SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Marschall HU) ;pers:(Matern S)"

Sökning: WFRF:(Marschall HU) > Matern S

  • Resultat 1-10 av 13
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  •  
2.
  •  
3.
  •  
4.
  •  
5.
  •  
6.
  •  
7.
  •  
8.
  • Nguyen, HN, et al. (författare)
  • Abnormal postprandial duodenal chyme transport in patients with long standing insulin dependent diabetes mellitus
  • 1997
  • Ingår i: Gut. - : BMJ. - 0017-5749 .- 1468-3288. ; 41:5, s. 624-631
  • Tidskriftsartikel (refereegranskat)abstract
    • AbstractBackground—Patients with long standing diabetes mellitus frequently have upper gut dysmotility. Gastroparesis has been well studied, whereas detailed data on duodenal motor function are limited.Aims—To characterise postprandial duodenal chyme transport in such patients.Methods—Intraluminal multiple impedance measurement, recently introduced as a novel technique for investigation of chyme transport, was used to study postprandial duodenal chyme flow in 10 patients with long standing insulin dependent diabetes mellitus with gastroparesis, and 10 healthy volunteers.Results—Four distinct transport patterns of chyme, termed bolus transport events (BTEs), were found in both groups and could be characterised as: short distance propulsive; simple long distance propulsive; retrograde; and complex long distance propulsive. Diabetic patients had significantly lower numbers of propulsive BTEs (p<0.01), and higher proportions of retrograde BTEs and complex long distance BTEs (p<0.05) than control subjects, whereas the proportion of simple long distance BTEs was significantly lower (p<0.05). The mean propagation velocities of the BTEs were similar in both groups.Conclusion—Abnormal postprandial duodenal chyme transport was found in patients with long standing insulin dependent diabetes mellitus. This is characterised by transport disorganisation and may result in disturbed chyme clearance.
  •  
9.
  •  
10.
  • Purucker, E, et al. (författare)
  • Increase in renal glutathione in cholestatic liver disease is due to a direct effect of bile acids
  • 2002
  • Ingår i: American journal of physiology. Renal physiology. - : American Physiological Society. - 1931-857X .- 1522-1466. ; 283:6, s. F1281-F1289
  • Tidskriftsartikel (refereegranskat)abstract
    • Hepatic synthesis and plasma levels of glutathione are markedly decreased in chronic liver disease. Because glutathione turnover is highest in kidneys, we examined whether changes in kidney glutathione occur in chronic cholestasis and whether they are related to kidney dysfunction in liver disease. Kidney and plasma GSH and GSSG were measured 1) in bile duct-ligated (BDL) rats; 2) in healthy rats after bile acid loading to mimic cholestasis; and 3) after irreversible inhibition of glutathione synthetase with buthionine-sulfoximine (BSO), where glutathione consumption, urinary volume, and sodium excretion were also estimated. In addition, γ-glutamylcysteine synthetase (γ-GCS) mRNA, protein, and enzymatic specific activity were measured in kidney tissue after BDL. After BDL, kidney GSH and GSSG increased within hours by 67 and 66%, respectively. The increases were not related to plasma glutathione, which decreased below control values. Intravenous bile acid loading caused identical increases in GSH and GSSG as occurred after BDL, when glycine- or taurine-conjugated dihydroxy bile acids were administered. Glutathione consumption, as estimated after blocking of de novo synthesis with BSO, was significantly increased after BDL (127 vs. 44 nmol · g−1· min−1). γ-GCS mRNA and enzymatic specific activity were significantly reduced 5 days after BDL, whereas protein concentrations did not change. The urinary sodium concentration was 70% lower in BDL than in control rats. Depletion of renal glutathione normalized sodium excretion by increasing urinary sodium concentration and urinary volume. The increase in kidney glutathione after BDL seems to be mediated by an increase in plasma bile acids and is critically related to sodium retention. The increase in GSH consumption despite reduced γ-GCS activity indicates a decreased GSH turnover tentatively due to reduced renal GSH efflux by competition with organic anions at membrane transport proteins.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 13

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy