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Objective Accumulating evidence suggests increased cardiovascular risk in women with polycystic ovarian syndrome (PCOS) due to a cluster of factors, such as obesity, lipid abnormalities, impaired glucose tolerance (IGT), and hypertension. Markers such as high-sensitivity C-reactive protein (hs-CRP) and plasminogen activator inhibitor-1 (PAI-1) can provide an adjunctive method for the assessment of cardiovascular risk and can indicate future coronary heart diseases in women with lean PCOS. Materials and Methods In this prospective case-control study, women clinically diagnosed with PCOS (n = 25) with normal body mass index (BMI) and age and BMI-matched healthy controls (n = 75) were enrolled. The quantitative data were expressed as mean ± standard deviation (SD). Unpaired Student's t -test was used to compare the values (PCOS vs. controls) and Pearson's correlation coefficient was used to elucidate the relationship between the variables. Results The mean level of fasting blood sugar, serum total cholesterol, low-density lipoprotein (LDL), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), hs-CRP, and PAI-1 were significantly increased in PCOS patients (p < 0.000) compared with the control patients. Of the reported cases, 54.16% had hs-CRP levels greater than 3 mg/L. When the cases were further divided into normal (n = 20) and IGT (n = 5), hs-CRP values were significantly higher in IGT group as compared with normal glucose tolerance (NGT) group. On bivariate correlation analysis, hs-CRP had significant correlations with PAI-1 (r = 0.41, p < 0.000), waist-to-hip ratio (WHR; r = 0.23, p = 0.02), fasting blood sugar (FBS; r = 0.26, p = 0.009), LDL (r = 0.20, p = 0.03), TSH (r = 0.42, p < 0.000), and LH-to-FSH ratio (r = 0.24, p = 0.01). Conclusion Women with lean phenotype of PCOS suffer from many metabolic abnormalities such as abdominal obesity, dyslipidemia, hyperandrogenemia, and insulin resistance. The findings of the study suggest that environment of ongoing low-grade inflammation due to infiltration further exacerbates the metabolic derangements and cardiovascular risk. The investigations as hs-CRP and PAI-1 will help in early identification, diagnosis, and management of cardiovascular diseases associated with lean type of PCOS. These markers can prove to be beneficial in monitoring any unfavorable changes in cardiometabolic profile of such patients. [ABSTRACT FROM AUTHOR]

The analysis of estrogen receptor (ER) expression in breast carcinomas plays a crucial role in determining the endocrine responsiveness of tumors for systemic adjuvant therapy. Conventionally, the ER levels in breast carcinomas had been detected using the dextran‐coated charcoal assay and radioimmunoassay, which are now substituted with safer and economic antibody‐based assays such as immunohistochemistry (IHC) and enzyme‐linked immunosorbent assay (ELISA). Despite a gold (Au) standard method, the IHC has been criticized for factors such as tissue fixation, antibody selection, and threshold staining for result interpretation that could falsify test accuracy and reproducibility. The quest for alternative methods of ER quantification in tissue samples paved the way for aptamer‐based diagnostics. Previously, we have isolated a DNA aptamer against human ER alpha (ERα) using an in vitro evolution system. In this study, we developed an electrochemical sensor using the 76‐nucleotide DNA ERα‐ aptamer for rapid, precise, and cost‐effective detection of ERα expression in human breast cancer patients. The aptasensor was constructed by covalently immobilizing the thiolated ERα‐ aptamer onto a screen‐printed Au electrode. Construction of aptasensors was confirmed through atomic force microscopy and differential pulse voltammetry measurements. A detection limit of 0.001 ng/ml was calculated for full‐length ERα (66.2 kDa) in a detection time of 10 min. Analysis of the cancerous breast tissue samples using the ELISA and aptasensor methods enabled distinctive classification of samples into the categories of ER −ve, weak ER +ve, and strong ER +ve samples. The current change of this aptasensor lies within 5% after a storage of 60 days at 4°C. Further studies on a reasonably large sample size are required to realize the clinical potential of the sensor. Rapid analysis of estrogen receptor (ER) expression in the breast tissue sample of human breast cancer patients using an electrochemical aptasensor comprising an immobilized 76‐nucleotide DNA aptamer of ER on gold electrode attached with a potentiostat for real‐time monitoring. [ABSTRACT FROM AUTHOR]

Aspirin and Clopidogrel are used in prophylaxis of patients undergoing percutaneous coronary intervention and long-term prevention of cardiovascular and cerebrovascular events. Clopidogrel resistance has been attributed to P2Y1 and P2Y12 adenosine diphosphate (ADP) receptor polymorphisms. This study enrolled 100 patients of coronary artery disease (CAD) who were on the maintenance dose of clopidogrel (75 mg OD) with or without aspirin. In addition, 10 received loading dose (300 mg) prior to percutaneous coronary intervention. Relevant clinical and drug history were elicited. ADP-induced platelet aggregation study and PCR-RFLP for P2Y1 (1622A > G) and P2Y12 (i-T744C) polymorphisms were performed. Two groups of controls were used for defining cut-off for platelet aggregation response. Follow-up data, wherever available was recorded. The most common pattern of aggregation response was disaggregation, either complete (46.4%) or partial (53.6%). A frequency of 13% clopidogrel non-responders and 19% semi-responders was found. All the cases were H1/H1 haplotype for P2Y12 gene polymorphism and 28 (29.2%) patients carried P2Y1 1622A > G (21(21.9%) AG and 7(7.3%) GG) gene polymorphism, the frequency being greater in clopidogrel responders compared to semi/non-responders but difference was not statistically significant. There was no statistically significant difference between responders and semi/non-responders in terms of the history of risk factor for CAD, concurrent atorvastatin use or past history of an acute vascular event. On follow up, the two patients who developed myocardial infarction/acute coronary syndromes (MI/ACS) were clopidogrel semi- and non-responder, respectively. Variability in clopidogrel response with 13% non-responders and 19% semi-responders was seen in this study with adverse outcome (MI/ACS) on follow up seen in two patients. Hence, poor response to clopidogrel may be related to increased likelihood of adverse long-term coronary event that may benefit from additional or alternative anti-platelet therapy. Clopidogrel resistance was not associated with ADP receptor P2Y1 and P2Y12 gene polymorphisms. Hence, it is postulated that clopidogrel resistance in CAD patients is multifactorial and not caused by single-gene polymorphisms. [ABSTRACT FROM AUTHOR]