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Pathak V.A.,National Institute of Immunohaematology ICMR | Ghosh K.,Surat Raktadan Kendra and Research Center

Anemia is the primary clinical manifestation of malarial infections and is responsible for the substantial rate of morbidity. The pathophysiology discussed till now catalogued several causes for malarial anemia among which ineffective erythropoiesis being remarkable one occurs silently in the bone marrow. A systematic literature search was performed and summarized information on erythropoietic response upon malaria infection and the factors responsible for the same. This review summarizes the clinical and experimental studies on patients, mouse models, and in vitro cell cultures reporting erythropoietic changes upon malaria infection as well as factors accountable for the same. Inadequate erythropoietic response during malaria infection may be the collective effect of various mediators generated by host immune response as well as parasite metabolites. The interplay between various modulators causing the pathophysiology needs to be explored further. Globin gene expression profiling upon malaria infection should also be looked into as abnormal production of globin chains could be a possible contributor to ineffective erythropoiesis. © 2016 Vrushali A. Pathak and Kanjaksha Ghosh. Source

Mirgal D.,National Institute of Immunohaematology ICMR | Ghosh K.,Surat Raktadan Kendra and Research Center | Mahanta J.,Regional Medical Research Center | Dutta P.,Regional Medical Research Center | Shetty S.,National Institute of Immunohaematology ICMR
Transactions of the Royal Society of Tropical Medicine and Hygiene

Background: Recent studies in experimental mice have shown that mild deficiency of methylenetetrahydrofolate reductase (MTHFR) enzyme confers protection against malaria, thus providing an important basis for the hypothesis that MTHFR polymorphism, i.e. C677T, might have been subjected to selection pressure against malaria. The present study was undertaken in a malaria endemic region in North East India to assess whether a similar selection advantage exists for other genes in folate metabolism pathway. Methods: A total of 401 subjects including 131 symptomatic malaria, 97 asymptomatic malaria and 173 normal healthy controls were analysed for nine polymorphisms (single-nucleotide polymorphisms [SNPs] in eight genes and insertion/deletion in one gene): MTHFR C677T, methionine synthase reductase (MTRR) A66G, glutamate carboxypeptidase II (GCPII) C1561T, cystathionine beta-synthase (CBS) 844ins68, reduced folate carrier-1 (RFC-1) G80A, serine hydroxymethyltransferase (SHMT) C1420T, methionine synthase (MTR) A2756G, MTHFR G1793A (D 919G), glycine N-methyltransferase (GNMT) 1289 by PCR-RFLP technique. Differences in frequencies of genotype distribution of each polymorphic marker between these groups were evaluated. Results: MTRR A2756G, SHMT C1420T, GCPII C1561T, MTRR A2756G and GNMT C1289T and RFC1 G80A polymorphisms showed significantly different prevalence between different groups analyzed. No significant differences were seen in the distribution of other polymorphisms. Conclusions: The study gives a clue for the possible selection of specific polymorphisms in the genes involved in the folate metabolism pathway by malaria parasite. © The Author 2016. Source

Antony H.A.,Jawaharlal Institute of Postgraduate Medical Education & Research | Pathak V.,National Institute of Immunohaematology NII | Parija S.C.,Jawaharlal Institute of Postgraduate Medical Education & Research | Ghosh K.,Surat Raktadan Kendra and Research Center | Bhattacherjee A.,SciGenom Labs Pvt Ltd.
Genomics Data

The emergence and distribution of drug resistance in malaria are serious public health concerns in tropical and subtropical regions of the world. However, the molecular mechanism of drug resistance remains unclear. In the present study, we performed a high-throughput RNA-Seq to identify and characterize the differentially expressed genes between the chloroquine (CQ) sensitive (3D7) and resistant (Dd2) strains of Plasmodium falciparum. The parasite cells were cultured in the presence and absence of CQ by in vitro method. Total RNA was isolated from the harvested parasite cells using TRIzol, and RNA-Seq was conducted using an Illumina HiSeq 2500 sequencing platform with paired-end reads and annotated using Tophat. The transcriptome analysis of P. falciparum revealed the expression of ~. 5000 genes, in which ~ 60% of the genes have unknown function. Cuffdiff program was used to identify the differentially expressed genes between the CQ-sensitive and resistant strains. Here, we furnish a detailed description of the experimental design, procedure, and analysis of the transcriptome sequencing data, that have been deposited in the National Center for Biotechnology Information (accession nos. PRJNA308455 and GSE77499). © 2016 The Authors. Source

Ali S.,National Institute of Immunohaematology ICMR | Shetty S.,National Institute of Immunohaematology ICMR | Ghosh K.,National Institute of Immunohaematology ICMR | Ghosh K.,Surat Raktadan Kendra and Research Center
Blood Cells, Molecules, and Diseases

Inherited macrothrombocytopenia is a subgroup of thrombocytopenias, and is characterised by the presence of giant platelets and decreased platelet count with variable bleeding manifestations. Bengal macrothrombocytopenia is a newly described entity, previously called asymptomatic constitutional macrothrombocytopenia (ACMT), presented with variable bleeding tendencies; with mild to severe thrombocytopenia and macro-platelets in their peripheral blood smear and it is not totally an innocuous condition as described previously. © 2016 Elsevier Inc. Source

Shukla R.V.,Surat Raktadan Kendra and Research Center | Patel T.G.,Surat Raktadan Kendra and Research Center | Gupte S.C.,Surat Raktadan Kendra and Research Center
Indian Journal of Hematology and Blood Transfusion

Contaminating white blood cells in stored platelet concentrate (PC) are the source of many pro-inflammatory cytokines. These are implicated in transfusion reactions. To study the release of interleukin (IL)-8 and tumor necrosis factor alpha (TNF-α) at different time interval in PC prepared by-platelet rich plasma (PRP) and buffy coat (BC) using different principles. Fifteen PCs were prepared by both the methods. The supernatants of PCs prepared by PRP and BC methods were collected aseptically after 1, 18, 65 and 112 h of preparation. pH, platelet and WBC counts were done. The supernatants were frozen in aliquots at −56 °C for measurement of IL-8 and TNF-α concentration using ELISA. The Mean ± SD value of WBC in PRP-PC was 7.4 ± 3.75 × 107 and in BC-PC 3.9 ± 2.2 × 107. The mean platelet counts were 6.05 ± 1.94 × 1010 and 6.54 ± 2.18 × 1010 respectively. The highest level of IL-8 in one hour was up to 30 pg/ml in both the type of PC. It increased up to 986 pg/ml in PRP-PC and 481 pg/ml in BC-PC at 112 h. IL-8 increased significantly during storage period of 5 days in both types of PCs (P0.000 and P0.01). TNF-α level remained low up to 18 h. The highest level was 72 pg/ml in PRP-PC and 57 pg/ml in BC-PC at 65 h. IL-8 levels significantly increased after one hour of storage and TNF-α. levels were low up to 18 h and then showed increase. The BC-PC had significantly low levels of IL-8 compared to PRP-PC (P0.0001). © 2014, Indian Society of Haematology & Transfusion Medicine. Source

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