检索结果-南通市图书馆

Small extracellular vesicles derived from cerebral endothelial cells with elevated microRNA 27a promote ischemic stroke recovery

引用

Neural Regeneration Research 2025年第1期20卷 224-233页

作者： Yi Zhang Zhongwu Liu Michael Chopp Michael Millman Yanfeng Li Pasquale Cepparulo Amy Kemper Chao Li Li Zhang Zheng Gang Zhang Department of Neurology Henry Ford HospitalDetroitMIUSA Department of Physics Oakland UniversityRochesterMIUSA Department of pathology Henry Ford HospitalDetroitMIUSA division of Pharmacology Department of NeuroscienceReproductive and Dentistry SciencesSchool of MedicineUniversity of Naples“Federico Ⅱ”NaplesItaly

Axonal remodeling is a critical aspect of ischemic brain repair processes and contributes to spontaneous functional *** previous in vitro study demonstrated that exosomes/small extracellular vesicles(sEVs)isolated from cerebral endothelial cells(CEC-sEVs)of ischemic brain promote axonal growth of embryonic cortical neurons and that microRNA 27a(miR-27a)is an elevated miRNA in ischemic *** the present study,we investigated whether normal CEC-sEVs engineered to enrich their levels of miR-27a(27a-sEVs)further enhance axonal growth and improve neurological outcomes after ischemic stroke when compared with treatment with non-engineered CEC-sEVs.27a-sEVs were isolated from the conditioned medium of healthy mouse CECs transfected with a lentiviral miR-27a expression *** EVs isolated from CECs transfected with a scramble vector(Scra-sEVs)were used as a *** male mice were subjected to permanent middle cerebral artery occlusion and then were randomly treated with 27a-sEVs or *** array of behavior assays was used to measure neurological *** with treatment of ischemic stroke with Scra-sEVs,treatment with 27a-sEVs significantly augmented axons and spines in the peri-infarct zone and in the corticospinal tract of the spinal grey matter of the denervated side,and significantly improved neurological *** vitro studies demonstrated that CEC-sEVs carrying reduced miR-27a abolished 27a-sEV-augmented axonal *** analysis revealed that 27a-sEVs systemically administered preferentially localized to the pre-synaptic active zone,while quantitative reverse transcription-polymerase chain reaction and Western Blot analysis showed elevated miR-27a,and reduced axonal inhibitory proteins Semaphorin 6A and Ras Homolog Family Member A in the peri-infarct *** of the Clathrin-dependent endocytosis pathway substantially reduced neuronal internalization of *** data provide evidence that 27a-sEVs have

关键词： axonal remodeling cerebral endothelial cells exosomes miR-27a mitochondria Semaphorin 6A small extracellular vesicles stroke

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Oligodendroglial heterogeneity in health,disease,and recovery:deeper insights into myelin dynamics

引用

Neural Regeneration Research 2025年第11期20卷 3179-3192页

作者： Pieter-Jan Serneels Julie D.De Schutter Lies De Groef Lieve Moons Steven Bergmans KU Leuven Leuven Brain InstituteDepartment of BiologyAnimal Physiology and Neurobiology DivisionNeural Circuit Development&Regeneration Research GroupLeuvenBelgium KU Leuven Leuven Brain InstituteDepartment of BiologyAnimal Physiology and Neurobiology DivisionCellular Communication&Neurodegeneration Research GroupLeuvenBelgium

Decades of research asserted that the oligodendroglial lineage comprises two cell types:oligodendrocyte precursor cells and ***,recent studies employing single-cell RNA sequencing techniques have uncovered novel cell states,prompting a revision of the existing *** forward,the oligodendroglial lineage should be delineated into five distinct cell states:oligodendrocyte precursor cells,committed oligodendrocyte precursor cells,newly formed oligodendrocytes,myelin-forming oligodendrocytes,and mature *** new classification system enables a deeper understanding of the oligodendroglia in both physiological and pathological *** this uniform terminology will facilitate comparison and integration of data across ***,including the consolidation of findings from various demyelinating models,is essential to better understand the pathogenesis of demyelinating ***,comparing injury models across species with varying regenerative capacities can provide insights that may lead to new therapeutic strategies to overcome remyelination ***,by standardizing terminology and synthesizing data from diverse studies across different animal models,we can enhance our understanding of myelin pathology in central nervous system disorders such as multiple sclerosis,Alzheimer's disease,and amyotrophic lateral sclerosis,all of which involve oligodendroglial and myelin dysfunction.

关键词： animal models demyelination fish mammals multiple sclerosis myelin neurodegeneration oligodendrocytes oligodendroglial lineage remyelination

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Growth-inhibitory Effects of Curcumin on Ovary Cancer Cells and Its Mechanisms

引用

Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第1期24卷 55-58页

作者：郑丽端童强松吴翠环 Department of pathology Department of pediatric Surgery

To study the growth inhibitory effects of curcumin on human ovary cancer A2780 cells in vitro and its molecular mechanisms, the growth inhibition rates of A2780 cancer cells, after being treated with 10 μmol/L-50 μmol/L curcumin for 6-24 h, were examined by MTT method. The morphological changes of cancer cells were observed under inversion microscopy. Cellular apoptotic rates were determined by using TUNEL. The protein expression levels of bcl 2, p53 and MDM2 in cancer cells were examined by SP immunohistochemistry. After being treated by various concentrations of curcumin, the growth of cancer cells was inhibited significantly. Some cancer cells presented characteristic morphological changes of apoptosis. The rates of apoptosis were 6.41 % -28.48 % ( P <0.01). The expression of bcl 2 and p53 was decreased, which depended on the action time ( P <0.01). There were no obvious changes in MDM2 expression. It was concluded that curcumin could significantly inhibit the growth of ovary cancer cells. The induction of apoptosis by down re gulating the expression of bcl 2 and p53 was probably one of its molecular mechanisms.

关键词： curcumin ovary cancer gene expression apoptosis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Incidence and localization of lymphoid follicles in early colorectal neoplasms

引用

World Journal of Gastroenterology 2005年第43期11卷 6863-6866页

作者： Kuang-I Fu Yasushi Sano Shigeharu Kato Takahiro Fujii Ikura Koba Takayuki Yoshino Atsushi Ochiai Shigeaki Yoshida Takahiro Fujimori division of Gastrointestinal Oncology and Digestive Endoscopy division of pathology Department of Surgical and Molecular pathology

AIM： TO investigate the incidence and Iocalizations of lymphoid follicles （LFs） in early colorectal neoplasms in human beings. METHODS： From July 1992 to September 1999, a total of 1 324 early colorectal neoplasms were removed endoscopically or surgically at our hospital; 1 031 （77.9%） were available for analysis in this study. Localization of LFs was defined histologically： as submucosal LFs, if located under the muscularis mucosa; and as intramucosal LFs, if located across or over the muscularis RESULTS： Histologically, the materials included 903 intramucosal neoplasms and 128 submucosal cancers. Overall incidence of LFs was 27.2% （280/1 031）. The incidence of LFs was significantly higher in females （33.6% vs 24.9%, P = 0.0064）, the right-sided colon （32.2% vs 25.6%, P = 0.0403） and in flat or depressed type lesions （34.6% vs 25.2%, P〈O.O001） as compared to males, left-sided colon and protruding type lesions, respectively. The incidences of intramucosal neoplasms and submucosal cancers were 24.3% and 43.8%, respectively （P〈O.O001）. Localizations of LFs （intramucosal LF/submucosal LF） in depressed, flat, and protruding types were 1/24, 14/36, and 131/74, respectively. CONCLUSION： The incidence of LFs in early human colorectal neoplasms significantly differs by gender, location, macroscopic type, and histology. Moreover,localization significantly differs by macroscopic type.

关键词： Lymphoid follicle Early colorectal neoplasm Carcinogenesis

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Expression of Ki-67,p53,and K-ras in chronic pancreatitis and pancreatic ductal adenocarcinoma

引用

World Journal of Gastroenterology 2005年第43期11卷 6765-6769页

作者： Seok Jeong Don Haeng Lee Jung Il Lee Jin-Woo Lee Kye Sook Kwon Pum-Soo Kim Hyung Gil Kim Yong Woon Shin Young Soo Kim Young Bae Kim division of Gastroenterology Department of pathology

AIM： To examine surgical specimens of pancreas with either chronic pancreatitis or pancreatic cancer in order to study whether ductal hyperplasia and dysplasia in pancreas represent precursor lesions for pancreatic cancer. METHODS： We examined expression of Ki-67, CEA, p53, and K-ras, in the surgical specimens of pancreas with adenocarcinomas （n = 11） and chronic pancreatitis （n = 12）. Cellular proliferation was assessed by Ki-67 proliferation index using the proliferation marker Ki-67. In specimens with pancreas cancer, we divided pancreas epithelium into normal （n = 7）, ductal hyperplasia （n = 3）, dysplasia （n = 4）, and cancerous lesion （n = 11） after hematoxylin and eosin staining, Ki-67, and CEA immunohistochemical staining. In cases with chronic pancreatitis, the specimen was pathologically examined as in cases with pancreas cancer, and they were also determined as normal （n = 10）, ductal hyperplasia （n = 4）, or dysplasia （n = 5）. p53 and K-ras expression were also studied by immunohistochemical staining. RESULTS： In pancreatic cancer, the Ki-67 index was 3.73±3.58 in normal site, 6.62±4.39 in ductal hyperplasia, 13.47：1：4.02 in dysplasia and 37.03±10.05 in cancer tissue, respectively. Overall, p53 was positive in normal ducts, ductal hyperplasia, dysplasia, and carcinoma cells in 0 of 14 （0%）, 0 of 7 （0%）, 7 of 9 （78%）, and 10 of 11 （91%）, respectively, and K-ras was positive in 0 of 8 （0%）, 1 of 3 （33%）, 4 of 6 （67%）, 4 of 5 （80%）, respectively. CONCLUSION： Our results favorably support the hypothesis that ductal hyperplasia and dysplasia of the pancreas might be precursor lesions for pancreas cancer. Further evaluation of oncogenes by the molecular study is needed.

关键词： Ki-67 p53 K-ras Chronic pancreatitis Pancreatic ductal adenocarcinoma

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Hepatitis C virus and type 2 diabetes

引用

World Journal of Gastroenterology 2009年第13期15卷 1537-1547页

作者： Francesco Negro Mahnaz Alaei division of Gastroenterology Hepatology and Clinical PathologyUniversity Hospitals division of Clinical pathology University Hospitals

This review focuses on the relationship between hepatitis C virus(HCV) infection and glucose metabolism ***-sectional and longitudinal studies have shown that the chronic HCV infection is associated with an increased risk of developing insulin resistance(IR) and type 2 diabetes(T2D).The direct effect of HCV on the insulin signaling has been analyzed in experimental *** currently available data should be considered as preliminary,HCV seems to affect glucose metabolism via mechanisms that involve cellular pathways that have been implicated in the host innate immune *** and T2D not only accelerate the histological and clinical progression of chronic hepatitis C,but also reduce the early and sustained virological response to interferon-alpha-based ***,a detailed knowledge of the mechanisms underlying the HCV-associated glucose metabolism derangements is warranted,in order to improve the clinical management of chronic hepatitis C patients.

关键词： Hepatitis C Fibrosis Insulin resistance Insulin signaling Type 2 diabetes

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Carcinoid tumor of the duodenum and accessory papilla associated with polycythemia vera

引用

World Journal of Gastroenterology 2005年第24期11卷 3794-3796页

作者： Horng-Yuan Wang Ming-Jen Chen Tsen-Long Yang Ming-Chih Chang Yu-Jan Chan division of Gastroenterology Department of Surgery division of Hematology Department of pathology

Carcinoid tumors have been reported in a wide range of organs but most frequently involve the gastrointestinal tract; however, duodenal carcinoid tumors are rare. We report a 50-year-old male patient complaining of multiple melenas for 3 wk. The panendoscopy and endoscopic retrograde cholangiopancreaticography revealed swelling accessory papilla with an ulcer. The biopsy taken showed a carcinoid tumor. The lesion was removed by wide resection. Patient was found to have an abnormal blood cell count during the follow-up period with elevated levels of hemoglobin and hematocrit of 21.2 g/dL and 63.5%,respectively, thrombocytosis of 501 000/μL, and leukocytosis of 20 410/μL. He was diagnosed as a polycythemia vera by a hematologist after further evaluation. He received periodic phlebotomy and hydroxyurea treatment. The response was good and his hematocrit was stabilized by periodic phlebotomy in the range of 44-49% during the last 2 years. The possible origin of UGI bleeding by a duodenal carcinoid tumor, although rare, should be considered. There has been one case report of a duodenal carcinoid tumor that involved accessory papilla of the pancreas divisum and one case report of metastatic carcinoid tumor associated with polycythemia vera. It is different in our patient as compared with the latter report, which mentioned a polycythemia vera patient who was found to have a metastatic carcinoid in the 17 years follow-up period. Chemotherapy had been given before the carcinoid tumor was revealed. Our patient had no previous chemotherapy for polycythemia vera before he was found to have duodenal carcinoid tumor; this excludes the possibility of chemotherapy induced carcinoid tumor, although it had been suspected in the previous report. In our patient, the existence of both diseases may be by predisposition of each other since both diseases have an increased incidence of other neoplasm, or they may be coexistent incidentally.

关键词： Carcinoid tumor Accessory papilla Polycythemia vera

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Inflammasome links traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease

引用

Neural Regeneration Research 2025年第6期20卷 1644-1664页

作者： Gabriela Seplovich Yazan Bouchi Juan Pablo de Rivero Vaccari Jennifer C.Munoz Pareja Andrew Reisner Laura Blackwell Yehia Mechref Kevin K.Wang J.Adrian Tyndall Binu Tharakan Firas Kobeissy Department of Surgery Morehouse School of MedicineAtlantaGAUSA Department of Neurobiology Center for NeurotraumaMultiomics&Biomarkers(CNMB)Neuroscience InstituteMorehouse School of MedicineAtlantaGAUSA Department of Neurological Surgery and the Miami Project to Cure Paralysis University of Miami Miller School of MedicineMiamiFLUSA division of pediatric Critical Care Department of PediatricsUniversity of Miami Miller School of MedicineMiamiFLUSA Department of pediatrics Emory UniversityAtlantaGAUSA Department of Neurosurgery Children’s Healthcare of AtlantaAtlantaGAUSA Department of Chemistry and Biochemistry Texas Tech UniversityLubbockTXUSA Morehouse School of Medicine AtlantaGAUSA

Traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease are three distinct neurological disorders that share common pathophysiological mechanisms involving neuroinflammation. One sequela of neuroinflammation includes the pathologic hyperphosphorylation of tau protein, an endogenous microtubule-associated protein that protects the integrity of neuronal cytoskeletons. Tau hyperphosphorylation results in protein misfolding and subsequent accumulation of tau tangles forming neurotoxic aggregates. These misfolded proteins are characteristic of traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease and can lead to downstream neuroinflammatory processes, including assembly and activation of the inflammasome complex. Inflammasomes refer to a family of multimeric protein units that, upon activation, release a cascade of signaling molecules resulting in caspase-induced cell death and inflammation mediated by the release of interleukin-1β cytokine. One specific inflammasome, the NOD-like receptor protein 3, has been proposed to be a key regulator of tau phosphorylation where it has been shown that prolonged NOD-like receptor protein 3 activation acts as a causal factor in pathological tau accumulation and spreading. This review begins by describing the epidemiology and pathophysiology of traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease. Next, we highlight neuroinflammation as an overriding theme and discuss the role of the NOD-like receptor protein 3 inflammasome in the formation of tau deposits and how such tauopathic entities spread throughout the brain. We then propose a novel framework linking traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease as inflammasomedependent pathologies that exist along a temporal continuum. Finally, we discuss potential therapeutic targets that may intercept this pathway and ultimately minimize long-term neurological decline.

关键词： Alzheimer's disease caspase-1 chronic traumatic encephalopathy inflammasomes neurodegeneration neuroinflammation NLRP1 NLRP3 pyroptosis tauopathy traumatic brain injury

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Radiological response and inflammation scores predict tumour recurrence in patients treated with transarterial chemoembolization before liver transplantation

引用

World Journal of Gastroenterology 2017年第20期23卷 3690-3701页

作者： Daniele Nicolini Andrea Agostini Roberto Montalti Federico Mocchegiani Cinzia Mincarelli Alessandra Mandolesi Nicola L Robertson Roberto Candelari Andrea Giovagnoni Marco Vivarelli division of Hepatobiliary and Transplant Surgery Department of Experimental and Clinical MedicinePolytechnic University of Marche division of General and pediatric Radiology Department of Radiological SciencesPolytechnic University of Marche division of Interventional Radiology Department of Radiological SciencesPolytechnic University of Marche division of pathology Department of PathologyPolytechnic University of Marche division of Radiology Department of RadiologyMemorial Sloan Kettering Cancer Center

To investigate the prognostic value of the radiological response after transarterial chemoembolization (TACE) and inflammatory markers in patients affected by hepatocellular carcinoma (HCC) awaiting liver transplantation (LT).METHODSWe retrospectively evaluated the preoperative predictors of HCC recurrence in 70 patients treated with conventional (n = 16) or doxorubicin-eluting bead TACE (n = 54) before LT. The patient and tumour characteristics, including the static and dynamic alpha-fetoprotein, neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio (PLR) measurements, were recorded. Treatment response was classified according to the modified Response Evaluation Criteria in Solid Tumours (mRECIST) and the European Association for the Study of the Liver (EASL) criteria as complete response (CR), partial response (PR), stable disease or progressive disease. After examination of the explanted livers, histological necrosis was classified as complete (100% of the cumulative tumour area), partial (50%-99%) or minimal (pathology as the reference standard, mRECIST criteria correctly classified necrosis in 72.9% (51/70) of patients and EASL criteria in 68.6% (48/70) of cases. The mRECIST non-response to TACE [Exp(b) = 9.2, p = 0.012], exceeding UCSF criteria before

关键词： Liver transplantation Recurrence-free survival Hepatocellular carcinoma Radiological response Locoregional therapies Inflammatory markers Selection criteria

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Analysis of CD117-negative gastrointestinal stromal tumors

引用

World Journal of Gastroenterology 2005年第7期11卷 1052-1055页

作者： Chin-Yuan Tzen Bey-Liing Mau Departments of pathology division of General Internal Medicine

AIM: To identify the gastrointestinal stromal tumors(GISTs) that are negative for CD117 expression by immunohistochemistry and to characterize their malignant ***: A total of 108 primary mesenchymal tumors of the gastrointestinal tract were screened to select CD117-negative tumors, from which KIT(exons 9, 11, 13, and 17)and PDGFRA (exons 10, 12, 14, and 18) were sequenced to identify GISTs. Tumor recurrence and distant metastasis were used as the criteria of ***: The result showed that approximately 25%(29/108) of the gastrointestinal mesenchymal tumors were negative for CD117 and approximately 6% (7/108)of the tumors were CD117-negative GISTs. All these CD117-negative tumors had a mutated KITand a wildtype PDGFRA. All CD117-negative GISTs with mutations at codons 557/558 of KIThad mitotic counts ＞10/50 high power field, and 75% (3/4) of them showed multiple recurrence or distant ***: CD1 17-negative KITmutated GISTs account for approximately 6% of the gastrointestinal mesenchymal tumors. Tumor recurrence or distant metastasis correlates to both theKITmutations at codons 557/558 and the mitotic counts, but not to the tumor size.

关键词： Gastrointestinal stromal tumor CD117 KIT mutation Tumor recurrence Distant metastasis

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：