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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 2 year carcinogenicity bioassay using B6C3F1 mice, one male mouse developed clinical signs near termination of the study, comprising skin sores around the prepuce, penile prolapse and urine scalding. The predominant finding at necropsy was a markedly distended urinary bladder filled with numerous crystallized particles. Microscopically, there was subacute cystitis with marked hyperplasia of the transitional epithelium. X-ray diffraction analysis of the crystals showed a diffraction pattern characteristic of struvite (ammonium magnesium phosphate). The implications of the spontaneous occurrence of bladder stones in rodents on long-term toxicology studies are discussed.
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PMID:Struvite urolithiasis in a B6C3F1 mouse. 144 6

The iv pathogenicity and toxigenicity of Protaminobacter rubrum was studied in New Zealand White rabbits and CF1 BR mice. Following a probe study, nine groups of six rabbits each were injected iv with; 1 ml of viable-cell suspension (VCS) at concentrations of 2.23 x 10(8), 10(6), 10(4) and 10(2) organisms/ml; the cell-free supernatant (CFS; in which the test organism had been cultured to a concentration of approximately 3 x 10(10) cells/ml) at dilutions of 1:100, 1:10,000 and 1:1,000,000 in phosphate buffered saline (PBS); uninoculated culture medium; or uninoculated PBS. Rabbits were observed daily for 14 days and body weights were recorded on days 0, 7 and 14. Body temperatures were recorded in two rabbits per group until 18 hr after dosing. On day 14, each rabbit was killed. Blood samples, sections of liver and spleen, and any tissues presenting lesions possibly indicating an infection were excised and cultured for P. rubrum. Deaths occurred in the probe study following 1 ml iv injection of VCS at a concentration of 2.5 x 10(10) organisms/ml or of undiluted CFS in which P. rubrum had been grown to a concentration of approximately 2.5 x 10(10) organisms/ml. Blood and tissue samples obtained less than 24 hr after treatment from rabbits in the VCS group tested positive for P. rubrum, which would be expected after iv administration of such a high concentration of cells. No deaths occurred, no adverse effects on body-weight gain were seen, and in no instance was P. rubrum recovered from blood or tissue cultures in the definitive study. Overt signs of infection or toxinosis were limited to transient reduced activity in the highest two VCS concentration groups, and the highest CFS group. Modestly elevated body temperatures were also recorded for rabbits that received the highest two concentrations of either VCS or CFS. A similar 14-day study was carried out in mice. Four groups of 20 Crl: COBS CF1 BR mice received a single iv injection of 0.1 ml of VCS (2.5 x 10(10) organisms/ml), CFS in which the test organism was cultured to approximately 2.5 x 10(10) cells/ml, uninoculated culture medium or uninoculated PBS. The mice were observed daily and body weights were recorded on days 0, 7 and 14. On day 14, each mouse was killed and blood samples as well as liver and spleen sections were obtained and cultured. In this study no deaths occurred, and signs of infection or toxinosis were limited to reduced activity and ptosis for all mice in the VCS and CFS groups.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Safety evaluation of Protaminobacter rubrum: intravenous pathogenicity and toxigenicity study in rabbits and mice. 195 22

Serum calcium, magnesium and phosphate values of ewes recently affected by vaginal prolapse were compared with unaffected ewes in four flocks. Subclinical hypocalcaemia was demonstrated in some affected and unaffected ewes in three flocks. Magnesium and phosphate values were normal. In two flocks the body condition of ewes recently affected by vaginal prolapse was variable and reflected the variation in condition found in the flock. In a third flock affected ewes had significantly lower body condition scores than unaffected ewes (P less than 0.001). Analysis of the fourth flock was not possible. Oestrogenic mycotoxins were not detected in any of the feed samples taken from these flocks. The following year the management, nutrition and energy, and the protein and calcium status of ewes in 12 flocks of greyface/mule ewes with a history of a regular high (greater than 3 per cent) or low (less than 1 per cent) prevalence of vaginal prolapse were compared. A high prevalence was not associated with any particular feedstuff. A high or intermediate (1 to 3 per cent) prevalence of vaginal prolapse was found in three of the four flocks managed as a single group and these three flocks were fed on an unrestricted basis. Body condition scoring and beta-hydroxybutyrate estimation confirmed that ewes in these flocks were overfed. The prevalence of vaginal prolapse in the flocks was not related to the serum albumin, calcium or urea of the ewes. Therefore subclinical hypocalcaemia was probably a consequence of vaginal prolapse rather than a cause.
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PMID:Nutritional factors associated with vaginal prolapse in ewes. 203 22

A sensitive and selective high-performance liquid chromatographic (HPLC) method for the determination of bupivacaine and its two metabolites, desbutyl- and 4'-hydroxybupivacaine, in human serum and urine is described. Bupivacaine, both metabolites and the internal standard, etidocaine, are extracted with diethyl ether and then back-extracted into an acidic aqueous phase. After subsequent extraction into diethyl ether, evaporation and reconstitution in the mobile phase, bupivacaine and the metabolites are determined by HPLC using a reversed-phase C8 column with tetrahydrofuran-potassium phosphate buffer (8:92, v/v, pH 2.4) as the mobile phase. The sensitivity of the method is 10 micrograms/l for bupivacaine and both metabolites and the extraction efficiencies are 95, 54 and 92% for bupivacaine and desbutyl- and 4'-hydroxybupivacaine, respectively. The reproducibility of the method is good, the coefficients of variation varying between 1.8 and 7.4% in the concentration range 0.10-2.00 mg/l. The procedure was applied to human serum and urine samples from two elderly women who had been operated on under epidural analgesia (plain bupivacaine, 1.5 mg/kg) because of uterine prolapse.
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PMID:Simultaneous determination of bupivacaine and its two metabolites, desbutyl- and 4'-hydroxybupivacaine, in human serum and urine. 355 65

The successful management of faecal incontinence can dramatically improve the quality of life of affected children. The introduction of the non-refluxing, catheterisable appendico-caecostomy provides the opportunity to treat previously resistant patients. Over a 6-year period, 29 children had a Malone antegrade continent stoma for enema administration (MACE). Incontinence was related to spina bifida in 12 children, ano-rectal anomaly in 12, Hirschprung's disease in 2, followed excision of a pelvic tumour in 2, and was secondary to intractable chronic constipation in 1. The conduit was fashioned from the appendix (20), a caecal tube (8), or a gastric tube (1). Surgical complications were stomal stenosis (11), wound infection (1), anastomotic leak (1), MACE stoma prolapse (1), and a pressure sore (1). Colonic irrigation was achieved with washouts of saline (24), saline plus phosphate (4), and saline plus Picolax (1). Twenty-three patients have complete control of bowel function, but 4 still soil. Two remain incontinent, 1 of whom is still being instructed. One child subsequently had a colostomy, but still uses the MACE stoma. Successful bowel management requires motivation, dedication, commitment, and the input of a clinical nurse specialist. The MACE is a relatively straightforward operative procedure that provides an effective washout technique that is acceptable to both parents and children.
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PMID:The Malone antegrade colonic enema procedure: outcome and lessons of 6 years' experience. 963 20

Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is an autosomal recessive disorder defined clinically by severe gastrointestinal dysmotility; cachexia; ptosis, ophthalmoparesis, or both; peripheral neuropathy; leukoencephalopathy; and mitochondrial abnormalities. The disease is caused by mutations in the thymidine phosphorylase (TP) gene. TP protein catalyzes phosphorolysis of thymidine to thymine and deoxyribose 1-phosphate. We identified 21 probands (35 patients) who fulfilled our clinical criteria for MNGIE. MNGIE has clinically homogeneous features but varies in age at onset and rate of progression. Gastrointestinal dysmotility is the most prominent manifestation, with recurrent diarrhea, borborygmi, and intestinal pseudo-obstruction. Patients usually die in early adulthood (mean, 37.6 years; range, 26-58 years). Cerebral leukodystrophy is characteristic. Mitochondrial DNA (mtDNA) has depletion, multiple deletions, or both. We have identified 16 TP mutations. Homozygous or compound heterozygous mutations were present in all patients tested. Leukocyte TP activity was reduced drastically in all patients tested, 0.009 +/- 0.021 micromol/hr/mg (mean +/- SD; n = 16), compared with controls, 0.67 +/- 0.21 micromol/hr/mg (n = 19). MNGIE is a recognizable clinical syndrome caused by mutations in thymidine phosphorylase. Severe reduction of TP activity in leukocytes is diagnostic. Altered mitochondrial nucleoside and nucleotide pools may impair mtDNA replication, repair, or both.
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PMID:Mitochondrial neurogastrointestinal encephalomyopathy: an autosomal recessive disorder due to thymidine phosphorylase mutations. 1085 45

Bone defects were created in rabbit medial femoral condyle in a model where subchondral bone was completely removed or about 2 mm of subchondral bone was maintained. Groups without augmentation and augmented with autogenous bone, polymethylmethacrylate, or calcium phosphate cement were sacrificed at 3, 12, and 24 weeks for evaluation of articular cartilage and observation of bone formation. In the model in which subchondral bone was completely removed, collapse of the subchondral bone together with exfoliation and prolapse of cartilage developed early in all cases. In the model in which 2 mm of subchondral bone was maintained, degeneration of articular cartilage developed at 12 weeks in the group augmented with polymethylmethacrylate, showing a significant difference when compared to the contralateral untreated control group. The group augmented with calcium phosphate cement did not demonstrate any evident difference from the control group. Mechanical properties after subchondral replacement did not differ between the groups augmented with polymethylmethacrylate and calcium phosphate cement, although calcium phosphate cement was considered histologically superior. Calcium phosphate cement was a reliable subchondral replacement material when the bone defect is adjacent to the articular cartilage.
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PMID:Effects on articular cartilage of subchondral replacement with polymethylmethacrylate and calcium phosphate cement. 1177 7

Here we report on a patient with findings of acrocephaly, craniosynostosis, low frontal hairline, ptosis of eyelids, deviated nasal septum, broad great toes, moderate hallux valgus, bilateral symmetrical complete soft tissue syndactyly of toes 2 and 3, and partial soft tissue syndactyly of toes 4 and 5 consistent with the diagnosis of Saethre-Chotzen syndrome. Additionally, the patient had some unusual findings as part of generalized dysfunction of the renal tubules including hypophosphatemia with renal phosphate wasting, normocalcemic hypercalciuria, hypomagnesemia with renal magnesium wasting, low-molecular-weight proteinuria, decreased serum PTH levels, osteopenia, and nephrolithiasis. In the light of these findings, the diagnosis of incomplete renal Fanconi syndrome was made. In conclusion, on the basis of the present findings, it is difficult to say whether renal tubular dysfunction are somehow connected to the Saethre-Chotzen syndrome or not. Therefore, we consider that this is probably just a coincident. However, further studies may show the connection between renal tubular dysfunction and Saethre-Chotzen syndrome.
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PMID:Saethre-Chotzen syndrome presenting with incomplete renal Fanconi syndrome. 1221 32

In bony defects of the cranium, bone healing may be complicated by prolapse of surrounding tissue into the defect. This tissue acts as a potential obstruction to the migration of osteogenic cells, resulting in impaired bone formation. It has been shown in previous studies that when a membrane composed of resorbable polymers (LactoSorb) is placed over a cranial bone defect, it inhibits connective tissue from entering the wound and improves the rate and quality of the bony regenerate. This study is an extension of this work and specifically evaluated the effects of differing calcium-based surface coatings on membrane-covered cranial defects in the rabbit model. In non-critical size, full-thickness defects of the mature rabbit calvarium, four differently treated LactoSorb membranes were evaluated in each animal model over a 1-year postoperative period. The surface coatings (three treated, one untreated) consisted of a base-powdered material of calcium sodium phosphate (Osteostim, EBI, NJ), which were applied by different methods (pressed, brushed, one-sided versus two-sided). Evaluation consisted of cross-sectional histologic assessment of the cranial detects determining the quantitative bony fill and the presence of residual polymer material and calcium sodium phosphate. This study produced the following findings: (1) cranial defect regeneration occurs faster with calcium-coated membranes and is complete by 3 months; (2) no difference could be seen between the different methods of calcium sodium phosphate coating; (3) the calcium sodium phosphate coatings did not inhibit resorption of the biodegradable membranes for those systems that had coatings on one side; however, systems completely covered showed delayed resorption; and (4) the calcium sodium phosphate coatings did not produce any inflammatory reactions. These findings suggest that, in addition to inhibiting connective tissue from entering the wound site, the calcium coatings on resorbable devices may have beneficial effects in selected clinical conditions, especially in conditions where faster bone regeneration is necessary.
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PMID:Compartmentalized bone regeneration of cranial defects with biodegradable barriers--effects of calcium sodium phosphate surface coatings on LactoSorb. 1221 98

Comparable pathological changes in the mitral valve have been described in dogs, pigs and human patients with myxomatous mitral valve disease (MMVD), i.e., primary mitral valve prolapse. The progressive myxomatous changes are probably a response to repeated impact on the leaflets, and endothelial stress or damage probably plays a central role in the pathogenesis. Little, however, is known about the vasoactive substances that mediate the subendothelial changes. The aim of this study was to investigate the expression of nitric oxide synthase (NOS) in canine mitral valve leaflets and to relate the findings to MMVD changes. The mitral valve was taken post mortem from 12 dogs (six males and six females) and a whole valve NADPH (the reduced form of nicotinamide-adenine dinucleotide phosphate) diaphorase (NADPH-d) reaction was performed. Macroscopical (semiquantitative) and microscopical (computer image analysis) evaluations of the staining due to NADPH-d activity were performed at four specific areas of the valve and related to microscopical signs of MMVD and gross signs of thickening or prolapse, or both. Macroscopically, the NADPH-d colour grade was correlated with the degree of MMVD (P=0.01). In addition, endothelial NADPH-d staining intensity was correlated with macroscopical signs of disease (P=0.004) as well as with collagen degeneration (P=0.008) and deposition of mucopolysaccharides (P=0.02). Age, gender and specific area of the valve did not seem to influence the NADPH-d activity. In conclusion, increased NADPH-d activity, suggesting increased NOS expression, was found in areas of the mitral valve with myxomatous changes. This indicates that nitric oxide (NO) may play a role in the pathogenesis of MMVD in dogs.
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PMID:Increased NADPH-diaphorase activity in canine myxomatous mitral valve leaflets. 1292 17


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