However, few groups have explored the potential interaction between surgical margin status and other cancer characteristics, specifically pathological stage. We addressed the first degree of interaction between positive surgical margins and other established adverse predictors of biochemical recurrence CX-6258 nmr after radical prostatectomy.
Materials and Methods: We used univariate and multivariate analysis to test the effect of surgical
margin status on biochemical recurrence in 4,490 patients treated at a single institution between 1992 and 2008. We systematically tested all first-degree interactions between surgical margin status, and pretreatment prostate specific antigen, pT and pN stage, and radical prostatectomy Gleason sum. If interactions were significant, we quantified the effect on Evofosfamide datasheet the biochemical recurrence rate.
Results: Overall 850 patients (18.9%) had positive surgical margins. In those with negative vs positive surgical margins the 5-year biochemical recurrence-free survival rate was 95% vs 83%, 74% vs 62% and 47%
vs 29% for pT2, pT3a and pT3b disease, respectively. In multivariate models only the pT stage-surgical margin status interaction achieved independent predictor status (p = 0.003). Negative vs positive surgical margin multivariate HRs were 1 vs 2.9, 2.3 vs 4.3 and 4.1 vs 5.6 in pT2, pT3a and pT3b cases, respectively.
Conclusions: Compared to negative surgical margins, positive surgical margins increase the absolute biochemical recurrence 5-year rate by 12%
to 18%. More importantly, Liproxstatin-1 supplier positive surgical margins may substantially worsen the prognosis beyond that of the original pathological disease stage.”
“BACKGROUND: Subarachnoid hemorrhage (SAH) is the stroke subtype with the highest mortality and morbidity. Which molecular events mediate brain damage after SAH is not well understood.
OBJECTIVE: To investigate the role of proinflammatory bradykinin B(1) and B(2) receptors for the pathophysiology of SAH.
METHODS: B(1) and B(2) receptor knockout or wild-type mice were subjected to SAH by endovascular puncture. Intracranial pressure, regional cerebral blood flow, and mean arterial blood pressure were continuously monitored up to 60 minutes after SAH. Brain water content was quantified 24 hours after SAH; mortality, neurological function, and body weight were assessed daily for 7 days after hemorrhage.
RESULTS: Intracranial pressure, regional cerebral blood flow, and mean arterial blood pressure did not differ between groups. Mortality was 60% in wild-type mice and 82% in B(1)R(-/-) mice but only 20% in B(2)R(-/-) animals (P < .05). B(2)R(-/-) mice also exhibited less severe neurological deficits (P < .05), a less pronounced loss of body weight (P < .05), and significantly less brain edema formation (P < .05) compared with wild-type mice.
CONCLUSION: Signaling mediated by bradykinin B(2) receptors contributes to mortality and secondary brain damage after SAH in mice.