Our findings are consistent with outcomes of studies in non-healthcare domains, but are contrary to a study of ED physicians, suggesting differential responses to interruptions by physicians and nurses. Future studies on interruptions in healthcare should thus be discipline specific. Though the effect of interruptions on intervention length is only about 2 min, in an ED setting, this can increase patient risks and costs. To better focus efforts to reduce interruptions future research should focus on further separation of interruption type (eg, urgent vs routine or unnecessary).
Introduction Bladder outlet obstruction (BOO) was caused by a series of histological and biochemical changes in the bladder wall, through the inflammation process in the bladder wall, hypertrophy and fibrosis. ADSC has an important role in bladder regeneration. Methods and materials This study was an experimental randomized study using male Wistar rats which were monitored at 2 and 4 weeks to determine the effect of ADSC therapy on TGF-β1 type I collagen, and degree of fibrosis. Result Rats were divided into 5 groups. In the week 2 BOO group, 1 sample included in the category of moderate fibrosis, 1 sample that was given ADSC with mild fibrosis category, 3 samples included in severe fibrosis category, 3 samples that were given ADSC included in the category of moderate fibrosis. The concentration of TGF-β1 in the hADSC therapy group was significantly lower than the control group at the 2nd and 4th week of monitoring (p2 = 0.048, p4 = 0.048), and also with more type I collagen on 2nd and the 4th week (p2 = 0.048, p4 = 0.048). Conclusion ADSC therapy can reduce the concentration of TGF-β1, type I collagen, and degree of fibrosis in the male Wistar BOO model.
Background: Priapism induces regulation of Transforming Growth Factor-β1 (TGF-β1) expression and collagen-type-1 deposition. This will replace the normal corpora cavernosa with fibrotic tissue which eventually resulted in erectile dysfunction. It is also known that the fibrosis process of corpora cavernosa is related to Renin-Angiotensin II System (RAS). Angiotensin II receptor blockers (ARB), especially losartan, inhibit the inflammation process and fibrotic tissue formation. This study evaluated the effect of losartan in reducing fibrosis in priapism by evaluating TGF-β1 and collagen-type-1 in cavernous tissue and determined the effect of losartan in preventing fibrosis in priapism model of Wistar rats assessed by the metavir score. Methods: A total of eighteen male Wistar rats mean were divided into five groups. For the priapism models, we applied negative pressure on the penis to make an artificial erection to mimic the priapism process. The control groups were observed and the treatment groups were orally given losartan 15 mg/kg/day. Corpora cavernosa was harvested for TGF-β1 and collagen-type-1 measurement using an enzyme-linked immunosorbent assay (ELISA). The fibrotic tissue of each rat was then collected and assessed histopathologically with the metavir scoring system. Results: Penile TGF-β1 concentration in the losartan-treated group was not significantly different on day 10 and day 28 of observation (p10=0,30; p28=0,17). Meanwhile, collagen-type-1 concentration was significantly lower compared to control group (p10=0,002; p28=0,01). There was a significant difference in metavir scores in rats that received losartan and those who did not (p<0,05). Conclusion: Losartan could suppress the fibrosis process in the priapism model. It could decrease the collagen type 1 deposition during corpora cavernosa tissue regeneration. Based on the metavir score, the group receiving losartan therapy was better than the control group.
Development of hyperplastic nodules in the transition zone of the prostate is the characteristic of Benign prostatic enlargement (BPE). Men with hypertension have a high risk of severe lower urinary tract syndrome (LUTS). This restrospective cohort analytic study investigated the association between LUTS and BPE in hypertension patients. Subjects were BPE patients with primary hypertension who visited the urology clinic of Dr. Hasan Sadikin General Hospital Bandung that were sampled consecutively from 2017 to 2020. Three hundred and twenty-four patients from the urology department participated in the study. These patients were categorized into mild LUTS (IPSS 1-7) (n=37, 11.4%), moderate LUTS (IPSS 8-19) (n=169, 52.2%), and severe LUTS (IPSS 20-35) (n=118, 36.4%). A positive correlation (r = 0.761, p = 0.000) and weak positive correlation (r = 0.152, p = 0.006) were found between systolic blood pressure and prostate volume and between LUTS and systolic blood pressure, respectively. In addition, there was also a weak positive correlation between diastolic blood pressure and prostate volume (r = 0.065, p = 0.245) and LUTS (r = 0.015, p = 0.784). Thus, there is an association between hypertension and prostate enlargement and the severity of lower urinary tract symptoms
Background: Priapism induces regulation of Transforming Growth Factor-β1 (TGF-β1) expression and collagen-type-1 deposition. This will replace the normal corpora cavernosa with fibrotic tissue which eventually resulted in erectile dysfunction. It is also known that the fibrosis process of corpora cavernosa is related to Renin-Angiotensin II System (RAS). Angiotensin II receptor blockers (ARB), especially losartan, inhibit the inflammation process and fibrotic tissue formation. This study evaluated the effect of losartan in reducing fibrosis in priapism by evaluating TGF-β1 and collagen-type-1 in cavernous tissue and determined the effect of losartan in preventing fibrosis in priapism model of Wistar rats assessed by the metavir score. Methods: A total of eighteen male Wistar rats mean were divided into five groups. For the priapism models, we applied negative pressure on the penis to make an artificial erection to mimic the priapism process. The control groups were observed and the treatment groups were orally given losartan 15 mg/kg/day. Corpora cavernosa was harvested for TGF-β1 and collagen-type-1 measurement using an enzyme-linked immunosorbent assay (ELISA). The fibrotic tissue of each rat was then collected and assessed histopathologically with the metavir scoring system. Results: Penile TGF-β1 concentration in the losartan-treated group was not significantly different on day 10 and day 28 of observation (p10=0,30; p28=0,17). Meanwhile, collagen-type-1 concentration was significantly lower compared to control group (p10=0,002; p28=0,01). There was a significant difference in metavir scores in rats that received losartan and those who did not (p<0,05). Conclusion: Losartan could suppress the fibrosis process in the priapism model. It could decrease the collagen type 1 deposition during corpora cavernosa tissue regeneration. Based on the metavir score, the group receiving losartan therapy was better than the control group.
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