Measuring beverage consumption in US children and adolescents: a systematic review.

Beverage consumption habits are associated with weight outcomes for children and adolescents. Many studies have examined youth's beverage consumption, but little is known about what methods are commonly used to assess youth beverage consumption and whether these strategies are valid and reliable. This study aimed to systematically review articles assessing beverage consumption among children and adolescents. We searched PubMed and Scopus for English-language articles published between February 2007 and February 2017 that measured and reported on American youth's (ages 2-18 years) beverage consumption. Searches yielded 17,165 articles, of which 589 articles describing 615 measures were extracted. We examined the types of assessment methods used, characteristics of these methods (e.g. validity, reliability, and literacy level), characteristics of study samples, and beverages assessed. The most common assessment methods were questionnaires/screeners (used by 65.4% of articles) and recalls (24.4%). About three-quarters of articles did not address validity (70.5%) or reliability (79.5%) of any measures used. Study populations were diverse: 54.7% of articles included low-income children, and 90.2% included non-White children. The most commonly assessed beverage category was sugar-sweetened beverages. Findings suggest that improved measurement techniques and reporting are both needed to track progress towards a goal of ensuring all youth have healthy beverage consumption.

Usefulness of cytogenetics in leukemias.

Present study consists of cytogenetic evaluation in 141 cases referred to our centre for various leukemias. This includes 110 cases of CML, 10 of ALL, 16 of AML (M3), 2 of AML(M2), 2 of MDS and 1 of CMML. The conventional cytogenetic study was carried out in all the cases using G Banding technique. Of the 141 patients studied, 17 patients showed secondary chromosomal alterations along with primary chromosomal alterations. In two patients of CML with secondary chromosomal alteration t(4:9:22), molecular cytogenetic technique (FISH) has been carried out which has confirmed the primary observations revealed by the conventional cytogenetic technique. Other secondary alterations were numerous and would have been missed if only FISH or PCR technique would have been used for diagnosis. We observed from our study that advanced molecular techniques like FISH and PCR cannot replace the conventional cytogenetic study but are useful as supportive and confirmative diagnostic tools.

Activation of guanosine 3',5'-cyclic monophosphate (cGMP)-dependent protein kinase in rabbit aorta by nitroglycerin and sodium nitroprusside.

It is generally accepted that cGMP mediates the vascular relaxant effects of nitrovasodilators such as sodium nitroprusside (SNP) and nitroglycerin (NTG). It has been suggested that the relaxant effects of cGMP are mediated via activation of a specific, cGMP-dependent protein kinase (PKG). The objective of this study was to determine whether PKG can be activated by SNP and by NTG in intact strips of rabbit aorta and, if so, whether a good correlation exists between activation of PKG and relaxation of the arteries by the nitrovasodilators. PKG activity was measured by means of a recently described assay using a peptide substrate, BPDEtide, that exhibits good sensitivity and specificity for PKG compared with other protein kinases. Verification of the specificity of the assay for PKG was obtained using MonoQ chromatography to resolve soluble extracts of the rabbit aorta and subsequent immunoblotting to identify the kinase by means of a PKG-specific antibody. The role of PKG in vascular relaxation was investigated by simultaneously monitoring the effects of SNP and NTG on cGMP levels, PKG activity ratios and tension in isolated strips of rabbit aorta exposed to varying concentrations of the nitrovasodilators for varying times. The results indicate that PKG can be activated in a concentration- and time-dependent manner by both SNP and NTG in intact vascular preparations and that reasonably good correlations exist between PKG activation and relaxation in these experiments. Although a causal relationship between the two parameters has not been definitely established, these results are consistent with the proposed role for PKG as a mediator of the vascular relaxant effects of cGMP-elevating agents such as SNP and NTG.

Activation of guanosine 3',5'-cyclic monophosphate (cGMP)-dependent protein kinase in rat vas deferens and distal colon is not accompanied by inhibition of contraction.

There is good evidence that in vascular smooth muscle, the relaxant effects of sodium nitroprusside (SNP) are mediated by increases in cGMP levels and activation of cGMP-dependent protein kinase (PKG). However, in rat vas deferens and rat distal colon, cGMP-elevating agents such as SNP and atrial natriuretic factor (ANF) have been shown to elevate cGMP without inducing relaxation. The lack of relaxation might be explained by either lack of activation of PKG by these agents or low levels of PKG in these tissues. The object of the present study was to investigate these possibilities by simultaneously monitoring cGMP levels, PKG activity and contractility in isolated strips of rat vas deferens, rat proximal colon and distal colon exposed to high concentrations of SNP or ANF. Verification of the specificity of the assay for PKG was obtained using MonoQ chromatography to resolve soluble smooth muscle extracts, followed by immunoblotting with a PKG-specific antibody to identify the kinase. In rat vas deferens, 5 mM SNP increased cGMP levels (14-fold) and PKG activity ratios (3.4-fold) but did not inhibit phenylephrine-induced contractions. In both rat proximal and rat distal colon, 100 nM ANF significantly elevated cGMP levels and PKG activity ratios, but only in the proximal colon was inhibition of spontaneous contractions observed. Total PKG activity was much lower (approximately 16 pmol PO4/min/mg protein) in rat vas deferens, which was not relaxed by SNP, than in rabbit aorta (approximately 148 pmol PO4/min/mg), which was relaxed. However, in the rat proximal colon, despite low PKG levels (approximately 11 pmole/min/mg), ANF did inhibit contractions. Thus the inability of the cGMP-elevating agents SNP and ANF to inhibit contractions in rat vas deferens and rat distal colon cannot be explained by either of the possibilities suggested above.

Reentrant arrhythmias in the subacute infarction period. The proarrhythmic effect of flecainide acetate on functional reentrant circuits.

BACKGROUND: The Cardiac Arrhythmia Suppression Trial has shown that flecainide was associated with an increased incidence of sudden cardiac death in postinfarction patients. The exact mechanism(s) of the proarrhythmic effects of flecainide remain unclear. We performed a detailed analysis of the electrophysiological and proarrhythmic effects of flecainide in a well-characterized model of reentrant arrhythmias in the subacute phase of myocardial infarction. METHODS AND RESULTS: Sixteen dogs were studied 4 days after ligation of the left anterior descending coronary artery. Isochronal mapping of ventricular activation showed that flecainide facilitated both the induction and sustenance of ventricular tachycardia, especially at shorter basic cycle lengths. Flecainide had negligible effect on the length of the arc of functional conduction block but markedly depressed conduction of the common reentrant wave front that was usually oriented parallel to fiber axis. Whole heart mapping was analyzed in combination with basic measurements of the effects of flecainide on conduction and refractory properties of both normal and ischemic myocardia using a high-resolution cross electrode consisting of four orthogonal arms, each comprised of 16 poles with an interelectrode spacing of 500 microns. The electrode was especially designed to study the effects of the drug on anisotropic conduction as determined by a linear regression of activation time and distance in each direction. Flecainide resulted preferentially in more marked rate-dependent depression of conduction in ischemic compared with normal myocardium. On the other hand, the effect of flecainide on refractoriness in both normal and ischemic myocardia was negligible. CONCLUSIONS: Because flecainide caused no significant change in refractoriness in both normal and ischemic myocardia, there was no difference in the dimension of the potential reentrant pathway, that is, the continuous line of functional conduction block, around which the reentrant wave fronts circulate. Yet, flecainide resulted in significant rate-dependent slowing of conduction preferentially in ischemic myocardium. The additional slowing of conduction of the common reentrant wave front coupled with minimal changes in the length of the reentrant pathway allowed additional time for the wave front to reexcite normal myocardium on the proximal side of the arc of block. After flecainide, reentry could be induced in hearts in which reentry could not be induced during control. The same proarrhythmic mechanism explains the propensity of nonsustained figure-8 reentrant tachycardias to become sustained after flecainide.