Toxicology Reports最新文献

{"title":"Pre-treatment red cell index and metastasis status as independent predictors of overall survival in Jordanian breast cancer patients receiving chemotherapy","authors":"Amjad Z. Alrosan ,&nbsp;Tahani Alwidyan ,&nbsp;Ghaith B. Heilat ,&nbsp;Aseel O. Rataan ,&nbsp;Khaled Alrosan","doi":"10.1016/j.toxrep.2025.102077","DOIUrl":"10.1016/j.toxrep.2025.102077","url":null,"abstract":"<div><div>Breast cancer (BC) poses a global health challenge, necessitating accessible prognostic biomarkers. Systemic inflammatory markers from complete blood counts, such as neutrophil-to-lymphocyte ratio (NLR) and red cell index (RCI), have shown prognostic potential. This retrospective study evaluated the prognostic significance of pre-treatment NLR and RCI for overall survival (OS) in 144 Jordanian BC patients (KAUH, 2011–2025) undergoing chemotherapy. Kaplan-Meier analysis revealed that high pre-treatment NLR (≥ 4.25) and high RCI (≥ 0.02) were significantly associated with shorter OS. Multivariate Cox regression identified elevated pre-treatment RCI (≥ 0.02) and metastasis at diagnosis as independent predictors of increased mortality and worse OS. A significant association between high NLR and RCI values was also observed, suggesting a link between systemic inflammation and erythrocytic dysregulation. In conclusion, pre-treatment RCI and metastasis are strong independent predictors of OS in this cohort, with RCI demonstrating substantial prognostic value.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"15 ","pages":"Article 102077"},"PeriodicalIF":0.0,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144321005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of the sidelined pollutant: Reviving the fight against heavy metal contamination in an era of emerging contaminants","authors":"Odera R. Umeh ,&nbsp;Eziafakaego M. Ibo ,&nbsp;Chima I. Eke ,&nbsp;Hilda C. Afeku-Amenyo ,&nbsp;Duke U. Ophori","doi":"10.1016/j.toxrep.2025.102073","DOIUrl":"10.1016/j.toxrep.2025.102073","url":null,"abstract":"<div><div>Groundwater contamination by heavy metals (HMs) remains a pressing global concern, presenting substantial risks to humans, animals, plants, and the environment. Although emerging pollutants have received increasing attention, the adverse impacts of HM have not been adequately resolved. This comprehensive review examines the current state of knowledge regarding HM in groundwater, addressing sources, global trends, transport, fate, sampling techniques, modeling, quality control, toxicity, treatment, sustainable measures, and vital research gaps. HM research has continued to dwindle since 2022, these chemicals infiltrate groundwater systems through various pathways, and their mobility and bioavailability are affected by changes in climate, geological heterogeneity, and chemical properties. Moreover, HM may interact with other emerging contaminants to enhance migration and toxicity; however, little or no research has been conducted to fully understand cocktail migration mechanisms and impacts in groundwater systems. Despite the existence of various treatment techniques, no single approach has been universally accepted as the sole solution for completely removing HM from drinking water systems. There is a pressing need for standardized and advanced sampling methods, stringent quality control measures, and the incorporation of cutting-edge technologies such as smart water sensors that can detect both charged and uncharged contaminants, and nanotechnology for effective management. The increasing toxicity of HM and their harmful effects on human health and ecosystems emphasize the need for continuous and novel research involving sustainable remedial strategies, as the battle against metal contamination in groundwater systems requires constant dedication, innovative research, and a shared commitment to protecting our environment.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"15 ","pages":"Article 102073"},"PeriodicalIF":0.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144312966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transgenerational toxicity of Aroclor 1232 by inhalational route in mouse model","authors":"Sivaselvakumar Muthusamy ,&nbsp;Ramanujam Narayanan","doi":"10.1016/j.toxrep.2025.102072","DOIUrl":"10.1016/j.toxrep.2025.102072","url":null,"abstract":"<div><h3>Background</h3><div>Aroclor 1232 is a commercial mixture of polychlorinated biphenyls with inhalational toxicological implications as it contains semi-volatile congeners like PCB 77, along with highly lipophillic ones like PCB 180. We aimed to assess the trans-generational behavioral toxicities of this complex mixture in mice by inhalational dosing chamber. We also aimed to evaluate the penetrability of PCBs across placental and lactational routes in mice in this study.</div></div><div><h3>Methods</h3><div>We assessed the probable route of penetration in the first generation of litters using behavioral scores as surrogate markers of developmental toxicity. We also quantified plasma concentrations of key PCBs and anthropometric parameters for trans-generational comparability.</div></div><div><h3>Results</h3><div>PCBs are responsible for behavioral toxicities across one generation of mice by hazardous exposures via the inhalational route. Behavioral scores of F1 and F2generation mice indicated as surrogate endpoints that PCBs are concentrated in lactating milk more than placental route in the next generation of mice. No significant lethality or effects on anthropometrical parameters were detected across one generation although the congeners were detected in plasma of the litters when they were 12–14 weeks age.</div></div><div><h3>Conclusion</h3><div>PCBs may pose both indoor and outdoor volatile hazard by inhalational routes and cause behavioral deficits across one generation by transfer via lactational routes. PCB 77 is more evident of penetrating trans-generationally and produces behavioral toxicities in subsequent generations. They definitely carry inhalational hazard in workplaces and outdoor as environmental pollutants and neuroendocrine disruptors.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"15 ","pages":"Article 102072"},"PeriodicalIF":0.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144312965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Berberine nanoemulsion attenuates bisphenol A-induced metabolic impairment through NF-κB signaling in the liver of rat","authors":"Ali Hormozi ,&nbsp;Hossein Salehi ,&nbsp;Seyed Mohammad Ali Hosseini ,&nbsp;Shahnaz Rajabi ,&nbsp;Hamid Kabiri-Rad ,&nbsp;Aatena Mansori ,&nbsp;Tahora Fakhrtaha ,&nbsp;Saeed Samarghandian ,&nbsp;Tahereh Farkhondeh","doi":"10.1016/j.toxrep.2025.102069","DOIUrl":"10.1016/j.toxrep.2025.102069","url":null,"abstract":"<div><div>This study was designed to investigate the potential of Berberine nanoemulsion (BNE) to mitigate Bisphenol A (BPA)-induced liver damage in rats. Thirty-six adult Wistar rats were randomly divided into six groups and exposed to various doses of BPA and BNE for 30 days. The experimental groups included a control group, a BPA-only group, BNE-only group, and combinations of BNE with BPA at 5 and 10 mg/kg doses. After 30 days of treatment, the rats were anesthetized, and blood and liver samples were collected. Key metabolic parameters, including glucose, triglycerides (TG), total cholesterol (TC), aspartate aminotransferase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP) and white blood cell (WBC) counts, were measured. Oxidative stress was assessed by measuring malondialdehyde (MDA) and nitric oxide (NO) levels. Gene expression analysis of NF-κB and IL-1β were performed using quantitative PCR. Liver histopathology was also conducted to assess structural alterations. BPA exposure significantly elevated serum glucose, TG, TC, AST, ALT and ALP levels, liver levels of oxidative stress markers (NO and MDA) and also expression of pro-inflammatory cytokines IL-1β and NF-κB compared to the control group. BNE treatment (10 mg/kg) significantly reduced blood glucose, TG, AST, ALT and ALP levels in BPA-exposed rats compared to non-treated BPA group. Additionally, BNE decreased liver levels of NO and MDA and normalized the total WBC count compared to the non-treated BPA group. The expressions of IL-1β and NF-κB were significantly reduced in the BNE-treated groups versus the non-treated BPA group. Histopathological examination of the liver revealed that BNE treatment alleviated BPA-induced liver damage, showing minimal structural alterations in the liver tissue. Our study demonstrates that BNE effectively mitigates the metabolic and inflammatory consequences of BPA exposure in rats. These findings contribute to understanding BPA toxicity and suggest the clinical potential of BNE in managing BPA-induced metabolic disorders in humans, warranting further investigation.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"15 ","pages":"Article 102069"},"PeriodicalIF":0.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144580127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Insights into medication-induced liver injury: Understanding and management strategies\" [Toxicol. Rep. 14 (2025) 101976].","authors":"Vatsalya Tiwari, Shrishti Shandily, Jessielina Albert, Vaibhav Mishra, Manoj Dikkatwar, Rohit Singh, Sujit Kumar Sah, Sharad Chand","doi":"10.1016/j.toxrep.2025.102068","DOIUrl":"https://doi.org/10.1016/j.toxrep.2025.102068","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1016/j.toxrep.2025.101976.].</p>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"102068"},"PeriodicalIF":0.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12223416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144561247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sub-acute polyethylene microplastic inhalation exposure induced pulmonary toxicity in wistar rats through inflammation and oxidative stress.","authors":"Athaya Rahmanardi Muhammad, Muhammad Reva Aditya, Bayu Lestari, Hikmawan Wahyu Sulistomo","doi":"10.1016/j.toxrep.2025.102067","DOIUrl":"10.1016/j.toxrep.2025.102067","url":null,"abstract":"<p><p>Plastic waste, particularly polyethylene (PE) plastic bags and bottles, poses a significant environmental problem and health risk when degraded into microplastics. Recent atmospheric microplastic pollution increases inhalation exposure, necessitating a study on toxicity in the lungs. However, the inhalation toxicology of PE microplastics is poorly understood. This study used Wistar rats that are divided into control and PE group. The PE groups were exposed to PE microplastic through inhalation for 28 days with the daily dose of 15 mg/m³. Inflammatory marker such as Inflammatory exudate, Alveolar thickening, and NF-κB were in PE group increased significantly compared to control group. the increment of MDA and decrement of SOD in PE group revealed the oxidative stress occurred. These results suggest that sub-acute PE microplastic inhalation may contribute to inflammation pathogenesis via the NF-κB pathway as a result of oxidative stress.</p>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"102067"},"PeriodicalIF":0.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Occurrence and dietary risk assessment of chloramphenicol residues in honey products in Saudi Arabia.","authors":"Lulu Almutairi, Abdullah AlSayari, Somaiah Almubayedh, Sarah AlSubaie, Thamer AlMudhehi, Malak Almutairi, Amani S Alqahtani","doi":"10.1016/j.toxrep.2025.102066","DOIUrl":"10.1016/j.toxrep.2025.102066","url":null,"abstract":"<p><strong>Background: </strong>Chloramphenicol (CAP) is a broad-spectrum antibiotic with potentially fatal side effects, including suspected carcinogenicity and toxicity in sensitive individuals. Due to these risks, CAP has been banned in food-producing animals, including honey, by regulatory authorities worldwide. This study investigates the presence of CAP residues in honey products from the Saudi market and evaluates the associated dietary exposure risk.</p><p><strong>Methods: </strong>A total of 902 honey samples collected during 2018-2019 were retrieved from the Saudi Food and Drug Authority (SFDA) to investigate honey safety and chemical components. CAP was extracted using a validated liquid-liquid extraction method and quantified using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Dietary exposure was assessed using the margin of exposure (MOE) approach, with relevant data on honey consumption and body weight sourced from published studies.</p><p><strong>Results: </strong>CAP residues were detected in 54 (6 %) of the tested honey samples, with a mean concentration of 0.16 ± 0.032 µg/kg. The 95th percentile MOE for adults was 31,752 in the lower-bound scenario and 24,290 in the upper-bound scenario, exceeding the critical threshold of 10,000 established by the European Food Safety Authority, which indicates low public health concern and low priority for risk management.</p><p><strong>Conclusion: </strong>Our findings indicate a low health risk associated with honey consumption in Saudi Arabia, as MOE values exceeded the critical safety threshold. However, ongoing monitoring, stricter regulations, and enhanced awareness are recommended to ensure the safety and quality of honey products.</p>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"102066"},"PeriodicalIF":0.0,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12209939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144544974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of methamphetamine intoxication on acute kidney injury in Iraqi male addicts.","authors":"Sazan A Mirza, Nawar S Mohammed, Zahraa Q Ali, Aseel Sameer Mohamed","doi":"10.1016/j.toxrep.2025.102065","DOIUrl":"10.1016/j.toxrep.2025.102065","url":null,"abstract":"<p><p>Methamphetamine (METH), a synthetic derivative of amphetamine, is prescribed for disorders such as narcolepsy but is sometimes illicitly produced from over-the-counter drugs like pseudoephedrine to produce \"crystal meth.\" Consumption of METH can have a severe impact on a number of organ systems, including renal failure, neurotoxicity, pulmonary toxicity, and cardiotoxicity. Increased doses of METH can elevate blood pressure and heart rate, hence enhancing the chance of serious repercussions. Acute renal failure associated with METH is linked to kidney issues such as renal tubular necrosis, caused by reduced blood flow, and acute interstitial nephritis, which damages kidney tubules and impairs waste filtration. Biomarkers such as elevated serum levels of urea, creatinine, cystatin C, and neutrophil gelatinase-associated lipocalin (NGAL) indicate acute kidney injury (AKI). METH-induced renal failure often correlates with hyperthermia, hemodynamic instability, rhabdomyolysis, and nephropathies like necrotizing angiitis, tubular necrosis, and interstitial nephritis. This study investigates the association between kidney toxicity and AKI in Iraqi males with METH addiction. The research, carried out at Ibn-Rushed Psychiatric Hospital in Baghdad between January and August 2023, involved 168 males aged 22-43 who had been addicted for over 60 months. Additionally, 154 healthy males with no history of drug use served as controls. Drug test screening cards were utilized to confirm the diagnosis. Kidney function tests (urea, creatinine), total protein, serum albumin, sodium ions, cystatin C, creatine kinase, and NGAL levels were assessed. Results revealed significant differences between addicts and controls, particularly elevated cystatin C, creatine kinase, and NGAL levels in addicts. A ROC curve analysis demonstrated heightened sensitivity of kidney function tests to METH-induced renal damage. Histopathological examination of a deceased male, aged 41-year-old, with a seven-year history of METH abuse revealed evidence of acute kidney injury, accompanied by significantly elevated levels of renal function biomarkers. The findings suggest that prolonged methamphetamine use may have contributed to severe renal impairment, manifesting in both structural damage to the kidneys and a marked disruption in renal function. This study highlights the severe impact of METH on kidney function and underscores the importance of preventive measures and effective treatment strategies for managing METH addiction and mitigating its harmful effects.</p>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"102065"},"PeriodicalIF":0.0,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptotic- and non-ferroptotic mechanisms associated with doxorubicin-induced male reproductive dysfunction.","authors":"E O Ajani, T M Akhigbe, P A Oyedokun, C A Adegbola, D H Adeyemi, R E Akhigbe","doi":"10.1016/j.toxrep.2025.102064","DOIUrl":"10.1016/j.toxrep.2025.102064","url":null,"abstract":"<p><p>Despite the effectiveness of doxorubicin as a chemotherapeutic agent, it exerts toxicity on non-target organs, including the male reproductive organs. This review synthesizes current evidence on both ferroptotic and non-ferroptotic mechanisms underlying doxorubicin (DOX)-induced male reproductive dysfunction. DOX disrupts testicular function by inducing oxidative stress, lipid peroxidation, mitochondrial dysfunction, and apoptosis, particularly in Leydig, Sertoli, and spermatogenic cells. These effects result in reduced testosterone production, impaired spermatogenesis, and poor semen quality. Additionally, DOX alters the hypothalamic-pituitary-gonadal (HPG) axis and downregulates key enzymes involved in steroidogenesis, exacerbating hormonal imbalances and infertility risks. Emerging research highlights ferroptosis, iron-dependent cell death, as a major contributor to DOX-induced testicular damage, with evidence showing that antioxidant agents like melatonin and zinc oxide nanoparticles may offer protective effects. In addition, the results of this review reveal the necessity of investigating the potential of interventional strategies. This research highlights the need for integrative care approaches prioritizing cancer management and fertility preservation. This review aims to inform healthcare providers, patients, and policymakers about the significant consequences of doxorubicin therapy and open new therapeutic horizons for adjuvant therapies.</p>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"102064"},"PeriodicalIF":0.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genotoxic activity of glyphosate and co-formulants in glyphosate-based herbicides assessed by the micronucleus test in human mononuclear white blood cells.","authors":"Khadija Ramadhan Makame, Yazen Aljaber, Moustafa Sherif, Balázs Ádám, Károly Nagy","doi":"10.1016/j.toxrep.2025.102063","DOIUrl":"10.1016/j.toxrep.2025.102063","url":null,"abstract":"<p><p>Glyphosate-based herbicides (GBHs) are widely used and contribute to soil, water, and air contamination. Despite differing assessments of its carcinogenic potential, glyphosate toxicity may be enhanced by the co-formulants (adjuvants) used to improve its effectiveness. In this study, we investigated the genotoxic effects of glyphosate, alkyl dimethyl betaine (adjuvant A), and polyethoxylated tallow amine (adjuvant B) on human peripheral white blood cells using a cytokinesis block micronucleus (CBMN) assay. The experiments tested Glyphosate (0.1, 1, 10, and 100 μM) and adjuvants (at concentrations matching their levels in respective GBHs) in whole blood samples. The samples were exposed for 4 and 20 h with and without S9 metabolic treatment. The results showed that glyphosate and adjuvant A caused a statistically significant increase in the frequency of binucleated cells with micronuclei (BNMN%) only at 100 μM after 4-hour exposure without S9 treatment. Adjuvant B, however, induced a statistically significant increase in BNMN% starting at 1 μM after 4-hour exposure without S9 treatment. No significant effects were observed after 4 h of exposure with S9 or 20 h of exposure, with or without S9. The proliferation index (PI) showed no significant changes. This study concluded that the co-formulants in GBHs can induce genotoxic effects at low concentrations and short exposure times. This indicated that some surfactants in GBHs may be more toxic than glyphosate.</p>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"102063"},"PeriodicalIF":0.0,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12192614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144498087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}