone levels and the L-arginine-nitric oxide (NO) pathway, a key regulator of endothelial function. This case-control study compared 120 male workers with occupational lead exposure (in battery manufacturing and foundries) to 120 unexposed controls. Blood lead levels (BLLs) were quantified via inductively coupled plasma mass spectrometry (ICP-MS), while testosterone (total/free) and methylated arginine metabolites; asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), arginine, and citrulline were analyzed using LC-MS/MS. Statistical analyses included <i>t</i>-tests and Pearson correlations to assess associations. Lead-exposed workers had significantly higher BLLs (31.76 ± 13.31 vs 1.72 ± 0.87 μg/dL), lower total testosterone (388.23 ± 71.78 vs 477.36 ± 104.21 ng/dL), and reduced arginine/ADMA ratios (432.48 ± 191.27 vs 544.33 ± 187.19), indicating endothelial dysfunction. Strong inverse correlations were observed between exposure duration, classified as 6 months to 1 year, 1 to 5 years, and >5 years, to evaluate its association with BLL, testosterone levels, and arginine metabolism markers. This study demonstrated that chronic occupational lead exposure significantly disrupted testosterone secretion and impaired the L-arginine-NO pathway, highlighting its dual threat to reproductive and cardiovascular health. The robust inverse correlations between BLL, testosterone, and arginine/ADMA ratios underscore the endocrine-disrupting and endothelial-damaging effects of lead. These findings support the routine biomonitoring of BLL, testosterone, and methylated arginine metabolites in high-risk occupations to enable early intervention and mitigate long-term health risks.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"223-232"},"PeriodicalIF":1.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147646604","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":"Toxicological impact of tetrabromobisphenol-A on pregnant rats: Morphological, biochemical, and histopathological investigations.","authors":"Mevlahan Özkan, Eda Nur İnkaya, Evrim Arzu Koçkaya, Nurhayat Barlas","doi":"10.1177/07482337261438207","DOIUrl":"10.1177/07482337261438207","url":null,"abstract":"<p><p>Tetrabromobisphenol-A (TBBPA) is found in high concentrations in textiles, plastic polymers, flame retardants, and various industrial products. In this maternofetal study, we aimed to evaluate the potential effects of TBBPA on the mother, fetus, and placenta in pregnant rats. In the experimental design, three different gestational days (GD10, GD15, and GD20) were selected for evaluation in pregnant rats. For each gestational period, one control group (corn oil) and three TBBPA dose groups (20, 200, and 400 mg/kg) were established, resulting in a total of 12 experimental groups. Each group included six pregnant rats. We hypothesized that TBBPA exposure would lead to alterations in maternal and fetal hormonal and placental parameters when evaluated across different doses and gestational days. Placenta, kidney, liver, and ovary tissues were examined histopathologically. Levels of follicle-stimulating hormone (FSH), progesterone, luteinizing hormone (LH), and estrogen were analyzed. Estrogen from ovarian homogenates and testosterone from testicular homogenates of GD20 fetuses were also measured. We detected statistically significant differences in placental and fetal data. However, no severe effects were observed. Serum FSH levels were elevated in the GD20 group receiving 400 mg/kg, whereas LH levels increased in the GD15 group at both 200 and 400 mg/kg compared to controls. In GD20 female fetuses, estrogen levels decreased at 20 mg/kg but increased at 200 mg/kg relative to the control group. Histopathological examination of placental tissue revealed congestion, degeneration in the labyrinth region, cytoplasmic dissolution and pyknosis in giant cells, and degeneration in spongiotrophoblasts. No severe systemic toxicity was observed in our study. However, the mild to moderate level changes detected highlight the need for further investigation of TBBPA, especially considering the uncertainties regarding its effects during pregnancy.</p>","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"178-197"},"PeriodicalIF":1.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593935","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}