Physiological research最新文献

{"title":"Role of Carvedilol in Inhibiting the Proliferation and Migration of Vascular Smooth Muscle Cells by Upregulating microRNA-145 Expression.","authors":"G Yang, Z Zhang, X Ma, J Chen, H Shi, J Yang, Q Han","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The proliferation and migration of vascular smooth muscle cells (VSMCs) are the initial contributors to restenosis in patients undergoing percutaneous coronary intervention (PCI). MicroRNA-145 (miR-145) plays a significant role in this pathological process. Although carvedilol has been shown to inhibit VSMC proliferation and migration, the underlying mechanisms are not fully understood. The aim of our study is to examine whether carvedilol regulates the expression of miR-145 and thereby inhibits the proliferation and migrative capacity of VSMCs. VSMCs were cultured and transfected with either miR-145 mimics or miR-145 inhibitors. Cell proliferation was evaluated using the Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2?-deoxyuridine (EdU) assays, while wound healing and Transwell assays were used to assess the migration capacity. Protein expression levels were quantified using western blot analysis, and additionally, a luciferase reporter assay was performed to identify the target gene of miR-145. We found that carvedilol upregulated the expression of miR-145 and decreased the expression of Krüppel-like factor 4 (KLF4). Furthermore, miR-145 inhibited VSMC proliferation and migration. KLF4 was identified as a direct target of miR-145. Importantly, the inhibition of miR-145 attenuated the suppressive effects of carvedilol on VSMCs. In summary, our results in this study demonstrate that carvedilol exerts its inhibitory effects on VSMC proliferation and migration, at least in part, through the upregulation of miR-145. These findings suggest that miR-145 may be a key mediator in the therapeutic effects of carvedilol on VSMCs.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"577-588"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966092","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":"Protective Effects of Teucrium Polium Leaf Ethanolic Extract Against Nicotine-Induced Nephrotoxicity in Mice.","authors":"A Alatawi, S Maodaa, S Alarifi, A H Harrath, E M Al-Shaebi, D A Alhomoud, S A Alawwad, J S Ajarem","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This study aimed to examine the protective and antioxidant properties of a Teucrium polium leaf extract against acute kidney damage caused by nicotine in male mice. A total of 24 male Swiss albino mice were divided into four groups. The control group (oral solution of 0.9 % NaCl), the positive control group (injections of nicotine at a dosage of 2.5 mg/kg b.w.), the third group (received 100 mg/kg b.w. ethanolic extract of T. polium), and the fourth group (nicotine injections at a dosage of 2.5 mg/kg b.w + 100 mg/kg b.w. ethanolic extract of T. polium). GC-MS analysis of the plant extract revealed the presence of 16 active compounds. Nicotine administration resulted in a significant increase in kidney biomarkers, namely urea, uric acid, and creatinine, by 50 %, 207 %, and 129 %, respectively, compared to the control group, indicating nephrotoxicity. However, treatment with the T. polium extract improved these parameters by 77 %, 79 %, and 83 %, respectively. Furthermore, the nicotine group exhibited elevated levels of nitric oxide (NO) and malondialdehyde (MDA), which are indicators of oxidative stress, as well as decreased levels of glutathione (GSH) and reduced activity of superoxide dismutase (SOD). Conversely, the administration of the T. polium extract reversed these effects, suggesting its potential to enhance the antioxidant defense system. This finding was also supported by the improvements observed in the kidney TUNEL assay sections and the preservation of histopathological integrity. In conclusion, the T. polium extract demonstrates protective effects against nicotine-induced kidney damage by modulating oxidative stress and antioxidant defense mechanisms.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"623-633"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966067","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":"Trimethylamine N-oxide Induced Chronic Kidney Injury by Triggering PANoptosis.","authors":"D Shao, L Bai, Q Chen, Y Chen, Z Qiu, Y Liu, S Jin, Y Wu, J Dai","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Trimethylamine N-oxide (TMAO) is involved in the development of kidney disease. However, the specific mechanism by which it leads to kidney injury is unclear. This study explored the role of regulated cell death in TMAO-induced kidney injury. We constructed a TMAO-induced chronic kidney injury model by intraperitoneal injection of TMAO (100 micromol/kg/day for three months). Plasma creatinine (Cre) and urea nitrogen (BUN) levels were measured to evaluate kidney function. Masson staining was used to evaluate kidney pathological changes. The expression levels of regulated cell death-related proteins were measured using western blotting. Plasma Cre and BUN, the area of kidney fibrosis in the TMAO group significantly increased. The western blotting results showed cleaved-Caspase-8, Caspase-8, Caspase-1, NOD-like receptor protein 3 (NLRP3), interleukin-1beta (IL-1beta), cleaved-gasdermin D (cleaved-GSDMD), Z-DNA binding protein 1 (ZBP1), phosphorylation of receptor-interacting protein kinase 3 (RIP3) and mixed-lineage kinase domain-like pseudokinase (MLKL) significantly elevated in the TMAO group. The transferrin receptor 1 (TFR1), ferritin heavy chain (FTH), ferroportin (FPN), nuclear factor erythroid 2-related factor 2 (NRF2), and glutathione peroxidase 4 (GPX4) protein expression in kidney tissue of the TMAO group significantly up-regulated. However, there was no change in iron and MDA levels. The results suggested that PANoptosis, including pyroptosis, apoptosis, and necroptosis components, might be involved in TMAO-induced chronic kidney injury.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"613-622"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966121","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":"Glial Activation Enhances Spinal TRPV1 Receptor Sensitivity in a Paclitaxel Model of Neuropathic Pain.","authors":"J Slepicka, J Palecek","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Paclitaxel (PTX), a commonly used chemotherapeutic, frequently leads to chemotherapy-induced peripheral neuropathy (CIPN), characterized by persistent pain and neuronal hypersensitivity. While its effects on peripheral nerves are well-documented, paclitaxel also influences central nervous system pathways, particularly spinal synaptic transmission, through Toll-like receptor 4 (TLR4) activation and subsequent sensitization of transient receptor potential vanilloid 1 (TRPV1) receptors. In this study, we used an in vitro model of paclitaxel-induced neuropathic pain to investigate the role of glial activation in TRPV1 receptor function. Using whole-cell patch-clamp recordings from superficial dorsal horn neurons in acute spinal cord slices, we evaluated the effects of minocycline (MX), a glial cell inhibitor, and ISO-1, a macrophage migration inhibitory factor (MIF) antagonist, on paclitaxel-induced synaptic changes. Our results demonstrate that acute paclitaxel application enhances nociceptive signaling and impairs capsaicin-induced TRPV1 receptor tachyphylaxis, leading to sustained hyperactivity. Minocycline preincubation effectively mitigated paclitaxel-induced sensitization, restoring normal nociceptive signaling, whereas acute minocycline treatment failed to prevent these changes. ISO-1 in vitro co-incubation with paclitaxel did not affect the paclitaxel-induced changes. These findings offer novel insight into the intricate interactions among neuroinflammatory mediators, glial cell activation, and TRPV1 receptor sensitization in paclitaxel-induced neuropathic pain. The differential effects of acute versus prolonged pre-incubation minocycline application suggest the importance of sustained glial inhibition for effective outcomes and neuropathic pain management.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"677-691"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144965999","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":"Virtual Reality-Based Rehabilitation Therapy.","authors":"J Lorkowski, M Raulinajtys-Grzybek, M Pokorski","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This minireview describes recent advances in high-tech innovations on virtual reality (VR) aiding physical and cognitive recovery from neuromuscular disorders, notably useful for post-stroke rehabilitation. VR is a computer-generated technique that engulfs users in 3D multisensory interactive feedback. This technique creates simulations of realistic situations that can be manipulated by a user. It provides a spectrum of benefits in both physical and cognitive rehabilitation in the wake of neuromuscular episodes. VR engages and motivates patients to endure the unpleasant sequela of disease. Further, it enhances the acquisition of rehabilitative skills by caregivers and trains them in psychophysical health preservation. The benefits and user-friendliness of VR make it an increasingly welcome assistive neurological therapy tool. However, VR standardization, mechanisms, and, particularly, the long-term effects appear not to keep pace with its popularity and fast-progressing technical advances. Evidence-based studies on large groups of individuals are needed to settle these issues.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"563-569"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966050","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":"Pathophysiology of Clopidogrel in Ischemic Stroke, Role of Platelet microRNAs.","authors":"T Mičaník, O Slabý, T Kvasnička, P Bobčíková, J Vavrošová, E Augste, D Václavík","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Variation in response to clopidogrel represents a significant clinical challenge in patients with ischemic stroke. Genetic polymorphisms cytochrome P450 2C19 (CYP2C19) are a known cause of resistance to clopidogrel. Platelet microRNAs (miRNAs) can modulate the efficacy of antiplatelet therapy. This study focuses solely on clopidogrel because it is the most widely used alternative to aspirin in patients with aspirin intolerance or contraindications. Our aim was to investigate its pharmacogenomic and epigenetic modulation in a targeted and homogeneous cohort. CYP2C19 genotypes are commonly reported as *1/*1 (wild type), *1/*2 (intermediate metabolizer), *2/*2 (poor metabolizer) and *2/*3 (poor metabolizer). These denote the number and type of loss-of-function alleles that affect clopidogrel metabolism. Clopidogrel treatment is typically a component of broader secondary prevention strategies, including lifestyle modifications, statins, and control of blood pressure. Relevant bibliographic references have been added to support the background statements provided in the introduction and methodology. To evaluate the expression of selected platelet miRNAs (miR-126-3p, miR-19a-3p, miR-19b-3p, miR-22-3p, miR-185-5p) in patients with ischemic stroke in relation to the CYP2C19 genotype (*1/*1 ,*1/*2, *2/*2) during clopidogrel treatment. Seventy patients treated with clopidogrel (75 mg daily) were enrolled. Patients were genotyped for the CYP2C19 *2 and *3 alleles by real-time polymerase chain reaction (polymerase chain reaction (PCR)) and miRNA expression was measured in plasma. All abbreviations used throughout the manuscript have been defined at their first appearance for the sake of clarity. No significant differences in miRNA expression were found between the genotypic groups (p > 0.05). Patients with genotype *2/*2 (poor metabolizer) showed a trend towards higher levels of miR-126-3p and miR-185-5p (approximately 1.5 to 1.7 times) compared to *1/*1 (wild type). The clinical parameters did not differ significantly between the groups. Poor clopidogrel metabolizers can exhibit upregulation of some platelet miRNAs as a potential compensatory mechanism. This pilot study suggests a possible epigenetic modulation of the response to antiplatelet therapy through platelet miRNAs.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"669-675"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966007","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":"Analysis of Gene Expression Profiles Regulating Phenotypic Transformation of Vascular Smooth Muscle Cells by Endothelial Cell-Derived Exosomes.","authors":"T Kang, X Li, S Hang, Y Lu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To establish a co-culture cell model and implement high-throughput gene sequencing of exosomes, we preliminarily demonstrated that endothelial cell-derived exosomes play a role in modulating the phenotypic transformation of vascular smooth muscle cells (VSMCs) by means of differentially expressed long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs). Primary rat aortic endothelial cells (ECs) and VSMCs were cultured for morphological observation, immunofluorescence (IF), and western blotting (WB). A co-culture model was established using a transwell system. A comparative analysis of ?-smooth muscle actin (?-SM actin), a marker of the contractile phenotype, and vimentin, indicative of the synthetic phenotype, was conducted to assess the expression levels in both co-culture and control setups. Isolated exosomes were obtained using an exosome-specific isolation kit, followed by detailed characterization using transmission electron microscopy (TEM) for morphological assessment, nanoparticle tracking analysis (NTA) for size distribution, and WB for protein profiling. Primary aortic ECs were isolated, cultured, and characterized. In the Transwell co-culture model, VSMCs transitioned to a contractile phenotype, exhibiting increased alpha-smooth muscle actin (?-SMA, contractile marker) and decreased Vimentin (synthetic marker). Exosomes were extracted, purified, and characterized by their morphology, diameter, concentration, and marker proteins (CD9, CD63, and CD81). RNA-seq and bioinformatic analyses were conducted on muscle cells before and after treatment. The Transwell-based ECs-VSMCs co-culture model significantly upregulates contractile phenotype protein expression in VSMCs, promoting their transition to a contractile state. Differentially expressed exosomal genes, including lncRNAs and circRNAs, modulate proliferation, differentiation, and phenotypic transformation of VSMCs.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"589-599"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144966041","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":"Effects of Astaxanthin on Chronic Exercise Fatigue.","authors":"S Liu, K Daďová","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Astaxanthin is a natural, small-molecule compound with anti-inflammatory and antioxidant properties that has broad potential for use in alleviating exercise fatigue. This study investigated whether astaxanthin can attenuate the onset of fatigue, prolong the time to exhaustion, and enhance post-exercise recovery using a rat model of chronic exercise fatigue. Twenty male rats were trained for 8 weeks to establish the chronic exercise fatigue model. During training, 10 rats were randomly assigned to receive astaxanthin intragastrically and 10 rats received soybean oil alone. After the intervention, 5 rats from each group were divided into astaxanthin (AX) and control groups. The remaining rats were divided into astaxanthin-exercise (AXE) and exercise control groups, respectively, and underwent exhaustive exercise. Astaxanthin alleviated chronic exercise fatigue by improving antioxidant capacity (^CAT, GSH-Px, GSH/GSSG; p<0.05-0.01) and mitochondrial function (^MMP, ST3/ST4; p<0.01-0.001). It prolonged exercise endurance (^time to exhaustion; p<0.001), reduced muscle damage (ˇBUN, CK; p<0.01) and accelerated recovery (^Liver glycogen, NEFA; p<0.001). Astaxanthin appears to improve skeletal muscle antioxidant capacity and mitochondrial function in chronic exercise fatigue in rats, providing a theoretical basis for fatigue management in exercise training.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"657-667"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144965982","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":"Gut Hormone Levels During Mixed Liquid Meal Test in Short Bowel Syndrome, the Possible Influence on the Intestine Adaptation.","authors":"J Krizova, P Trachta, M Mraz, T Brutvan, D Hoskovec, P Dytrych, A Cinkajzlova, O Psenicka, M Haluzik","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Short bowel syndrome (SBS) is an intestinal disorder characterized by reduced length of the gut most due to intestinal resection, resulting in malabsorption, malnutrition, and water and electrolyte disturbances. Intestinal adaptation is a long-term process in which GIT hormones, growth peptides, cytokines etc. are involved. These mechanisms have not been fully clarified yet. The most important seem to be GLP-2 and other gut hormones. The aim of our study was to consider the changes of the levels of selected gut hormones and parameters of glucose homeostasis during the mixed liquid meal test in one year of follow up after the gut resection. Seventeen patients with SBS type I were included into our study. The meal test and measuring of selected parameters (GLP-2, GLP-1, ghrelin, insulin, glucagon, GIP, amylin) were conducted after 2 weeks, 6 and 12 months from its initiation, respectively. During one year of this study patients´ nutritional status improved due to sufficient parenteral nutrition, despite no change in body weight. Hormones possibly involved in intestinal adaptation (GLP-2, GLP-1, ghrelin) did not differ in meal test, neither levels nor AUC. Only higher insulin and glucose levels after one year of follow-up may indicate the beginning of intestinal adaptation process and improving intestinal functions. We conclude that impaired GLP-2 secretion is probably the main reason for the limited adaptation ability in patients with SBS type I.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"645-655"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144965991","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":"Platelet Membrane-Camouflaged Biomimetic Drug Delivery Systems for Ischemia-Reperfusion Injury: Targeted Therapeutic Strategies.","authors":"Chun Shi, Tong Li, Bensi Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This review summarizes the application of platelet membrane-coated biomimetic drug delivery systems in the treatment of various ischemia-reperfusion injuries (I/RI). Platelet membrane-coated nanoparticles, extracellular vesicles, microbubbles, microemulsions, as well as platelet membrane vesicles and their derivatives have shown significant promise for I/RI treatment. By leveraging the specific targeting, adhesive, and immune evasion properties of platelets, these systems enable the targeted delivery of therapeutic agents, such as antioxidants, anti-inflammatory agents, thrombolytics, and neuroprotective compounds, to ischemic tissues, while also offering diagnostic capabilities. However, challenges remain in bridging the gap between research and clinical application, such as scalability, maintaining bioactivity, and potential side effects. Future research should focus on improving scalability, stability, and safety. Furthermore, the context-specific selection or integration of delivery strategies is essential to meet the therapeutic demands of I/RI.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 4","pages":"551-562"},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144965971","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}