The objective of study was to evaluate and correlate the pathological characteristics of breast cancer patients with estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (Her2/neu) detected by immunohistochemistry and/or fluorescent in situ hybridization method. We have conducted 2 year study of 204 cases of breast cancer at HCG-Medisurge Hospitals, Ahmedabad from 2009 to 2011. Significant correlation was found in ER and PR expression whereas no correlation was found in hormonal receptors and Her2/neu expression. ER and PR positivity increased with advancing age in breast carcinoma patients while not affecting Her2/neu expression. The expression of hormone receptors were higher in infiltrating lobular carcinoma and infiltrating duct carcinoma subtypes of breast carcinoma as compared to other subtypes such medullary and in situ carcinoma. High-grade carcinoma patients were predominantly ER/PR negative and Her2/neu positive as compared to lower grade breast carcinoma whereas high-stage carcinoma patients were ER/PR positive and Her2/neu positive as compared to lower stage breast carcinoma.

The aim of study was to evaluate the effect of commonly used lisinopril, rosuvastatin and their combined action on site-specific nephrotoxicity in rats using clusterin and microalbumin nephrotoxic biomarkers and other related parameters using oral gavage. Rosuvastatin at 2 different doses showed increase in urinary microalbumin levels whereas lisinopril and its combination with rosuvastatin at 2 different doses did not show urinary microalbumin excretion indicating beneficial effects of lisinopril in terms of reducing microalbumin. Urinary clusterin levels significantly increased in high-dose treated animals of lisinopril and rosuvastatin. The use of lisinopril plus rosuvastatin at low dose also led to worsened renal function by raising urinary clusterin levels (217±4.6 ng/ml) when compared with the control (143±3.3 ng/ml). Renal histopathology showed multifocal regeneration of tubules indicating proximal tubule damaged. These results indicate that lisinopril (50 mg/kg), rosuvastatin (100 mg/kg), lisinopril+rosuvastatin (20+40 mg/kg) and lisinopril+rosuvastatin (50+100 mg/kg) showed toxicity only on proximal tubules.

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Despite of the superiority of combination of anthracycline and taxane-based chemotherapy over the anthracycline-based chemotherapy in the present study, further pivotal studies should be conducted to confirm the combination of anthracycline and taxane-based chemotherapy as a better neoadjuvant regimen for treatment of LABC tumors.

Urinary biomarkers have been used widely in preclinical toxicity studies to detect dys-functions and injuries of the kidney caused by drugs under development. While they have been well studied for evaluating nephrotoxicity, knowledge of sex differences in excretion levels of urinary biomarkers remains inadequate. We conducted experiments focused on effects of endogenous sex hormones on uri-nary biomarkers using intact and castrated male and female rats. Comparisons of the urinary biomarker excretion levels between intact male and female rats at 5, 7, 9 and 12 weeks of age revealed higher excre-tion levels of leucine aminopeptidase (LAP), γ-glutamyl transpeptidase (γGTP), total protein, liver-type fatty acid-binding protein (L-FABP), cystatin C (Cys-C) and β2-microglobulin (β2-MG), and lower excre-tion level of kidney injury molecule 1 (Kim-1), in male rats as compared to female rats. Orchidectomized male rats showed lower urinary excretion levels of alkaline phosphatase (ALP), LAP, γGTP, N-acetyl-β-D-glucosaminidase (NAG), glucose, total protein, L-FABP, Cys-C, β2-MG and neutrophil gelatinase-associated lipocalin (NGAL), and higher urinary excretion levels of clusterin (CLU) and Kim-1, than sham-operated male rats. On the other hand, no significant differences in the urinary biomarker excre-tion levels excluding ALP were observed between ovariectomized and sham-operated female rats. In the present study, we demonstrated the existence of sex differences in excretion levels of urinary biomarkers that are universally used in preclinical toxicity studies, and also that these differences, especially in relation to the urinary excretions of ALP, LAP, γGTP, total protein, L-FABP, Cys-C, and β2-MG, may closely relate to the endogenous testosterone.

Objective:Combination therapy of lisinopril and rosuvastatin may be an important concept in developing more effective strategies to treat and prevent atherosclerosis, coronary heart disease, and co-morbid metabolic disorders. The present study was designed to evaluate toxic effects of lisinopril and rosuvastatin alone or its combination therapy on hematological and biochemical analytes in Wistar rats.Materials and Methods:Forty-two rats were divided into seven groups, with each group comprising six rats. Rats were administered with lisinopril, rosuvastatin alone, or in-combination at two different doses. The blood samples were collected from rats after 21 days of oral administration of the drug/s and analyzed for various hematological and biochemical analytes.Results:Lisinopril alone and its combination treatment with rosuvastatin at high doses decreased hemoglobin and hematocrit. Rosuvastatin alone at high dose and its concomitant administration with lisinopril at two different doses showed increase in total white blood cells and absolute lymphocyte count and neutrophil count. Serum levels of aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin were significantly increased in rosuvastatin alone and its combination with lisinopril at both the doses. Besides this, lisinopril treatment decreased serum levels of sodium and increased the levels of potassium. Serum creatine kinase (CK) levels were increased in the animals treated with rosuvastatin at both the doses. However, increased serum CK level because of rosuvastatin became normal with co-administration of lisinopril at low doses.Conclusion:Our results indicate that administration of lisinopril with rosuvastatin does not ameliorate hepatotoxicity caused by rosuvastatin. However, combination treatment reduces serum CK levels elevated due to rosuvastatin, implicating protective effect of combination treatment on myopathy at low doses.

Numerous clinical studies reported effectiveness of add-on non-steroidal anti-inflammatory agents in patients with depression. In the present study, we investigated efficacy and safety of add-on aceclofenac alone or in-combination with serratiopeptidase to sertraline in patients with depression. A total of 102 patients with depression were assigned to three different treatment groups: A) add-on aceclofenac monotherapy (200mg/day) to sertraline B) add-on fixeddose combination (FDC) of aceclofenac and serratiopeptidase (200+30mg/ day) to sertraline C) sertraline (150mg/day). Efficacy measures included the HAM-D17 score, MADRS score and biomarkers levels like interleukin-6, cortisol and brain-derived neurotrophic factor (BDNF). Treatment with addon aceclofenac monotherapy or its combination with serratiopeptidase to sertraline showed significant reduction in HAM-D17 score at week 8 and week 12 as compared to sertraline monotherapy. Add-on therapies also showed reduction in MADRS score at week 12. Interleukin-6 levels significantly reduced in patients treated with add-on aceclofenac monotherapy or add-on FDC treatment with that of sertraline monotherapy at week 12. Both add-on treatments to sertraline also showed significant improvement in BDNF levels as compared to sertraline monotherapy at week 12.The antidepressant activity and neuroprotective potential of add-on aceclofenac monotherapy or its combination with serratiopeptidase to sertraline can be attributed to its capability of reducing IL-6 and cortisol levels and augmenting levels of BDNF.