Background: Impaired glucose metabolism and cystic fibrosis (CF)-related diabetes (CFRD) are associated with insufficient weight gain and impaired lung function in children and adolescents with CF. We have asked whether imminent CFRD may be a cause of poor growth in children and adolescents. Methods: A retrospective case control study including 32 patients with CF with or without diabetes was conducted. Sixteen pairs, matched according to age, gender and exocrine pancreatic insufficiency, were analysed. Standard deviation scores (SDS) of height, growth, weight, body mass index (BMI), forced vital capacity (FVC), forced expiratory volume in the first second (FEV1) and forced expiratory flow at 75% of expired FVC (FEF75) were recorded during a mean observation period of 13 years per patient. Results: SDS of height and weight were reduced in CF patients with diabetes compared to those without, not only at the point of diagnosis (both p < 0.05) but years before the evidence of diabetes. Afterwards there was a significant decline in height (p < 0.001) and weight (p < 0.01) SDS in CFRD patients and an increasing difference between the height and weight of CF patients with or without diabetes. In contrast, no significant reduction of BMI-SDS was observed in CFRD patients. All analysed lung function parameters showed a marked decline in CFRD patients starting 1 year prior to the diagnosis of diabetes. Conclusions: Deteriorating growth, reduced weight and impaired lung function are related to the development of CFRD and are obvious several years before the actual diagnosis of diabetes.

It is known that sensorimotor gating measured by the prepulse inhibition of the startle reflex (PPI) matures during childhood. Since certain disorders in children, for example, enuresis, show a significant loss in PPI, the PPI as a tool for investigating brainstem reflex control mechanism gains in importance. Therefore, it is crucial to know the natural course of PPI maturation in childhood. A total of 122 healthy children aged from 3-10 years and 10 healthy adults were examined. PPI was initiated by a 120 ms and a 60 ms prepulse and was measured by the EMG of M. orbicularis oculi. For the respective prepulse intervals, the PPI level in each age group increased from 3 to 9 or 10 years and showed a similar course. The findings confirm and extend knowledge about the maturation of PPI during childhood and emphasize the importance of age-dependent standard values when investigating PPI in children.

The anti-platelet drug clopidogrel has been shown to modulate adhesion molecule and cytokine expression, both playing an important role in the pathogenesis of atherosclerosis. The aim of this study was to investigate the impact of clopidogrel on the development and progression of atherosclerosis. ApoE(-/-) mice fed an atherogenic diet (cholesterol: 1 %) for 6 months received a daily dose of clopidogrel (1 mg/kg) by i.p. injection. Anti-platelet treatment was started immediately in one experimental group, and in another group clopidogrel was started 2 month after beginning of the atherogenic diet. Blood was analysed at days 30, 60 and 120 to monitor the lipid profile. After 6 months the aortic arch and brachiocephalic artery were analysed by Sudan IV staining for plaque size and by morphometry for luminal occlusion. Serum levels of various adhesion molecules were investigated by ELISA and the cellular infiltrate was analysed by immunofluorescence. After daily treatment with 1 mg/kg clopidogrel mice showed a significant reduction of atherosclerotic lesions in the thoracic aorta and within cross sections of the aortic arch [plaque formation 55.2 % (clopidogrel/start) vs. 76.5 % (untreated control) n = 8, P < 0.05]. After treatment with clopidogrel P-/E-selectin levels and cytokine levels of MCP-1 and PDGFβ were significantly reduced as compared to controls. The cellular infiltrate showed significantly reduced macrophage and T-cell infiltration in clopidogrel-treated animals. These results show that clopidogrel can effectively delay the development and progression of 'de-novo' atherosclerosis. However, once atherosclerotic lesions were already present, anti-platelet treatment alone did not result in reverse remodelling of these lesions.

Heterogeneity of ADHD is confirmed with a wide range of baseline PPI. The improvement of reduced baseline PPI through MPH suggests impaired sensorimotor gating in this subgroup.

SUMMARY Enteroendocrine regulatory peptides may play an important role in the adaptation of small bowel mucosa, and it is likely that they act interdependently with neural and luminal stimuli. We assessed their action in rats by morphometric evaluation of enteroendocrine cells after heterotopic accessory small bowel transplantation (SBT), in which the graft is shunted off from the intestinal passage and is entirely deprived of neural connections, and after orthotopic SBT It is likely that the control of the adaptive response and the transport capacity of small bowel mucosa depends on the interaction of neural, enteroendocrine, and luminal stimuli.'-3 Enteroglucagon has been suggested to be an effective agent for influencing growth after small bowel resection." After small intestinal bypass and small bowel resection gastric inhibitory peptide (GIP) shows a strong reaction. Buchan and coworkers' found a markedly reduced number of GIP positive cells in the functional jejunum after jejunoileal bypass and in the jejunum of rat after massive small bowel resection. In addition there is evidence that other gastrointestinal peptides play a significant role in the gastrointestinal regulatory systems that influence the transporting epithelium of the small bowel mucosa. In the rat model exclusion of nutritional stimuli to the small bowel mucosa during total parenteral nutrition (TPN) causes a marked decrease in cholecystokinin (CCK) positive cells in the duodenum and a decrease in neurotensin (NT)