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)

A subepithelial multilayer of abundant fusiform cells has been distinguished cytochemically in the urinary bladder and ureter in mice and rats. These distinctive cells stained selectively for carbonic anhydrase (CA) isozymes I and III. Immunonegativity for keratin and Na+,K+-ATPase differentiated the CA-positive cells from epithelial cells and their lack of immunoreactivity for actin distinguished them from smooth muscle cells. Immunostaining for vimentin, blue staining with the trichrome method, location in an exceptionally dense collagen stroma, and ultrastructural appearance related the multilayer cells to fibroblasts. A loosely collagenous, less cellular lamina propria separated the CA-positive suburothelial zone from the smooth muscle wall in the rodent urinary bladder. Ureter lacked the loose lamina propria, and the presence of such a collageneous layer in bladder therefore correlated with distensability of the organ. The presence of CA uniquely in the fibroblastoid cells applied intimately to ureter and bladder epithelium implies a specialized function of these cells, possibly one concerned with the barrier between blood and hypertonic urine. Cytochemical demonstration of keratin and fucose-rich glycoconjugate in the plasmalemma of superficial urothelial cells indicates a role for these components in passively maintaining the blood-urine barrier. The observed distribution of Na+,K+-ATPase in mid and deep urothelial cells implicates this enzyme and these cells in actively maintaining the urine's hypertonicity. Basal urothelial cells contained glycoconjugate with terminal galactose in their plasmalemma. Ultrastructural features suggesting involution of superficial urothelial cells further evidence restriction of active ion transport to the deeper cells.
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PMID:Evidence for the blood-urine barrier depending on urothelium and carbonic anhydrase positive fibroblasts. 244 48

Mesoblastic nephroma is an uncommon congenital tumor of infancy that rarely occurs in adults. We report three patients (two were female, one was male) who had mesoblastic nephroma of adulthood and who presented at 45, 64, and 66 years of age with hematuria, flank mass, and pain. All underwent nephrectomy without postoperative adjuvant therapy. The tumors were solitary yellow-tan masses with solid and cystic areas involving the renal cortex (three cases) with extension into the renal pelvis and calyces (two) and ureter (one). Microscopically, all consisted of uniform spindle cell proliferations with entrapped dilated renal tubules. Focal necrosis was present in two, but no atypia or mitoses were identified in any case. The spindle cells displayed cytoplasmic immunoreactivity for vimentin, desmin, panmuscle actin (HHF-35), and alpha-smooth-muscle actin, but were nonreactive for keratin (AE1/AE3), epithelial membrane antigen, and S-100 protein. Electron microscopy revealed the presence of smooth-muscle differentiation in two cases and undifferentiated mesenchyme in one. All tumors were DNA diploid by flow cytometry. The patients were free of recurrence 8 months-2 years postoperatively. Because surgical excision may be curative, mesoblastic nephroma in adult patients must be differentiated from spindle cell neoplasms of the kidney that require additional therapy.
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PMID:Mesoblastic nephroma of adulthood. Report of three cases. 839 55

An 86-year-old Caucasian female presented with two weeks history of discomfort discharging urine, occasional hematuria, and suprapubic pain. The patient had a history of left salpingo-oophorectomy for an ovarian tumor, performed four years earlier. Ultrasound showed a solid mass surrounding the orifice of the left ureter. Bladder washing cytology yielded single, loosely cohesive syncytial aggregates of rather uniform cells. A few discretely grooved nuclei ("coffee bean nuclei") were seen. Histologic examination revealed muscular tissue infiltrated by oval to round cells, arranged in solid and follicular structures. The tumor cells were immunoreactive for estrogen receptor, inhibin, vimentin, and calretinin. The use of antibodies to pancytokeratin, inhibin, estrogen receptor, S-100, calretinin, and chromagranin could help confirm granulosa cell tumor. To my knowledge, there was no previous report on bladder washing cytology of metastatic granulosa cell tumor.
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PMID:Bladder-washing cytology of metastatic ovarian granulosa cell tumor. 1211 30

Tubular cell damage is an important mediator of interstitial fibrosis in chronic renal diseases. Glomerular and tubular damage in genetic hypertension was therefore studied. Tubular and glomerular damage was investigated in 10-, 40-, and 70-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) and compared with glomerular capillary pressure (P(GC)) and glomerulosclerosis in superficial (OC) and juxtamedullary (JMC). Tubular vimentin was used as criterion of tubular damage. Variation in tubular diameter was measured during change in perfusion pressure, and ureter ligation was used to demonstrate the relationship between tubular pressure and appearance of vimentin-positive cells. Tubular and glomerular damage was most pronounced in JMC and greater in SHR than in WKY. It was absent in 10-wk-old WKY and significantly higher in JMC of SHR compared with WKY at 70 wk of age. Numbers of vimentin-positive segments were 18 +/- 9 vs. 38 +/- 7% in JMC of 70-wk-old WKY and SHR (P < 0.02), and glomerulosclerosis was seen in 8 +/- 3 vs. 19 +/- 5% of glomeruli in JMC of 70-wk-old WKY and SHR, respectively (P < 0.01). P(GC) was 45 +/- 3 mmHg in JMC of WKY and 57 +/- 3 mmHg in JMC of 70-wk-old SHR (P < 0.001). Tubular diameter variation was greatest in SHR (P < 0.05) during pressure variation. Proteinuria was present only in 40- and 70-wk-old SHR and did not correlate with tissue damage. Tubular and glomerular damage in both strains develops in parallel and may be caused by a common mechanism, which may be glomerular capillary and tubular wall stretch during acute blood pressure variation which is greatest in JMC in SHR.
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PMID:Glomerular and tubular damage in normotensive and hypertensive rats. 1553 68

We report a rare case of intra-abdominal fibromatosis of the jejunal mesentery. A 71-year-old man, who was incidentally diagnosed with left hydronephrosis, was found to have a tumor near the duodeno-jejunal junction. The tumor appeared to invade the intestinal wall and was obstructing the left ureter. The tumor was indefinite in diagnosis preoperatively. The patient underwent an en-bloc excision of the tumor by a partial duodeno-jejunectomy combined with a left nephrectomy. Microscopic examination of the tumor showed that non-dysplastic fibroblasts proliferating in the jejunal mesentery had infiltrated into the adjacent small intestines and ureter, resulting in a diagnosis of intra-abdominal fibromatosis. This diagnosis was supported by findings of immunohistochemical analyses showing positive staining for vimentin and smooth muscle actin and negativity for keratin, CD34, C-kit and S-100. To our knowledge, this is the first documented case of intra-abdominal fibromatosis of the jejunal mesentery completely resected with the operative procedure described herein. In cases of a preoperatively undiagnosed retroperitoneal or mesenteric tumor that invades adjacent structures, it is important to consider intra-abdominal fibromatosis as a possible differential diagnosis. This may be helpful in planning the appropriate therapeutic strategies including extended multi-organ resection in selected patients.
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PMID:Mesenteric fibromatosis successfully resected with duodeno-jejunectomy and nephrectomy. 1633 67

Nestin is an intermediate filament protein originally identified in neuroepithelial stem cells. This cytoskeletal-associated protein is also expressed in some non-neuronal organs including renal tubular cells and glomerular endothelial cells during kidney development. Little is known, however, about nestin expression in the kidney during injury. In this study, we find nestin expression induced in renal tubular and interstitial myofibroblasts in the adult rat kidney following unilateral ureteral obstruction. The degree of nestin expression was well correlated with the degree of tubulointerstitial fibrosis. Immunohistochemical identification of specific nephron segments showed that nestin was primarily expressed by proximal tubules, partially by distal tubules and thick ascending limbs of Henle but not by collecting ducts. The nestin-positive tubular cells also expressed vimentin and heat-shock protein 47 (HSP47) suggesting these cells reverted to a mesenchymal phenotype. Not all vimentin- or HSP-expressing cells expressed nestin; however, suggesting that nestin is distinct from these conventional mesenchymal markers. Nestin expression was also found associated with phenotypical changes in cultured renal cells induced by hypoxia or transforming growth factor-beta. Nestin expression was located in hypoxic regions of the kidney with an obstructed ureter. Our results indicate that nestin could be a novel marker for tubulointerstitial injury.
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PMID:Nestin expression in the kidney with an obstructed ureter. 1765 33

A 73-year-old woman who had undergone resection of urothelial carcinoma (UC) (G3 > G2) of the ureter was also found to have UC (G3) in the urinary bladder, spread throughout the urinary bladder with multiple foci of carcinoma in situ and small papillary cancers. Total cystectomy was therefore performed. On detailed microscopic examination of the extirpated urinary bladder, multiple minute cell nests, 14 in number and less than 2 mm in diameter each, consisting of cells harboring small nuclei and clear cytoplasm, were incidentally detected within the sub-mucosal layer and the proper muscle layer, mainly in the posterior wall of the urinary bladder. Some cell nests were clearly associated with ganglion cells. The cells in minute nests were positive on Grimelius staining and also strongly positive on staining with antibodies to chromogranin A, neuron-specific enolase (NSE), synaptophysin, and vimentin on immunohistochemical staining. In addition, sustentacular cells in the minute cell nests were positive for S100 protein. Staining with antibodies to pancytokeratin AE1/AE3, glial fibrillary acidic protein, and p53 was negative in the cell nests. Based on these findings, the multiple minute foci were diagnosed as paraganglionic cells (PGCs) incidentally detected in the urinary bladder of an elderly woman, in association with UC. Although PGCs are rarely detected in adult human urinary bladder on routine histopathological examination, the possibility of their existence should be kept in mind by pathologists, especially in coexistence with UC. This is the first case of PGCs associated with UC in the human urinary bladder in the English literature.
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PMID:Multiple minute nests of incidentally detected paraganglionic cells associated with urothelial carcinoma of the urinary bladder in a 73-year-old woman. 1847 Jun 83

The author presents a unique case of a synchronous triple carcinoma of kidney, ureter, and urinary bladder. A 73-year-old man was admitted to our hospital because of hematuria and lumbago. Endoscopy and imaging modalities revealed a bladder tumor, a left ureter tumor, and a left kidney tumor. No other tumors were found in the body by imaging modalities. Cystectomy and left nephroureterectomy were performed. The bladder tumor was a large polypoid tumor consisting of pleomorphic sarcomatoid carcinoma (80%) and high-grade papillary urothelial carcinoma (20%), both invading the deep muscle layer. There were gradual merges between the two. The sarcomatous component was composed of malignant spindle, polygonal, and giant cells. Lymphovascular permeation was pronounced. Immunohistochemically, the sarcomatous element was positive for vimentin and various types of cytokeratins (CK), while the urothelial carcinoma element was positive for various types of CK and negative for vimentin. The ureter tumor was small and obstructed the ureter lumen. It was a pure squamous cell carcinoma without a urothelial component. The ureter tumor invaded the adventitia. A mild degree of lymphovascular invasion was recognized. Immunohistochemically, the tumor cells were positive for various types of CK but negative for vimentin. In the kidney, almost the entire kidney parenchyma was replaced by a tumor. The renal pelvis was broadly erosive but was free of apparent tumors. Histologically, the renal tumor was a pure squamous cell carcinoma without a urothelial component. Broad necrosis was present, and lymphovascular permeation was pronounced. The renal pelvis and calices were devoid of apparent tumor cells, but renal squamous cell carcinoma was present just beneath the pelvis and calices. Immunohistochemically, the kidney tumor was positive for various types of CK and negative for vimentin.
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PMID:Synchronous squamous cell carcinoma of the kidney, squamous cell carcinoma of the ureter, and sarcomatoid carcinoma of the urinary bladder: a case report. 1976 8

Primary osteosarcoma of the ureter is an extremely rare disease. Herein, the authors report a case of extraosseous osteosarcoma arising in the ureter of a 64-year-old woman. Ureteroscopy showed a papillary mass that protruded into and almost completely occluded the lumen. The tumor was successfully removed, and pathologic analysis identified mitotically active spindle cells and focal areas that contained osteoid. The tumor cells were strongly positive for vimentin but negative for cytokeratin (CK), CK7, CK20 and leukocyte-common antigen, supporting a diagnosis of high-grade extraosseous osteosarcoma of the ureter. The patient recovered well from surgery and exhibited no evidence of local recurrence or distant metastasis 6 months after the surgery. To the best of our knowledge, this is only the third reported case of primary osteosarcoma of the ureter.
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PMID:Primary osteosarcoma of the ureter. 2239 11

Primary carcinoid tumors are uncommon neoplasms in the kidney. The current study presents a case of primary carcinoid tumor of the kidney in a 49-year-old female who suffered from painless gross hematuria for half a month. Left hydronephrosis, a horseshoe kidney and a space-occupying lesion of the left ureter were found by abdominal computed tomography scans and ultrasonic testing. Surgery was performed and an oval tumor was found under the left ureter; the tumor and left kidney were excised completely. The neoplasm was composed of solid nests of cells, trabeculae, adenoid structures and anastomosing cords in a loose and myxoid background. The tumor cells, which were consistent in volume, exhibited centrally oval nuclei with inconspicuous nucleoli, and eosinophilic finely granular cytoplasm. Upon immunohistochemical staining, the neoplastic cells were positive for AE1/AE3, vimentin, synaptophysin, chromogranin A, estrogen receptor and progesterone receptor, while being negative for epithelial membrane antigen, inhibin A, cluster of differentiation (CD)99, S-100 and CD10. Based on the histological characteristics, a diagnosis of primary carcinoid tumor of the left kidney was formed. The patient did not receive further treatment. The total follow-up period was 18 months after the surgery and repeated imaging examinations every 6 months revealed no recurrence.
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PMID:Primary carcinoid tumor of the kidney with estrogen and progesterone receptor expression. 2617 Oct 49


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