Results 41 to 50 of about 39,321 (195)

Evaluation of Alpha-Thalassemia Mutations in Cases with Hypochromic Microcytic Anemia: The İstanbul Perspective

open access: yesTurkish Journal of Hematology, 2015
INTRODUCTION: Alpha thalassemia syndromes are caused by mutations on one or more of the four α-globin genes. Mutations could be either more commonly deletional or non-deletional. As some deletions (3.7 and 4.2) cause α+-thalassemia, some cause (
Zeynep Karakaş   +11 more
doaj   +1 more source

Chronic hyperplastic anemia as an independent risk factor for atherosclerotic lesions: a lesson from thalassemia intermedia [PDF]

open access: yes, 2010
Introduction. Cardiovascular involvement represents a well-known complication and the primary cause of mortality, both in transfusion-dependent beta thalassemia major (β-TM) and in transfusion-independent beta thalassemia intermedia (β-TI ...
Alessandra Spiga   +7 more
core   +1 more source

Nonsense-mediated decay mechanism is a possible modifying factor of clinical outcome in nonsense cd39 beta thalassemia genotype [PDF]

open access: yes, 2012
Nonsense-mediated mRNA decay (NMD) is a surveillance system to prevent the synthesis of non-functional proteins. In β-thalassemia, NMD may have a role in clinical outcome.
ATTANASIO, Massimo   +11 more
core   +1 more source

Alpha globin gene alterations modifying the phenotype of homozygous beta thalassaemia

open access: yeseJHaem
The phenotype of β‐thalassemia varies widely. The primary determinant is the type of beta‐globin gene mutation; however, there are secondary and tertiary modifiers also as associated alpha mutations, polymorphisms, as well as coinheritance of mutations ...
Jyoti Shaw   +7 more
doaj   +1 more source

Effects of vitamin e and zinc supplementation on antioxidants in beta thalassemia major patients [PDF]

open access: yes, 2011
Objective: In beta thalassemic patients, tissue damage occurs due to oxidative stress and it happens because of the accumulation of iron in the body. This study was conducted to determine the effect of zinc and vitamin E supplementation on antioxidant ...
Aboomardani, M.   +5 more
core   +1 more source

Prevalence of Co-Inheritance of Alpha-Thalassemia with Beta-Thalassemia and Beta-Hemoglobinopathy in Ahvaz City

open access: yesJournal of Ardabil University of Medical Sciences, 2013
Background: Co-inheritance of hemoglobin gene defects is a rare important status that can lead to double heterozygote or homozygote with significant clinical manifestations. Such conditions can be observed in co-inheritance of alpha-thalassemia with beta-
Najmaddin Saki   +8 more
doaj  

Low prevalence of an acute phase response in asymptomatic children from a malaria-endemic area of Papua New Guinea [PDF]

open access: yes, 2007
Levels of C-reactive protein (CRP), a classic marker for the acute phase response (APR), were measured in children with asymptomatic malaria infection in the Amele region of Papua New Guinea (PNG).
Day, KP   +6 more
core  

Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells [PDF]

open access: yes, 2006
Antioxidant phytochemicals are investigated as novel treatments for supportive therapy in b-thalassemia. The dietary indicaxanthin was assessed for its protective effects on human b-thalassemic RBCs submitted in vitro to oxidative haemolysis by cumene ...
Allegra, M.   +4 more
core   +1 more source

Revealing the molecular signatures of host-pathogen interactions. [PDF]

open access: yes, 2011
Advances in sequencing technology and genome-wide association studies are now revealing the complex interactions between hosts and pathogen through genomic variation signatures, which arise from evolutionary co ...
C Herdtweck   +53 more
core   +13 more sources

Alpha- Thalassemia: An Overview

open access: yesScholars Journal of Applied Medical Sciences, 2023
Alpha-Thalassemia is the commonest hereditary monogenic disease worldwide. α-thalassemia is caused by α-globin gene losses and categorized into α-thalassemia 1 and α-thalassemia 2 depending on how many α-globin genes are functioning. Α thalassemia 1 is defined by inactivation of both α-globin genes on a chromosome, while in α-thalassemia 2, one gene is
openaire   +1 more source

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