Hari S. Sharma

ORCID: 0000-0003-4446-0749
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About
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Research Areas
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Cardiac Ischemia and Reperfusion
  • Spinal Cord Injury Research
  • Neonatal Respiratory Health Research
  • Cardiac Arrest and Resuscitation
  • Heme Oxygenase-1 and Carbon Monoxide
  • Pulmonary Hypertension Research and Treatments
  • Congenital Heart Disease Studies
  • Asthma and respiratory diseases
  • Thermal Regulation in Medicine
  • Nitric Oxide and Endothelin Effects
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Anesthesia and Neurotoxicity Research
  • Congenital Diaphragmatic Hernia Studies
  • Cardiac Fibrosis and Remodeling
  • Angiogenesis and VEGF in Cancer
  • Adipose Tissue and Metabolism
  • S100 Proteins and Annexins
  • Congenital heart defects research
  • Fibroblast Growth Factor Research
  • Mitochondrial Function and Pathology
  • Heat shock proteins research
  • Thermoregulation and physiological responses
  • Apelin-related biomedical research
  • Traumatic Brain Injury Research

Saint Michael's Medical Center
2024

New York Medical College
2024

Erasmus MC
2003-2024

Uppsala University Hospital
1997-2023

Rotterdam University of Applied Sciences
2005-2023

Erasmus University Rotterdam
1996-2022

Uppsala University
2003-2017

Amsterdam UMC Location Vrije Universiteit Amsterdam
2011-2014

Capital Medical University
2013

Vanderbilt University Medical Center
2013

The late stages of age-related maculopathy (ARM), especially neovascular macular degeneration (ARMD), can severely affect central vision and are the main cause blindness in elderly Western world. It has been shown that angiogenic growth factors present membranes ARMD. However, it is not known if play a role onset neovascularisation.In order to elucidate involvement initiation neovascularisation early ARM, expression patterns VEGF, TGF-beta, b-FGF, PDGF-AA on 18 human maculae with 11 control...

10.1136/bjo.81.2.154 article EN British Journal of Ophthalmology 1997-02-01

Chronic airways inflammation is one of the features chronic obstructive pulmonary disease (COPD). We demonstrated previously that bronchiolar epithelium in COPD contains increased numbers macrophages and mast cells. Transforming growth factor β1 (TGF- β1) may be involved this influx because it has chemotactic activity for In study, we examined expression patterns TGF- β1, β receptors type I II RI RII) by immunohistochemistry mRNA situ hybridization peripheral lung tissue 14 current or...

10.1164/ajrccm.158.6.9803053 article EN American Journal of Respiratory and Critical Care Medicine 1998-12-01

Epithelial cells form a tight barrier against environmental stimuli via junctions (TJs) and adherence (AJs). Defects in TJ AJ proteins may cause changes epithelial morphology integrity potentially lead to faster trafficking of inflammatory through the epithelium. Bronchial fragility has been reported asthmatic patients, but little is known about expression asthma. We studied zonula occludens-1 (ZO-1) E-cadherin, alpha-catenin, beta-catenin bronchial biopsies from nonatopic nonasthmatic...

10.1139/y08-004 article EN Canadian Journal of Physiology and Pharmacology 2008-03-01

Ongoing inflammatory processes resulting in airway and vascular remodelling characterise chronic obstructive pulmonary disease (COPD). Vascular endothelial growth factor (VEGF) its receptors VEGFR-1 (Flt-1) VEGFR-2 (KDR/Flk-1) could play a role tissue angiogenesis COPD.The cellular expression pattern of VEGF, Flt-1, KDR/Flk-1 was examined by immunohistochemistry central peripheral lung tissues obtained from ex-smokers with COPD (forced expiratory volume 1 second (FEV(1)) <75% predicted; n =...

10.1136/thx.2004.023986 article EN Thorax 2005-01-29

The molecular basis of myocardial adaptation to ischemia and reperfusion is poorly understood. It thought that nuclear proto-oncogenes act as third messengers, converting cytoplasmic signal transduction into long-term changes gene expression. We studied the expression six (Egr-1, c-fos, fosB, c-jun, junB, c-myc) in myocardium subjected anesthetized pigs. Stunning was achieved by two 10-minute left anterior descending coronary artery occlusions separated 30 minutes reperfusion. Hearts were...

10.1161/01.res.71.6.1351 article EN Circulation Research 1992-12-01

Remodeling of airways and blood vessels is an important feature in chronic obstructive pulmonary disease (COPD). By using immunohistochemical analysis, we examined bronchial expression patterns various extracellular matrix (ECM) components such as collagens (subtypes I, III, IV), fibronectin, laminin β2 patients with COPD (forced expiratory volume 1 second [FEV1] ≤75%; n = 15) without (FEV1 =≥85%; 16) correlated data lung function. Quantitative analysis revealed enhanced levels (P < .01)...

10.1309/jc477fael1ykv54w article EN American Journal of Clinical Pathology 2006-11-01

Pulmonary hypoplasia accompanied by pulmonary hypertension resistant to treatment is an important feature of congenital diaphragmatic hernia (CDH). The pathogenesis the vascular abnormalities in CDH remains be elucidated at molecular level. Vascular endothelial growth factor (VEGF), cell specific mitogen, known play a role angiogenesis and remodelling but there are no data on VEGF expression patients with CDH.Necroscopic lung specimens from 21 seven age matched control newborn infants...

10.1136/thx.54.5.427 article EN Thorax 1999-05-01

Section:ChooseTop of pageAbstract <<Materials and MethodsResultsDiscussionReferencesCITING ARTICLES

10.1165/ajrcmb.18.6.2924 article EN American Journal of Respiratory Cell and Molecular Biology 1998-06-01

Abstract An important feature of chronic obstructive pulmonary disease (COPD) is airway remodelling, the molecular mechanisms which are poorly understood. In this study, role fibroblast growth factors (FGF‐1 and FGF‐2) their receptor, FGFR‐1, was assessed in bronchial wall remodelling patients with COPD (FEV 1 &lt; 75%; n = 15) without &gt; 85%; 16). FGF‐1 FGFR‐1 were immunolocalized epithelium, smooth muscle (ASM), submucosal glandular vascular muscle. Quantitative digital image analysis...

10.1002/path.1748 article EN The Journal of Pathology 2005-03-16

Fresh bovine, porcine and canine hearts were homogenized mitogens for mesoderm‐derived cells purified in three different steps. Extraction by two ammonium sulfate precipitations was followed cation‐exchange chromatography heparin‐Sepharose affinity chromatography. A fraction from heart (eluted at 1.1 M NaCl) increased mitotic activity serum‐deprived cultures of aortic endothelial smooth muscle cells, human fibroblasts. This mitogenic is potentiated heparin inhibited γ‐interferon. The showed...

10.1111/j.1432-1033.1989.tb14694.x article EN European Journal of Biochemistry 1989-04-01

Section:ChooseTop of pageAbstract <<Materials and MethodsResultsDiscussionReferencesCITING ARTICLES

10.1165/ajrcmb.23.1.3765 article EN American Journal of Respiratory Cell and Molecular Biology 2000-07-01

Congenital heart disease (CHD) leading to increased pulmonary blood pressure and flow is an important cause of plexogenic arteriopathy (PPA). This type tends progress irreversible stage, hallmarked histologically by the emergence a number characteristic lesions, which include concentric laminar intimal proliferation fibrosis, plexiform lesions. The pathogenesis these connote very poor prognosis, not well understood. Since endothelial cell has been demonstrated in it was hypothesized that...

10.1002/(sici)1096-9896(200006)191:2<202::aid-path608>3.0.co;2-d article EN The Journal of Pathology 2000-01-01

Mediators of myocardial inflammation, predominantly cytokines, have for many years been implicated in the healing processes after infarction. In recent years, however, more attention has paid to possibility that inflammation may result deleterious complications The proinflammatory cytokines mediate dysfunction associated with infarction, severe congestive heart failure, and sepsis. A growing body literature suggests inflammatory mediators could play a crucial role ischemia-reperfusion...

10.1080/09629359791668 article EN cc-by Mediators of Inflammation 1997-01-01
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