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Background: Early pregnancy losses can be a distressing experience both for the parents and the treating clinician. We aim to explore the role of chemokine receptor 4 (CXCR4) in early pregnancy losses by comparing its expression among patients with spontaneous miscarriages and patients undergoing termination of viable pregnancies for unwanted pregnancies. Aim: The aim of the study was to investigate the expression of CXCR4 in early pregnancy losses and correlate the various clinical parameters with differential expression of the above receptor in the chorionic villi and maternal decidua. Study and Setting: The present study is a case-“control study done in a tertiary care center. Methodology: Fifty patients attending outdoor and antenatal clinic of the hospital aged 18-“40 years with spontaneous miscarriage under 20 weeks of gestational age were included as cases and compared with fifty females of comparable age group (18-“40 years) seeking medical termination of pregnancy as controls. Chorionic villi and decidua obtained from the cases and controls were analyzed for CXCR4 expression. Statistical Analysis: The results were analyzed using mean ± standard deviation, percentiles values, Chi-square test, and P value to determine the association of CXCR4 expression in decidua and chorionic villi of cases versus controls. Results: CXCR4 expression was significantly downregulated in cases as compared to the controls with P < 0.001. The mean normalized ratio of CXCR4 expression to housekeeping gene (β Actin) expression in the case group was 1.607 ± 1.108 and in the control group, it was 2.506 ± 1.457. There was a strong correlation between the expression of CXCR4 and maternal age. With increasing age, the expression of CXCR4 was more downregulated in both the cases and control groups (P < 0.001). The expression of CXCR4 was elevated in controls as compared to cases in

CONTEXT: In majority of couples experiencing recurrent pregnancy loss (RPL), etiology is still unknown. Two genetic factors have been suggested to underlie miscarriage in a subset of patients, namely skewed X chromosome inactivation in females and Y chromosome microdeletions in their partners. In males, microdeletions of the Y chromosome are known to cause spermatogenetic failure and male infertility. AIMS: The aim of the study was to find out the role of Y chromosome microdeletion in male partners of couples experiencing RPL. SETTINGS AND DESIGN: University hospital and genetic laboratory. Prospective case–control study. SUBJECTS AND METHODS: 59 couples with a history of RPL and 20 fertile controls (FC) with no miscarriage were included in the study. The study subjects were divided into male partners of RPL couples with abnormal semen parameters (AS) (n = 8), and couples with normal semen parameters (NS) (n = 51). Fertile controls with normal semen parameters were (FC) (n = 20). Y chromosome microdeletion was performed on 40 male partners of RPL and 20 FC. STATISTICAL ANALYSIS USED: Chi-square test. P

Background: Male infertility is a multifactorial disorder which affects approximately 10% of couples at childbearing age with substantial clinical and social impact. Genetic variation and environmental factors contribute to susceptibility to spermatogenic impairment in humans. The A386G (T54A) polymorphism of the autosomal gene, DAZL, has shown susceptibility to spermatogenic failure in Taiwanese population. However, no such association has been seen in infertile patients from Italy and South India. Aim: This study aims to find out the possible association between A386G (T54A) polymorphism of the autosomal gene, DAZL and idiopathic male infertility in patients from North India. DESIGN: Case-control study. Materials and Methods: The prevalence of A386G (T54A) polymorphism was determined in 165 idiopathic infertile azoo-/oligospermic patients and 200 fertile healthy control men. PCR-RFLP analysis was employed to determine the genotypes. PCR amplicons were subjected to restriction digestion with AluI as this mutation created a restriction site (AGCT), and separated on a 12% polyacrylamide gel. Results: Analysis of 165 idiopathic infertile azoo-/oligospermic and 200 fertile control men revealed only one case of the variant as a heterozygote in the control population. Single Nucleotide Polymorphism (SNP) was absent in the infertile patients. Conclusion: As in the report from Italy and South India, our results illustrate the rarity of this mutation. Apparently, this mutation is of recent origin and/or has poor selective value. Its preponderance in infertile patients from Taiwan (all heterozygotes) suggests a founder effect and also that its low selective value could be due to impaired spermatogenesis.