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PubMed1981

Primary epiduritis.

An infant, born with multiple anomalies of the gastrointestinal tract, required intravenous hyperalimentation for virtually his entire life. His course was characterized by multiple episodes of sepsis or phlebitis, culminating in death five and one-half months after birth. The brain and spinal cord at necropsy were normal on gross inspection. However, microscopic study showed inflammation of the dura surrounding the spinal cord with sparing of the spinal and cerebral subarachnoid spaces.

Digestive System Abnormalities↗
PubMed1953

Hallux valgus.

Explore the source record for details and available documents.

Digestive System Abnormalities↗
PubMed1995

Double duplication in a nonrotational colon. Study of a case associated with mucinous adenoma.

Duplications of gastrointestinal tract are unusual anomalies, especially in the colon. We report a case with two colonic duplications in a 20 year old woman who complained of recurrent backache associated with left lower quadrant abdominal pain. Neither physical examination nor laboratory test alterations were detected. Roentgenographic examination showed organic scolinosis, no intestinal gas and a mass with central hyperdensity and thickened wall in the descending colon area on the CT scan. Laparotomy was performed in which 22 cm of ascending colon and terminal ileum sited on left side, was excised. Pathological study revealed two unrelated and cystic duplications without communication to intestinal lumen. Their epithelial lining were of colonic or gastric types and showed a mucinous adenoma; the remaining layers were normal except for eosinophilic inflammatory infiltrate with Charcot-Leyden like crystaloids. In conclusion, we present a double spherical colonic duplication type I associated to a mucinous adenoma on a non-rotational ascending colon in a patient with organic scoliosis.

Adenoma↗
PubMed2003

Redundant early and overlapping larval roles of Xsox17 subgroup genes in Xenopus endoderm development.

We have used antisense morpholino oligos to establish the developmental roles of three Xsox17 proteins in Xenopus development (Xsox17alpha(1), alpha(2) and beta). We show that their synthesis can be inhibited with modest amounts of oligo. The inhibition of each individually produces defects in late midgut development. Loss of activity of the Xsox17alpha proteins additionally inhibits hindgut formation, and inhibiting Xsox17alpha(1) disrupts foregut development with variable penetrance. When all Xsox17 activity is inhibited cell movements are halted during late gastrulation and the transcription of several endodermally expressed genes is reduced. Thus the Xsox17 proteins have redundant roles in early development of the endoderm and partly distinct roles during later organogenesis.

5' Untranslated Regions↗
PubMed2002

[Gastrointestinal system duplications in children (19 cases)].

UNLABELLED: Digestive duplications are a rare condition in children, characterized by an important anatomoclinical polymorphism. Diagnosis suspected on clinics and evoked by radiology, require histological confirmation. PATIENTS AND METHODS: Nineteen children with duplications were managed in our department, from 1989 to 2001: their hospital chart was retrospectively studied. RESULTS: Ten of our patients were less than one year of age, ten were boys and nine were girls. Clinical signs consisted of pain and abdominal mass, with some transit disturbs, and these signs led to ultrasonography and tomodensitometry. In one case alimentary tract duplication was revealed by digestive hemorrhage, leading to scintigraphic study. The digestive duplications were localized on the stomach in one case, the duodenum in two cases, the jejuno-ileum in twelve cases, the colon in two cases, and the rectum in two cases. Five digestive duplications were tubular, with one communicating duplication. All cases benefited from surgical treatment, and resection procedure was chosen according to duplication type and site. Histological study showed eight cases of ectopic mucosa, six ectopic gastric mucosa and two pancreatic ectopic mucosa. CONCLUSION: Diagnosis and surgical precocious treatment of digestive duplications are the only way to warn complications of this benign pathology.

Biopsy↗
PubMed2003

[Agenesis of the gallbladder].

Isolated agenesis of the gallbladder (AG) is a rare anomaly. Twenty-three percent of the patients are symptomatic and present with right upper abdominal pain, nausea and fatty food intolerance. The condition is frequently mistaken with excluded or sclero-atrophic gallbladder, regardless of the imaging modality used. Consequently, AG leads often to unnecessary and potentially dangerous surgery. During laparoscopy, the absence of normal anatomical structures and the impossibility of pulling on the gallbladder to dissect the triangle of Callot represent an increased risk of iatrogenic injury to biliary or portal structures. The aim of this study is to discuss the pitfalls of the available radiological exams and the management of this rare condition. We describe two cases of AG, with a review of the literature. A high index of suspicion is necessary when interpreting the radiological images. In case of doubt, a MRI-cholangiography is mandatory. Because of possible inherited transmission, relatives with a history of biliary symptoms should be investigated, even when asymptomatic.

Adult↗
PubMed1996

Renal agenesis and the absence of enteric neurons in mice lacking GDNF.

Glial-cell-line-derived neurotrophic factor (GDNF) is a potent survival factor for dopaminergic neurons and motor neurons in culture. It also protects these neurons from degeneration in vitro, and improves symptoms like Parkinson's disease induced pharmacologically in rodents and monkeys. Thus GDNF might have beneficial effects in the treatment of Parkinson's disease and amyotrophic lateral sclerosis. To examine the physiological role of GDNF in the development of the mammalian nervous system, we have generated mice defective in GDNF expression by using homologous recombination in embryonic stem cells to delete each of its two coding exons. GDNF-null mice, regardless of their targeted mutation, display complete renal agencies owing to lack of induction of the ureteric bud, an early step in kidney development. These mice also have no enteric neurons, which probably explains the observed pyloric stenosis and dilation of their duodenum. However, ablation of the GDNF gene does not affect the differentiation and survival of dopaminergic neurons, at least during embryonic development.

Animals↗
PubMed2006

Type ID unconventional myosin controls left-right asymmetry in Drosophila.

Breaking left-right symmetry in Bilateria embryos is a major event in body plan organization that leads to polarized adult morphology, directional organ looping, and heart and brain function. However, the molecular nature of the determinant(s) responsible for the invariant orientation of the left-right axis (situs choice) remains largely unknown. Mutations producing a complete reversal of left-right asymmetry (situs inversus) are instrumental for identifying mechanisms controlling handedness, yet only one such mutation has been found in mice (inversin) and snails. Here we identify the conserved type ID unconventional myosin 31DF gene (Myo31DF) as a unique situs inversus locus in Drosophila. Myo31DF mutations reverse the dextral looping of genitalia, a prominent left-right marker in adult flies. Genetic mosaic analysis pinpoints the A8 segment of the genital disc as a left-right organizer and reveals an anterior-posterior compartmentalization of Myo31DF function that directs dextral development and represses a sinistral default state. As expected of a determinant, Myo31DF has a trigger-like function and is expressed symmetrically in the organizer, and its symmetrical overexpression does not impair left-right asymmetry. Thus Myo31DF is a dextral gene with actin-based motor activity controlling situs choice. Like mouse inversin, Myo31DF interacts and colocalizes with beta-catenin, suggesting that situs inversus genes can direct left-right development through the adherens junction.

Actins↗
PubMed2006

An unconventional myosin in Drosophila reverses the default handedness in visceral organs.

The internal organs of animals often have left-right asymmetry. Although the formation of the anterior-posterior and dorsal-ventral axes in Drosophila is well understood, left-right asymmetry has not been extensively studied. Here we find that the handedness of the embryonic gut and the adult gut and testes is reversed (not randomized) in viable and fertile homozygous Myo31DF mutants. Myo31DF encodes an unconventional myosin, Drosophila MyoIA (also referred to as MyoID in mammals; refs 3, 4), and is the first actin-based motor protein to be implicated in left-right patterning. We find that Myo31DF is required in the hindgut epithelium for normal embryonic handedness. Disruption of actin filaments in the hindgut epithelium randomizes the handedness of the embryonic gut, suggesting that Myo31DF function requires the actin cytoskeleton. Consistent with this, we find that Myo31DF colocalizes with the cytoskeleton. Overexpression of Myo61F, another myosin I (ref. 4), reverses the handedness of the embryonic gut, and its knockdown also causes a left-right patterning defect. These two unconventional myosin I proteins may have antagonistic functions in left-right patterning. We suggest that the actin cytoskeleton and myosin I proteins may be crucial for generating left-right asymmetry in invertebrates.

Actins↗
PubMed2006

Enteric duplication cyst resembling umbilical cord cyst.

We report a case of a neonatal male with a prenatal diagnosis of umbilical cord cyst that was finally diagnosed as an ileal duplication cyst after post-natal surgical exploration of the umbilical mass. To our knowledge, a similar case has never been reported previously. Although this form of presentation of enteric duplication cyst is exceptional, it should be taken into consideration when evaluating suspected umbilical cord cysts.

Adult↗
PubMed1999

Case report: Colonic duplication: a rare cause of obstruction.

Complete duplication of the entire large bowel with partial ileal involvement is very rare and diagnosis can often be difficult as illustrated by this case report. We also review the other clinical associations of this rare condition and briefly discuss the embryology of duplications of the gastrointestinal tract.

Child↗
PubMed2003

Intestinal obstruction in neonatal/pediatric surgery.

Intestinal obstruction in the newborn infant and older child may be due to a variety of conditions, including atresia and stenosis, annular pancreas, malrotation, duplication cyst, meconium ileus, meconium plug syndrome and neonatal small left colon syndrome, Hirschsprung's disease, neoplasia, trauma, and other rarer causes. The mode of presentation can be acute or more chronic with systemic upset due to shock. Neonates, more so than older children, with unrecognized intestinal obstruction deteriorate rapidly, show an increase of associated morbidity and mortality and appropriate surgical treatment becomes more hazardous. Early diagnosis depends largely on the prompt detection of obstructive manifestations by the clinician and the subsequent accurate interpretation of radiographic findings and other investigations, leading to definitive treatment, which should always be preceded by appropriate resuscitation/preparation of the infant/child. Management of intestinal obstruction will almost always be surgical, apart from some notable exceptions and all are discussed in more detail. With the advent of pediatric and neonatal intensive care and multidisciplinary care, the morbidity and mortality of cases of intestinal obstruction reported in current series is generally extremely low and mainly determined by the coexistence of other major congenital anomalies (eg, cardiac), delays in diagnosis and treatment or coexisting medical conditions. Newer treatments and future developments may reduce the residual mortality in such cases as ultrashort-bowel syndrome.

Child↗
PubMed2000

The late nonfunctioning duodenal atresia repair--a second look.

BACKGROUND/PURPOSE: In 1986, the authors reported on 3 newborns who had repair of their duodenal atresia, and between 6 and 18 months postoperatively an anastomotic obstruction developed in each suddenly. After prolonged medical and surgical treatments it became apparent that the duodenal atresia repair was functionally obstructed and plication of the dilated atonic proximal duodenum was curative. Since then, 2 more patients became so obstructed at 5 and 24 years postoperatively. The aim of this study was to report the very late occurrence of a functional obstruction of a newborn duodenal atresia repair. METHODS: The 2 additional histories and surgical repairs were reviewed. RESULTS: The 5-year old boy was cured immediately with plication only of his dilated proximal duodenum. The 24-year-old nurse had a very stormy 2-year course with several bypass operations, which did not relieve her abdominal pain and bile vomiting until they were taken down and her dilated proximal duodenum was plicated, after which she made a good recovery. Both remain well. CONCLUSION: An uncommon, very late, sudden, apparently anastomotic, postoperative, newborn, duodenal atresia repair obstruction caused by proximal, dilated, duodenal atony, and dysfunction can occur many years later and responds to duodenal plication alone.

Adult↗