Surface Hydrophobicity Properties of Rabbit Stomach In Vitro

Dr, Mack; Aw, Neumann; Policova, Zdenka; Pm, Sherman

doi:10.1203/00006450-199402000-00017

Cited by 9 publications

(2 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, GMSH was higher in antral than in corpus mucosa in both H pylori infected and uninfected patients. Such differences were not observed in the first study using endoscopic biopsy specimens of human gastric mucosa,9 but antral was found to be higher than corpus GMSH in both the pig43 and the rabbit 24. Although our data cannot shed much light on these differences we suspect that they might in part be physiological.…”

Section: Discussioncontrasting

confidence: 77%

See 1 more Smart Citation

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Hackelsberger

Platzer

Nilius

et al. 1998

Gut

View full text Add to dashboard Cite

Background-Gastric mucosal surface hydrophobicity (GMSH) is an essential component of the mucosal defence system that is decreased by Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in elderly subjects, and may thus reflect diminished mucosal resistance. Aims-To investigate whether aging decreases GMSH. Patients-One hundred and twenty patients without peptic ulcer disease were divided into three age groups: I (41 years or below); II (41-64 years); and III (65 years or above). Methods-Biopsy specimens were taken from the antrum, corpus, and cardia for histology (Sydney system), urease testing for H pylori, and for contact angle measurement of GMSH with a goniometer. The presence of specific H pylori antibodies was checked by immunoblotting. Results-Fifty two patients (43%) were infected, and 68 were uninfected with H pylori. GMSH at all biopsy sites was lower in H pylori infected subjects (p=0.0001), but also decreased with age independently of infection status (p=0.0001). The most notable decrease in GMSH occurred between age groups I and II in those with, and between age groups II and III in those without, H pylori infection. GMSH was greater in antral than in corpus mucosa in both infected (p=0.0001) and uninfected patients (p=0.0003). Conclusions-A physiological decrease in GMSH with aging may contribute to the risk of ulcer development in the elderly, and may act synergistically with H pylori and/or NSAIDs on gastric mucosal defence. (Gut 1998;43:465-469)

show abstract

Section: Discussioncontrasting

confidence: 77%

“…In rabbit corpus mucosa the mean contact angle in suckling animals (76.4°) increases after weaning (84.2°) but decreases sharply in adult animals (36.1°) 24. According to the commonly accepted model proposed by Lichtenberger et al , GMSH is determined by a mucous gel layer of adsorbed surface active phospholipids (SAPL) 6.…”

Section: Discussionmentioning

confidence: 99%

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Hackelsberger

Platzer

Nilius

et al. 1998

Gut

View full text Add to dashboard Cite

show abstract

Prospects for gene therapy in ornithine carbamoyltransferase deficiency and other urea cycle disorders

Robinson

Batshaw

et al. 1995

Ment. Retard. Dev. Disabil. Res. Rev.

View full text Add to dashboard Cite

Although individually inborn errors of metabolism are rare, collectively they contribute significantly to morbidity and mortality in the pediatric age group. There are several reasons why, out of these inborn errors of metabolism, urea cycle disorders have emerged as potentially good candidates for the development of gene therapy. Studies have initially focused on ornithine carbamoyltransferase (OCT) deficiency in part because there are mouse models of this disease and in part because this disease is particularly resistant to current therapies. Both in vivo and ex vivo approaches to gene therapy are being developed for the treatment of urea cycle disorders. Ex vivo gene therapy is appealing because of the long‐term expression that can be achieved, but there are clear limitations to this approach. In vivo gene therapy using adenoviral vectors is attractive for several reasons, including the fact that the virus can be administered by intravenous injection, the high levels of expression observed after a single injection, and the rapidity of that expression. Studies of transgene expression in the mouse models of OCT deficiency (OCTD) have been encouraging, but have also provided evidence that the immune system may be involved in mediating two limiting aspects of this technology, transient gene expression and inflammation. Although deletions in adenoviral early genes should limit adenoviral late gene expression and subsequent viral replication, there is in vitro and in vivo evidence of late gene expression after infection with adenoviruses deleted of some of the early genes. Future studies will focus on systematically defining the components of the virus that are recognized by the immune system and mutating these gene products. The development of an approach to gene therapy that safely, stably, and efficiently transduces gene expression holds the promise of revolutionizing the treatment of inborn errors of urea synthesis. © 1995 Wiley‐Liss, Inc.

show abstract

Glycogen storage disease type I: pathophysiology of liver adenomas

Lee

2002

Eur J Pediatr

View full text Add to dashboard Cite

show abstract

Surface Hydrophobicity Properties of Rabbit Stomach In Vitro

Cited by 9 publications

References 29 publications

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Prospects for gene therapy in ornithine carbamoyltransferase deficiency and other urea cycle disorders

Glycogen storage disease type I: pathophysiology of liver adenomas

Contact Info

Product

Resources

About