Young Vets Group

1. ۱٫   J. M. FINLAY, M.D., F.R.C.P.(C); and
2. 2.   K. J. R. WIGHTMAN, M.D., F.R.C.P.(C), F.A.C.P.
3. Requests for reprints should be addressed to J. M. Finlay, M.D., Department of Medicine,

100 College Street, Toronto, Ontario, Canada

.

Excerpt

Metabolic balance studies and the more recent radioactive isotopic tracer technics provide reasonably accurate methods for measuring the intestinal absorption of fat,^{1, 2, 3, 4} nitrogenous materials,^{1, 2} water^{5, 6} and electrolytes.^{2, 7, 8, 9, 10, 11, 12, 13} However, the available methods for the measurement of carbohydrate absorption have certain disadvantages. For example, the oral glucose tolerance test has been criticized because the blood levels obtained reflect many metabolic processes and not simply intestinal absorption.³⁸ In the second method, in which carbohydrate absorption is measured directly, the small bowel is intubated during repeated fluoroscopic examinations and its lumen is

This 100-word excerpt has been provided in the absence of an abstract.

Summario in Interlingua

Le test del tolerantia de xylosa esseva studiate como medio pro evalutar le absorption de hydrato de carbon in un gruppo de patientes con varie typos de disordine intestinal. Le test es executate per le administration de 25 g de d-xylosa dissolvite in 500 cm³ de aqua, con le patiente in stato jejun, sequite per le mesuration del nivellos sanguinee de d-xylosa a intervallos de un hora durante cinque horas e del excretion urinari de d-xylosa pro le complete periodo de cinque horas. Le responsa obtenite in individuos normal es reproducibile e non es alterate per le administration oral de cortisona, de maniera que un alteration occurrente in patientes sub tractamento con steroides es probabilemente interpretabile como expression de un meliorate absorption e non como effecto del metabolismo intermediari. Patientes con diarrhea sed sin steatorrhea responde normalmente in le test. Patientes adulte con active sprue idiopathic ante le tractamento revela un deprimite curva de xylosa in le sanguine e basse nivellos del substantia in le urina. Tractamento a bon successo o remission spontanee restaura le normalitate del responsa. Quando le tractamento es interrumpite e un recidiva occurre, le responsa in le test redeveni anormal.

Multes del patientes con steatorrhea secundari causate per lesiones intestinal etc. habeva un responsa normal in le test. In casos sporadic, il habeva mesmo excessivemente alte nivellos sanguinee, non explicabile super le base de morbo renal. Iste resultatos suggere que studios additional del metabolismo intermediari de d-xylosa es requirite, specialmente in patientes qui suffre de diabete mellite, disordines hepatic, e dysfunction renal. Tal studios es in progresso.

Es concludite que le test es de valor in steatorrhea idiopathic como medio pro establir le diagnose e estimar le resultatos del therapia. Illo pote esser de adjuta in distinguer patientes qui suffre de steatorrhea secundari, sed illo es multo minus adjuvante in sequer le progresso de tal casos.

Cell, 09 December 2010
Copyright © ۲۰۱۰ Elsevier Inc. All rights reserved.
10.1016/j.cell.2010.11.039

Katarina Moravcevic, Jeannine M. Mendrola, Karl R. Schmitz, Yu-Hsiu Wang, David Slochower, Paul A. Janmey, Mark A. Lemmon

In Duchenne muscular dystrophy (DMD), dystrophin mutation leads to progressive lethal skeletal muscle degeneration. For unknown reasons, dystrophin deficiency does not recapitulate DMD in mice (mdx), which have mild skeletal muscle defects and potent regenerative capacity. We postulated that human DMD progression is a consequence of loss of functional muscle stem cells (MuSC), and the mild mouse mdx phenotype results from greater MuSC reserve fueled by longer telomeres. We report that mdx mice lacking the RNA component of telomerase (mdx/mTR) have shortened telomeres in muscle cells and severe muscular dystrophy that progressively worsens with age. Muscle wasting severity parallels a decline in MuSC regenerative capacity and is ameliorated histologically by transplantation of wild-type MuSC. These data show that DMD progression results, in part, from a cell-autonomous failure of MuSC to maintain the damage-repair cycle initiated by dystrophin deficiency. The essential role of MuSC function has therapeutic implications for DMD.