PURPOSE: To assess how radiologic intervention altered the hospital course of patients undergoing continent urinary diversion. METHODS: Thirty-seven consecutive patients with bladder cancer invading the muscular layer were treated with total cystectomy and construction of a continent urinary reservoir. Eleven of 37 patients suffered early and late anastomotic leakage; six had prolonged extraperitoneal leakage at the urethroenteric anastomosis, three had prolonged intraperitoneal pouch leaks, and two had delayed ureteroenteric leaks. Seven of these patients required radiologic intervention. RESULTS: Intervention in the form of drainage catheter manipulation (n = 4), percutaneous nephrostomy (n = 4), or ureteral stent placement (n = 2) resulted in cessation of leakage without surgical intervention in all seven patients. Intraperitoneal pouch leaks were more difficult to control than extraperitoneal leakage and required longer drainage intervals. CONCLUSION: Interventional radiologic procedures played a key role in the management of continent urinary diversion complications, obviating the need for repeat surgical intervention in all instances.

Adult↗

PubMedDate not supplied

Complement resistance of tumor cells: basal and induced mechanisms.

Clinical and experimental studies have suggested that complement may play a role in tumor cytotoxicity. However, the efficiency of complement-mediated tumor cell lysis is hampered by various protective mechanisms, which may be divided into two categories: basal and induced mechanisms. The basal mechanisms are spontaneously expressed in cells without a need for prior activation, whereas the induced mechanisms develop in cells subjected to stimulation with cytokines, hormones, drugs or with sublytic doses of complement and other pore-formers. Membrane-associated complement regulatory proteins, such as CD55 (DAF, Decay-Accelerating Factor), CD46 (MCP, Membrane Cofactor Protein), CD35 (CR1, Complement Receptor type 1) and CD59, which serve as an important mechanism of self protection and render autologous cells insensitive to the action of complement. appear to be over-expressed on certain tumors. Furthermore, tumor cells secrete several soluble complement inhibitors. Tumor cells may also express proteases that degrade complement proteins, such as C3, or ecto-protein kinases which can phosphorylate complement components, such as C9. Besides this basal resistance, nucleated cells resist, to some extent, complement damage by removing the membrane attack complexes (MAC) from their surface. Several biochemical pathways, including protein phosphorylation, activation of G-proteins and turnover of phosphoinositides have been implicated in resistance to complement. Calcium ion influx and activation of protein kinase C (PKC) and of mitogen-activated protein kinase (MAPK) have also been demonstrated to be associated with the complement-induced enhanced resistance to lysis. The complete elucidation of the molecular mechanisms involved in basal and induced tumor cell resistance will enable the development of strategies for interfering with these evasion mechanisms and the use of the cytotoxic complement system against tumor cells.

Animals↗

PubMedDate not supplied

Intracellular signaling pathways mediated by the gonadotropin-releasing hormone (GnRH) receptor.

The hypothalamic gonadotropin-releasing hormone (GnRH) is a key regulator of the reproductive system, triggering the synthesis and release of LH and FSH in the pituitary. GnRH transmits its signal via two specific serpentine receptors that belong to the large group of G-protein coupled receptors (GPCRs). Here we review the intracellular signaling pathways mediated by the GnRH receptor (GnRHR). In pituitary-derived alpha T3-1 cells, a widely used model for GnRH action, GnRHR signaling includes activation of mitogen-activated protein kinase (MAPK) cascades, which provide an important link for the transmission of signals from the cell surface to the nucleus and play a role in the regulation of gonadotropin transcription. Activation of ERK--one of the MAPK cascades--by GnRH in these cells depends mainly on the phosphorylation of Raf1 by PKC, supported by a pathway involving c-Src, dynamin, and Ras. On the other hand, the activation of JNK, another MAPK cascade, involves PKC, c-Src, CDC42/Rac1, and probably MEKK1. The GnRHR is also expressed in non-pituitary cells and was found to be involved in the inhibition of cell proliferation in certain cells. Therefore, GnRHR represents a potential target for GnRH-analogs used for cancer treatment. Interestingly, the signaling mechanism of the GnRHR in other cell types significantly differs from that in pituitary cells. Studies conducted in GnRHR-expressing COS7 cells have shown that GnRHR transmits its signals mainly via Gi, EGF receptor, c-Src, and is not dependent on PKC. Understanding the signaling mechanisms elicited by GnRHR can shed light on the mechanism of action of GnRH in pituitary and extra-pituitary tissues.

Animals↗

PubMedDate not supplied

Factors affecting the utilization of homecare supports by caregiving relatives of Alzheimer patients.

Thirty-six homecare patients with dementia of Alzheimer type (DAT) and their caregiving relatives were studied to determine the factors influencing their use or nonuse of available medical, institutional, instrumental, and legal supports. The rate of utilization of homecare support was found to be surprisingly low. Only when the burden of providing care had become intolerable did relatives resort to homecare support (homecare allowance, counseling, outpatient services, etc.). The main reason for the low utilization was poor knowledge regarding the availability of homecare supports. Since all of the DAT patients were under the care of a family doctor, this information deficit could best be overcome by improved counseling from personal physicians.

Aged↗

PubMedDate not supplied

CD44s, E-cadherin and PCNA as markers for progression in renal cell carcinoma.

CD44s, E-cadherin and PCNA play an important role in the tumorigenesis of renal cell carcinoma (RCC), although their significance in the clinical progression of RCC is still not clear. In n = 137 cases of operatively resected RCC the expression of CD44s, E-cadherin and PCNA was semiquantitatively analyzed by the APAAP immunohistochemical method. The mean observation period of the n = 74 (54%) of patients with no evidence of disease was 52.6 months and for the n = 63 (46%) patients with progressive disease was 18.7 months. The mean progression free period occurring with absent or low levels of CD44s and PCNA expression was 79 and 118+ months, and with strong expression was 12 and 18 months (p < 0.001), respectively. With strong E-cadherin expression the progression free period was 110+ months, and with low expression 61 months (p = 0.01). A high CD44s/E-cadherin ratio and an above average PCNA expression were identified as independent prognostic parameters for the progression tendency of RCC.

Antigens, CD↗