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PubMedDate not supplied

Hyperammonemia during total parenteral nutrition in children.

Serial blood ammonia (NH3) determinations in 19 low birth weight (LBW) infants, 14 term neonates and 12 children receiving total parenteral nutrition (TPN) have shown that 73% of patients had one or more elevated NH3 values (greater than 150 micrograms/dl). The mean blood NH3 was 220 +/- 13 micrograms/dl in LBW infants, 180 +/- 9 micrograms/dl in 10 infants, and 140 +/- 7 micrograms/dl in children. All of these values are significantly higher than normal (p less than 0.001). There was no difference in incidence or mean blood ammonia concentration between patients receiving casein hydrolysate and those receiving a crystalline amino acid solution. Only four patients were symptomatic and several infants remained fully alert despite blood NH3 concentration in excess of 400 micrograms/dl. One infant who had sustained hyperammonemia was given another amino acid source (Travasol) containing 1.2 mmol/dl of arginine; blood NH3 promptly fell to the normal range. However, six of seven additional infants had hyperammonemia while receiving Travasol (mean = 184 micrograms/dl). Hyperammonemia is common during TPN in children, often is not recognized clinically, and occurs with equal frequency in infants and older children. The high levels observed in LBW infants may be due to hepatic immaturity. Blood NH3 concentration should be monitored frequently during TPN. Persistent hyperammonemia should be treated by decreasing protein content of the infusate. The role of supplemental arginine is unclear.

Adolescent↗
PubMedDate not supplied

A communicating intestinal duplication in a Sprague-Dawley rat.

Duplications of the gastrointestinal tract are exceedingly rare in laboratory animals. We report a case of a communicating intestinal duplication in a 17-wk-old Sprague-Dawley (SD) rat. The duplication was present in the mesenteric border of the ileum, and both proximal and distal ends were communicated with the lumen of ileum. Histologically, the duplicated portion had a thick muscle wall and a mucosa similar to that of the small intestine. This is the first reported case of intestinal duplication in an SD rat.

Animals↗
PubMedDate not supplied

A congenital ciliated epithelial cyst on the stomach of a B6C3F1 mouse.

Congenital anomalies of the alimentary tract are rare lesions in laboratory animals. We describe a congenital cyst attached to the greater curvature of the forestomach in a B6C3F1 mouse. The inner surface of the cyst was mostly covered with cuboidal or pseudostratified ciliated epithelium and was focally covered with the flat cuboidal epithelium. The base of the cyst appeared to be inserted between the layers of the outer longitudinal muscle layer of the forestomach, although no smooth muscle layer was evident in the free surface of the cyst wall. The cyst resembled duplication of the alimentary tract, as it was lined with ciliated epithelium and had developed at the greater curvature of the forestomach. Since the smooth muscle layer did not completely cover the whole wall and the cyst did not communicate with the gastric lumen, the cyst was not thought to be a standard duplication but rather a simple congenital cyst.

Animals↗
PubMed1996

Drosophila brachyenteron regulates gene activity and morphogenesis in the gut.

Chromosomal region 68D/E is required for various aspects of Drosophila gut development; within this region maps the Brachyury homolog T-related gene (Trg), DNA of which rescues the hindgut defects of deficiency 68D/E. From a screen of 13,000 mutagenized chromosomes we identified six non-complementing alleles that are lethal over deficiencies of 68D/E and show a hindgut phenotype. These mutations constitute an allelic series and are all rescued to viability by a Trg transgene. We have named the mutant alleles and the genetic locus they define brachyenteron (byn); phenotypic characterization of the strongest alleles allows determination of the role of byn in embryogenesis. byn expression is activated by tailless, but byn does not regulate itself. byn expression in the hindgut and anal pad primordia is required for the regulation of genes encoding transcription factors (even-skipped, engrailed, caudal, AbdominalB and orthopedia) and cell signaling molecules (wingless and decapentaplegic). In byn mutant embryos, the defective program of gene activity in these primordia is followed by apoptosis (initiated by reaper expression and completed by macrophage engulfment), resulting in severely reduced hindgut and anal pads. Although byn is not expressed in the midgut or the Malpighian tubules, it is required for the formation of midgut constrictions and for the elongation of the Malpighian tubules.

Alleles↗
PubMed2002

Depletion of definitive gut endoderm in Sox17-null mutant mice.

In the mouse, the definitive endoderm is derived from the epiblast during gastrulation, and, at the early organogenesis stage, forms the primitive gut tube, which gives rise to the digestive tract, liver, pancreas and associated visceral organs. The transcription factors, Sox17 (a Sry-related HMG box factor) and its upstream factors, Mixer (homeobox factor) and Casanova (a novel Sox factor), have been shown to function as endoderm determinants in Xenopus and zebrafish, respectively. However, whether the mammalian orthologues of these genes are also involved with endoderm formation is not known. We show that Sox17(-/-) mutant embryos are deficient of gut endoderm. The earliest recognisable defect is the reduced occupancy by the definitive endoderm in the posterior and lateral region of the prospective mid- and hindgut of the headfold-stage embryo. The prospective foregut develops properly until the late neural plate stage. Thereafter, elevated levels of apoptosis lead to a reduction in the population of the definitive endoderm in the foregut. In addition, the mid- and hindgut tissues fail to expand. These are accompanied by the replacement of the definitive endoderm in the lateral region of the entire length of the embryonic gut by cells that resemble the visceral endoderm. In the chimeras, although Sox17-null ES cells can contribute unrestrictedly to ectodermal and mesodermal tissues, few of them could colonise the foregut endoderm and they are completely excluded from the mid- and hindgut endoderm. Our findings indicate an important role of Sox17 in endoderm development in the mouse, highlighting the idea that the molecular mechanism for endoderm formation is likely to be conserved among vertebrates.

Animals↗
PubMed2002

The Drosophila gap junction channel gene innexin 2 controls foregut development in response to Wingless signalling.

In invertebrates, the direct communication of neighbouring cells is mediated by gap junctions, which are composed of oligomers of the innexin family of transmembrane proteins. Studies of the few known innexin mutants in Drosophila and C. elegans have shown that innexin proteins, which are structurally analogous to the connexins in vertebrates, play a major structural role as gap junctional core components in electric signal transmission. We show that Drosophila innexin 2 mutants display a feeding defect that originates from a failure of epithelial cells to migrate and invaginate during proventriculus organogenesis. The proventriculus is a valve-like organ that regulates food passage from the foregut into the midgut. Immunohistological studies indicate that innexin 2 is functionally required to establish a primordial structure of the proventriculus, the keyhole, during the regionalisation of the embryonic foregut tube, which is under the control of Wingless and Hedgehog signalling. Our genetic lack- and gain-of-function studies, and experiments in Dorsophila tissue culture cells provide strong evidence that innexin 2 is a target gene of Wingless signalling in the proventricular cells. This is the first evidence, to our knowledge, that an invertebrate gap junction gene controls epithelial tissue and organ morphogenesis in response to the conserved WNT signalling cascade.

Animals↗
PubMedDate not supplied

The association of congenital hypothyroidism and congenital gastrointestinal anomalies in Down's syndrome infants.

OBJECTIVE: To study the prevalence of congenital hypothyroidism in infants with Down's syndrome and to verify whether there is an association with other congenital defects. METHODS: This is a prospective study of 112 Down patients, less than 1 year of age, who attended Songklanagarind Hospital from January 1991 to December 1996. Free T4 and TSH determinations were performed in all Down infants. Information on karyotype, sex, maternal age and other congenital anomalies was collected. RESULTS: Congenital hypothyroidism was detected in 17 patients (15.2%); 3 overt congenital hypothyroidism; 6 persistent compensated hypothyroidism; and 8 transient compensated hypothyroidism. Nine of the 20 patients (45%) with congenital gastrointestinal anomalies had congenital hypothyroidism, while 8 out of 92 patients (8.7%) without congenital gastrointestinal anomalies had congenital hypothyroidism. The odds ratio was 8.59 (95% confidence interval 2.4-31.6; p = 0.0001). CONCLUSION: Congenital hypothyroidism has a relatively high prevalence rate in Down infants and tends to occur in Down patients with gastrointestinal anomalies.

Congenital Hypothyroidism↗
PubMed2000

Pancreatic disorders in the newborn.

Except for the hyperinsulinism associated with the infant of a diabetic mother (accounting for about 5 percent of NICU admissions annually), pancreatic disorders of the newborn are rare. Congenital anomalies (such as annular pancreas) and endocrine disorders (such as hyperinsulinism of nesidioblastosis or hyperglycemia of neonatal diabetes mellitus) present many challenges to the personnel caring for these infants and their families. The potential mortality and morbidity of these disorders make it imperative for nurses and nurse practitioners working with infants to recognize and understand pancreatic dysfunction so that appropriate and timely intervention can prevent complications of brain injury and developmental delay. The home care needs of these infants and the extensive teaching needs of their parents require skilled nursing care to ensure a safe discharge.

Diabetes Mellitus↗
PubMed2000

The stomach.

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Digestive System↗