S Agrawal

Banaras Hindu University, Vārānasi, Uttar Pradesh, India

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Publications (36)81.42 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to investigate the HLA-G 14-bp insertion/deletion (I/D) polymorphism among end-stage renal disease (ESRD) patients. Cytomegalovirus (CMV) infection, acute allograft rejection (AR) and overall survival after renal transplantation was investigated in 300 ESRD patients and 302 age, sex and ethnicity-matched controls. Sequencing was performed to evaluate the impact of HLA-G promoter region single-nucleotide polymorphisms (SNPs) whereas semi-quantitative PCR method was used to determine the probable HLA-G expression pattern among ESRD and AR cases. Further, soluble human leukocyte antigen (HLA)-G (sHLA-G) expression levels were compared in AR vs non-AR cases in the light of HLA-G 14-bp I/D polymorphism. Increased risk was found for 14-bp D/D (deletion-DD) genotype and 14-bp D allele [DD: odds ratio (OR) = 1.46, 95% confidence interval (CI) = 1.03-2.06, P value = 0.0358; D: OR = 1.29, 95% CI = 1.03-1.62, P value = 0.0277], respectively for ESRD and CMV infection (DD: OR = 2.70, 95% CI = 1.45-5.05, P value = 0.0021; D: OR = 1.94, 95% CI = 1.22-3.08, P value = 0.0052). Nearly fourfold (OR = 3.62, 95%CI = 1.61-8.14, p = 0.0039) risk was observed for 14-bp I/I (insertion-II) genotype for AR. Survival analysis showed increased overall survival (OS) (AR or death) for 14-bp D/D genotype. HLA-G promoter region sequencing was carried out among 60 ESRD patients and 100 normal controls which showed increased risk for -964 G>A, -725 C>G/T and -486 A>C SNPs. -964 G>A and -725 C>G/T SNPs showed risk association for AR patients. High level of HLA-G transcripts was observed among non-AR patients. Further soluble HLA-G (sHLA-G) showed increased levels in ESRD patients (mean ± SEM; 62.16 ± 2.43 U/ml) as compared to controls (mean ± SEM; 21.06 ± 3.89 U/ml) (P = <0.0001). The 14-bp I/I, 14-bp I/D and 14-bp D/D genotypes showed significantly higher levels of sHLA-G among non-AR as compared to AR patients.
    Tissue Antigens 11/2013; 82(5):317-26. · 2.35 Impact Factor
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    ABSTRACT: The trophoblast cells at the maternal-fetal interface express an unusual combination of human leukocyte antigen (HLA)-C, HLA-E and HLA-G. Altered expression of HLA-G on the extravillous cytotrophoblast has been implicated in the etiology of recurrent miscarriages (RMs). We have assessed HLA-G expression in extravillous cytotrophoblast in cell cultures prepared from RM patients and compared with those of first-trimester voluntarily terminated normal pregnancies (control). Glucocorticoids, dexamethasone and hydrocortisone were examined for their role in modulation of the HLA-G expression. HLA-G promoter and 3'UTR variants were investigated for their effect on the transcription of HLA-G. Cultured cytotrophoblast cells from the first-trimester RM patients were treated with dexamethasone and hydrocortisone (dose concentration 0-1000 ng/ml). HLA-G gene transcription was determined by semiquantitative and quantitative real-time polymerase chain reaction (RT-PCR), while protein expression was determined by a specific enzyme-linked immunosorbent assay (ELISA), flow cytometry and western blot analyses. HLA-G polymorphisms were detected by PCR and/or sequence-based typing. Low level of HLA-G was observed in untreated trophoblast cells obtained from RM patients as compared with controls. Upon treatment with glucocorticoids, the expression of HLA-G in these cells was up-regulated in a dose-dependent manner (P < 0.05), with no change in cellular proliferation and viability. There was no significant association between HLA-G polymorphism in RM patients and controls. HLA-G is minimally expressed in cultured trophoblast cells of RM patients. It can be up-regulated upon exposure with both dexamethasone and hydrocortisone. Glucocorticoids have the potential to modulate HLA-G expression in vitro, and can be further examined for their therapeutic applicability in RM.
    Tissue Antigens 05/2012; 80(2):126-35. · 2.35 Impact Factor
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    ABSTRACT: The aim of this study was to determine whether or not interleukin-1 alpha (IL-1a), interleukin-1 beta (IL-1b) and IL-1 receptor antagonist (IL-1RA) polymorphisms are associated with risk of unexplained recurrent pregnancy loss (RPL) among North Indian women. This retrospective case–control study examine 200 well-characterized RPL cases for IL-1 gene cluster variants, determined by restriction fragment length polymorphism-PCR. The observed allele, genotype and haplotype distributions were compared with those obtained from 300 ethnically matched negative controls. Invariant distribution of IL-1 gene cluster single-nucleotide polymorphisms was observed among RPL cases and controls. Meta-analysis of IL-1b _511, +3953 and IL-1RN 86-bp variable number tandem repeat from the reported literature and this study did not reveal any significant association with the risk of RPL. In conclusion, no significant difference between RPL and control groups was observed at the allele, genotype or haplotype levels when tested for association using the dominant, recessive and additive models of inheritance for IL-1 gene cluster variants. As far as is known, this is the first report from India pertaining to IL-1 gene cluster variants’ association with the risk of RPL from North India.
    Reproductive biomedicine online 03/2012; 24(3):342-51. · 2.68 Impact Factor
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    ABSTRACT: Recurrent miscarriage (RM), defined as three or more consecutive losses before the 20th week of gestation, affects 0.5-2% of pregnant women. In over 80% of cases, RM remains unexplained after investigations, suggesting the involvement of genetic factors. The present study investigates the common polymorphisms of chemokine receptors CCR5 (NG_012637.1:g.5303A>G) and CX3CR1 (NG_016362.1:g.21065C>T, Thr280Met and NG_016362.1:g.20971G>A, Val249Ile) and their association with recurrent miscarriages (RM) among north Indian women. In a retrospective case-control study 200 well characterized patients with unexplained RM and 300 controls were genotyped for three polymorphic markers of CCR5 and CX3CR1 by restriction digestion of PCR amplified fragments. Alleles and genotypes of CX3CR1 Val249Ile revealed statistically significant associations with RM cases when compared with the controls. The homozygous variant genotype Ile/Ile was found to be significantly higher among patients (p=0.0002) when compared with the homozygous wild type Val/Val genotype. The haplotype of CX3CR1 that carried major alleles of Thr280Met and Val249Ile (T-V) showed statistically significant protective association (p<0.0001, OR=0.41, 95% CI=0.31-0.54). The haplotype A-T-V (all wild type alleles) revealed a statistically significant protective association (p<0.0001, OR=0.41, 95% CI=0.34-0.62), whereas the haplotypes G-T-I, A-T-I and A-M-V modified the risk of RM 1.9-fold, 5.5-fold and 5.1-fold respectively. A common polymorphism of CX3CR1 gene, Val240Ile is associated with the risk of RM in north Indian women. Risk of RM may also be modified by the presence of haplotypes T-I, M-V, G-T-I, A-T-I and A-M-V.
    Cytokine 08/2011; 56(2):239-44. · 2.87 Impact Factor
  • F Parveen, R M Faridi, S Alam, S Agrawal
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    ABSTRACT: This study investigated the association of common polymorphisms of the endothelial nitric oxide synthase (eNOS) gene with recurrent miscarriage (RM) among North Indian women. A total of 200 patients with unexplained recurrent miscarriages and 300 controls were genotyped for six polymorphic regions of eNOS by PCR, re-sequencing and RFLP. The GG genotype of 12862A>G, the G allele of Glu298Asp and the aa genotype of intron 4VNTR increased the risk of RM by ∼1.8-fold, ∼3.5-fold and ∼2-fold, respectively (odds ratio (OR) 1.84, 95% confidence intervals (CI) 1.19-2.86, P=0.0066; OR 3.58, 95% CI 2.12-6.03, P<0.0001; and OR 2.23, 95% CI 1.04-4.77, P=0.0493). Two haplotypes were found to have a significant protective effect against RM (OR 0.63, 95% CI 0.48-0.82, P=0.0009; and OR 0.4, 95% CI 0.19-0.81, P=0.0149) and another was found to increase the risk of RM by ∼2-fold (OR 2.12, 95% CI 1.16-3.89 P=0.0195). In conclusion three common polymorphisms of eNOS gene, 12862A>G, Glu298Asp and intron 4VNTR increase the risk of RM in North Indian women. Risk of RM may also be modified by the presence of particular haplotypes.
    Reproductive biomedicine online 04/2011; 23(1):124-31. · 2.68 Impact Factor
  • R M Faridi, S Agrawal
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    ABSTRACT: Decidual natural killer (NK) cells play key developmental roles at the feto-maternal interface. Individual differences in NK-cell interactions are dependent on the combinations of variable killer immunoglobulin-like receptor (KIR) and HLA class-I gene products. As different receptor-ligand interactions may result in altered NK-cell-mediated immunity against pathogens, it is proposed that the relationship between these genes may be important in a state such as recurrent miscarriage (RM). We had earlier reported that the predisposition to RM is influenced by the maternal KIR gene content. In the present study, we have attempted to extend our findings in the light of contribution from the paternal antigens on the outcome of pregnancy, since maternal NK cells may potentially encounter non-self-paternal HLA-C alleles on trophoblasts. All HLA-C allotypes fall into two major KIR epitopes--C1 (HLA-C*01/*03/*07/*08/*12/*14/*16) and C2 (HLA-C*02/*04/*05/*06/*15/*17/*18)--on the basis of a dimorphism at position 80 of the α1 domain. PCR-sequence specific primer-based genotyping was used to determine the maternal KIR gene content and HLA-C genotypes down to allele level in couples experiencing RM and controls. KIR2DL1 with both partners homozygous for HLA C2 was significantly higher in control couples when compared with the patients [P = 0.0004, odds ratio (OR) = 0.28, 95% confidence interval (CI) = 0.13-0.58]. The activating KIR2DS2 with both partners homozygous for HLA C1 was significantly higher in patients when compared with the controls (P = 0.002, OR = 2.83, 95% CI = 1.47-5.40). Our results represented the 'top-end' of the activation spectrum of KIR-HLA-C compound genotype for NK cells and this may contribute to the immunological etiology of RM.
    Human Reproduction 02/2011; 26(2):491-7. · 4.59 Impact Factor
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    ABSTRACT: The aim of the study was to study the distribution of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism, and its association with steroid responsiveness in children with idiopathic nephrotic syndrome (INS). One hundred twenty-five children with INS were classified into two groups: steroid-sensitive nephrotic syndrome (SSNS: n = 90) and steroid-resistant nephrotic syndrome (SRNS: n=35). The control group consisted of 150 unrelated healthy children. Genomic DNA was extracted from peripheral leucocytes by the standard salting-out method. ACE genotyping was performed and ACE genotypes DD, ID, and II were compared between different groups. The frequency distribution of the DD genotype was significantly increased in children with INS compared to control subjects (P = 0.0012) while the difference was not significant (P = 0.071) between SSNS and control subjects. The frequency distribution of the DD genotype was significantly high in the SRNS group compared to control subjects (P < 0.0001). The distribution of the DD genotype was high in SRNS compared to SSNS group patients (P = 0.016). In conclusion, the presence of the DD genotype may predict risk for steroid resistance in childhood INS.
    Indian Journal of Nephrology 01/2011; 21(1):26-9.
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    ABSTRACT: Allelic variants of the detoxification genes that have impaired biotransformation functions may increase susceptibility to reproductive toxicity leading to endometriosis, recurrent miscarriage (RM) or poor pregnancy outcome. In the present study, we have investigated CYP1A1, CYP2D6, GSTT1, GSTP1 and GSTM1, which are involved in the phase I and phase II detoxification systems, in relation to their role in the etiology of unexplained RMs. In a case-control study, we have investigated 200 females with RM and 300 age and ethnically matched healthy controls with successful reproductive history from North India. The frequencies of phase I wild-type genotypes of CYP1A1 and CYP2D6 in RM cases were 0.56 and 0.60, whereas in controls these were 0.68 and 0.65, respectively (both P < 0.05). The GSTM1 null-genotype frequencies were 0.66 and 0.84 among RM cases and controls, respectively, the GSTT1 null-genotype frequencies were 0.52 and 0.45 (P < 0.005) and the GSTP1 variant allele frequencies were 0.23 and 0.20, respectively. In conclusion, we observed significant protective effects of phase I wild-type genotypes and association of the GSTT1 null genotype with RM. Through combined analyses we have highlighted the importance of the balance of phase I/phase II detoxification systems, in the etiology of RM.
    Molecular Human Reproduction 11/2009; 16(3):207-14. · 3.48 Impact Factor
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    ABSTRACT: Polymorphisms in paraoxonase 1 (PON1) coding for PON1 enzyme have been studied as genetic markers of coronary artery disease (CAD). PON1 Q192R and PON1 L55M polymorphisms have been analyzed extensively, but data on association and role of these polymorphisms in the etiology of CAD are conflicting. In this study, we tested the genetic association between PON1 Q192R and PON1 L55M polymorphisms and CAD among north Indians. Two hundred eighty-five angiographically proven patients with coronary artery disease and 200 sex-matched and ethnically matched controls were genotyped for 2 PON1 polymorphisms by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Genotype/ allele frequencies were compared in patients and controls using the chi-square test. At PON1-192 locus, there were significant differences between patients and controls (P< 0.05), leading to significant odds ratios for RR genotype (OR= 1.92, CI: 1.19-3.10) and *R allele (OR= 1.30, CI: 1.00-1.70). These odds ratios were higher in the sub-sample of smokers (2.84 and 1.45, respectively). Binary logistic regression analysis also confirmed that *R allele carriers (QR and RR) have a higher risk of CAD (OR= 3.54, CI: 1.67-5.53). PON1-55 locus did not show significant differences between patients and controls, but LL genotype and *L allele were significant risk factors in the nonsmoker group. RL haplotype was also significantly associated with CAD risk (OR= 1.44, CI: 1.08-1.93). PON1-192R allele and RR genotype are significantly associated with CAD patients from the north Indian population (Uttar Pradesh). This association was stronger in smokers, supporting the conclusion that an interaction between PON1 activity and smoking augments CAD risk. Further studies with larger sample size are warranted to confirm these associations in different Indian populations.
    Indian Journal of Medical Sciences 08/2009; 63(8):335-44.
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    ABSTRACT: Cytokines and intercellular adhesion molecule (ICAM) play a crucial role in the pathogenesis of primary kidney disease and progression to end-stage renal disease (ESRD). Cytokine secretion is reported to be dependent on the single nucleotide polymorphisms located in the cytokine genes. The role of different polymorphisms in cytokines and ICAM genes as probable susceptibility factors for ESRD has been explored in the present study. The study was conducted on 258 ESRD patients and on ethnically matched 569 controls. Individuals were genotyped for interleukin (IL)-6 (G174C), IL-4 (C590T), tumor necrosis factor-alpha (TNF-alpha) (-G308A and -G238A) and ICAM-1 (A469G) gene polymorphisms using standard polymerase chain reaction-restriction fragment length polymorphism-based method. We observed significant difference in the genotype frequencies of the TNF-alpha-308AA [P = 0.001; odds ratios (OR) = 7.61, 95% confidence intervals (CI) = 2.1-27.9] and TNF-alpha-238AA (P = 0.001; OR = 5.8, 95% CI = 2.2-15.1). Furthermore, C allele of IL-6 -G174C and G allele of ICAM-1 A469G were significantly different in ESRD patients when compared with controls (P = 0.0001; OR = 5.5, 95% CI = 3.9-7.7 and P < 0.0001; OR = 3.8, 95% CI = 3.1-4.7). For the IL-4 C590T polymorphism, although the homozygous mutant genotype (TT) was not found to be significantly associated with ESRD, a statistically significant association with T allele (P = 0.008) was observed. Furthermore, combined analysis showed a higher risk in ESRD patients with high IL-4- and low IL-6-producing genotypes, low IL-4- and low IL-6-producing genotypes and high-producing genotype of TNF-alpha (308 and 238) with the increased risk of 6.47-, 3.7- and 3.3-fold, respectively. Our results suggest that IL-6, IL-4, TNF-alpha and ICAM gene polymorphisms are implicated in ESRD.
    Tissue Antigens 07/2009; 74(2):147-55. · 2.35 Impact Factor
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    ABSTRACT: Understanding of the immune events and mechanisms occurring at the feto-maternal interface is likely to help in understanding the ability of the fetus to survive within the maternal body. Evidence supporting extensive roles of natural killer cells during pregnancy gives rise to a possibility that these NK cells can be mis-regulated and involved in fetal allograft rejection. Killer immunoglobulin-like receptors (KIR) play an important role in regulating the NK cell activity through their activating and inhibiting isoforms. Since there exists a considerable, genetically determined variation in the repertoire of KIR receptors between different individuals, a particular maternal KIR repertoire may predispose to recurrent miscarriages (RMs). Gene-specific PCR amplification (PCR-SSP) was used to determine the individual KIR genotypes in women experiencing RM and controls. A higher prevalence of activating KIR genes was seen in patients than in controls. Among women experiencing RM, the BB genotypes were more prevalent (P < 0.0001, OR = 4.4, 95% CI = 2.89-6.69) compared with controls. Our results indicate that the balance between inhibitory and activating receptor-mediated signals present in natural killer cells is inclined toward a more activating state that may contribute to pregnancy loss.
    Human Reproduction 03/2009; 24(7):1758-64. · 4.59 Impact Factor
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    ABSTRACT: India is like a microcosm of the world in terms of its diversity; religion, climate and ethnicity which leads to genetic variations in the populations. As a highly polymorphic marker, the human leukocyte antigen (HLA) system plays an important role in the genetic differentiation studies. To assess the genetic diversity of HLA class II loci, we studied a total of 1336 individuals from north India using DNA-based techniques. The study included four endogamous castes (Kayastha, Mathurs, Rastogies and Vaishyas), two inbreeding Muslim populations (Shias and Sunnis) from north India and three northeast Indian populations (Lachung, Mech and Rajbanshi). A total of 36 alleles were observed at DRB1 locus in both Hindu castes and Muslims from north, while 21 alleles were seen in northeast Indians. At the DQA1 locus, the number of alleles ranged from 11 to 17 in the studied populations. The total number of alleles at DQB1 was 19, 12 and 20 in the studied castes, Muslims and northeastern populations, respectively. The most frequent haplotypes observed in all the studied populations were DRB1*0701-DQA1*0201-DQB1*0201 and DRB1*1501-DQA1*0103-DQB1*0601. Upon comparing our results with other world populations, we observed the presence of Caucasoid element in north Indian population. However, differential admixturing among Sunnis and Shias with the other north Indians was evident. Northeastern populations showed genetic affinity with Mongoloids from southeast Asia. When genetic distances were calculated, we found the north Indians and northeastern populations to be markedly unrelated.
    Tissue Antigens 09/2008; 72(2):120-30. · 2.35 Impact Factor
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    ABSTRACT: Polymorphisms in genes coding for chemokine receptors, CCR2 and CCR5 have been studied as genetic markers of coronary artery disease (CAD). V64Ile polymorphism in CCR2 has been implicated in the manifestation of myocardial infarction in different populations, but data on association of the CCR5 deletion variant in etiology of CAD are conflicting. In the present study we tested genetic association between CCR5 Delta32 polymorphism and CAD among North Indians (Uttar Pradesh). Two hundred angiographically proven patients with coronary artery disease and two hundred age, sex and ethnically matched controls were genotyped for CCR5 Delta32 polymorphism by polymerase chain reaction. Genotype/allele frequencies were compared in patients and controls using the chi-square test. The frequency of the heterozygote genotype in the population, including both patient and control group, was 3% and the frequency of the mutant allele Delta32 was 1.5%. CAD patients had a three times higher (4.6% vs. 1.5%) frequency of heterozygote genotype but the differences were statistically not significant. Association analysis did not achieve statistical significance, though odds ratio of 3.13 was observed for heterozygote genotype. The allele frequency of the CCR5 Delta32 polymorphism in CAD patients is 2.25% and 0.75% among controls but the differences were not significant. Overall this fits well with the pattern of CCR5 Delta32 allele frequency in Indian subcontinent where it varies from 1 to 3%. The heterozygote (+/ Delta32) genotype does not seem to have any protective role against development of CAD in this population. In fact, North Indian CAD had a higher frequency of CCR5 Delta32 allele suggesting a possible susceptibility trend (odds ratio 3.08, CI 0.83-11.46, chi-square 2.167, NS).
    International journal of cardiology 03/2008; 124(2):254-8. · 6.18 Impact Factor
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    ABSTRACT: We report here the capacity of three analogs of Splenopentin, to up regulate transcription of the HLA -B7 gene in the K562 cell line. These cells normally do not transcribe the HLA class I genes. The Splenopentin analogs used in this study are effective at very low molar concentrations and are non-toxic to cells at these levels. Electrophoretic Mobility Shift assays indicate that this transcriptional up regulation of HLA class I genes may be related to the appearance of novel class I promoter binding factors induced in the nuclei of treated cells.
    International Union of Biochemistry and Molecular Biology Life 01/2008; 41(3):521 - 528. · 2.79 Impact Factor
  • P Tripathi, S Agrawal
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    ABSTRACT: After the discovery of human immunodeficiency virus (HIV) and its role in the causation of most devastating epidemic acquired immune deficiency syndrome (AIDS), there has been an increasing trend to decipher the mechanism of infection and to understand why it cannot be controlled by our immune system. By evolution, our immune system has been empowered and enough trained to recognize, elicit immune response and remove antigens and pathogens from the body. Simultaneously, HIV has also gained enough mechanism to escape the natural immune response. On one hand, it downregulates HLA class I antigens, which may present viral antigens to specific CD8 + T cells; on the other hand, the viral genome get mutated very readily under the selection pressure of specific cytotoxic T lymphocytes. The high mutation rate and convertibility of its genotype makes it a moving target and poses a prime hurdle in vaccine development. This review explains how HIV enters into the cell, how it resists the host immune response and how HIV manages to escape from it and establish in the human body.
    Indian Journal of Medical Microbiology 11/2007; 25(4):311-22. · 1.04 Impact Factor
  • S Agrawal, F Khan, U Bharadwaj
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    ABSTRACT: Human leucocyte antigen (HLA) loci widely known for their role in generation of immune responses by encoding cell-surface heterodimers are often considered to be effective for the purpose of reconstructing human phylogenies due to high degree of polymorphism and less recombination. In the present study, we have made an attempt to study HLA class II loci (DRB1, DQA1 and DQB1) in inferring phylogenetic relationship based on both phylogenetic and haplotype approach. In the phylogenetic approach, the compiled database of 19 populations got segregated and finely resolved in three basal clusters with very high bootstrap values corresponding to four geo-ethnic groups of Africans, Orientals, Americans and Caucasians. Maximum- likelihood phylogram has placed North Indian Hindus alongside other Caucasian populations. Haplotype analysis revealed high range of haplotype diversity with nearly 144 observed haplotypes. The haplotype distribution suggested that numbers of Caucasian-specific haplotypes are frequently found among north Indian Hindus. Our results indicate that if the property of less recombination is explored to assign extended haplotypes, followed by strong interpretation based on more logistic statistical model, then there is a high possibility that HLA class II loci can infer exact and accurate phylogenetic assessments as revealed by mtDNA and Y-chromosome markers.
    International Journal of Immunogenetics 09/2007; 34(4):247-52. · 1.34 Impact Factor
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    S Talwar, F Khan, S Nityanand, S Agrawal
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    ABSTRACT: Information regarding the chimeric status of hematopoietic stem cell transplantation (HSCT) recipients is of great significance when comparing different conditioning and prophylactic therapies. In recent years, short tandem repeats/variable number tandem repeats (STRs/VNTRs) have emerged as the best tool for chimerism monitoring. However, the polymorphisms of STR/VNTR markers vary within and between ethnic groups. The issue is further complicated in a heterogeneous population such as occurs in the Indian subcontinent. In the present study, we attempted to devise a robust scheme to identify a set of polymorphic STRs/VNTRs most suitable for chimerism evaluation in north Indian HCST recipients. At first, we did genotyping of 11 STR and one VNTR in 1000 randomly chosen north Indian individuals to quantify different diversity parameters. Resulting data indicated that ApoB3'HVR, FES, VWA, D3S1358 and D16S310 were most polymorphic loci with the average heterozygosity being 0.756+/-0.17. Furthermore, all markers were genotyped in 77 HLA-matched donor-recipient pairs to evaluate the informativeness in differentiating donor's and recipient's cells. A panel of seven markers (ApoB3HVR-D3S1358-HUM-THO1-VWF-1-D16S310-FES-VWA) differentiated 98.70% of donor-recipient pairs. This set of markers also successfully monitored the graft status in 14 HSCT cases during multiple time points following HSCT. The results were compared to the commercially available AmpF/STR SGM Plus multiplex PCR kit (Applied Biosystems, Foster City, CA, USA). Our findings established that the panel of seven markers we identified was more cost-effective and informative.
    Bone Marrow Transplantation 06/2007; 39(9):529-35. · 3.47 Impact Factor
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    ABSTRACT: Little data are available on cellular immune responses during infection with hepatitis E virus (HEV). We therefore mapped CD4 T-cell epitopes in open reading frame (ORF)2 and ORF3 proteins of HEV using lymphocyte proliferation assays and overlapping peptide libraries. Proliferation of peripheral blood mononuclear cells from 40 patients with acute hepatitis E and 21 healthy controls with recombinant HEV ORF2 protein or pools of overlapping HEV ORF2/ORF3 peptides was measured. HLA-DQB1 and HLA-DRB1 alleles were also determined. Mononuclear cells from patients with hepatitis E more often showed significant proliferation on stimulation with recombinant ORF2 protein than controls (32/40 vs 7/21), and had higher median (range) stimulation indices [2.6 (0.9-15.2) vs 1.3 (0.6-12.9)]. Peptide pools corresponding to amino acids 73-156, 289-372, 361-444 and 505-588 of HEV ORF2 protein were associated with significant proliferation. Individual peptides in these pools did not show a clear pattern of stimulation. HEV ORF3 peptide pools did not induce proliferative responses. Lymphocyte proliferation in response to the peptide pool corresponding to amino acids 289-372 of HEV ORF2 protein was associated with presence of HLA-DRB1 allele 010X. These data on mapping of T-cell epitopes in HEV proteins may prove useful for designing HEV vaccines and for studying the immunopathogenesis of hepatitis E.
    Journal of Viral Hepatitis 05/2007; 14(4):283-92. · 3.31 Impact Factor
  • A Abbas, S Javed, S Agrawal
    International Journal of Gynecology & Obstetrics 06/2006; 93(2):148-9. · 1.56 Impact Factor
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    ABSTRACT: Abstract The FHIT gene is a relatively newly discovered tumor suppressor gene, which is located on the chromosome 3p14.2. The gene encompasses the FRA3B fragile site. The gene has been implicated in the pathogenesis of various carcinomas, particularly cancers of the stomach and oral squamous cell carcinomas. The protein encoded by the gene bears a significant homology to a group of proteins that have a histidine triad motif, designated HIT proteins. The function of the protein remains essentially unknown. Loss of heterozygosity and microsatellite instability are responsible for FHIT gene alterations. A mutation in a gene will invariably give abnormal transcripts and contribute to the pathogenesis of cancer. A better understanding of FHIT mutations will also help us to understand the pathogenesis of the multistep process of carcinogenesis. Therapeutic potentials of Fhit can also be explored. Replacement of FHIT cDNA in human cancer cell lines has resulted in the suppression of tumor growth. This opens the possibility of therapeutic potentials using recombinant vectors carrying the FHIT gene.
    Asia-Pacific Journal of Clinical Oncology 06/2006; 2(2):73-79. · 1.06 Impact Factor

Publication Stats

410 Citations
81.42 Total Impact Points


  • 2013
    • Banaras Hindu University
      • Department of Anatomy
      Vārānasi, Uttar Pradesh, India
  • 1990–2013
    • Sanjay Gandhi Post Graduate Institute of Medical Sciences
      • Department of Medical Genetics
      Lakhnau, Uttar Pradesh, India
  • 2009
    • Loughborough University
      • School of Sport, Exercise and Health Sciences
      Loughborough, ENG, United Kingdom
  • 2006
    • Era's Lucknow Medical College and Hospital
      Lakhnau, Uttar Pradesh, India