Serological Detection of Rh-Del Phenotype among Rh-Negative Blood Donors at National Blood Center, Yangon, Myanmar.

BACKGROUND: Red cell Rhesus (Rh) antigen expression is influenced by the genetic polymorphism of RHD and RHCE genes and reveals serologically different reactions of RhD variants such as partial D, weak D, and Rh-Del. Serologically, Rh-Del type can only be detected by an adsorption-elution technique, and it might be mistyped as Rh-negative. The prevalence of Rh-Del has not been reported yet in Myanmar. METHOD: A total of 222 Rh-negative blood donors in the National Blood Center were tested for weak D and Rh-Del by indirect antihuman globulin and adsorption-elution method, respectively. RhCE typing was performed among Rh-negative and Rh-Del. RESULTS: Of them, 75.2% (167/222) were Rh-negative, 15.8% (35/222) were Rh-Del, and 9% (20/222) were weak D. Of 202 blood donors (167 true Rh-negative and 35 Rh-Del), all of the Rh-Del positives were C-antigen-positive with 94.3% Ccee phenotype (33/35) and 5.7% CCee (2/35). Most of the Rh-negative donors (80.2%) were ccee phenotype (134/167). CONCLUSION: About half of Rh-Del subjects were repeated donors, and attention was needed to avoid transfusion of truly Rh-negative patients to prevent alloimmunization. It is recommended to do Rh-Del typing of Rh-negative donors who are C-antigen-positive and consider moving them to the Rh-positive pool. Further study is needed to clarify the alloimmunization status for transfusion of Rh-Del blood to Rh-negative recipients. Molecular markers for RhD-negative and D variants should be established in the Myanmar population to improve selection of antisera for Rh typing and enhance safety of the transfusion services.

microRNA-27a and microRNA-146a SNP in cerebral malaria.

BACKGROUND: During Plasmodium falciparum infection, microRNA expression alters in brain tissue of mice with cerebral malaria compared to noninfected controls. MicroRNA regulates gene expression post-transcriptionally to influence biological processes. Cerebral malaria pathology caused mainly by the immunological disorder. We hypothesize that single-nucleotide polymorphism in a microRNA influences microRNA biogenesis or target gene recognition and altering susceptibility to cerebral malaria. METHODS: We performed a literature search based on immunological mechanism and applied microRNA-related single-nucleotide polymorphisms database to examine candidate microRNA SNPs possibly responsible for cerebral malaria. MicroRNA-27a and microRNA-146a are supposed to involve in cerebral malaria pathology. To assess the relationship of microRNA SNP to cerebral malaria outcome, we performed TaqMan Genotyping Assays in 110 cerebral malaria and 207 uncomplicated malaria cases for three candidate microRNA SNPs (rs895819 of microRNA-27a, rs57095329 and rs2910164 of microRNA-146a). RESULTS: Our study detected no significant difference in genotype and allele frequency of individual microRNA SNPs as well as in haplotypes of microRNA-146a between these two groups of malaria patients in Thailand. Hardy-Weinberg disequilibrium of rs57095329 in the cerebral malaria group showed a heterozygous excess which might be due to natural selection. CONCLUSION: Our data supported that the candidate microRNA SNPs have no major role to develop cerebral malaria.

Prevalence of Anemia and Hemoglobin Disorders Among School Children in Myanmar.

The prevalence of anemia is high in the population of Myanmar and hypochromic microcytic anemia (HMA) is predominant. The objective of our study was to determine the prevalence of anemia and causes of HMA among school children. A cross-sectional study was conducted on 239 children from Thanlyin and Insein Townships, Yangon Region, Myanmar. Complete blood count (CBC) and blood film morphology was examined on venous blood samples. Hypochromic microcytic anemia cases were subsequently analyzed for serum ferritin and cellulose acetate hemoglobin (Hb) electrophoresis. The prevalence of anemia was 46.4%; 27.6% had mild, while 18.8% had moderate anemia, and no case of severe anemia was detected. The mean Hb concentration was 11.7 ± 0.9 g/dL. The younger age group (8-11 years) had a significantly higher prevalence of anemia than the older age group (12-15 years) (p = 0.029). Blood film morphology revealed a 50.6% red blood cell (RBC) disorder; HMA was the most common type (70.2%). Out of 85 children with HMA, three children (3.5%) had iron deficiency and all had comorbidity with Hb AE (ßA/ßE) (Hb E trait). Hemoglobin electrophoresis illustrated that Hb AA (ßA/ßA) (31, 36.5%) and Hb AE (ßA/ßE) trait (31, 36.5%) were the most common types followed by ß-thalassemia (ß-thal) trait (19, 22.3%) and Hb EE (ßE/ßE) (homozygous Hb E; HBB: c.79G>A) (three, 3.5%). Hematocrit [or packed cell volume (PCV)], mean corpuscular volume (MCV), mean corpuscular Hb (MCH) and mean corpuscular Hb concentration (MCHC), showed a significant difference between Hb AE, Hb EE and ß-thal trait (p = 0.029, 0.023, 0.015 and 0.01, respectively). Our findings will provide valuable information for the management of anemia in the Myanmar school-age population.

Molecular basis of human cerebral malaria development.

Cerebral malaria is still a deleterious health problem in tropical countries. The wide spread of malarial drug resistance and the lack of an effective vaccine are obstacles for disease management and prevention. Parasite and human genetic factors play important roles in malaria susceptibility and disease severity. The malaria parasite exerted a potent selective signature on the human genome, which is apparent in the genetic polymorphism landscape of genes related to pathogenesis. Currently, much genomic data and a novel body of knowledge, including the identification of microRNAs, are being increasingly accumulated for the development of laboratory testing cassettes for cerebral malaria prevention. Therefore, understanding of the underlying complex molecular basis of cerebral malaria is important for the design of strategy for cerebral malaria treatment and control.