Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5 Άγιος Νικόλαος
Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com

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Τρίτη 19 Ιανουαρίου 2016

Effects of a community-oriented obesity prevention programme on indicators of body fatness in preschool and primary school children: main results from the IDEFICS study

BACKGROUND/OBJECTIVES: Childhood obesity is a major public health concern but evidence-based approaches to tackle this epidemic sustainably are still lacking. The Identification and prevention of Dietary- and lifestyle-induced health EFfects In Children and infantS (IDEFICS) study investigated the aetiology of childhood obesity and developed a primary prevention programme. Here, we report on the effects of the IDEFICS intervention on indicators of body fatness. SUBJECTS/METHODS: The intervention modules addressed the community, school and parental level, focusing on diet, physical activity and stress-related lifestyle factors. A cohort of 16,228 children aged 2-9.9 years – about 2000 per country – was equally divided over intervention and control regions. (Participating countries were Sweden, Germany, Estonia, Hungary, Cyprus, Italy, Spain and Belgium.) We compared the prevalence of overweight/obesity and mean values of body mass index z-score, per cent body fat and waist-to-height ratio over 2 years of follow-up. Mixed models adjusting for age and socioeconomic status of the parents and with an additional random effect for country accounted for the clustered study design. RESULTS: The prevalence of overweight and obesity increased in both the intervention and control group from 18.0% at baseline to 22.9% at follow-up in the control group and from 19.0% to 23.6% in the intervention group. The difference in changes between control and intervention was not statistically significant. For the cohort as a whole, the changes in indicators of body fatness did not show any clinically relevant differences between the intervention and control groups. Changes in favour of intervention treatment in some indicators were counterbalanced by changes in favour of the control group in some other indicators. CONCLUSIONS: Over the 2-year-observation period, the IDEFICS primary prevention programme for childhood obesity has not been successful in reducing the prevalence of overweight and obesity nor in improving indicators of body fatness in the target population as a whole.

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Belgische VIP’s brengen ISA verder

Draagvlak creëren voor ISA. Dat was een belangrijke doelstelling van het organiseren van demonstratieritten met een ISA-auto voor belangrijke Belgen én van een ISA-proef in Gent. Ook aan de Gentse proef deden VIP's mee, zoals de Gentse burgemeester en de rector van de universiteit. Door deze aanpak kreeg ISA veel publiciteit en groeide de bekendheid. Een bericht uit de Belgische ISA-stad.

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A novel case presenting with an unusual ureteral diverticular lesion similar to adenomyomatous hyperplasia of the gallbladder

We present the first case of an unusual ureteral diverticular lesion demonstrating similarities to adenomyomatous hyperplasia of the gallbladder. A 68-year-old asymptomatic Japanese man with high prostate-specific antigen levels was clinically evaluated. Left hydronephrosis and benign prostatic hyperplasia were detected. A bilateral retrograde pyelogram revealed that the upper and middle portions of the left ureter exhibited an irregular narrow lumen and some pooling of contrast material, which was compatible with ureteral pseudodiverticulosis. Although no malignant cells were seen on cytology, computed tomography detected a fusiform shaped lesion with a circumferential thick wall including multiple diverticulae. Left nephroureterectomy was performed because malignancy could not be ruled out. Pathology demonstrated that the ureteral lesion showed a localized thick wall consisting of multilocules and/or multicysts and a hyperplastic muscularis propria. The cysts were mostly seen in the muscularis propria or a deeper site. The inner layers of the cysts were lined with normal urothelium, and some cysts opened onto the mucosal surface, indicating that they were derived from invaginated mucosal epithelium. We believe that this lesion may be a novel form of diverticular disorder demonstrating similarities to adenomyomatous hyperplasia of the gallbladder.

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miR-1, regulated by LMP1, suppresses tumour growth and metastasis by targeting K-ras in nasopharyngeal carcinoma

Summary

There is evidence to show that downregulation of miR-1 expression is closely related to cancer progression, including in nasopharyngeal carcinoma (NPC). However, the molecular mechanisms underlying miR-1 downregulation in NPC remain largely unknown, especially its association with Epstein–Barr virus (EBV). In this study we found that restoration of miR-1 dramatically inhibited cell invasion in vitro, together with tumour growth and metastasis in vivo. Importantly, we found that LMP1, an Epstein–Barr virus (EBV)-associated protein, suppressed miR-1 expression. Furthermore, we identified K-ras as a novel direct target of miR-1. Our results demonstrated for the first time that miR-1 was suppressed by LMP1 and its tumour-suppressive effects were mediated chiefly by repressing K-ras expression. We propose that miR-1 could serve as an independent biomarker to identify patients with different clinical characteristics.

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Reduced AMPKα2 protein expression restores glucose-induced insulin secretion in islets from calorie-restricted rats

Summary

In a state of caloric restriction (CR), improved insulin action was associated with the activation of AMP-activated kinase (AMPK). Here, we verified whether AMPK was involved in impaired β-cell function in islets from rats subjected to CR for 21 days.

Eight-week-old male rats were distributed into a control (CTL) group that was fed an isocaloric diet ad libitum or a CR group that received 60% of the food consumed by the CTL group. From days 18–21, CTL and CR rats were treated with sense (CTLS and CRS) or antisense (CTLAS and CRAS) AMPKα2 oligonucleotides.

Caloric restriction was associated with decreased body weight, perigonadal fat pads and insulinaemia, while higher glucose tolerance was observed in CRS rats. Antisense treatment normalized insulinaemia and glucose tolerance in CRAS rats and increased cholesterolaemia in CRAS and CTLAS groups. These effects were associated with reduced pAMPK/AMPK protein expression in the liver of rats treated with antisense oligonucleotides. Additionally, CRS islets showed higher pAMPK/AMPK content and lower glucose-induced insulin release. As expected, antisense oligonucleotides against AMPKα2 efficiently reduced pAMPK/AMPK protein in CRAS and CTLAS islets. The lower AMPK content in CRAS islets normalized the insulin secretion in islets exposed to 16.7 mM glucose. In addition, CTLAS islets presented higher insulin secretion at 2.8 and 16.7 mM glucose. These findings support the hypothesis that higher AMPK protein expression is involved in impaired β-cell function in islets from rats subjected to CR for 21 days.

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Characterization of lesion formation in marmosets following inhalational challenge with different strains of Burkholderia pseudomallei

Summary

The marmoset model of melioidosis was used to explore whether there was any difference in the disease presentation and/or the lesion formation following inhalational challenge with one of four strains of Burkholderia pseudomallei (K96243, 1026b, HBPUB10303a and HBPUB10134a). Marmosets were challenged with a range of bacterial doses and bacterial load, histological and physiological features were determined temporally following lethal disease. Melioidosis presented as an acute, febrile disease with bacteraemia, bacterial dissemination, necrotizing hepatitis, splenitis and pneumonia which was independent of the challenge strain. Generally, there were no major differences in the manifestation of melioidosis following challenge by the different strains of B. pseudomallei; however, there were some differences in the time to death and the severity of the pathological features. The pathological features observed in the liver and spleen of animals challenged with B. pseudomallei strain 1026b were statistically less severe (P < 0.05) and less frequent. However, more severe foci of disease were evident in the lungs of animals challenged with strain 1026b. In all cases, the lesions developed from small areas of bacteria-infected macrophages surrounded by non-infected neutrophils into large lesions with both immune cell types infected. The marmoset model was a useful tool enabling the distinction of subtle difference in the pathological response to B. pseudomallei.

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Multiple pathways regulate Cten in colorectal cancer without a Tensin switch

Summary

CTEN/TNS4 is a member of the Tensin gene family. It localizes to focal adhesions and induces cell motility. The mechanisms regulating Cten expression are unclear although we have shown regulation by Kras in the colon and pancreas. In normal mammary cell lines, it is reportedly upregulated by epidermal growth factor receptor (EGFR) and STAT3 signalling and upregulation is accompanied by downregulation of Tensin 3 (Tensin switch). In this study, we investigated the roles of EGFR and STAT3 signalling in the regulation of Cten in colorectal cancer (CRC). In addition, we investigated calpain – a regulator of focal adhesion-associated proteins whose relevance to Cten has not been investigated. CRC cell lines were stimulated with epidermal growth factor (EGF). This resulted in an increase in Cten and Tensin 3 protein. Kras was knocked down and this resulted in downregulation of Cten and Tensin 3. We next investigated the role of STAT3 signalling. Activation and knockdown of STAT3 resulted in downregulation and upregulation, respectively, of Cten. Inhibition of calpain resulted in upregulation of both Cten and Tensin 3. As the regulators of Cten also seemed to regulate Tensin 3, we tested the interaction between Cten and Tensin 3. Cten was forcibly expressed or knocked down resulting, respectively, in upregulation and downregulation of Tensin 3. We conclude that in CRC, Cten is upregulated by EGFR and Kras but downregulated by STAT3. We show that calpain may be a negative regulator of Cten and that a Tensin switch does not occur and, if anything, Cten stabilizes Tensin 3.

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