Amer Alnajar
About
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Co-founder/Chief Medical Officer
Hoboken, New Jersey, United States
Résumé
Jobs
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Co-founder/Chief Medical OfficerVytalize HealthAug 2014 - Current (11 years 11 months)Vytalize Health is a leading value-based care platform helping primary care doctors strengthen relationships with their patients through data-driven, holistic, and personalized care. Vytalize provides an all-in-one solution including value-based incentives, smart technology, and a virtual and in-home clinic that enables small and large independent practices to succeed in value-based care arrangements. Vytalize's care delivery model transforms the healthcare experience for more than a hundred thousand Medicare beneficiaries across 16 states by helping them manage their chronic conditions in collaboration with their doctors. Learn more at www.vytalizehealth.com or email info@vytalizehealth.com- Resident DoctorHahnemann University HospitalJul 2012 - Jul 2014 (2 years 1 month)Internal Medicine
Education
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- DDrexel University College of MedicineDrexel University College of MedicineJan 2007 - Dec 2012 (6 years)
- Lehigh UniversityLehigh UniversityJan 2004 - Dec 2007 (4 years)
Publications
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- The LIM-Only Protein FHL2 Attenuates Lung Inflammation during Bleomycin-Induced FibrosisPLOS ONENov 2013Fibrogenesis is usually initiated when regenerative processes have failed and/or chronic inflammation occurs. It is characterised by the activation of tissue fibroblasts and dysregulated synthesis of extracellular matrix proteins. FHL2 (four-and-a-half LIM domain protein 2) is a scaffolding protein that interacts with numerous cellular proteins, regulating signalling cascades and gene transcription. It is involved in tissue remodelling and tumour progression. Recent data suggest that FHL2 might support fibrogenesis by maintaining the transcriptional expression of alpha smooth muscle actin and the excessive synthesis and assembly of matrix proteins in activated fibroblasts. Here, we present evidence that FHL2 does not promote bleomycin-induc
- HExpression and regulation of nicotine receptor and osteopontin isoforms in human pancreatic ductal adenocarcinomaHistology and HistopathologyJul 2011Osteopontin (OPN) is a secreted phospho-protein that confers on cancer cells a migratory phenotype. We have recently shown that nicotine, a risk factor in pancreatic ductal adenocarcinoma (PDA), induces an alpha7-nicotine acetylcholine receptor (α7-nAChR)-mediated increase of OPN in PDA cells. In this study, we tested nicotine's effect on the expression of OPN splice variants (OPNa, b, c) in PDA cells. We also analyzed the correlation between patients' smoking history with OPN and α7-nAChR levels. RT-PCR and UV-light-illumination of ethidium-bromide staining were used to examine the mRNA expression in tissue and PDA cells treated with or without nicotine (3-300 nM). Localization of total OPN, OPNc and α7-nAChR was analyzed by immunohistoche
- SExpression of a prometastatic splice variant of osteopontin, OPNC, in human pancreatic ductal adenocarcinoma.Surgery JournalAug 2009Osteopontin (OPN) is a secreted phosphoprotein that confers on cancer cells a migratory phenotype. We demonstrated recently that nicotine, a major risk factor in pancreatic ductal adenocarcinoma (PDA), increases OPN expression in PDA cells. An OPN splice variant, OPNc, supports anchorage independence and maybe the most potent OPN isoform to convey metastatic behavior. In this study, we tested the effect of nicotine on OPNc expression and analyzed the correlation between total OPN/OPNc levels and patients' smoking history.
- IInduction of osteopontin expression by nicotine and cigarette smoke in the pancreas and pancreatic ductal adenocarcinomaIJC International Journal of CancerFeb 2009Pancreatic ductal adenocarcinoma (PDA) is a lethal disease with etiological association with cigarette smoking. Nicotine, an important component of cigarettes, exists at high concentrations in the bloodstream of smokers. Osteopontin (OPN) is a secreted phosphoprotein that confers on cancer cells a migratory phenotype and activates signaling pathways that induce cell survival, proliferation, invasion, and metastasis. Here, we investigated the potential molecular basis of nicotine's role in PDA through studying its effect on OPN. Nicotine significantly (p < 0.02) increased OPN mRNA and protein secretion in PDA cells through activation of the OPN gene promoter. The OPN mRNA induction was inhibited by the nicotinic acetylcholine receptor antago