The role of parental motivation in family-based treatment for childhood obesity

This study investigated the role of parental motivation (importance, confidence and readiness) for predicting dropout and outcome from family-based behavioral treatment for childhood obesity. Parent and child demographics, adherence to treatment, and weight loss parameters were also explored as potential predictors. Eighty-four obese children (BMI-standard deviation scores (SDS) >2.14) and a participating parent with each child started treatment consisting of 12 weeks of group and individual treatment sessions (24 sessions total) delivered over a period of 18 weeks. Sixty-one families (73%) completed treatment and attended follow-up at 1 year after treatment. Child session attendance and completion of self-monitoring records served as measures of adherence. In regression analyses, parent reports (pretreatment) of confidence for doing well in treatment was the strongest predictor of treatment completion (P = 0.003) as well as early treatment response (weight loss at week 5) (P = 0.003). This variable remained a significant predictor of child weight loss at post-treatment (P = 0.014), but was not associated with child outcome at 1-year follow-up (P > 0.05). The only significant predictor of child weight loss at that point was child baseline weight (P = 0.001). However, pretreatment parent ratings of importance of and readiness for treatment did not predict dropout or weight loss at any point. The results underscore the importance of addressing parental motivation, specifically parental confidence for changing lifestyle related behaviors, early in the treatment process. Doing so may reduce treatment dropout and enhance treatment outcome.     

The Sperm Whale,Physeter macrocephalus,in the Eastern Mediterranean Sea

Abstract

After the successful establishment of free–living populations of Rose–ringed Parakeets (Psittacula krameri) and Common Mynas (Acridotheres tristis) in Jeddah, an overview of all exotic birds imported into Jeddah in the first three months of 1990 is given.     

MiR-21-5p but not miR-1-3p expression is modulated by preconditioning in a rat model of myocardial infarction

Molecular Biology Reports - Isoflurane (Iso) preconditioning (PC) is known to be cardioprotective against ischemia/reperfusion (I/R) injury. It was previously shown that microRNA-21-5p (miR-21-5p)...     

Large aggregates are the major soluble Aβ species in AD brain fractionated with density gradient ultracentrifugation

Soluble amyloid-β (Aβ) aggregates of various sizes, ranging from dimers to large protofibrils, have been associated with neurotoxicity and synaptic dysfunction in Alzheimer's Disease (AD). To investigate the properties of biologically relevant Aβ species, brain extracts from amyloid β protein precursor (AβPP) transgenic mice and AD patients as well as synthetic Aβ preparations were separated by size under native conditions with density gradient ultracentrifugation. The fractionated samples were then analyzed with atomic force microscopy (AFM), ELISA, and MTT cell viability assay. Based on AFM appearance and immunoreactivity to our protofibril selective antibody mAb158, synthetic Aβ42 was divided in four fractions, with large aggregates in fraction 1 and the smallest species in fraction 4. Synthetic Aβ aggregates from fractions 2 and 3 proved to be most toxic in an MTT assay. In AβPP transgenic mouse brain, the most abundant soluble Aβ species were found in fraction 2 and consisted mainly of Aβ40. Also in AD brains, Aβ was mainly found in fraction 2 but primarily as Aβ42. All biologically derived Aβ from fraction 2 was immunologically discriminated from smaller species with mAb158. Thus, the predominant species of biologically derived soluble Aβ, natively separated by density gradient ultracentrifugation, were found to match the size of the neurotoxic, 80-500 kDa synthetic Aβ protofibrils and were equally detected with mAb158.     

High-throughput genotyping of unknown genomic terrain in complex plant genomes: lessons from a case study

Novel high-throughput genotyping technologies have facilitated rapid genotyping of single nucleotide polymorphisms in non-model organisms. Most plant species have complex genomes with a large proportion of their genes having one or more paralogous copies due to single gene duplications and ancient or recent polyploidization events. These paralogous gene copies are potential sources of genotyping errors, and hence genotyping of plant genomes is inherently difficult. Here we present a case study that exemplifies paralog-related problems in high-throughput genotyping of plant genomes. We used the MassARRAY genotyping platform to genotype the LpIRI locus in L. perenne populations; this gene is thought to be involved in low-temperature stress tolerance. The dissection of the molecular genetics underlying the genotyping results provides a good example of how unknown paralogs can mask the true genotype of the locus, instructive to the non-specialist plant researcher and breeder.     

Role of nitric oxide synthase isoforms in glucose-stimulated insulin release

The role of islet constitutive nitric oxide synthase (cNOS) in insulin-releasing mechanisms is controversial. By measuring enzyme activities and protein expression of NOS isoforms [i.e., cNOS and inducible NOS (iNOS)] in islets of Langerhans cells in relation to insulin secretion, we show that glucose dose-dependently stimulates islet activities of both cNOS and iNOS, that cNOS-derived nitric oxide (NO) strongly inhibits glucose-stimulated insulin release, and that short-term hyperglycemia in mice induces islet iNOS activity. Moreover, addition of NO gas or an NO donor inhibited glucose-stimulated insulin release, and different NOS inhibitors effected a potentiation. These effects were evident also in K+-depolarized islets in the presence of the ATP-sensitive K+ channel opener diazoxide. Furthermore, our results emphasize the necessity of measuring islet NOS activity when using NOS inhibitors, because certain concentrations of certain NOS inhibitors might unexpectedly stimulate islet NO production. This is shown by the observation that 0.5 mmol/l of the NOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA) stimulated cNOS activity in parallel with an inhibition of the first phase of glucose-stimulated insulin release in perifused rats islets, whereas 5.0 mmol/l of L-NMMA markedly suppressed cNOS activity concomitant with a great potentiation of the insulin secretory response. The data strongly suggest, but do not definitely prove, that glucose indeed has the ability to stimulate both cNOS and iNOS in the islets and that NO might serve as a negative feedback inhibitor of glucose-stimulated insulin release. The results also suggest that hyperglycemia-evoked islet NOS activity might be one of multiple factors involved in the impairment of glucose-stimulated insulin release in type II diabetes mellitus.     

Inhibition of the thrombin–fibrinogen reaction by a macromolecular factor from rat liver

1. The supernatant obtained by centrifugation of a rat liver homogenate at 100000g for 1h contained a heat-labile macromolecular inhibitor of the thrombin-fibrinogen reaction. 2. The inhibitor was purified to electrophoretic homogeneity by repeated preparative polyacrylamide disc electrophoresis. Inhibition was observed with purified inhibitor equivalent to about 1mug of protein/ml. 3. The inhibitor had a pI of 3.50-3.75, a molecular weight (from sodium dodecyl sulphate-polyacrylamide-gel electrophoresis) of 72000+/-3000 and was inactivated by p-hydroxymercuribenzoate or 5,5'-dithiobis-(2-nitrobenzoic acid). 4. Kinetic studies revealed a non-competitive inhibition, with the inhibitor probably acting on the thrombin-fibrinogen complex.     

Morphine-Induced Preconditioning: Involvement of Protein Kinase A and Mitochondrial Permeability Transition Pore

Background

Morphine induces myocardial preconditioning (M-PC) via activation of mitochondrial large conductance Ca²⁺-sensitive potassium (mK_Ca) channels. An upstream regulator of mK_Ca channels is protein kinase A (PKA). Furthermore, mK_Ca channel activation regulates mitochondrial bioenergetics and thereby prevents opening of the mitochondrial permeability transition pore (mPTP). Here, we investigated in the rat heart in vivo whether 1) M-PC is mediated by activation of PKA, and 2) pharmacological opening of the mPTP abolishes the cardioprotective effect of M-PC and 3) M-PC is critically dependent on STAT3 activation, which is located upstream of mPTP within the signalling pathway.

Methods

Male Wistar rats were randomised to six groups (each n = 6). All animals underwent 25 minutes of regional myocardial ischemia and 120 minutes of reperfusion. Control animals (Con) were not further treated. Morphine preconditioning was initiated by intravenous administration of 0.3 mg/kg morphine (M-PC). The PKA blocker H-89 (10 μg/kg) was investigated with and without morphine (H-89+M-PC, H-89). We determined the effect of mPTP opening with atractyloside (5 mg/kg) with and without morphine (Atr+M-PC, Atr). Furthermore, the effect of morphine on PKA activity was tested in isolated adult rat cardiomyocytes. In further experiments in isolated hearts we tested the protective properties of morphine in the presence of STAT3 inhibition, and whether pharmacological prevention of the mPTP-opening by cyclosporine A (CsA) is cardioprotective in the presence of STAT3 inhibition.

Results

Morphine reduced infarct size from 64±5% to 39±9% (P<0.05 vs. Con). H-89 completely blocked preconditioning by morphine (64±9%; P<0.05 vs. M-PC), but H-89 itself had not effect on infarct size (61±10%; P>0.05 vs. Con). Also, atractyloside abolished infarct size reduction of morphine completely (65±9%; P<0.05 vs. M-PC) but had no influence on infarct size itself (64±5%; P>0.05 vs. Con). In isolated hearts STAT3 inhibitor Stattic completely abolished morphine-induced preconditioning. Administration of Stattic and mPTP inhibitor cyclosporine A reduced infarct size to 31±6% (Stat+CsA, P<0.05 vs. Con). Cyclosporine A alone reduced infarct size to 26±7% (CsA P<0.05 vs. Con). In cardiomyocytes, PKA activity was increased by morphine.

Conclusion

Our data suggest that morphine-induced cardioprotection is mediated by STAT3-activation and inhibition of mPTP, with STA3 located upstream of mPTP. There is some evidence that protein kinase A is involved within the signalling pathway.