[Laparoscopic partial nephrectomy for renal leiomyoma: a case report].

A 60-year-old man visited our hospital with a complaint of right renal incidentaloma which was pointed out on abdominal ultrasonography for a medical check-up. Abdominal computed tomography showed a renal tumor in the right kidney, which was a slightly high-dense relative to the renal parenchyma and was enhanced in the arterial phase. The tumor had grown gradually from 1.

[A case of small cell carcinoma of the renal pelvis].

A 77-year-old man visited our hospital with a chief complaint of asymptomatic gross hematuria. He was diagnosed with right renal pelvic tumor (7 cm) involving right renal hilar and inter-aortocaval lymph node metastases by radiological evaluation, and cytologic examination of urine indicated small cell carcinoma. After neoadjuvant chemotherapy with gemcitabine and cisplatin, right nephroureterctomy with bladder cuff, and right renal hilar and inter-aortocaval lymph node dissection was performed.

Targeting granzyme B to tumor cells using a yoked human chorionic gonadotropin.

Purpose: Luteinizing hormone receptor (LHR) is found in abundance on human ovarian, breast, endometrial and prostate carcinomas but at only low levels on non-gonadal tissues. To selectively kill LHR-expressing tumors, granzyme B (GrB) was linked to a protein in which both chains of human chorionic gonadotropin were yoked together (YCG).

Methods: GrB-YCG was expressed and secreted from insect Sf9 cells.

Recombinant CPE fused to tumor necrosis factor targets human ovarian cancer cells expressing the claudin-3 and claudin-4 receptors.

Using gene expression profiling, others and we have recently found that claudin-3 (CLDN3) and claudin-4 (CLDN4) are two of the most highly and consistently up-regulated genes in ovarian carcinomas. Because these tight junction proteins are the naturally occurring receptors for Clostridium perfringens enterotoxin (CPE), in this study, we used the COOH-terminal 30 amino acids of the CPE (CPE(290-319)), a fragment that is known to retain full binding affinity but have no cytolytic effect, to target tumor necrosis factor (TNF) to ovarian cancers. We constructed a pET32-based vector that expressed the fusion protein, designated here as CPE(290-319)-TNF, in which CPE(290-319) was fused to TNF at its NH(2)-terminal end.

Basic fibroblast growth factor causes urinary bladder overactivity through gap junction generation in the smooth muscle.

Overactive bladder is a highly prevalent clinical condition that is often caused by bladder outlet obstruction (BOO). Increased coupling of bladder smooth muscle cells (BSMC) via gap junctions has been hypothesized as a mechanism for myogenic bladder overactivity in BOO, although little is known about the regulatory system underlying such changes. Here, we report the involvement of basic fibroblast growth factor (bFGF) and connexin 43, a bladder gap junction protein, in bladder overactivity.