Glutamergic Action on Alpha-Melanocyte-Stimulating Hormone Release from the Rat Hypothalamus

Release of α-melanocyte-stimulating hormone (α-MSH) synthesized in the hypothalamus is regulated by monoaminergic neuronal systems. An endogenous dopaminergic system inhibits α-MSH release (1, 2) whilst serotoninergic systems exert a biphasic effect on peptide release (3). The toxic effects of neonatal peripheral administration of monosodium glutamate on hypothalamic neurons containing proopiomelanocortin- (POMC-) derived peptides (4, 5) suggest additionally the presence of glutamate receptors on or indirectly influencing the POMC neuron. By comparison of the effect of the excitatory amino-acid agonists N-methyl-D-aspartate (NMDA), quisqualate and kainate on the release of α-MSH from superfused slices of rat hypothalamus, we have demonstrated a stimulatory glutamergic action on α-MSH release mediated through NMDA-type receptors.     

Diagnosis,treatment and prevention of type 2 diabetes mellitus in children and adolescents

During the last two decades, there have been several reports of an increasing incidence of type 2 diabetes mellitus (T2DM) in children and adolescents, especially among those belonging to minority ethnic groups. This trend, which parallels the increases in prevalence and degree of pediatric obesity, has caused great concern, even though T2DM remains a relatively rare disease in children. Youth T2DM differs not only from type 1 diabetes in children, from which it is sometimes difficult to differentiate, but also from T2DM in adults, since it appears to be an aggressive disease with rapidly progressive β-cell decline, high treatment failure rate, and accelerated development of complications. Despite the recent research, many aspects of youth T2DM still remain unknown, regarding both its pathophysiology and risk factor contribution, and its optimal management and prevention. Current management approaches include lifestyle changes, such as improved diet and increased physical activity, together with pharmacological interventions, including metformin, insulin, and the recently approved glucagon-like peptide-1 analog liraglutide. What is more important for everyone to realize though, from patients, families and physicians to schools, health services and policy-makers alike, is that T2DM is a largely preventable disease that will be addressed effectively only if its major contributor (i.e., pediatric obesity) is confronted and prevented at every possible stage of life, from conception until adulthood. Therefore, relevant comprehensive, coordinated, and innovative strategies are urgently needed.     

Clinical association between chronic periodontitis and the leukocyte extravasation inhibitors developmental endothelial locus‐1 and pentraxin‐3

This clinical study aimed to determine whether periodontal disease is associated with expression of developmental endothelial locus‐1 (Del‐1) and pentraxin‐3 (PTX‐3), endogenous inhibitors of leukocyte extravasation in humans. Expression of DEL1, PTX3, interleukin‐17A (IL17A), and lymphocyte function‐associated antigen‐1 (LFA1) was determined, using RT‐PCR and melting curve analysis, in biopsies of gingival tissues from 95 patients: 42 with moderate periodontitis; 40 with severe periodontitis; and 13 healthy controls. Relative expression of DEL1 and PTX3 was statistically significantly weaker in patients with periodontitis than in the control subjects. On the contrary, both IL17A and LFA1 showed statistically significant stronger expression in patients with periodontitis than in healthy controls. Correlation analysis, performed using Spearman's test, showed that expression of DEL1 was statistically significantly linked to periodontitis (ρ = ?0.103) and to age (ρ = ?0.134), but not to the gender of the patient, and that expression of PTX3 was significantly correlated with periodontitis (ρ = ?0.354). Expression of neutrophil extravasation inhibitors DEL1 and PTX3 show significant, but weak, association with the clinical manifestation of chronic periodontitis.     

Regression of Atherosclerosis

Atherosclerotic cardiovascular disease (CVD) is a complex disorder that leads to premature death and hospitalization. Several drugs have been, or are currently being tested for their ability to reduce cardiovascular mortality and/or promote regression of atherosclerotic lesions. In addition to "hard end point" clinical trials in which total and cardiovascular mortality as well as risk of incident myocardial infarction are considered as outcomes, trials with surrogate end points using imaging biomarkers can rapidly assess the efficacy of new cardiovascular drugs. Low-density lipoprotein-based therapies with statins have been shown to promote atherosclerosis regression, and several other drugs targeting high-density lipoproteins or inflammation/oxidation are currently being tested in both outcomes and imaging trials in which atherosclerosis regression is anticipated. In this review, we focus on the latest progress in CVD and highlight novel drugs that tackle atherosclerosis as well as the currently used and upcoming imaging techniques to optimally measure atherosclerosis progression.