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BACKGROUND/OBJECTIVE: The recent rapid increase in childhood obesity rates suggests that a consideration of the role of the schools in addressing this problem is necessary. 'Fits me' program functions to promote eating daily and healthy breakfast among elementary school children. METHODS: Separate children groups were sampled each year by clusters from seven regions around Israel. They filled a self-administered questionnaire at the beginning of 2003, before the program started, and in 2003-2005, after the program. A separate sample was collected in 2006 in a case-control structure. The answer to the question: 'what do you eat for breakfast?' considered as a healthy breakfast if it included one of the following food items: A sandwich (not including chocolate, jam or butter), cereals, vegetable, fruit, egg and dairy product. RESULTS: As compared with 2003 before the program, more children reported eating daily breakfast over the years (51-65% before and until 2005, respectively, P for trend<0.01). Odds ratio (OR) and 95% confidence interval (95% CI) for eating a healthy breakfast, in 2006 in the intervention (n=417) vs controls (n=572), adjusted for sex and age were OR=1.53 (95% CI: 1.15-2.04). However, only a third of 75% of the children who ate a healthy breakfast in the intervention group estimated that they were eating a healthy breakfast. CONCLUSIONS: After implementation an educational program to promote daily and healthy breakfast eating, the goal of a healthier breakfast was achieved. However, one should strive to define an exact definition of a healthy breakfast.

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Gonadotropin-releasing hormone (GnRH), which is essential for reproductive function, is made by neurones that migrate from the nasal region into the brain during early embryonic development. This migration begins in chick when the olfactory pit is formed. This is approximately the time that GnRH neurones can be detected immunocytochemically. The present study investigated (i). how early in development the GnRH gene is expressed and (ii). the sites of its expression. Accordingly, reverse transcriptase-polymerase chain reaction (PCR) and in situ hybridization were performed on chick embryos before gastrulation up until the stage by which GnRH neurones have begun to migrate into the central nervous system. Primers were made to the 5'- and 3'-UTR region of the message for cGnRH-I, the form of the peptide that is essential for reproductive function in the chicken. PCR product was found in all stages and the sequences of products from all stages were identical. Thus, the GnRH gene is expressed continuously throughout embryonic development. In situ hybridization with a digoxygenin labelled riboprobe revealed staining along the primitive streak immediately before gastrulation. In later stages, cGnRH-I gene expression was seen in association with the anterior neural ridge. The expression was subsequently restricted to a narrow, clearly defined region, which is associated with the presumptive nasal cavity and olfactory placode. Later, GnRH neurones could be seen in their migratory routes by both in situ hybridization and immunocytochemistry. Expression of the GnRH gene has been described in preimplantation stages in mammals and there is evidence that the neuropeptide plays a role in formation and maintenance of the placenta. What role (if any) it may play in early avian development remains unknown. The demonstration of sites of GnRH expression during the early period of neurulation suggests that GnRH neurones arise before olfactory placode formation.

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There is evidence that the incidence and severity of asthma are increasing worldwide, but there are limited data on asthma in Israel. The aim of this study was to investigate the prevalence and severity of asthma and asthma symptoms in 13-14 yr-old schoolchildren in Israel. The self-completed questionnaire used was a modified version of that developed by the International Study of Asthma and Allergies in Childhood (ISAAC), and was administered to a national sample of 12,918 children. The prevalence of asthma ever, wheezing ever and wheezing in the last 12 months were 13.7, 23.8 and 17.9% respectively. Significantly higher rates of a history of asthma and asthma symptoms were observed in Jews compared with Arabs. Although asthma ever was more prevalent in males than in females, asthma symptoms were significantly more common in females. The type of area of residence had no effect on the prevalence of wheezing. The ethnic differences in the prevalence of asthma persisted after controlling for sex, district of residence and level of urbanization. The prevalence of both asthma and asthma symptoms in Israel are slightly above the mean reported from 10 other countries in Europe and the Far-East.

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GnRH cells are first detected in the olfactory placode of the mouse on Gestational Day 11.5 (E11.5). Between E12.5 and E15.5 they migrate across the nasal septum and by E16.5 attain their adult distribution within the forebrain. In the present study, we used immunocytochemistry at the light and electron microscopic level to study the biochemical and morphological differentiation of gonadotropin-releasing hormone (GnRH) neurons and the cellular associations that they make during this migratory process. On E12.5, when the majority of GnRH cells are still in the nasal septum, only 15% of the population can process the pro-GnRH precursor to the amidated decapeptide. Two days later (E14.5), when most of the cells have advanced into the forebrain, 79% contain mature GnRH. In keeping with these light microscopic observations, ultrastructural analysis reveals that on E12.5 GnRH immunologic reaction product is confined to the outer nuclear envelope and rough endoplasmic reticulum. By E14.5 these migratory cells in the nasal septum have more reaction product in the rough endoplasmic reticulum and some of the Golgi cisternae are also immunopositive. Neurosecretory granules, some of which are immunoreactive, also appear at this stage. We had anticipated that the expression of GAP-43 would coincide with axonal elongation and pathfinding in GnRH neurons. Instead, GAP-43 was expressed at the early migratory stage of GnRH cells and its expression declined rapidly after these neurons had entered the forebrain and commenced axonal outgrowth. Hence, on E12.5, 62.3% of GnRH cells in the nasal septum are immunopositive for GAP-43, while only 12.6% of the forebrain population at the same embryonic stages express the protein. Similarly, on E14.5 GAP-43 is expressed in 50.7% of the nasal septum GnRH cells but only 11.6% of cells in the E14.5 forebrain express this protein. While in the nasal septum, GnRH neurons migrate only within the confines of the olfactory and vomeronasal axonal fascicles. During this part of the migratory route, the cells maintain close membrane apposition with each other and with the axons and ensheathing glia of the nerve fascicles. Once in the forebrain, GnRH neurons no longer maintain these associations, nor do they follow any defined anatomical structure. These findings indicate that although GnRH cells express their unique neuropeptide early in their ontogeny, their differentiation continues and is coordinated with their migration.(ABSTRACT TRUNCATED AT 400 WORDS)

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This study was undertaken to determine whether gonadotropin-releasing hormone (GnRH) neurons in the mutant hypogonadal (hpg) mouse can establish axonal connections with their target despite their failure to synthesize and secrete the GnRH neuropeptide. Normal and hpg males received intraperitoneal injections of the retrograde tracer Fluoro-Gold. This tracer does not cross the blood-brain-barrier and hence is taken up only by neurons in the central nervous system whose axons terminate on fenestrated capillaries, such as the capillaries of the median eminence. The brains of the injected animals were processed for in situ hybridization to visualize GnRH transcribing cells. In 3 hpg males 64.1 +/- 5.6% of GnRH transcribing cells contained Fluoro-Gold, while 55.8 +/- 6.4% of the cells in 3 normal males had Fluoro-Gold. Thus, we have demonstrated that secretory-deficient GnRH neurons can establish axonal connections with their primary secretory target, the median eminence. We conclude that the capability of GnRH neurons to recognize and interact with their target is not dependent upon their neurosecretory function.

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Some aspects of reproductive function in the GnRH-deficient hypogonadal (hpg) mutant mouse can be restored by transplanting normal fetal brain tissue containing GnRH cells into the central nervous system of adult hpg mice. However, hpg males showing physiological response to the graft fail to display sexual behavior and are infertile. We hypothesized that the reproductive deficit of these males is due to insufficient perinatal exposure to testicular androgens as a consequence of the GnRH deficiency. To test this hypothesis we androgenized hpg males by giving them neonatal injections of testosterone propionate (TP). Controls consisted of hpg males not androgenized neonatally and of normal males. All three groups received a TP implant in adulthood, and their copulatory behavior and reproductive capability were recorded. In addition, other hpg males, not androgenized neonatally, received fetal brain transplants containing GnRH neurons and were also tested for copulatory behavior and reproductive capability before and after receiving a TP implant. Three of 8 neonatally androgenized hpg males expressed the full repertoire of male sexual behavior, including intromission and ejaculation, and sired several litters. Three of 7 control hpg males that were not androgenized neonatally but received TP implants in adulthood also displayed mounting and intromission, but there was no evidence of ejaculation, and these males failed to impregnate normal females. Of the 8 hpg males that responded to a fetal transplant with testicular growth, only 1 displayed mounting behavior. However, when given a TP implant, 4 of 8 hpg males with grafts displayed mounting and intromissions.(ABSTRACT TRUNCATED AT 250 WORDS)

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Gonadotropin-releasing hormone (GnRH) neurons are derived from the olfactory placode and migrate into the CNS during embryogenesis. During this migration the GnRH neuronal population follows a very specific pathway through the nasal septum and forebrain with individual neurons 'stopping' at various points along the way. Following migration GnRH neurons elaborate axonal projections, the major one to the median eminence. The function of this neurosecretory connection can then be assessed by activation of the pituitary-gonadal axis. In previous experiments we had demonstrated that grafted post-migratory GnRH neurons could send axons to the median eminence and initiate gonadal development in hypogonadal (hpg) mice that lack GnRH. In the present experiment, grafts derived from the embryonic nasal septum, which contains the migratory population of GnRH neurons, were used to determine if the transplanted GnRH neurons could (1) continue their migration in the adult host brain, (2) elaborate axons to their normal target in the host and (3) stimulate the host pituitary-gonadal axis to induce gonadal development. Nasal tissue from normal mouse embryos was implanted into the preoptic area (n = 8), anterior hypothalamus (n = 3) or third ventricle (n = 1) of adult hpg males. Following survival of 10 days to 10 weeks, the distribution of GnRH immunoreactive elements was assessed and testicular weight recorded. Surviving GnRH neurons were few in number and were found within the graft (n = 3), the host brain (n = 2) or both (n = 1). Four grafts resulted in specific outgrowth of GnRH axons through the host parenchyma to the median eminence.(ABSTRACT TRUNCATED AT 250 WORDS)

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