Metabolic syndrome in patients with chronic obstructive pulmonary disease: frequency and relationship with systemic inflammation.

BACKGROUND: Metabolic syndrome (MetS) is frequent in patients with chronic obstructive pulmonary disease (COPD). Systemic inflammation plays an important role in both COPD and MetS. The aim of this study was to assess the frequency of MetS in COPD patients and to evaluate the status of systemic inflammation in COPD patients with MetS and those without MetS. METHODS: This cross-sectional study included 98 consecutive stable COPD patients. The MetS was defined using the criteria of the International Diabetes Federation. Components of MetS and markers of systemic inflammation: C-reactive protein (CRP), fibrinogen, and leukocyte count were measured. All patients underwent spirometry. The staging of COPD was made according to the Global initiative for chronic obstructive lung disease (GOLD) criteria. RESULTS: MetS was present in 37.8 % COPD patients. The frequencies of MetS in patients with GOLD stages I, II, III, and IV were 33.3 %, 48.8 %, 31.6 %, and 23.1 %, respectively. MetS frequencies were not significantly different between GOLD stages. The multivariate logistic regression analysis revealed leukocyte count and CRP level as significant independent predictors of the presence of Mets in COPD patients (OR =1.321, 95%CI: 1.007-1.628, p =0.009 and OR =1.184, 95%CI: 1.020-1.376, p =0.027 respectively). CONCLUSIONS: This study shows that MetS is frequent in patients with COPD. Systemic inflammatory markers are higher in COPD patients with MetS than in patients without MetS. These findings suggest that physicians should screen COPD patients for associated MetS and elevated circulatory inflammatory markers. Management of these disorders should reduce the risk of cardiovascular morbidity and mortality in these patients. Hippokratia 2016, 20(2):110-114.

GPNMB cooperates with neuropilin-1 to promote mammary tumor growth and engages integrin α5ß1 for efficient breast cancer metastasis.

Glycoprotein nmb (GPNMB) promotes breast tumor growth and metastasis and its expression in tumor epithelium correlates with poor prognosis in breast cancer patients. Despite its biological and clinical significance, little is known regarding the molecular mechanisms engaged by GPNMB. Herein, we show that GPNMB engages distinct functional domains and mechanisms to promote primary tumor growth and metastasis. We demonstrate that neuropilin-1 (NRP-1) expression is increased in breast cancer cells that overexpress GPNMB. Interestingly, the GPNMB-driven increase in NRP-1 expression potentiated vascular endothelial growth factor signaling in breast cancer cells and was required for the growth, but not metastasis, of these cells in vivo. Interrogation of RNAseq data sets revealed a positive correlation between GPNMB and NRP-1 levels in human breast tumors. Furthermore, we ascribe pro-growth and pro-metastatic functions of GPNMB to its ability to bind α5ß1 integrin and increase downstream signaling in breast cancer cells. We show that GPNMB enhances breast cancer cell adhesion to fibronectin, increases α5ß1 expression and associates with this receptor through its RGD motif. GPNMB recruitment into integrin complexes activates Src and Fak signaling pathways in an RGD-dependent manner. Importantly, both the RGD motif and cytoplasmic tail of GPNMB are required to promote primary mammary tumor growth; however, only mutation of the RGD motif impaired the formation of lung metastases. Together, these findings identify novel and distinct molecular mediators of GPNMB-induced breast cancer growth and metastasis.

The role of gut hormones in appetite regulation (review).

Eating process is an aggregate of complex and different forms of behavior. Its regulation is based on energy homeostasis and appetite control which includes two components: the homeostatic and the hedonistic control. Important signals in appetite regulation are gut-derived hormones. They are produced by enteroendocrine cells in response to nutrient and energy intake, and achieve their effects by influencing brain structures involved in food intake regulation. The key brain structure involved in this process is the hypothalamus. Gut hormones reach the hypothalamus from the circulation or by the vagal nerve via the nucleus of the solitary tract. Among gut peptides, ghrelin is the only orexigenic hormone, leading to an increase in food intake and body weight. All others, such as cholecystokinin, glucagon like peptide-1, oxyntomodulin, peptide tyrosine tyrosine or pancreatic polypeptide, are anorexigenic, leading to decrease in food intake. Also, gut-derived endocannabinoids exert orexigenic effect on appetite. Keeping in mind the growing problem of obesity, the crucial issue when considering gut derived peptides is to understand their mechanisms of acting because of potential role in clinical therapy, and discovering long-lasting gut peptides or their analogues, with no or minimal side effects.

Nonlinear magnetic electron tripolar vortices in streaming plasmas.

Magnetic electron modes in nonuniform magnetized and unmagnetized streaming plasmas, with characteristic frequencies between the ion and electron plasma frequencies and at spatial scales of the order of the collisionless skin depth, are studied. Two coupled equations, for the perturbed (in the case of magnetized plasma) or self-generated (for the unmagnetized plasma case) magnetic field, and the temperature, are solved in the strongly nonlinear regime and stationary traveling solutions in the form of tripolar vortices are found.

[The importance of changes in the septal Q wave induced by exercise in the detection of ischemic heart disease]. / Vrednost promene septumskog talasa Q izazvane fizickim opterecenjem u otkrivanju ishemijske bolesti srca.

Among the numerous variables measured by the electrocardiogram during exercise little attention has been paid to the "septal" Q wave. We examined changes of the "septal" Q wave amplitude during exercise in 43 patients with chest pain. Coronary arteriography showed significant changes in 23 patients and normal arteries in 20. The Q wave amplitude was measured in leads V4-V6 immediately before and at the peak of submaximal bicycle exercise. The amplitude of "septal" Q wave increased during exercise in 11 (55%) patients, and decreased or was not changed in 9 (45%) of the normal subjects (p greater than 0.05). However, the Q wave amplitude increased in 6 (26%) patients, and decreased or was not changed in 17 (74%) patients with ischaemic heart disease (p less than 0.05). Thus, the sensitivity of Q wave analysis in the detection of coronary disease was 74% (p less than 0.05), but specificity was only 55% (p greater than 0.05).