The authors review the literature, pointing out the anatomy of the duodenojejunal angle, the etiology, and the predisposing factors, as well as diagnostic and therapeutic strategies.

Neural tube defects (NTDs) are a group of congenital malformations of the central nervous system occurring at an average rate of 1 per 1,000 human pregnancies worldwide. Numerous genetic and environmental factors are discussed to be relevant in their etiology. In mice, mutants in >200 genes including the planar cell polarity (PCP) pathway are known to cause NTDs, and recently, heterozygous mutations in the human VANGL1 gene have been described in a small subset of patients with NTDs. We performed a VANGL1 mutation analysis in 144 unrelated individuals with NTDs from Slovakia, Romania and Germany and identified 3 heterozygous missense mutations: c.613G>A (p.Gly205Arg) with an open spina bifida (lumbosacral meningomyelocele), c.557G>A (p.Arg186His) with a closed spina bifida (tethered cord and spinal lipoma) and c.518G>A (p.Arg173His) with an unknown NTD. The c.613G>A mutation was also found in a healthy sibling. None of the mutations were described previously. Findings support that heterozygous VANGL1 mutations represent hypomorphs or conditional mutants predisposing to NTDs and occur at a frequency of approximately 2.1% of open and closed spinal NTDs. The mutations (p.Arg173His, p.Arg186His, p.Gly205Arg) modified conserved regions of the VANGL1 protein and shared similarities with previously described mutants, providing further evidence for the presence of mutational hot spots in these patients.

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We conclude that clostridial myonecrosis should be considered in unclear abdominal infections, even if the patient's history is not typical as in the present case.

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)