1.
[Importance of annexin V in kidney diseases].
Jakubowska, A, Kiliś-Pstrusińska, K
Postepy higieny i medycyny doswiadczalnej (Online). 2015;:153-7
Abstract
Annexin V (AnV) belongs to a cytoplasmic calcium binding protein family found in many body tissues, including distal tubule cells and glomerular epithelial cells. The biological role of this protein discovered so far is connected with apoptosis. AnV is considered as an early marker of that process and is used in one of the most frequently applied apoptosis detection methods, consisting in the detection of biochemical and morphological changes in cells. Measuring the AnV level may help understand many renal processes. Elevated AnV levels have been found in both acute and chronic renal conditions. Applying AnV to identify cells in the early phase of apoptosis in acute pyelonephritis caused by Escherichia coli showed that hemolysins of pathogenic bacteria stimulate the death of tubular cells and that the intensification of the process depends on the level of the toxin and its activity time. Studies on the mechanisms of reperfusion injury in acute renal injury have revealed protective activity of a synthetic AnV homodimer with regard to tubular cells. AnV was also used in diabetic nephropathy to study the influence of metabolic disorders on the intensification of apoptosis in renal tubular cells. Additionally, the suitability of AnV measurement as a biochemical marker of atherosclerosis in patients with a chronic renal condition was evaluated. It was also used to study the causes of immunodeficiency in patients diagnosed with the above-mentioned condition. There have been few papers published so far on the significance of AnV in children with renal conditions. The prognostic value of AnV and T cell apoptosis was evaluated in children with nephrotic syndrome.
2.
Fenofibrate and extended-release niacin improve the endothelial protective effects of HDL in patients with metabolic syndrome.
Gomaraschi, M, Ossoli, A, Adorni, MP, Damonte, E, Niesor, E, Veglia, F, Franceschini, G, Benghozi, R, Calabresi, L
Vascular pharmacology. 2015;:80-86
Abstract
BACKGROUND Fibrates and niacin are at present the most effective therapies to increase plasma levels of high density lipoprotein-cholesterol (HDL-C); to date, limited data are available on their effects on HDL protective functions. METHODS AND RESULTS Within a multicenter, randomized, open-label, cross-over study, 37 patients with metabolic syndrome received 6weeks' treatment with fenofibrate or extended-release niacin (ER niacin), with a 4weeks' wash-out period. HDL ability to preserve endothelial cell homeostasis was assessed by incubating cultured endothelial cells with HDL isolated from patients at baseline and after each treatment. HDL isolated from patients at baseline were as effective as control HDL in inhibiting vascular cell adhesion molecule-1 (VCAM-1) expression, but less efficient in promoting endothelial cell nitric oxide (NO) release. Both fenofibrate and ER niacin increased HDL ability to inhibit TNFα-induced VCAM-1 expression (+7% and +11%, respectively). Fenofibrate and ER niacin also improved the impaired HDL ability to induce the expression of endothelial nitric oxide synthase and NO production (+10% and +8%, respectively). Interestingly, HDL isolated after treatment showed an ability to promote endothelial NO release similar to HDL isolated from controls. No differences were observed between the two drugs. With both drugs, HDL function was improved irrespective of baseline HDL-C levels. CONCLUSION Treatment with fenofibrate or ER niacin in patients with metabolic syndrome not only increased HDL-C levels but also improved the endothelial protective effects of HDL.
3.
Life-style and metformin for the prevention of endometrial pathology in postmenopausal women.
Campagnoli, C, Abbà, C, Ambroggio, S, Brucato, T, Pasanisi, P
Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 2013;(2):119-24
Abstract
In western women, the endometrium is frequently exposed, even after menopause, to the endogenous hormonal stimulation. Such a stimulation increases the risk of pathologic conditions such as endometrial hyperplasia and type I (endometrioid) endometrial adenocarcinoma. Metabolic syndrome, obesity, insulin resistance and type II diabetes promote the endometrial stimulation, and are recognized risk factors for endometrial cancer. Furthermore, chronic hyperinsulinemia linked both to obesity and metabolic syndrome influences endometrial proliferation through direct and indirect actions. Intentional weight loss, calorie restriction and physical activity are associated with a reduced risk of the endometrial pathology. Biological mechanisms include reduction in insulin and sex steroid hormone levels. In addition to life-style modifications, the antidiabetic metformin may be proposed as preventive agent. Metformin reduces the metabolic syndrome, lowers insulin and testosterone levels in postmenopausal women, and it is a potent inhibitor of endometrial cancer cell proliferation.
4.
Nonalcoholic fatty liver disease: molecular pathways and therapeutic strategies.
Huang, YY, Gusdon, AM, Qu, S
Lipids in health and disease. 2013;:171
Abstract
Along with rising numbers of patients with metabolic syndrome, the prevalence of nonalcoholic fatty liver disease (NAFLD) has increased in proportion with the obesity epidemic. While there are no established treatments for NAFLD, current research is targeting new molecular mechanisms that underlie NAFLD and associated metabolic disorders. This review discusses some of these emerging molecular mechanisms and their therapeutic implications for the treatment of NAFLD. The basic research that has identified potential molecular targets for pharmacotherapy will be outlined.
5.
[Galstena therapy of some hepatobiliary diseases].
Munushkin, ON
Klinicheskaia meditsina. 2001;(12):38-41
Abstract
Galstena was given to 10 patients with chronic cholecystitis, 15 patients with chronic hepatitis and 15 patients with fatty degeneration of the liver for 30 days in a dose 10 drops 3 times a day 30 min before meal. The effect of the drug was assessed in relation to biliary inflammation and motility, inflammation and metabolism in a hepatic cell. It was found that galstena improves motor function of the biliary tract and exocrine function of the liver, reduces activity of mesenchymo-inflammatory syndrome and fatty degeneration of the liver.