Impact of Bariatric Surgery on Carotid Intima-Media Thickness in Patients with Morbid Obesity: a Prospective Study and Review of the Literature

Obesity Surgery - One of the main causes of mortality among obese patients is cardiovascular disease (CVD). Carotid intima-media thickness (CIMT) is an independent predictor for atherosclerosis and...     

Effect of recombinant β-defensin 1 protein on human sperm motility and viability

The reduction of sperm motility and subsequently reduced ability to undergo capacitation and acrosome reaction are considered as common causes of male infertility. The β-defensin family is a group of well-known secretory proteins with antimicrobial activity that contribute to the process of “sperm maturation” during the passage of spermatozoa in the epididymis when spermatozoa attain its motility. One member of this family is “β-defensin 1” which is present in seminal plasma and spermatozoa. The aim of this study was the incubation of human processed spermatozoa with recombinant β-defensin 1 (500 ng/ml) for 1, 2 and 3 hr at 37°C under 5% CO₂ atmosphere and assessment of sperm viability and motility in 59 semen samples. The analysis of semen samples such as sperm concentration, motility, viability, morphology and semen volume was performed according to the World Health Organization (2010; World health organization laboratory manual for the examination and processing of human semen (p. 287). Geneva, Switzerland: World Health Organization) criteria. The result of the current study shows that the incubation of spermatozoa with recombinant β-defensin significantly maintained percentage of sperm viability and motility compared to processed spermatozoa incubate in the absence of β-defensin in the studied time intervals (p < .05). Therefore, we concluded that recombinant β-defensin 1 protein as an agent with antimicrobial activity can maintain sperm viability and motility in in vitro condition.     

Evaluation of psychiatric illness in Iranian stoma patients

Introduction

The objective of this study was to assess the nonpsychotic psychiatric disorders of stoma patients in Iran.

Method

In this cross-sectional study, patients referred to the Iranian Ostomy Association from 2005 to 2006 filled the 28-item General Health Questionnaire (GHQ) in Farsi as a screening instrument to identify cases of nonpsychotic psychiatric morbidity.

Results

A total of 155 patients participated in the study, of whom 79 (51%) were female and 76 (49%) were male. Fifty-five percent of the patients (n=86) had psychiatric problems. The females' mean GHQ score was significantly higher than that of males (P=.001). Psychiatric disorder was significantly more frequent among patients with the following specifications: educational level of high school or lower (P=.001), mucosal hemorrhage of the ostomy (P=.03), stomal stenosis (P=.012), and history of psychiatric drug consumption (P=.000). GHQ score decreased as stoma age increased (P=.032; r=−.177).

Discussion

Similar to other complications, psychiatric problems are prevalent in Iranian stoma patients. Our findings highlight the need for special support.     

Genes and pathways downstream of telomerase in melanoma metastasis

Recent studies have demonstrated a role for telomerase in driving tumor progression, but its mechanism of action remains unclear. Here we show that stable, ribozyme-mediated suppression of mouse telomerase RNA reduced telomerase RNA expression, telomerase activity, and telomere length, which significantly reduced tumor invasion and metastatic potential. Our studies reveal that previously unidentified effects of telomerase may mediate its tumor-promoting effects. First, reducing telomerase activity induced a more dendritic morphology, accompanied by increased melanin content and increased expression of tyrosinase, a key enzyme in melanin biosynthesis. Second, gene expression profiling revealed that telomerase targeting down-regulated expression of several glycolytic pathway genes, with a corresponding decrease in glucose consumption and lactate production. Thus, telomerase activity controls the glycolytic pathway, potentially altering the energy state of tumor cells and thereby modulating tyrosinase activity and melanin production. These studies have important implications for understanding the mechanisms by which telomerase promotes tumor invasion and metastasis.     

Footbath as a safe,simple, and non-pharmacological method to improve sleep quality of menopausal women

Due to the adverse effects of medication we decided to provide a safe, economic, and easy intervention to decrease sleep problems in menopausal women. This trial aimed to determine the effect of footbath on sleep disturbance in postmenopausal women. One hundred menopausal women were randomly stratified using a permuted block randomization procedure by Random Allocation Software, and assigned to one of two study groups: control (without intervention, n = 50) and intervention (footbath, n = 50). The footbath group was asked to lie their feet into the warm water for 20 min in a container with a depth of 10 cm one hour before the usual sleeping time for 6 weeks. To assess sleep quality, we used the Pittsburgh sleep quality index (PSQI). To evaluate severity of menopause symptoms, the Greene scale was applied. Before the intervention, 96% of the subjects in the footbath group and 94% in the control group were poor sleepers. The results of analysis of covariance showed significant improvement in sleep quality and decrease in severity of menopause signs in the footbath group compared to the control group. At the baseline, there was a statistically significant correlation between the severity of menopause signs and the global score of PSQI in all study individuals (p ≤ .001, r = .464). The present study findings showed that footbath intervention enhanced sleep quality in menopausal women. Thus, footbath as a safe, simple, and non-pharmacological application can improve quality of life in postmenopausal women and inhibit problems due to inadequate sleep quality.     

Organ-specific metastasis of breast cancer: molecular and cellular mechanisms underlying lung metastasis

Background

Breast cancer (BC) is the most common type of cancer in women and the second cause of cancer-related mortality world-wide. The majority of BC-related deaths is due to metastasis. Bone, lung, brain and liver are the primary target sites of BC metastasis. The clinical implications and mechanisms underlying bone metastasis have been reviewed before. Given the fact that BC lung metastasis (BCLM) usually produces symptoms only after the lungs have been vastly occupied with metastatic tumor masses, it is of paramount importance for diagnostic and prognostic, as well as therapeutic purposes to comprehend the molecular and cellular mechanisms underlying BCLM. Here, we review current insights into the organ-specificity of BC metastasis, including the role of cancer stem cells in triggering BC spread, the traveling of tumor cells in the blood stream and their migration across endothelial barriers, their adaptation to the lung microenvironment and the initiation of metastatic colonization within the lung.

Conclusions

Detailed understanding of the mechanisms underlying BCLM will shed a new light on the identification of novel molecular targets to impede daunting pulmonary metastases in patients with breast cancer.

     

Atorvastatin Inhibits Viability and Migration of MCF7 Breast Cancer Cells

Objective: Atorvastatin is commonly used as a lipid lowering drug. The emerging interest in  statins as anticancer agents is based on their pleiotropic effects on cancer cells. Among the statins, atorvastatin, and in cancers, breast malignancies have received less attention in preclinical investigations. In order to enhance the efficacy of cancer treatment,  adjuvant, less expensive therapeutic strategies have been recently noticed. In this case, we investigated the in-vitro effect of atorvastatin on viability and migration of MCF7 breast cancer cell line. Methods: We tested the cytotoxicity of atorvastatin on breast cancer cells survival by MTT assay. Annexin-V / PI staining and then flow cytometry of cancer cells in addition to quantitative real-time PCR tests quantified the apoptosis and necrosis of cancer cells. We figured out the impact of atorvastatin on cancer cell migration capability through scratch-wound healing assay and transwell migration examination. Inverted light microscope and fluorescent imaging displayed the morphological changes following treatment of MCF7 cells with atorvastatin. Result: We resulted that atorvastatin can trigger MCF7 cancer cells to undergo necrosis and caspase-dependent apoptosis based on the viable/dead cell number, mitotic cell cycle, gene expression, and morphological assays. The results were dose- and time-dependent and the half- maximal inhibitory concentration of atorvastatin for cancer cells’ viability inhibition was 9.1 μM/L(nM/mL). Moreover, the migration of MCF7 cells were inhibited in the treated group as we figured out in two- and three-dimensional migration methods. Conclusion:In-vitro inspection of drug-cancer cell interactions paves the way  for future in-vivo research studies. These in-vitro results revealed that atorvastatin has anti-viability and anti-migration effects on breast cancer cells.