Histology and histopathology最新文献

{"title":"The effectiveness of edible bird's nest in lowering VEGF, CD31, and PDGFR-β levels in diabetic retinopathy in rats with type 1 diabetes.","authors":"Manaras Komolkriengkrai, Udomlak Matsathit, Nualpun Sirinupong, Wipapan Khimmaktong","doi":"10.14670/HH-18-825","DOIUrl":"https://doi.org/10.14670/HH-18-825","url":null,"abstract":"<p><strong>Aims: </strong>Diabetic eye disease, known as diabetic retinopathy (DR), is one of the problems that can arise from having high blood sugar for an extended period. This study aimed to investigate the effect of the edible bird's nest (EBN) on retinal angiogenesis in diabetic rats.</p><p><strong>Methods: </strong>The 50 rats were separated into five different groups, each containing 10 rats: control, diabetes (DM), bird's nest-fed diabetes (75 mg/kg Body weight; BW), (EBN 75), (150 mg/kg BW) (EBN 150), and glyburide (GR) for an eight-week study. H&E and Masson's trichrome staining were utilized to investigate the retinal tissue and vascular changes. The immunofluorescence study was used to detect angiogenic protein expression. The vascular corrosion cast/SEM method was also used to evaluate capillary plexus formation within the retinal layer.</p><p><strong>Results: </strong>From histological studies, DM rats have thinning of the retinal layer. Remarkably, the retinal vessels displayed dilations resembling ruptured blood vessels. The expression of vascular endothelial growth factor (VEGF) (30.51±2.62), cluster of differentiation 31 (CD31) (28.18±0.22), and platelet-derived growth factor receptor beta (PDGFR-β) (141.67±0.97) were increased. EBN 75 exhibited some small improvements in their blood vessels and eye tissue. At a dose of 150 mg/kg BW, EBN proved to be more effective. There was a significant decrease in VEGF and CD31 expression compared with the diabetic group (<i>p</i><0.001 and <i>p</i><0.01, respectively).</p><p><strong>Conclusions: </strong>These studies have demonstrated that EBN can lower the growth levels of VEGF, CD31, and PDGFR-β, which results in a decrease in angiogenesis and a recovery from a variety of diabetic retinopathy-related diseases.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18825"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Upregulation of LY6K induced by FTO-mediated demethylation promotes the tumorigenesis and metastasis of oral squamous cell carcinoma via CAV-1-mediated ERK1/2 signaling activation.","authors":"Chen Xu, Rujuan Gong, Haibing Yang","doi":"10.14670/HH-18-725","DOIUrl":"10.14670/HH-18-725","url":null,"abstract":"<p><p>Lymphocyte antigen 6 complex locus K (LY6K) has been demonstrated to play a significant role in cancers and identified as a therapeutic biomarker for head and neck squamous cell carcinoma. However, the role of LY6K in oral squamous cell carcinoma (OSCC) has not been explored. The current study discovered that LY6K was aberrantly upregulated in OSCC cell lines and tissues and that high LY6K expression significantly correlated with poorer survival of OSCC patients. Through stable knockdown of LY6K, we found that the growth, colony formation, migration, and invasion of OSCC cells were substantially suppressed. In addition, tumor growth and lung metastasis <i>in vivo</i> were effectively inhibited by LY6K depletion. Mechanically, LY6K binds with CAV-1 and activates CAV-1-mediated MAPK/ERK signaling to exert its oncogenic effects on OSCC. In addition, LY6K expression in OSCC was discovered to be regulated by FTO-mediated RNA N6-methyladenosine (m⁶A) modification in an IGF2BP1-dependent manner. Generally, LY6K expression was upregulated by FTO-mediated demethylation in OSCC, which promoted the tumorigenesis and metastasis of OSCC via activating the CAV-1-mediated ERK1/2 signaling pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1359-1370"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140101501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA-binding protein DND1 participates in migration, invasion, and EMT of prostate cancer cells by degrading CLIC4.","authors":"Wei Zhang, Qian Xu, Chunmei Shi, Xinfeng Chen, Cheng Shen, Yong Zhang, Bing Zheng, Hua Zhu","doi":"10.14670/HH-18-720","DOIUrl":"10.14670/HH-18-720","url":null,"abstract":"<p><p>Dead-End 1 (DND1) is an RNA-binding protein (RBP) with regulatory functions in multiple cancers, including gastric and colorectal. Nevertheless, the role that DND1 plays in prostatic cancer (PCa) as well as the hidden molecular mechanism is still obscure. The gene expression of DND1 and survival analyses in PCa were analyzed by the UALCAN database. Expression of DND1 and chloride intracellular channel 4 (CLIC4) were detected by qRT-PCR and western blot analysis. The Cell Counting Kit-8 assay and EDU staining were employed for the estimation of cell viability. The capabilities of cells to migrate and invade were appraised by the wound healing assay as well as the Transwell assay, while epithelial-mesenchymal transition (EMT) was measured by immunofluorescence and western blot assay. The interaction of DND1 and CLIC4 was predicted by PCTA, linkedomics, and RPISeq databases. It was discovered that DND1 expression was elevated in PCa cells. DND1 silencing had suppressive impacts on the proliferative, migrative, and invasive capabilities as well as EMT in DU145 and 22Rv1 cells. Mechanistically, bioinformatic analysis demonstrated that DND1 was negatively correlated with CLIC4 and that DND1 protein could bind to CLIC4 mRNA. Additionally, the CLIC4 level was reduced in PCa cells. CLIC4 depletion countervailed the suppressive impacts of DND1 deficiency on the capabilities of DU145 and 22Rv1 cells to proliferate, migrate, and invade as well as the process of EMT. These results suggested that DND1 silencing repressed the proliferation, migration, invasion, and EMT in PCa by regulating the mRNA level of CLIC4.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1343-1358"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intratumoral T cells are associated with prognosis and chemotherapy benefit in gastric cancer.","authors":"Lu Liu, Qianwen Chen, Chen He, Feilan Xie, Shengyuan Su, Lijun Wang, Jintao Liu","doi":"10.14670/HH-18-824","DOIUrl":"10.14670/HH-18-824","url":null,"abstract":"<p><p>Tumor-infiltrating lymphocytes (TILs) have been described in various malignancies and viewed as a sign of anti-tumor immunity, so they are frequently thought to be implicated in the prognosis of cancers. However, little information is available on the association of the distribution pattern of TILs with clinical outcomes in gastric cancer (GC). TIL densities at different regions were assessed immunohistochemically in 59 GC patients to analyze their relationship with clinicopathological characteristics. We found that GC patients in the high-density TIL group were significantly associated with reduced tumor invasion depth, absence of lymph node metastasis, earlier TNM stage, and improved progression-free survival (PFS). Both intratumoral CD3+ TILs and pathological T stage were identified as having an independent prognostic value. Additionally, GC patients with a high density of intratumoral CD3+ TILs were found to gain more benefit from chemotherapy. Overall, these results underscored the predictive power of intratumoral TILs in survival prognosis and chemotherapy benefit for GC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18824"},"PeriodicalIF":2.5,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BATF is involved in the malignant phenotype and epithelial-mesenchymal transition of colon cancer cells via ERK/PD-L1 signaling.","authors":"Xiaoqiong Chen, Huaqian Dong, Liping Jin","doi":"10.14670/HH-18-823","DOIUrl":"https://doi.org/10.14670/HH-18-823","url":null,"abstract":"<p><strong>Objective: </strong>Transcription factors have emerged as primary regulators in colon cancer. Basic Leucine Zipper Transcription Factor (BATF) was found to be differentially expressed in colon cancer. This study aimed to explore the impact of BATF on the malignant phenotype and epithelial-mesenchymal transition (EMT) process.</p><p><strong>Methods: </strong>Based on The Cancer Genome Atlas (TCGA) data, the correlation between BATF and patients' overall prognosis was analyzed. BATF expression in epithelial and colon cancer cells was evaluated. By knocking down its levels in colon cancer cells, its effects on the malignant phenotype, apoptosis, EMT progression, and ERK/PD-L1 were evaluated. Cells were treated with ERK/PD-L1 agonists, and the BATF cell regulation was re-examined.</p><p><strong>Results: </strong>BATF levels were negatively correlated with patients' overall survival. BATF is upregulated in colon cancer cell lines, and BATF knockdown in HCT116 cells suppressed the malignant cellular phenotypes (proliferation, migration, and invasion) and increased apoptosis. BATF knockdown inhibited EMT and ERK/PD-L1 signaling activation, whereas upon agonist treatment, BATF potency was disrupted.</p><p><strong>Conclusion: </strong>This study revealed that BATF is involved in the malignant phenotype and EMT of colon cancer cells, and this process may be mediated by ERK/PD-L1 signaling.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18823"},"PeriodicalIF":2.5,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G protein-gated inwardly rectifying K+ (GIRK/Kir3) channels: Molecular, cellular, and subcellular diversity.","authors":"Alejandro Martín-Belmonte, Carolina Aguado, Rocio Alfaro-Ruíz, Rafael Luján","doi":"10.14670/HH-18-822","DOIUrl":"10.14670/HH-18-822","url":null,"abstract":"<p><p>G protein-gated inwardly rectifying K⁺ (GIRK/K_ir3) channels are mainly expressed in excitable cells such as neurons and atrial myocytes, where they can respond to a wide variety of neurotransmitters. Four GIRK subunits have been found in mammals (GIRK1-4) and act as downstream targets for various Gαi/o-linked G protein-coupled receptors (GPCRs). Activation of GIRK channels produces a postsynaptic efflux of potassium from the cell, responsible for hyperpolarization/inhibition of the neuron. A growing body of evidence suggests that dysregulation of GIRK signalling can lead to excessive or deficient neuronal excitability, which contributes to neurological diseases and disorders. Therefore, GIRK channels are proposed as new pharmacological targets. The function of GIRK channels in neurons is not only determined by their biophysical properties but also by their cellular and subcellular localization patterns and densities on the neuronal surface. GIRK channels can be located within several subcellular compartments, where they have many different functional implications. This subcellular localization changes dynamically along the neuronal surface in response to drug intake. Ongoing research is focusing on determining the proteins that form macromolecular complexes with GIRK channels and are responsible for fast and precise signalling under physiological conditions, and how their alteration is implicated in pathological conditions. In this review, the distinct regional, cellular, and subcellular distribution of GIRK channel subunits in the brain will be discussed in view of their possible functional and pathological implications.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18822"},"PeriodicalIF":2.5,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Golgi method. A historical through contemporary view.","authors":"Ignacio González-Burgos","doi":"10.14670/HH-18-821","DOIUrl":"https://doi.org/10.14670/HH-18-821","url":null,"abstract":"<p><p>Knowledge regarding the biology of the nervous system and its functions has gone through various theoretical, methodological, and interpretative stages throughout history, depending largely on technical advances that have allowed us not only to approach old questions from new perspectives but also to address new ones. One advance that constituted a watershed in the history of neuroscience was the appearance of a chrome-silver staining technique called the <i>Golgi method</i> that allowed the complete, three-dimensional observation of nerve cells. Discovered by Camilo Golgi and, later, modified significantly and employed by Santiago Ramón y Cajal, Golgi's method was crucial in demonstrating the veracity of the Neuronal Theory over the earlier Reticular Theory, and in revealing numerous findings related to the human brain and those of many other animal species, which continue to be analyzed today. Despite a period of scientific recession in the first half of the 20^th century, the use of the Golgi method prevailed and even expanded in the second half of that century and into the 21^st, as researchers continued to use it in its original or modified form and in combination with emerging methodologies. Currently, there are no signs of any decline in its use.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18821"},"PeriodicalIF":2.5,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRIP1 is a downstream target of YY1 in promoting OGD/R-induced H9c2 cardiomyocyte injury and mitochondrial dysfunction.","authors":"Wanliu Zhang, Jingqian Lu, Yan Gao, Qianhong Song, Shihua Luo, Yi Li","doi":"10.14670/HH-18-820","DOIUrl":"10.14670/HH-18-820","url":null,"abstract":"<p><strong>Background and objective: </strong>From a clinical standpoint, myocardial ischemia/reperfusion injury (MIRI) has always been an enormous challenge for the treatment of acute myocardial infarction (AMI). Molecular targeting therapy may help overcome this challenge. The present work aimed to elucidate the possible involvement of Yin-Yang 1 (YY1)/nuclear receptor-interacting protein 1 (NRIP1) and discover the molecular mechanism of MIRI.</p><p><strong>Methods: </strong>Herein, a cardiomyocyte ischemia/reperfusion (I/R) model was established via oxygen-glucose deprivation/re-oxygenation (OGD/R) damage in H9c2 cardiomyocytes. Reverse transcription-quantitative PCR and western blotting were conducted to measure the levels of YY1 and NRIP1 at the RNA and protein levels, respectively. H9c2 cell viability and apoptosis were assayed using the Cell Counting Kit-8, flow cytometry, and western blotting. In addition, superoxide dismutase, glutathione peroxidase, and malondialdehyde levels were analyzed as markers of oxidative stress. Additionally, mitochondrial membrane potential, which was measured via JC-1 staining, ATP content, Complex I activity, mitochondrial DNA copy number, and mitochondrial permeability transition pore (mPTP) opening rate were analyzed to evaluate mitochondrial activity. Moreover, luciferase reporter and chromatin immunoprecipitation assays experimentally validated the predicted affinity of YY1 with the NRIP1 promoter according to the HumanTFDB online tool.</p><p><strong>Results: </strong>YY1/NRIP1 were both highly expressed in OGD/R-injured H9c2 cardiomyocytes. Downregulation of NRIP1 improved cell viability, whereas it inhibited cell apoptosis and oxidative stress, and suppressed mitochondrial dysfunction in OGD/R-injured H9c2 cardiomyocytes. Importantly, it was verified that YY1 could bind to the NRIP1 promoter to positively regulate NRIP1 expression. The protective effects of NRIP1 knockdown against cardiomyocyte damage and mitochondrial dysfunction in OGD/R-injured H9c2 cardiomyocytes were partly abolished through overexpression of YY1.</p><p><strong>Conclusion: </strong>NRIP1 emerged as a downstream target of YY1 in promoting OGD/R-induced H9c2 cardiomyocyte injury and mitochondrial dysfunction, providing novel ideas for targeted treatments to alleviate MIRI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18820"},"PeriodicalIF":2.5,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of morphology, apoptosis, and cell proliferation of the uterus in postmenopausal women.","authors":"Weronika Ratajczak, Malwina Łazowska, Maria Laszczyńska, Aleksandra Rył, Anna Lubkowska, Małgorzta Zimny, Andrzej Kram, Olimpia Sipak","doi":"10.14670/HH-18-819","DOIUrl":"https://doi.org/10.14670/HH-18-819","url":null,"abstract":"<p><strong>Background: </strong>The aim of this study was to evaluate the morphology (atrophy and fibrosis), apopto-sis, and cell proliferation in the uterine wall. The research material came from postmenopausal women who had undergone hysterectomy due to uterine myomas or prolapse of the reproductive organ and were not taking menopausal hormone therapy (MTH).</p><p><strong>Material and methods: </strong>The collected material was divided into three groups. Group I (n=18) con-sisted of uterine sections taken 1 to 5 years after the last menstruation, Group II (n=17) 6 to 10 years after the last menstruation, and Group III (n=15) over 11 years after the last menstruation. To assess morphology and fibrosis, the uterine sections were subjected to hematoxylin and eosin (HE) staining and to Mallory's staining. In addition, we performed a histochemical examination to identify apopto-sis in endometrial and myometrial cells using the TUNEL method. An immunohistochemical analysis of endometrial and myometrial cells was also performed to detect the location of the proliferating cell nuclear antigen (PCNA).</p><p><strong>Results: </strong>Differences in apoptosis were only found in the myometrium between Group I and Group III, and were strongest in Group I myometrial cells, and weakest in Group III. Neither the endome-trium nor the myometrium showed statistically significant differences in the overall percentage of PCNA(+) cells between groups.</p><p><strong>Conclusion: </strong>Morphological changes in the endometrial and myometrial layers of postmenopausal uteri increased with time since the last menstruation.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18819"},"PeriodicalIF":2.5,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNMT1 silencing induces KIR2DL1/2/3 expression via methylation to alleviate graft-versus-host disease after allogeneic hematopoietic stem cell transplantation.","authors":"Ping Zhang, Shuling Yu, Miao Zhou, Xiao Yan, Huiling Zhu, Lixia Sheng, Yi Zhang, Shujun Yang, Guifang Ouyang","doi":"10.14670/HH-18-818","DOIUrl":"https://doi.org/10.14670/HH-18-818","url":null,"abstract":"<p><p>Natural killer (NK) cells are the promoters in graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT), while demethylation can regulate NK cell function. We explored the mechanism of demethylation regulating NK cell function to affect GVHD after allo-HSCT. BALB/c mice were transfused with C57BL/6 mouse-derived NK and bone marrow cells to establish GVHD models, followed by isolation and <i>in-vitro</i> expansion of NK cells. NK cell purity, cytokine levels, proliferation, and cytokine-producing NK cell levels were measured via flow cytometry. KIR2DL1/2/3 methylation was tested by Methylation-specific polymerase chain reaction (MSP), with determination of mouse survival and GVHD scores. KIR2DL1/2/3 and DNMT1 expression was detected through qRT-PCR and/or western blot. Methylation levels were upregulated and KIR2DL1/2/3 expression was downregulated in GVHD mouse model-derived NK cells following IL-2 stimulation. DNMT1 silencing promoted KIR2DL1/2/3 expression, proliferation, and the secretion of Granzyme, Perforin, and Interferon-γ (IFN-γ) in C57BL/6 mouse-derived NK cells. DNMT1 silencing also enhanced mouse survival, reduced GVHD scores, promoted KIR2DL1/2/3 expression on the NK cell surface, and increased the secretion of Granzyme, Perforin, IFN-γ, and the number of cytokine-producing NK cells in the spleen, liver, and lung tissues of the models. Collectively, DNMT1 silencing induced KIR2DL1/2/3 expression in NK cells through reducing methylation to alleviate GVHD after allo-HSCT.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18818"},"PeriodicalIF":2.5,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}