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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an industrial pig production unit 101 sows were culled because of reproduction failure. All the sows had a previous history of MMA, PHS, SUGD. All the sows were crosses of the two breeds Large White and Landrace. 101 sows were examined postmortem for pathologic changes. Changes were found in the kidney (38.6%), pyelum (49.5%), ureter (52.5%), bladder (100%), urethra (100%), uterus (50.5%), cervix (31.7%), vagina (28.7%), ovaries (51.5%), mammary gland (100%). Since 100% of the pathologic findings happened simultaneously in the urinary tract as well as in the mammary gland and just over 50% of the investigated cases had pathologic changes in the genital organs as well, the results suggest that MMA, PHS, and SUGD must be regarded as different manifestations of the same pathological entity of the urogenital organs of the sow. The authors introduce the term SUGD to denominate the conflicting terminology around the periparturient reproductive failure syndrome complex.
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PMID:[Pathological changes in the urogenital tract and mammae of culled sows from an industrial pig production unit]. 779 73

Obstructive and nonobstructive forms of hydronephrosis (increased diameter of the renal pelvis and calyces) and hydroureter (dilatation of the ureter) are the most frequently detected antenatal abnormalities, yet the underlying molecular mechanisms are largely undefined. Hedgehog (Hh) proteins control tissue patterning and cell differentiation by promoting GLI-dependent transcriptional activation and by inhibiting the processing of GLI3 to a transcriptional repressor. Genetic mutations that generate a truncated GLI3 protein similar in size to the repressor in humans with Pallister-Hall syndrome (PHS; a disorder whose characteristics include renal abnormalities) and hydroureter implicate Hh-dependent signaling in ureter morphogenesis and function. Here, we determined that Hh signaling controls 2 cell populations required for the initiation and transmission of coordinated ureter contractions. Tissue-specific inactivation of the Hh cell surface effector Smoothened (Smo) in the renal pelvic and upper ureteric mesenchyme resulted in nonobstructive hydronephrosis and hydroureter characterized by ureter dyskinesia. Mutant mice had reduced expression of markers of cell populations implicated in the coordination of unidirectional ureter peristalsis (specifically, Kit and hyperpolarization-activation cation-3 channel [Hcn3]), but exhibited normal epithelial and smooth muscle cell differentiation. Kit deficiency in a mouse model of PHS suggested a pathogenic role for GLI3 repressor in Smo-deficient embryos; indeed, genetic inactivation of Gli3 in Smo-deficient mice rescued their hydronephrosis, hydroureter, Kit and Hcn3 expression, and ureter peristalsis. Together, these data demonstrate that Hh signaling controls Kit and Hcn3 expression and ureter peristalsis.
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PMID:GLI3 repressor controls functional development of the mouse ureter. 2133 39