Institution
Tehran University of Medical Sciences
Education•Tehran, Iran•
About: Tehran University of Medical Sciences is a education organization based out in Tehran, Iran. It is known for research contribution in the topics: Population & Medicine. The organization has 35661 authors who have published 57234 publications receiving 878523 citations. The organization is also known as: TUMS.
Topics: Population, Medicine, Cancer, Randomized controlled trial, Health care
Papers published on a yearly basis
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TL;DR: The model indicates that decreasing the incarceration rate in people who inject drugs and providing opioid agonist therapy could reduce the burden of HIV in this population of prisoners.
455 citations
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Iran University of Medical Sciences1, Tehran University of Medical Sciences2, Tabriz University of Medical Sciences3, Shahid Beheshti University of Medical Sciences and Health Services4, Kermanshah University of Medical Sciences5, University of Alcalá6, Yale University7, NewYork–Presbyterian Hospital8, Universidad Católica San Antonio de Murcia9, Brigham and Women's Hospital10, Virginia Commonwealth University11, University of Nebraska Medical Center12, Icahn School of Medicine at Mount Sinai13, University of Liverpool14, Aalborg University15
TL;DR: In this paper, the authors evaluated the effects of intermediate-dose vs standard-dose prophylactic anticoagulation among patients with COVID-19 admitted to the intensive care unit (ICU).
Abstract: Importance Thrombotic events are commonly reported in critically ill patients with COVID-19. Limited data exist to guide the intensity of antithrombotic prophylaxis. Objective To evaluate the effects of intermediate-dose vs standard-dose prophylactic anticoagulation among patients with COVID-19 admitted to the intensive care unit (ICU). Design, Setting, and Participants Multicenter randomized trial with a 2 × 2 factorial design performed in 10 academic centers in Iran comparing intermediate-dose vs standard-dose prophylactic anticoagulation (first hypothesis) and statin therapy vs matching placebo (second hypothesis; not reported in this article) among adult patients admitted to the ICU with COVID-19. Patients were recruited between July 29, 2020, and November 19, 2020. The final follow-up date for the 30-day primary outcome was December 19, 2020. Interventions Intermediate-dose (enoxaparin, 1 mg/kg daily) (n = 276) vs standard prophylactic anticoagulation (enoxaparin, 40 mg daily) (n = 286), with modification according to body weight and creatinine clearance. The assigned treatments were planned to be continued until completion of 30-day follow-up. Main Outcomes and Measures The primary efficacy outcome was a composite of venous or arterial thrombosis, treatment with extracorporeal membrane oxygenation, or mortality within 30 days, assessed in randomized patients who met the eligibility criteria and received at least 1 dose of the assigned treatment. Prespecified safety outcomes included major bleeding according to the Bleeding Academic Research Consortium (type 3 or 5 definition), powered for noninferiority (a noninferiority margin of 1.8 based on odds ratio), and severe thrombocytopenia (platelet count Results Among 600 randomized patients, 562 (93.7%) were included in the primary analysis (median [interquartile range] age, 62 [50-71] years; 237 [42.2%] women). The primary efficacy outcome occurred in 126 patients (45.7%) in the intermediate-dose group and 126 patients (44.1%) in the standard-dose prophylaxis group (absolute risk difference, 1.5% [95% CI, −6.6% to 9.8%]; odds ratio, 1.06 [95% CI, 0.76-1.48];P = .70). Major bleeding occurred in 7 patients (2.5%) in the intermediate-dose group and 4 patients (1.4%) in the standard-dose prophylaxis group (risk difference, 1.1% [1-sided 97.5% CI, −∞ to 3.4%]; odds ratio, 1.83 [1-sided 97.5% CI, 0.00-5.93]), not meeting the noninferiority criteria (Pfor noninferiority >.99). Severe thrombocytopenia occurred only in patients assigned to the intermediate-dose group (6 vs 0 patients; risk difference, 2.2% [95% CI, 0.4%-3.8%];P = .01). Conclusions and Relevance Among patients admitted to the ICU with COVID-19, intermediate-dose prophylactic anticoagulation, compared with standard-dose prophylactic anticoagulation, did not result in a significant difference in the primary outcome of a composite of adjudicated venous or arterial thrombosis, treatment with extracorporeal membrane oxygenation, or mortality within 30 days. These results do not support the routine empirical use of intermediate-dose prophylactic anticoagulation in unselected patients admitted to the ICU with COVID-19. Trial Registration ClinicalTrials.gov Identifier:NCT04486508
447 citations
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University College London1, University of California, Los Angeles2, Pasteur Institute3, University Medical Center Freiburg4, University of Düsseldorf5, Selçuk University6, Ege University7, Istanbul University8, Marmara University9, Newcastle University10, Boston Children's Hospital11, University of Milan12, Tehran University of Medical Sciences13, St George's Hospital14, Sultan Qaboos University15, University of California, San Francisco16, National Institutes of Health17
TL;DR: In this paper, the authors identify a gene that is mutated or deleted in autosomal recessive hyper-IgE syndrome and perform genome-wide single nucleotide polymorphism analysis to locate copy number variations and homozygous haplotypes.
Abstract: Background The genetic etiologies of the hyper-IgE syndromes are diverse. Approximately 60% to 70% of patients with hyper-IgE syndrome have dominant mutations in STAT3, and a single patient was reported to have a homozygous TYK2 mutation. In the remaining patients with hyper-IgE syndrome, the genetic etiology has not yet been identified. Objectives We aimed to identify a gene that is mutated or deleted in autosomal recessive hyper-IgE syndrome. Methods We performed genome-wide single nucleotide polymorphism analysis for 9 patients with autosomal-recessive hyper-IgE syndrome to locate copy number variations and homozygous haplotypes. Homozygosity mapping was performed with 12 patients from 7 additional families. The candidate gene was analyzed by genomic and cDNA sequencing to identify causative alleles in a total of 27 patients with autosomal-recessive hyper-IgE syndrome. Results Subtelomeric biallelic microdeletions were identified in 5 patients at the terminus of chromosome 9p. In all 5 patients, the deleted interval involved dedicator of cytokinesis 8 (DOCK8) , encoding a protein implicated in the regulation of the actin cytoskeleton. Sequencing of patients without large deletions revealed 16 patients from 9 unrelated families with distinct homozygous mutations in DOCK8 causing premature termination, frameshift, splice site disruption, and single exon deletions and microdeletions. DOCK8 deficiency was associated with impaired activation of CD4 + and CD8 + T cells. Conclusion Autosomal-recessive mutations in DOCK8 are responsible for many, although not all, cases of autosomal-recessive hyper-IgE syndrome. DOCK8 disruption is associated with a phenotype of severe cellular immunodeficiency characterized by susceptibility to viral infections, atopic eczema, defective T-cell activation and T h 17 cell differentiation, and impaired eosinophil homeostasis and dysregulation of IgE.
441 citations
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TL;DR: Considering the potential applications of NPs in many fields and the growing apprehensions of FDA about the toxic potential of nanoproducts, the need of the hour to look for new internationally agreed free of bias toxicological models by focusing more on in vivo studies.
Abstract: Nanotechnology is a rapidly growing field having potential applications in many areas. Nanoparticles (NPs) have been studied for cell toxicity, immunotoxicity, and genotoxicity. Tetrazolium-based assays such as MTT, MTS, and WST-1 are used to determine cell viability. Cell inflammatory response induced by NPs is checked by measuring inflammatory biomarkers, such as IL-8, IL-6, and tumor necrosis factor, using ELISA. Lactate dehydrogenase (LDH) assay is used for cell membrane integrity. Different types of cell cultures, including cancer cell lines have been employed as in vitro toxicity models. It has been generally agreed that NPs interfere with either assay materials or with detection systems. So far, toxicity data generated by employing such models are conflicting and inconsistent. Therefore, on the basis of available experimental models, it may be difficult to judge and list some of the more valuable NPs as more toxic to biological systems and vice versa. Considering the potential applications of NPs in many fields and the growing apprehensions of FDA about the toxic potential of nanoproducts, it is the need of the hour to look for new internationally agreed free of bias toxicological models by focusing more on in vivo studies.
440 citations
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TL;DR: It is suggested that HAX1 is a major regulator of myeloid homeostasis and underline the significance of genetic control of apoptosis in neutrophil development.
Abstract: Autosomal recessive severe congenital neutropenia (SCN) constitutes a primary immunodeficiency syndrome associated with increased apoptosis in myeloid cells, yet the underlying genetic defect remains unknown. Using a positional cloning approach and candidate gene evaluation, we identified a recurrent homozygous germline mutation in HAX1 in three pedigrees. After further molecular screening of individuals with SCN, we identified 19 additional affected individuals with homozygous HAX1 mutations, including three belonging to the original pedigree described by Kostmann. HAX1 encodes the mitochondrial protein HAX1, which has been assigned functions in signal transduction and cytoskeletal control. Here, we show that HAX1 is critical for maintaining the inner mitochondrial membrane potential and protecting against apoptosis in myeloid cells. Our findings suggest that HAX1 is a major regulator of myeloid homeostasis and underline the significance of genetic control of apoptosis in neutrophil development.
439 citations
Authors
Showing all 35946 results
Name | H-index | Papers | Citations |
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Graeme J. Hankey | 137 | 844 | 143373 |
Paul D.P. Pharoah | 130 | 794 | 71338 |
Jerome Ritz | 120 | 644 | 47987 |
Reza Malekzadeh | 118 | 900 | 139272 |
Robert N. Weinreb | 117 | 1124 | 59101 |
Javad Parvizi | 111 | 969 | 51075 |
Omid C. Farokhzad | 110 | 329 | 64226 |
Ali Mohammadi | 106 | 1149 | 54596 |
Alexander R. Vaccaro | 102 | 1179 | 39346 |
John R. Speakman | 95 | 667 | 34484 |
Philip J. Devereaux | 94 | 443 | 110428 |
Rafael Lozano | 94 | 265 | 126513 |
Mohammad Abdollahi | 90 | 1045 | 35531 |
Ingmar Skoog | 89 | 458 | 28998 |
Morteza Mahmoudi | 83 | 334 | 26229 |