Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.
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PMID:Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system. 171 Jun 5

Immunohistochemical and immunochemical analyses were performed on a monoclonal antibody designated 1-2B7B which was derived from immunizing mice with human prostate epithelial tissue. The 1-2B7B antigen was expressed not only along the acinous basement membrane zone (BMZ) of the prostate and testis, but also along the BMZ of the epithelia of several other organs including the skin, oesophagus, urinary bladder, ureter, stomach, intestine and bile duct. The antigenic epitope was not expressed in these tissues of lower mammals. Immunoelectron microscopic studies on normal human skin revealed that the 1-2B7B antigen was localized mainly just beneath the hemidesmosomes of basal keratinocytes, but not beneath melanocytes. Indirect immunofluorescence and immunoelectron microscopic studies on 1 M NaCl-split skin confirmed that this antigen was not separated from the cytoplasmic membrane of basal cells after salt treatment. SDS polyacrylamide gel electrophoresis of immunochemically purified protein from the epidermis demonstrated the molecular weight of the antigen to be 120 kDa. 1-2B7B monoclonal antibody should be a useful probe for studying the pathomechanism of some blistering diseases, as well as the assembly and function of the epidermal-dermal junction.
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PMID:1-2B7B: monoclonal antibody reacting to the 120 kDa polypeptide component of human epidermal hemidesmosomes. 192 54

Monoclonal antibodies against basement membrane (BM) were generated using the matrix deposited by cultured rabbit corneal epithelial cells as immunogen. BM antibodies were identified by immunofluorescent staining of frozen tissue sections and of extracellular matrix of living cultured cells. BM localization was confirmed by immunoelectron microscopy. Antibody AE26 immunoprecipitates a 140,000 Mr component from radiolabeled corneal epithelial cells and recognizes this component plus a 95,000 Mr band on Western blots. The antigen resists extraction by high and low salt and by nonionic detergents, but is solubilized in 4 M urea/1% mercaptoethanol. On isoelectric focusing and nonequilibrium pH gradient gels, AE26 antigen migrates to the acidic region (pI less than 3). The molecule is destroyed by trypsin, but is insensitive to bacterial collagenase. In frozen tissue sections, AE26 stains only BM of stratified epithelia plus trachea, ureter, lung, and intestine, but no other epithelial or nonepithelial BM. AE26 antigen is detected on Western blots of cornea, skin, and lung extracts, but not liver, kidney, or muscle, indicating that this is not due to masking of the epitope. This tissue distribution is different from any previously described BM molecule. Although we have not ruled out the possibility that AE26 recognizes a modification or fragment of a known BM component (particularly entactin), the acidic pI, collagenase resistance, and unusual tissue specificity suggest that AE26 recognizes a new BM protein. The BM heterogeneity demonstrated by AE26 may play a structural role or provide positional signals to the overlying epithelium.
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PMID:Tissue-specific distribution of a novel component of epithelial basement membranes. 219 81

The use of a collagen sponge tube graft as a material for segmental ureteral replacement was investigated. The structural design of the collagen sponge graft was achieved by cell culture on the matrix. MGH-U1 cells, derived from bladder cell carcinoma, were grown in vitro on the collagen sponge matrix with excellent biocompatibility and without evidence of cytotoxicity. The collagen sponge demonstrated biodegradability when implanted subcutaneously in dogs. However, a urine exposure test of collagen sponge in rat bladders revealed extensive salt deposits on its surface in some rats, as observed by crystallographic examination. Segmental ureteral replacements by collagen sponge tube grafts, accompanied by ureteral splint catheters, were performed in dogs. There was extensive uro-epithelial cell regeneration on the inner surface of the collagen grafts, without evidence of severe hydronephrosis, 5 to 12 weeks following the procedure. The results indicate the potential for ureteral replacement by collagen sponge tube grafts, which would act as non-toxic, biodegradable scaffolds inducing the regenerative activity of the ureter.
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PMID:Ureteral replacement using collagen sponge tube grafts. 398 29

1. The capacity of adaptation of toads (Bufo bufo) to environments of high salinity was studied and the relative importance of skin, kidney and urinary bladder in controlling the balance of water and salt was assessed.2. Toads were kept in NaCl solutions of 20, 50, 110, 150 and 220 mM and studied in their fourth week of adaptation. A group of animals considered as ;control' was kept in wet soil with free access to water. Plasma, ureter urine, and bladder and colon contents were analysed for sodium, potassium, chloride and osmolality, and total body sodium and water were determined. Absorption of water and (22)Na through the skin, and water flow and sodium excretion through the ureter, of intact animals was studied. Hydrosmotic water transport through the isolated urinary bladder of ;control' and adapted animals was determined. The effects of pitressin and aldosterone on the water and sodium balance are described.3. The survival rates of toads kept in saline concentrations up to 150 mM were identical to that of ;control' animals, but half of the animals kept in 220 mM died within 4 weeks.4. There is a linear correlation between the sodium concentrations and osmolality of plasma and of the external media.5. The sodium concentration in colon contents rose with rising external concentrations, up to values higher than the values in plasma.6. Sodium concentrations and osmolalities of ureter and bladder urine increased in adapted animals, the values for bladder urine becoming much higher than those for ureter urine in animals adapted to 110, 150 and 220 mM.7. Total body water, as a percentage of total weight was kept within very narrow limits, although the total body sodium increased with adaptation.8. Absorption of water through the skin for the same osmotic gradients was smaller in adapted than in ;control' animals.9. The ureteral output of water of toads adapted to 110 and 150 mM-NaCl was larger than the water absorption through the skin.10. Skin absorption of sodium was lower in animals adapted to concentrated saline solutions than in ;control' animals.11. Sodium output by the ureter was identical to skin absorption in ;control' animals adapted to 20, 50 and 110 mM-NaCl but was higher in animals adapted to 150 mM-NaCl.12. Aldosterone increased the absorption of sodium in ;control' and adapted toads, but at all dose levels absorption by control was greater than by adapted animals.13. The stimulation of water absorption by vasopressin in vivo or in isolated bladders was not modified in animals adapted to high salinities.
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PMID:Salt adaptation in Bufo bufo. 463 11

Chronic pyelonephritis was induced in young adult cats by the intravenous injection of a human or a feline strain of Escherichia coli after ligation of one ureter for 24 or 48 h. In the 3 cats infected with the feline strain, scarred kidneys from the obstructed side were removed at necropsy 3, 4 and 5 months later. Collagen was extracted from pyelonephritic and normal kidney tissue with dilute acetic acid and limited proteolysis with pepsin. Scarred kidneys gave higher yields of both acid-soluble collagen (normal = 0.57 +/- 0.12 mg per g tissue; scarred = 0.88 +/- 0.10 mg per g tissue) and pepsin-solubilized collagen (normal = 9.69 +/- 1.79 mg per g tissue; scarred = 20.02 +/- 2.84 mg per g tissue). There was no significant increase in the collagen yield from the kidneys of the 2 cats in which mild focal lesions were found 14 and 16 months after infection with the human strain of E. coli. Pepsin released collagens were separated by fractional salt precipitation and identified by agarose gel chromatography and polyacrylamide gel electrophoresis. Normal kidney was shown to contain collagen of Types I, IV and V (AB). The Type IV collagen extracted consisted of a mixture of 4 major pepsin-resistant chains of apparent molecular weights of 150 000, 115 000, 85 000 and 60 000. The collagen extracted from scarred kidneys was predominantly Type I, only trace amounts of Type IV and V components being present. These findings suggest that basement membrane collagens of the kidney are selectively degraded during the atrophy and scarring of chronic feline pyelonephritis and are preferentially replaced by interstitial Type I collagen.
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PMID:Experimental pyelonephritis in the cat: 3. Collagen alterations in renal fibrosis. 684 96

Specific features of antihypertensive action of two new isoprenoid compounds, i.e. 5-nicotinooxymethyl -gamma - tocopherylnicotinate (NNT) and decaprenoic ethylester (EDP) were studied in rats. NNT and EDP were very similar to each other in their pharmacological features as far as we studied. Both NNT and EDP did not affect blood pressure in normotensive animals but significantly reduced blood pressure in SHR and DOCA/salt hypertensive animals in the acute studies with single dosing of 1 to 10 mg/kg (p.o.). Their antihypertensive action was mild but long-lasting and cumulated by the repeated administration. The chronic administration of NNT and EDP at oral doses of 0.2 and 2 mg/kg once a day completely suppressed the development of hypertension in rats unilaterally nephrectomized and treated with DOCA/salt and in SHR which were unilaterally ureter-ligated to accelerate the progress of their genetic hypertension. The mechanism of their antihypertensive action remains to be solved.
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PMID:Antihypertensive actions of isoprenoids. 707 84

Partial obstruction of the left ureter was created in seven dogs. Renal function was studied 3 weeks later. Total renal blood flow (RBF) and intrarenal blood flow distribution were studied using the microsphere technique. Glomerular filtration rate (GFR), effective renal plasma flow (CPAH) and the excretion of sodium and osmolar substances were determined using the clearance technique. RBF, GFR and CPAH in the hydronephrotic kidney were reduced to approximately 30% of the same parameters in the contralateral kidney. Urinary sodium excretion was consistently lower in the hydronephrotic than in the contralateral kidney. Volume expansion with isotonic saline solution revealed that this reduction of sodium excretion from the hydronephrotic kidney was out of proportion to the extent of GFR reduction. The contralateral unobstructed kidney did not compensate for this salt retention by increasing its sodium excretion.
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PMID:Renal function in dogs with chronic moderate unilateral ureteral obstruction. 713 86

The prevalence of kidney stones has steadily risen during this century; passage of a calculus and a positive family history increase the probability of recurrence. Findings from recent studies on the cause of renal calculi have stressed crystallization and crystal aggregation of stone minerals from supersaturated urine, rather than excessive organic matrix. Absence of normal urine inhibitors of calcium salts is also stressed. Formation of calcium oxalate stones is the major problem. Therapy with decreased calcium and oxalate intake, thiazides, phosphate salts and allopurinol in various combinations has substantially decreased the prevalence of recurrent stones. The rationale for the use of allopurinol is that uric acid salts enhance the tendency for calcium oxalate to crystallize from supersaturated urine. The hypercalciuria seen in 30 percent to 40 percent of patients with oxalate stones is usually caused by intestinal hyperabsorption of calcium. Although patients with uric acid calculi constitute only a small fraction of those in whom stones form, they represent a group in whom good medical therapy, based on sound physiologic principles, has proved extremely successful. Renal tubular syndromes lead to nephrocalcinosis and lithiasis through hypercalciuria, alkaline urine and hypocitraturia, the latter an inhibitor of calcium salt precipitation. Recent advances in surgical techniques are discussed, including the rationale for removing staghorn calculi. The ileal ureter and coagulum pyelolithotomy deserve special emphasis.
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PMID:Kidney stones. 738 35

Human genital skin fibroblasts contain both the full-length 110 K androgen receptor protein (AR-B, apparent M(r) approximately 110,000) and an 87 K N-terminally truncated AR isoform (AR-A, apparent M(r) approximately 87,000). These two AR species are structurally analogous to the A- and B-isoforms of the progesterone receptor (PR). We examined the distribution pattern of human AR isoforms in a variety of fetal and adult tissues by Western blot analysis. Relative levels of immunoreactive AR proteins in high salt tissue extracts were estimated by densitometry in comparison to a standard normal genital skin fibroblast preparation. High AR levels (AR-A + AR-B = 0.8-7.7) were present in male and female reproductive tissues from mid-trimester fetuses, including penis, prostate, testis, epididymis, scrotal skin, labial skin, uterus/cervix, and ovary. AR-A and AR-B (0.08-0.9) also were found in 14 non-genital fetal tissues (bladder, fat, lung, great vessel, trachea, muscle, scalp skin, kidney, thyroid, intestine, thymus, ureter, stomach and rectum). AR-A accounted for 4-26% of the AR protein detected in these tissues. Ten other fetal tissues had low levels of AR-B (0.02-0.3) and little or no detectable AR-A. AR-B also was the predominant or only immunoreactive AR species found in 17 adult human tissues. AR levels in adult reproductive tissues (prostate, endometrium, ovary, uterus, fallopian tube, testis, seminal vesicle, myometrium, and ejaculatory duct) ranged from 0.1 to 2.2. Immunoreactive AR (0.4-0.8) also was present in specimens of prostate carcinoma, endometrial carcinoma, thyroid carcinoma and kidney. Lower levels of AR (0.03-0.1) were detected in adult breast, colon, lung and adrenal gland specimens. This study demonstrates that immunoreactive AR protein is present in a wide variety of human fetal and adult tissues and that two AR isoforms are expressed in many tissues.
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PMID:A and B forms of the androgen receptor are expressed in a variety of human tissues. 880 38


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