Life Science Journal Impact Factor & Information
Current impact factor: 0.17
Impact Factor Rankings
|2015 Impact Factor
||Available summer 2015
|2012 Impact Factor
|2011 Impact Factor
|2010 Impact Factor
Impact factor over time
Publications in this journal
To determine whether polycystic ovarian syndrome (PCOS) is a causative factor in
dysregulation of leptin levels in obese subjects and to identify effect of PCOS on the relationship of serum leptin
with hormonal, metabolic and anthropometric parameters in obese PCOS women. Methods: A cross sectional study
in Jinnah Postgraduate Medical Center Karachi, Pakistan recruited twenty nine obese (BMI >30 kg/m2) and 20
normal-weight (BMI <25 kg/m2) PCOS women together with twenty seven normal cycling (NC) obese (BMI >30
kg/m2) and 25 normal-weight females (BMI <25 kg/m2). Serum leptin, prolactin, follicle stimulatimg hormone
(FSH), lutenizing hormone (LH), free testosterone, estradiol (E2) and fasting blood glucose (FBG) levels were
measured by Radioimmunoassay. Results: Mean serum leptin levels were higher in obese compared to normalweight
PCOS (54.00 ± 9.33 vs. 26.08±2.44 ng/ml; p <0.01) and in obese compared to normal-weight NC (51.54
±9.19 vs. 25.39 ± 2.37 ng/ml; p <0.01). Significantly lower level of FSH, LH, E2 (p <0.01), was observed in both
groups of PCOS as compared to non-PCOS while higher levels of testosterone, progesterone and FBG were found in
obese PCOS in comparison to obese NC (p <0.01). Leptin levels correlated with BMI in all four groups. There was a
significant correlation of FBG with obese NC (r=0.42, p<0.05) and normal-weight and obese groups of PCOS
(r=0.45, p<0.05; r=0.58, p<0.05 respectively). The leptin level correlated with E2 and testosterone in obese PCOS
subjects (p<0.05; p<0.05 respectively). Conclusion: It seems that leptin has a role in pathogenesis of PCOS in obese
Life Science Journal 03/2015; 12(4).
Life Science Journal 03/2015;
Objectives: Y chromosome microdeletion in azoospermia factor (AZF) region is frequently observed in azoospermic/severe oligozoospermic infertile men. We aim to investigate AZF microdeletions in infertile men and the concomitant testicular pathology. Also, we aim to identify the potential variation of AZF microdeletions between blood and seminal fluid genomic DNA. Materials and Methods: Fifty azoospermic/sever oligozoospermic infertile males and 50 healthy fertile males were enrolled in this study. Blood and seminal fluid genomic DNA were investigated for microdeletion in AZF loci. Additionally, testicular biopsies were examined to evaluate the testicular pathology. Results: Twenty two percent of patients have at least one microdeletion in one or more loci of the AZF sub-regions. While 16 microdeletions were found in the blood’s DNA, 19 microdeletions were found in the semen’s DNA. The microdeletion was found in different loci among the cases, one case had deletions in both AZFb and AZFc loci. The frequency of both AZFb and AZFc microdeletions in blood’s DNA and semen’s DNA was (14%), (16%) respectively. The testicular biopsies revealed variable histological changes ranged from hyalinized seminiferous tubules to arrested spermatogenesis. Conclusions: AZF microdeletions are frequently seen in primary non-obstructive male infertility and are usually associated with impaired spermatogenesis and variable degrees of testicular histological changes.
Life Science Journal 01/2015; 12(1):29-37.
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