Association of 2B-adrenergic receptor gene polymorphism with disturbances of cardiac conduction

In this work we for the first time revealed on clinical - genetic material association between hereditary disturbances of cardiac conduction and polymorphism of 2-adrenergic receptor gene.     

FGF23 contributes to insulin sensitivity in obese adolescents - preliminary results

Fibroblast growth factor‐23 (FGF23) is a hormonal regulator of circulating phosphate and vitamin D levels. Recent investigations revealed that besides a key role in the pathogenesis of calcium–phosphorus disorders, in some patients FGF23 may be an indicator of cardiovascular complications. As a ‘hormone‐like’ factor, it may also be involved in some metabolic processes, especially in the metabolism of glucose and fat. Its potential contribution to metabolic syndrome (MS) development has not been confirmed yet. Objective The study was to examine the possible correlations between FGF23 serum levels and body composition, blood pressure and selected parameters of glucose, insulin and fat metabolism in adolescents with simple obesity. Patients and design In 68 (35 female) adolescents (mean age 13·9 years) with simple obesity [mean BMI SDS 4·9 (95% CI 4·4–5·4)], the levels of FGF23, total cholesterol, low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol and triglycerides were measured. Standard oral glucose tolerance tests were performed with the assessment of fasting and after 120′ postload glucose and insulin levels; the insulin resistance index HOMA‐IR was calculated. Results Regardless of gender, there was a significant inverse correlation between FGF23 and fasting insulin level (r = ?0·3), as well as HOMA‐IR (r = ?0·29). Multiple regression model showed the independent association between FGF23 and HOMA‐IR. Conclusion FGF23 seems to be a novel factor contributing to insulin sensitivity. Further investigations are needed to define its role in the development of MS.     

Theoretical explanations for maintenance of behaviour change: a systematic review of behaviour theories

Background: Behaviour change interventions are effective in supporting individuals in achieving temporary behaviour change. Behaviour change maintenance, however, is rarely attained. The aim of this review was to identify and synthesise current theoretical explanations for behaviour change maintenance to inform future research and practice.

Methods: Potentially relevant theories were identified through systematic searches of electronic databases (Ovid MEDLINE, Embase, PsycINFO). In addition, an existing database of 80 theories was searched, and 25 theory experts were consulted. Theories were included if they formulated hypotheses about behaviour change maintenance. Included theories were synthesised thematically to ascertain overarching explanations for behaviour change maintenance. Initial theoretical themes were cross-validated.

Findings: One hundred and seventeen behaviour theories were identified, of which 100 met the inclusion criteria. Five overarching, interconnected themes representing theoretical explanations for behaviour change maintenance emerged. Theoretical explanations of behaviour change maintenance focus on the differential nature and role of motives, self-regulation, resources (psychological and physical), habits, and environmental and social influences from initiation to maintenance.

Discussion: There are distinct patterns of theoretical explanations for behaviour change and for behaviour change maintenance. The findings from this review can guide the development and evaluation of interventions promoting maintenance of health behaviours and help in the development of an integrated theory of behaviour change maintenance.     

Prostaglandin and cyclic nucleotide levels in patients with peptic ulcer and chronic gastritis with secretory insufficiency

A study of prostaglandins (PGE2 and PGF2) and cyclic nucleotides (cAMP, cGMP) in the blood and gastric mucosa biopsies was carried out. In peptic ulcer the level of cyclic nucleotides in the blood and gastric mucosa was on an increase. The level of prostaglandins increased in the blood and decreased in the gastric mucosa. A decrease in the level of prostaglandins and cAMP in the blood and gastric mucosa was noted in patients with chronic atrophic histamine refractory gastritis with a simultaneous rise of the cAMP level. It was shown that stable stimulation of cyclic nucleotides resulting in an increase of gastric acid production, might cause ulcer development and exacerbation of disease. In patients with chronic atrophic gastritis changes of prostaglandins and cyclic nucleotides as compared to those in patients with peptic ulcer, were contrary.     

Study of spontaneous acetylcholine-dependent tachyarrhythmias using isolated specimens of the right canine atrium by bilateral mapping of the spread of excitation

The authors examined tachycardias induced by administering acetylcholine (AC), 1-2 micrograms into the artery of sinus node (ASN) of an isolated specimen of the canine right atrium, which had spontaneous automatism. Bilateral multielectrode mapping was employed. The episodes of tachycardia occurred during AC-induced arrest of sinus rhythm. In 81% of the cases, episodes of arrhythmia consisted of 2-3 beats, in 19%, 6-150 beats. The mapping revealed a focal picture of activation during short-term episodes of arrhythmia and transition from a focal type of activation to the re-entry in most cases of "prolonged" episodes. With this, excitation circulation might be detected only on one side of the specimen, in the presence of the focal activation picture, on the other. Focus-re-entry transition is proposed to be caused by a mechanism associated with heterogeneous refractoriness of atrial tissue.     

Cell surface IL-1α trafficking is specifically inhibited by interferon-γ, and associates with the membrane via IL-1R2 and GPI anchors

IL-1 is a powerful cytokine that drives inflammation and modulates adaptive immunity. Both IL-1α and IL-1β are translated as proforms that require cleavage for full cytokine activity and release, while IL-1α is reported to occur as an alternative plasma membrane-associated form on many cell types. However, the existence of cell surface IL-1α (csIL-1α) is contested, how IL-1α tethers to the membrane is unknown, and signaling pathways controlling trafficking are not specified. Using a robust and fully validated system, we show that macrophages present bona fide csIL-1α after ligation of TLRs. Pro-IL-1α tethers to the plasma membrane in part through IL-1R2 or via association with a glycosylphosphatidylinositol-anchored protein, and can be cleaved, activated, and released by proteases. csIL-1α requires de novo protein synthesis and its trafficking to the plasma membrane is exquisitely sensitive to inhibition by IFN-γ, independent of expression level. We also reveal how prior csIL-1α detection could occur through inadvertent cell permeabilisation, and that senescent cells do not drive the senescent-associated secretory phenotype via csIL-1α, but rather via soluble IL-1α. We believe these data are important for determining the local or systemic context in which IL-1α can contribute to disease and/or physiological processes.