Journal of Research in Medical Sciences
Volume:25 Issue: 1, Jan 2020

Osteoporosis is known as reduction of bone density, which is diagnosed using dual‑energy X‑ray absorptiometry. Although some studies have shown high body mass index (BMI) as a protective factor for osteoporosis and fracture risks, some other studies demonstrated obesity as a risk factor for osteoporosis. The aim of this study is to evaluate the relationship between BMI and bone mineral density (BMD) in premenopausal and postmenopausal females. Furthermore, we determined the correlation between BMI and fracture risk in postmenopausal females.

In this study, we evaluated the relationship between the age and BMI with 10‑year probability fracture risk (estimated using fracture risk assessment tool) and BMD in the L1–L4 spine and femoral neck. Data were collected from BMD center, Askariye Hospital, Isfahan, Iran, from May 2016 to July 2017.

The study consisted of 1361 individuals, including 305 premenopausal females and 1056 postmenopausal females. The results showed a statistically significant increase of BMD (P < 0.001) and a decrease of fracture risk (β = −0.158, R2 = 0.518) with an increase of BMI in postmenopausal females. Moreover, lumbar spine and femoral neck BMD were significantly higher in individuals with BMI ≥30 than in those with BMI <25 in both premenopausal and postmenopausal females (P < 0.001). In addition, older postmenopausal females indicated significantly lower L1–L4 BMD (r = −0.280, P < 0.05) and femoral neck BMD (r = −0.358, P < 0.05).

The results showed a positive correlation between BMI and BMD of the spine and femoral neck which did not differ by menopausal status. However, there was a correlation between BMI and fracture risk in postmenopausal females.

Cholangiocarcinoma (CCA) is a neglected disease prevalent in developing countries with high burden and mortality rate, and there is no effective treatment. We aimed to investigate β‑eudesmol molecular target of action in human CCA cell lines using the selected key molecules of apoptotic pathways.

Two CCA cell lines (HuH28 and HuCCT1) were assessed at different time points after β‑eudesmol treatment for mRNA and protein expression profiles of caspase‑3, ‑8, ‑9, p53, p21, Bcl‑2, and Bax by real‑time polymerase chain reaction and western blot, respectively.

β‑eudesmol induced expressions of p21 and p53 in mRNA/protein level in HuH28 and HuCCT1 cells. These CCA cells also expressed caspase‑3, ‑8, ‑9 and bax (mRNA and/or protein level) among others after β‑eudesmol treatment indicating its role in both intrinsic and extrinsic caspase‑dependent apoptotic pathways.

The study demonstrated that β‑eudesmol induced the expression of apoptosis pathway proteins, suggesting its potential role in promoting the caspase‑dependent apoptotic pathway, and induction of the cell cycle arrest in CCA cell lines. β‑eudesmol can be considered as a potential compound for further investigation as an anti‑CCA agent.

Despite huge efforts, the underlying molecular mechanisms of diabetic nephropathy (DN) are yet elusive, and holistic views have rarely been generated. Considering the complexity of DN pathogenesis, the integration of datasets from different molecular types to construct a multilayer map of DN can provide a comprehensive insight toward the disease mechanisms and also can generate new knowledge. Here, we have re‑analyzed two mRNA microarray datasets related to glomerular and tubulointerstitial compartments of human diabetic kidneys.

The quality of the datasets was confirmed by unsupervised hierarchical clustering and principal component analysis. For each dataset, differentially expressed (DE) genes were identified, and transcription factors (TFs) regulating these genes and kinases phosphorylating the TFs were enriched. Furthermore, microRNAs (miRNAs) targeting the DE genes, TFs, and kinases were detected. Based on the harvested genes for glomeruli and tubulointerstitium, key signaling pathways and biological processes involved in diseases pathogenesis were recognized. In addition, the interaction of different elements in each kidney compartment was depicted in multilayer networks, and topology analysis was performed to identify key nodes. Central miRNAs whose target genes were most likely to be related to DN were selected, and their expressions were quantitatively measured in a streptozotocin‑induced DN mouse model.

Among the examined miRNAs, miR‑208a‑3p and miR‑496a‑3p are, for the first time, found to be significantly overexpressed in the cortex of diabetic kidneys compared to controls.

We predict that miR‑208 is involved in oxygen metabolism and regulation of cellular energy balance. Furthermore, miR‑496 potentially regulates protein metabolism and ion transport. However, their exact functions remain to be investigated in future studies. Taken together, starting from transcriptomics data, we have generated multilayer interaction networks and introduced novel players in DN.

Acute kidney injury is a high‑risk complication in a variety of clinical situations mostly due to ischemia–reperfusion (IR) injuries. The novel idea of remote ischemic preconditioning (rIPC) was proposed to prevent serious ischemia sequels. To address the controversy of previous reports, the current study was performed to assess the effect of rIPC on kidney IR injury.

Male BALB/c mice were exposed to either rIPC or sham intervention, 24 h before kidney IR. In two independent sets of experiments, rIPC was accomplished by inducing three cycles of 5 min ischemia with 5 min reperfusion intervals through the ligation of the left external iliac artery or infrarenal abdominal aorta. Kidney IR injury was performed by left renal pedicle occlusion for 35 min and simultaneous right nephrectomy. After 48 h, mice were sacrificed for the assessment of kidney function and structure.

According to the serum urea and creatinine, as well as histopathological measures, none of the exploited rIPC procedures could significantly protect against kidney IR injury.

Based on our findings and the divergent results of previous animal and human studies, it can be concluded that the renoprotective effects of rIPC are minimal, if any, and are not robustly detectable.

Pathogenesis of cardiovascular diseases (CVDs) may be indicated by lipoprotein‑associated phospholipase A2 (Lp‑PLA2), serving as an inflammatory biomarker. However, the general dietary predictors of Lp‑PLA2 have not been investigated so far. The aim of the present study is to investigate the relationship between the serum levels of Lp‑PLA2 and dietary patterns in adults with cardiovascular risk factors.

Dietary patterns extracted using factor analysis and serum levels of Lp‑PAL2 in 470 adults aged 40–70 years who participated in the 5th phase of the Tehran Lipid and Glucose Study (2011–2014) were determined. Associations between the dietary patterns and serum levels of Lp‑PAL2 considering some confounder factors were evaluated.

The results showed that Western and semi‑Mediterranean dietary patterns had significant effects on changes in Lp‑PLA2 levels in univariate analyses. In multivariate analyses, after adjusting for age, sex, total cholesterol, low‑density lipoprotein cholesterol, body mass index and physical activity, energy intake, hormone therapy for women, and taking blood lipid‑lowering drugs as potential confounders, the Western dietary pattern remained a significant factor influencing the Lp‑PLA2 level (β value: 1.65, 95% confidence interval: 1.12, 1.89; P < 0.05). Moreover, after adjustment for the mentioned confounder factors, the effect of the semi‑Mediterranean dietary pattern on Lp‑PLA2 disappeared.

It can be concluded that the Western dietary pattern is associated with higher Lp‑PLA2 levels. We recommend that adults eat less carbonated drinks, fast foods, salty snacks, mayonnaise, and organ meat to counteract increased serum Lp‑PLA2 levels, which are directly associated with vascular inflammation and CVDs.

Inflammation is an important mechanism in the pathogenesis of delirium. Since delirium might reduce by anti‑inflammatory effects of omega‑3 fatty acids. Based on this respect, a study was conducted to indicate the effect of omega‑3 fatty acids in the prevention of delirium in mechanically ventilated patients.

This study is a randomized, double‑blind, placebo‑controlled clinical trial. One hundred and sixty‑eight mechanically ventilated patients were selected in the investigation. Patients were randomly allocated to receive either 2 g of omega‑3 syrup or placebo once a day. Twice daily delirium was assessed due to Confusion Assessment Method and the Richmond Agitation‑Sedation Scale. The number of days with delirium during the first 10 days of admission was the primary outcome. Secondary outcomes had been included duration of mechanical ventilation, length of intensive care unit (ICU) stay, and mortality.

Patient‑days with delirium (P = 0.032), the number of ICU stay (P = 0.02), and mechanical ventilation (P = 0.042) days in omega‑3 group significantly were lower than control group. Mortality was not significantly different between two groups.

Omega‑3 fatty acids can reduce the risk of delirium in mechanically ventilated patients.