The association between the self-perception period of overactive bladder symptoms and overactive bladder symptom scores in a non-treated population and related sociodemographic and lifestyle factors.

AIMS: To investigate the association between the self-perception period of OAB symptoms (SP-OAB) and the overactive bladder symptom score (OABSS), along with related sociodemographic and lifestyle factors. METHODS: This was a cross-sectional study comprised of 192 men aged 40 years and older who participated in a prostate examination survey between February and May 2009 and proved to have OAB. Survey questionnaires included items on the OABSS and the SP-OAB assessed by the OABSS. Various sociodemographic and lifestyle factors were also included. RESULTS: The average SP-OAB period was 24.72 ± 45.75 months and became significantly longer as the severity of OAB increased in correlation analysis (coefficient = 0.501, p < 0.001). Age, education, income, regular check-up, health maintenance and occupation were all risk factors in both OABSS and SP-OAB in univariate analysis. Body mass index (BMI), family size and SP-OAB were risk factors for OABSS in univariate analysis. Age and regular check-ups were factors in both OABSS and SP-OAB in multivariate analysis. BMI, income and SP-OAB were risk factors for OABSS. CONCLUSION: These findings suggest that the SP-OAB is an independent risk factor for OAB progression and that various sociodemographic and lifestyle factors affect OABSS. The self-perception period should be considered in the treatment and prevention of OAB symptoms.

Sociodemographic and lifestyle factors affecting the self-perception period of lower urinary tract symptoms of international prostate symptom score items.

AIMS: This study investigated the influence of sociodemographic and lifestyle factors on the lower urinary tract symptom (LUTS) self-perception period and International Prostate Symptom Score. METHOD: This cross-sectional study examined 209 men aged ≥ 40 years with non-treated LUTS who participated in a prostate examination survey. Questions included International Prostate Symptom Score (IPSS) items with self-perception periods for each item. Sociodemographic and lifestyle factors were also assessed. Participants were divided by mild LUTS (IPSS less than 8) and moderate-to-severe LUTS (IPSS 8 or higher). RESULTS: Self-perception period of the moderate-to-severe LUTS (n = 110) was affected by BMI; the self-perception period of the mild LUTS (n = 90) was affected by age, income, occupation and concomitant disease. Moderate-to-severe LUTS were affected by self-perception period (p = 0.03). Self-perception period was affected by concern for health (p = 0.005) by multivariate analysis, and self-perception period of mild LUTS was affected by BMI (p = 0.012). Moderate-to-severe LUTS were affected by age, number of family members, concern for health and drinking (p < 0.05, respectively) by multivariate analysis. CONCLUSION: Lower urinary tract symptom was affected by self-perception period. In moderate-to-severe LUTS, age, concern for health and drinking were affecting factors of self-perception period.

Caspase-mediated cleavage of p130cas in etoposide-induced apoptotic Rat-1 cells.

Apoptosis causes characteristic morphological changes in cells, including membrane blebbing, cell detachment from the extracellular matrix, and loss of cell-cell contacts. We investigated the changes in focal adhesion proteins during etoposide-induced apoptosis in Rat-1 cells and found that during apoptosis, p130cas (Crk-associated substrate [Cas]) is cleaved by caspase-3. Sequence analysis showed that Cas contains 10 DXXD consensus sites preferred by caspase-3. We identified two of these sites (DVPD(416)G and DSPD(748)G) in vitro, and point mutations substituting the Asp of DVPD(416)G and DSPD(748)G with Glu blocked caspase-3-mediated cleavage. Cleavage at DVPD(416)G generated a 74-kDa fragment, which was in turn cleaved at DSPD(748)G, yielding 47- and 31-kDa fragments. Immunofluorescence microscopy revealed well-developed focal adhesion sites in control cells that dramatically declined in number in etoposide-treated cells. Cas cleavage correlated temporally with the onset of apoptosis and coincided with the loss of p125FAK (focal adhesion kinase [FAK]) from focal adhesion sites and the attenuation of Cas-paxillin interactions. Considering that Cas associates with FAK, paxillin, and other molecules involved in the integrin signaling pathway, these results suggest that caspase-mediated cleavage of Cas contributes to the disassembly of focal adhesion complexes and interrupts survival signals from the extracellular matrix.

Degradation of focal adhesion proteins paxillin and p130cas by caspases or calpains in apoptotic rat-1 and L929 cells.

Immunofluorescence microscopy revealed the rearrangement and gradual dissociation of paxillin from focal adhesion sites during apoptosis. In vitro, cleavage of paxillin by caspase-3 generated a 42-kDa fragment, among other products, while cleavage by calpain generated a different set of fragments. In Rat-1 cells, cleavage of paxillin by caspase-3 was suppressed by zVAD-fmk or zDEVD-cmk, making caspase-3 a likely executioner during etoposide-induced apoptosis. In contrast, the cleavage of paxillin and p130cas in apoptotic L929 cells was blocked by calpain-specific inhibitors, which also reduced the death rate by 23 to 44%. Therefore, The disassembly and degradation of p130cas and paxillin during apoptosis may controlled by both caspases and calpains, depending upon their cellular contexts. Our findings also suggest that focal adhesion proteins paxillin and p130cas take part in integrin-mediated signaling for cell survival, and that their cleavage by caspase and/or calpain may not only disrupt focal adhesion complexes, but may also impede cell survival signaling.

Degradation of focal adhesion proteins during nocodazole-induced apoptosis in rat-1 cells.

Nocodazole, a microtubule-disrupting agent, induced apoptosis in Rat-1 cells, as indicated by changes in cell morphology, DNA fragmentation, and eventual cell death. During nocodazole-induced apoptosis, normally flat cells became rounded in shape and detached from the extracellular matrix. These morphological changes appeared to be closely associated with degradation of focal adhesion proteins, including p130cas, p125(FAK) and paxillin. p130cas was also degraded in cells treated with staurosporine or etoposide, suggesting that degradation of focal adhesion proteins is a characteristic feature of apoptosis. Nocodazole-induced apoptosis was antagonized by Bcl-2: degradation of focal adhesion proteins was suppressed and cell viability was enhanced in bcl-2 over-expressing cells, even in the presence of nocodazole. Further study of the molecular mechanism of Bcl-2 activation should provide an understanding of the apoptosis induced by disruption of the microtubule network.