Background: Serological testing for extended RHCcEe, Kell, Kidd and Duffy blood grouping from multitransfused patients may not give correct blood grouping of the recipient. Hence molecular testing for these blood groups was compared with serological groups in a cohort of multitransfused thalassemia mjor and sickle cell anaemia patients. Objective: Molecular genotyping of antigens of Rh (D, C, c, E, e), Kell (K, k), Duffy (Fy a , Fy b) and Kidd (Jk a , Jk b) blood group antigens by PCR and PCR-RFLP methods and comparison of predicted genotypes with their serological phenotypes. Materials and methods: A cohort of multitransfused thalassemia and sickle cell anemia patient were serologically and molecularly tested for RHCc, RHEe, K, k Fy a , Fy b , Jk a and Jk b antigens and compared. Serological testing was done by tube agglutination and molecular testing was done either by allele specific PCR or by RFLP technique just before next transfusion. Results: In more than 80% of the cases recipient's molecular testing blood groups were at variance with serologically tested blood groups (p < 0.0001). Mixed field reactions in serological typing were common. In sickle cell anemia patients no discrepancy was found. Molecular technique results were checked by Sanger's sequencing. Discussion: Extended phenotyping in multitransfused thalassemia patients by serological technique often donot detect the exact red cell phenotype of the recipient and molecular techniques for such grouping is preferable, especially in multitransfused thalassemia patients where red cells from previous transfusions continues to be present in significant numbers whenever the testing is done.

An otherwise healthy male child of 9 years presented with paroxysmal fever and diffuse abdominal pain along with loss of appetite and nausea lasting for 3-4days every 4-6 weeks for last 2 years. He also has stretchable skin and hypermobile joint which he inherited from his mother who never suffered any paroxysmal attack of the kind.  Work up for acute intermittent porphyria, lead poisoning and familial mediterranean fever was negative. A novel harmful sequence change in NLRP12 gene was detected and a diagnosis of NLRP12 associated autoinflammatory syndrome was made. This sequence change with disease has not yet been reported in the literature and is the first such case of NLRP12 related autoinflammatory syndrome from India.

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Background Hepatitis‐E virus (HEV) is an emerging infectious threat to blood safety. The enormity of the transmission of HEV and its clinical consequence are issues currently under debate. This study aimed to evaluate the prevalence of HEV‐RNA in blood donors in western India. Materials and Methods We screened 13 050 blood donors for HEV using HEV‐RNA screening of 10 mini‐pools using RealStar HEV RT‐PCR Kit (95% limit of detection (LOD): 4.7 IU/ml). Furthermore, all HEV‐RNA‐positive donors were investigated for the presence of IgM/IgG antibody along with liver function tests. Results Of the 13 050 blood donations, 7 (0.53%) were found to be HEV‐RNA positive, and the prevalence of HEV nucleic acid testing yield cases among blood donors was 1 in 1864. All seven HEV‐RNA‐positive samples were tested with anti‐HEV IgM and anti‐HEV IgG antibodies; this resulted in two (28.5%) positive anti‐HEV IgM and two (28.5%) positive anti‐HEV IgG antibodies. Hepatic activity was measured, with two of seven HEV‐RNA‐positive donors demonstrating abnormal serum glutamic oxaloacetic transaminase (SGOT) andserum glutamic pyruvic transaminase (SGPT). Two HEV‐RNA‐positive blood donors who had abnormal SGOT and SGPT were found to have a high HEV viral load. Furthermore, we were able to follow up two HEV‐RNA donors, and both were HEV‐RNA positive and had anti‐HEV IgM and anti‐HEV IgG antibodies; moreover, their liver function tests were also abnormal. One of the HEV‐RNA donors with high viral load did show hepatitis‐E‐like virus on electron microscopy. Conclusion Our studies indicate that there is a significant risk of blood‐borne transmission of HEV. This finding may help to provide a direction towards the safety of blood transfusions in clinical settings in countries like India, which fall under the endemic category for HEV infection.

The quantity of mesenchymal stem/stromal cells (MSCs) required for a particular therapy demands their subsequent expansion through ex vivo culture. During in vitro multiplication, they undergo replicative senescence which may alter their genetic stability. Therefore, this study was aimed to analyze cellular, molecular, and chromosomal alterations in Wharton’s jelly-derived MSCs (WJ-MSCs) during their in vitro sequential passages, where WJ-MSCs were sequentially passaged up to P14 and cells were evaluated at an interval of P2, P6, P10, and P14. They were examined for their morphology, tumorigenicity, surface markers, stemness markers, DNA damage, chromosomal aberration, and telomere length. We have processed five full-term delivered human umbilical cord samples to obtain WJ-MSCs. Morphological appearance observed at initial stages was small fine spindle-shaped WJ-MSCs which were transformed to flat, long, and broader cells in later passages. The cell proliferation rate was gradually decreased after the 10th passage. WJ-MSCs have expressed stemness markers OCT-4 and NANOG, while they showed high expression of positive surface markers CD90 and CD105 and lower expression of CD34 and CD45. They were non-tumorigenic with slow cellular aging during subsequent passages. There was no chromosomal abnormality up to the 14th passage, while increase in comet score and decrease in telomere length were observed in later passages. Hence, our study suggests that early and middle passaged (less than P10) WJ-MSCs are good candidates for clinical administration for treatment.