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Exploring pre-degenerative alterations in humans using induced pluripotent stem cell-derived dopaminergic neurons

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Neural Regeneration Research 2017年第7期12卷 1068-1070页

作者： Federica Bono Chiara Fiorentini division of Pharmacology Department of Molecular andTranslational Medicine University of Brescia Brescia Italy

Understanding the cellular and molecular mechanisms underlying human neurological disorders is hindered by both the complexity of the disorders and the lack of suitable experimental models recapitulating key pathological features of the *** is a crucial issue since a limited understanding of pathogenic mechanisms precludes the development of drugs counteracting the progression of the *** neurological disorders,

关键词： in Exploring pre-degenerative alterations in humans using induced pluripotent stem cell-derived dopaminergic neurons stem DAT been that of cell PSC

Endogenous DNA Damage and Repair Enzymes—A short summary of the scientific achievements of Tomas Lindahl,Nobel Laureate in Chemistry 2015

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genomics, Proteomics & Bioinformatics 2016年第3期14卷 122-125页

作者： Arne Klungland Yun-Gui Yang Department of Microbiology Division of Diagnostics and InterventionInstitute of Clinical MedicineOslo University Hospital Department of molecular medicine Faculty of MedicineInstitute of Basic Medical SciencesUniversity of Oslo CAS Key Laboratory of genomic and Precision medicine Collaborative Innovation Center of Genetics and DevelopmentBeijing Institute of GenomicsChinese Academy of Sciences

Tomas Lindahl completed his medical studies at Karolinska Institute in ***,his work has always been dedicated to unraveling fundamental mechanisms of DNA decay and DNA *** research is characterized with groundbreaking discoveries on the instability of our genome,the identification of novel DNA repair activities,the characterization of DNA repair pathways,and the association to diseases,throughout his 40 years of scientific career.

关键词： DNA repair completed career instability decay dedicated summary Clare breaking

Why some tumours trigger neovascularisation and others don't:the story thus far

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Chinese Journal of Cancer 2016年第2期35卷 69-79页

作者： Omanma Adighibe Russell D.Leek Marta Fernandez-Mercado Jiangting Hu Cameron Snell Kevin C.Gatter Adrian L.Harris Francesco Pezzella Radcliffe Department of medicine Nuffield Division of Laboratory ScienceJohn Radcliffe HospitalUniversity of Oxford Radcliffe Department of medicine Leukaemia and Lymphoma Research Molecular Haematology UnitNuffield Division of Laboratory ScienceJohn Radcliffe Hospital Biodonostia Research Institute Department of Medical Oncology Molecular Oncology LaboratoriesWeatherall Institute of Molecular MedicineJohn Radcliffe Hospital

Background:Angiogenesis is not essential for tumours to develop and expand,as cancer can also grow in a nonangiogenic fashion,but why this type of growth occurs is ***,our data from mRNA transcription profiling did not show any differences in the classical angiogenic pathways,but differences were observed in mitochondrial metabolic pathways,suggesting a key role for metabolic *** then validated these results with mRNA profiling by investigating differential protein expression via immunohistochemistry in angiogenic and non-angiogenic non-small cell lung cancers(NSCLCs).Methods:Immunohistochemical staining for 35 angiogenesis- and hypoxia-related biomarkers were performed on a collection of 194 angiogenic and 73 non-angiogenic NSCLCs arranged on tissue *** of P53 was performed with frozen tissue samples of ***:The non-angiogenic tumours were distinguished from the angiogenic ones by having higher levels of proteins associated with ephrin pathways,mitochondria,cell biogenesis,and hypoxia-inducible factor 1(HIF1) regulation by oxygen and transcription of HIF-controlled genes but lower levels of proteins involved in the stroma,cell-cell signaling and adhesion,integrins,and Delta-Notch and epidermal growth factor(EGF)-related ***,proteins classically associated with angiogenesis were present in both types of tumours at very comparable *** expression of P53 was strongly associated with non-angiogenic tumours.A pilot investigation showed that P53 mutations were observed in 32.0%of angiogenic cases but in 71.4%of non-angiogenic ***:Our observations thus far indicate that both angiogenic and non-angiogenic tumours experience hypoxia/HIF and vascular endothelial growth factor(VEGF) pathway protein expression in a comparable ***,angiogenesis does not ensue in the non-angiogenic ***,metabolic reprogramming seems to distinguish these two types of ne

关键词： Cancer, Angiogenesis, Hypoxia, Blood vessels

Systematic review and meta-analysis on the association of tuberculosis in Crohn's disease patients treated with tumor necrosis factor-α inhibitors(Anti-TNFα)

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World Journal of Gastroenterology 2018年第25期24卷 2764-2775页

作者： Brent L Cao Ahmad Qasem Robert C Sharp Latifa S Abdelli Saleh A Naser division of molecular Microbiology Burnett School of Biomedical Sciences College of Medicine University of Central Florida

AIM To perform a meta-analysis on the risk of developing Mycobacterium tuberculosis(TB) infection in Crohn's disease(CD) patients treated with tumor necrosis factoralpha(TNFα) *** A meta-analysis of randomized, double-blind, placebocontrolled trials of TNFα inhibitors for treatment of CD in adults was conducted. Arcsine transformation of TB incidence was performed to estimate risk difference. A novel epidemiologically-based correction(EBC) enabling inclusions of studies reporting no TB infection cases in placebo and treatment groups was developed to estimate relative *** Twenty-three clinical trial studies were identified, including 5669 patients. Six TB infection cases were reported across 5 studies, all from patients receiving TNFα inhibitors. Eighteen studies reported no TB infection cases in placebo and TNFα inhibitor treatment arms. TB infection risk was significantly increased among patients receiving TNFα inhibitors, with a risk difference of 0.028(95%CI: 0.0011-0.055). The odds ratio was 4.85(95%CI: 1.02-22.99) with EBC and 5.85(95%CI: 1.13-30.38) without *** The risk of TB infection is higher among CD patients receiving TNFα inhibitors. Understanding the immunopathogenesis of CD is crucial, since using TNFα inhibitors in these patients could favor mycobacterial infections, particularly Mycobacterium avium subspecies paratuberculosis, which ultimately could worsen their clinical condition.

关键词： Tuberculosis Tumor necrosis factor-alpha inhibitors Crohn’s Disease Meta-analysis Systematic review

Assessment of Biochemical and Antioxidative Status in Patients Suffering from Dengue Fever

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2015年第3期35卷 411-418页

作者： Mahmood Rasool Arif Malik Khalid Mahmud Khan Muhammad Saeed Qureshi Beenish Shabbir Sara Zahid Muhammad Asif Abdul Manan Sana Rashid Saima Rubab Khan Hafiz Muhammad Arsalan Rabail Alam Mahwish Arooj Mahmood Husain Qazi Adeel Gulzar Ahmed Chaudhary Adel Mohammed Abuzenadah Mohammed Hussain Al-Qahtani Sajjad Karim Center of Excellence in genomic medicine Research Faculty of Applied Medical SciencesKing Abdulaziz University Institute of molecular Biology and Biotechnology the University of Lahore Fatima Jinnah Medical College Sir Gangaram Hospital Lahore Institute of molecular Biology and Biotechnology the University of Lahore Department of Biotechnology and Informatics BUITEMS Quetta 87300 Pakistan Center for Research in molecular medicine the University of Lahore KACST Technology Innovation Center in Personalized medicine King Abdulaziz University Center of Excellence in genomic medicine Research Faculty of Applied Medical Sciences King Abdulaziz University

Summary：A multi-centred study was designed to collect dengue epidemiologic data from government and registered private hospitals/clinics and maintained archive of frozen specimens in bio-bank to be used for future dengue epidemic control program, and assess the epidemiology of dengue fever（DF） by evaluating biochemical and oxidative status of patients. ELISA Ig M antibodies test was done to confirm DF. From August 2010 to December 2011, 101 confirmed blood samples of DF patients referred to pathology lab of Jinnah Hospital Lahore were subjected to the epidemiologic assessment by evaluating the biochemical and physiological indices and alterations of circulating antioxidants. Clinical features of DF patients and effect of fever on blood components and serum proteins of liver were recorded. The hospital stay in DF, dengue hemorrhagic fever（DHF） and dengue shock syndrome（DSS） showed significant difference. Significant increases in serum alanine amino transferase（ALT）（P=0.000）, aspartate amino transferase（AST）（P=0.000）, alkaline phosphatase（ALP）（P=0.000）, malondialdehyde（MDA） along with significant decreases in total protein（TP）（P=0.000）, reduced glutathione（GSH）（P=0.000）, superoxide dismutase（SOD）, catalase（CAT）（P=0.000）, and sialic acid contents（P=0.016） were observed. A positive correlation existed between bound sialic acid levels, liver enzymes and circulating antioxidants（r=0.656, P=0.016）. In the present study, alterations of circulating antioxidants in DF suggest that DF might be a metabolic response to an acute, self-limiting tropical viral infection, and a consequence of the viral inflammatory process.

关键词： dengue fever alanine amino transferase aspartate amino transferase malondialdehyde superoxide dismutase catalase

Pro-resolving lipid mediator reduces amyloid-β42–induced gene expression in human monocyte–derived microglia

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Neural Regeneration Research 2025年第3期20卷 873-886页

作者： Ying Wang Xiang Zhang Henrik Biverstål Nicolas GBazan Shuai Tan Nailin Li Makiko Ohshima Marianne Schultzberg Xiaofei Li Department of Neurobiology Care Sciences&SocietyDivision of NeurogeriatricsKarolinska InstitutetStockholmSweden Department of Neurology Neuroscience CenterThe First Hospital of Jilin UniversityChangchunJilin ProvinceChina Department of Physiology and Pharmacology Karolinska InstitutetStockholmSweden Department of Biosciences and Nutrition Karolinska InstitutetHuddingeSweden Neuroscience Center of Excellence Louisiana State UniversityNew OrleansLAUSA Department of medicine SolnaClinical Pharmacology GroupKarolinska University HospitalStockholmSweden

Specialized pro-resolving lipid mediators including maresin 1 mediate resolution but the levels of these are reduced in Alzheimer's disease brain, suggesting that they constitute a novel target for the treatment of Alzheimer's disease to prevent/stop inflammation and combat disease pathology. Therefore, it is important to clarify whether they counteract the expression of genes and proteins induced by amyloid-β. With this objective, we analyzed the relevance of human monocyte–derived microglia for in vitro modeling of neuroinflammation and its resolution in the context of Alzheimer's disease and investigated the pro-resolving bioactivity of maresin 1 on amyloid-β42–induced Alzheimer's disease–like inflammation. Analysis of RNA-sequencing data and secreted proteins in supernatants from the monocyte-derived microglia showed that the monocyte-derived microglia resembled Alzheimer's disease–like neuroinflammation in human brain microglia after incubation with amyloid-β42. Maresin 1 restored homeostasis by down-regulating inflammatory pathway related gene expression induced by amyloid-β42 in monocyte-derived microglia, protection of maresin 1 against the effects of amyloid-β42 is mediated by a re-balancing of inflammatory transcriptional networks in which modulation of gene transcription in the nuclear factor-kappa B pathway plays a major part. We pinpointed molecular targets that are associated with both neuroinflammation in Alzheimer's disease and therapeutic targets by maresin 1. In conclusion, monocyte-derived microglia represent a relevant in vitro microglial model for studies on Alzheimer's disease-like inflammation and drug response for individual patients. Maresin 1 ameliorates amyloid-β42–induced changes in several genes of importance in Alzheimer's disease, highlighting its potential as a therapeutic target for Alzheimer's disease.

关键词： Alzheimer's disease amyloid-β maresin microglia monocyte neuroinflammation resolution RNA-sequencing specialized pro-resolving lipid mediator

Functional proteomics of adenosine triphosphatase system in the rat striatum during aging

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Neural Regeneration Research 2012年第1期7卷 6-12页

作者： Roberto Federico Villa Federica Ferrari Antonella Gorini Department of Forensic medicine and Pharmacological-Toxicological Sciences division of Pharmacological and Toxicological Sciences Laboratory of Pharmacology and molecular medicine of Central Nervous System University of Pavia

The maximum rates of adenosine triphosphatase （ATPase） systems related to energy consumption were systematically evaluated in synaptic plasma membranes isolated from the striata of male Wistar rats aged 2, 6, 12, 18, and 24 months, because of their key role in presynaptic nerve ending homeostasis. The following enzyme activities were evaluated： sodium-potassium-magnesium adenosine triphosphatase （Na^＋, K^＋, Mg^2＋-ATPase）; ouabain-insensitive magnesium adenosine triphosphatase （Mg^2＋-ATPase）; sodium-potassium adenosine triphosphatase （Na^＋, K^＋-ATPase）; direct magnesium adenosine triphosphatase （Mg^2＋-ATPase）; calcium-magnesium adenosine triphosphatase （Ca^2＋, Mg^2＋-ATPase）; and acetylcholinesterase. The results showed that Na~, K＋-ATPase decreased at 18 and 24 months, Ca^2＋, Mg^2＋-ATPase and acetylcholinesterase decreased from 6 months, while Mg^2＋-ATPase was unmodified. Therefore, ATPases vary independently during aging, suggesting that the ATPase enzyme systems are of neuropathological and pharmacological importance. This could be considered as an experimental model to study regeneration processes, because of the age-dependent modifications of specific synaptic plasma membranes. ATPases cause selective changes in some cerebral functions, especially bioenergetic systems. This could be of physiopathological significance, particularly in many central nervous system diseases, where, during regenerative processes, energy availability is essential.

关键词： ATPase synaptic plasma membranes aging striatum functional proteomics

Loss of Hox5 function results in myofibroblast mislocalization and distal lung matrix defects during postnatal development

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Science China(Life Sciences) 2018年第9期61卷 1030-1038页

作者： Steven M.Hrycaj Leilani Marty-Santos ANDrew J.Rasky Nicholas W.Lukacs Deneen M.Wellik Department of Internal medicine Division of Molecular Medicine and Genetics University of Michigan Department of Pathology University of Michigan Department of Cell and Developmental Biology University of Michigan

Alveologenesis is the final stage of lung development and is responsible for the formation of the principle gas exchange units called alveoli. The lung mesenchyme, in particular the alveolar myofibroblasts, are drivers of alveolar development, however,few key regulators that govern the proper distribution and behavior of these cells in the distal lung during alveologenesis have been identified. While Hox5 triple mutants(Hox5 aabbcc) exhibit neonatal lethality, four-allele, compound mutant mice(Hox5 AabbCc) are born in Mendelian ratios and are phenotypically normal at birth. However, they exhibit defects in alveologenesis characterized by a BPD-like phenotype by early postnatal stages that becomes more pronounced at adult stages. Invasive pulmonary functional analyses demonstrate significant increases in total lung volume and compliance and a decrease in elastance in Hox5 compound mutants. SMA+ myofibroblasts in the distal lung are distributed abnormally during peak stages of alveologenesis and aggregate, resulting in the formation of a disrupted elastin network. Examination of other key components of the distal lung ECM, as well as other epithelial cells and lipofibroblasts reveal no differences in distribution. Collectively, these data indicate that Hox5 genes play a critical role in alveolar development by governing the proper cellular behavior of myofibroblasts during alveologenesis.

关键词： Hox5 alveologenesis alveolar myofibroblasts lung ECM postnatal lung development

Human epidermal growth factor receptor targeted inhibitors for the treatment of ovarian cancer

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Cancer Biology & medicine 2018年第4期15卷 375-388页

作者： Maria Bonello ANDrew Harvey Sims Simon Peter Langdon Cancer Research UK Edinburgh Center and division of Pathology Laboratory MRC Institute of Genetics and Molecular Medicine University of Edinburgh

Ovarian cancer is the second most lethal gynecological cancer worldwide and while most patients respond to initial therapy, they often relapse with resistant disease. Human epidermal growth factor receptors(especially HER1/EGFR and HER2/ERBB2) are involved in disease progression; hence, strategies to inhibit their action could prove advantageous in ovarian cancer patients,especially in patients resistant to first line therapy. Monoclonal antibodies and tyrosine kinase inhibitors are two classes of drugs that act on these receptors. They have demonstrated valuable antitumor activity in multiple cancers and their possible use in ovarian cancer continues to be studied. In this review, we discuss the human epidermal growth factor receptor family; review emerging clinical studies on monoclonal antibodies and tyrosine kinase inhibitors targeting these receptors in ovarian cancer patients; and propose future research possibilities in this area.

关键词： Tyrosine kinase monoclonal antibodies ovarian cancer inhibitors HER receptors