In a DXA screening cohort, higher mean arterial pressure (MAP) as a continuous exposure was associated with greater odds of DXA-defined osteoporosis (OR 1.15 per +10 mmHg). This supports a blood-pressureburden perspective that complements claims-based hypertension definitions.
Although intensive blood pressure (BP) lowering after mechanical thrombectomy (MT) may adversely affect outcomes, the prognostic significance of post-recanalization BP variability remains unclear. This study aimed to evaluate the association between systolic blood pressure (SBP) variability after successful recanalization and 90-day functional outcomes following MT. Among 342 consecutive patients who underwent MT between May 2014 and June 2025, 280 patients who achieved successful recanalization were included in this retrospective analysis. SBP was recorded from immediately after recanalization up to 72 h thereafter. BP variability indices, including variability independent of the mean (VIM), time rate, and coefficient of variation, were calculated. The primary outcome was defined as a modified Rankin Scale (mRS) score of 4-6 at 90 days. Associations between SBP variability and outcomes were assessed using multivariable logistic regression models. Of the 280 patients, 104 (37.1%) experienced poor functional outcomes. Higher SBP variability was significantly associated with unfavorable outcomes. In time-segmented analyses, only SBP variability during the 24-72-h period remained significantly associated with poor outcomes (aOR per 10-unit increase in VIM [VIM/10], 1.89; 95% CI, 1.20-3.06, p = 0.005). Sensitivity analyses excluding patients who received antihypertensive therapy during 24-72 h and those with symptomatic intracranial hemorrhage confirmed the robustness of the association between 24-72 h VIM and poor outcomes (aOR VIM/10, 1.94; 95% CI, 1.26-3.11, p = 0.003). In conclusion, these findings highlight the clinical importance of stabilizing BP beyond the first 24 h after recanalization.
Although elevated soluble uric acid (SUA) levels enhance the production of IL-1β in macrophages stimulated with monosodium urate (MSU) crystals, the underlying mechanism remains unelucidated. The aim of this study was to examine the effects of SUA on inflammatory response-related gene expression in lipopolysaccharide-primed and MSU crystal-stimulated macrophages using mouse macrophage-like J774.1 cells. Differential gene expression in SUA-pretreated and untreated group cells was analyzed by RNA sequencing and quantitative reverse transcription-polymerase chain reaction. SUA upregulated the genes related to pro-inflammatory reactions and downregulated those related to anti-inflammatory reactions. SUA also upregulated M1 pro-inflammatory macrophage-related genes and enhanced mRNA expression of CD44 responsible for phagocytosis of MSU crystals. These results suggest that SUA enhances gouty inflammation via promoting the expression of genes related to pro-inflammatory reactions, polarization toward the M1 phenotype, and MSU crystal phagocytosis in macrophages. Enhanced expression of the transcription factor genes Nfkb1 and Stat1 may underlie the SUA-induced M1 polarization and resulting enhancement of inflammasome activation and IL-1β transcription.
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