UNASSIGNED: Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 1 (NLRP1) participates in neuroinflammation. This study aimed to identify serum NLRP as a potential prognostic biomarker of acute intracerebral hemorrhage (ICH).
UNASSIGNED: This prospective cohort study enrolled 145 patients with supratentorial ICH and 51 healthy controls. Serum NLRP1 levels were quantified on admission of all 145 patients, on days 1, 3, 5, 7, and 10 after stroke in 51 of 145 patients and at entry into the study of controls. Poststroke 6-month modified Rankin Scale (mRS) scores of 3-6 signified a poor prognosis.
UNASSIGNED: Compared to controls, patients had prominently increased serum NLRP1 levels until day 10 after ICH, with the highest levels at days 1 and 3. Serum NLRP1 levels were independently correlated with National Institutes of Health Stroke Scale (NIHSS) scores, hematoma volume and six-month mRS scores, and independently predicted six-month bad prognosis. A linear relationship was observed between serum NLRP1 levels and the risk of poor prognosis in a restricted cubic spline. Under the receiver operating characteristic (ROC) curve, serum NLRP levels efficiently discriminated poor prognosis. Serum NLRP1, NIHSS, and hematoma volume were merged into a prognosis prediction model, which was portrayed using a nomogram. Good performance of the model was verified using calibration curve, decision curve, and ROC curve.
UNASSIGNED: Serum NLRP1 levels are elevated during the early period following ICH and are independently related to hemorrhagic severity and poor prognosis, suggesting that serum NLRP1 may represent a promising prognostic biomarker of ICH.

Gout is triggered by high urate levels and causes inflammation, pain, and an impaired quality of life. Immersion in water at 20-30°C reduces inflammation and pain in arthritis. Yet, relationships of immersion in water at 20-30°C with urate levels and the nucleotide-binding domain (NOD)-like receptor protein 1 (NLRP1) inflammasome have never been clarified.
We aimed to investigate the effects of immersion in water at 20-30°C on urate levels, the NLRP1 inflammasome, pain, and quality of life among acute gout patients.
A community-based randomized control trial design was used with 2 parallel-intervention groups: immersion in water at 20-30°C (20 min/day for 4 weeks) group and a control group. In total, 76 eligible participants in Tomohon City, Indonesia, were assigned using block randomization. We analyze the results (coef. β) and 95% confidence intervals (CIs) using a generalized estimating equation model. We analyzed mediating effects using a path analysis.
Significant pain alleviation (β = -2.06 [95% CI = -2.67∼-1.45]; β = -2.42 [95% CI = -2.97∼-1.87]) and improved quality of life (β = 5.34 [95% CI = 3.12-7.57]; β = 9.93 [95% CI = 7.02-12.83]) were detected at 2 and 4 weeks of follow-up compared to the pre-test and control group. Urate levels (β = -0.34 [95% CI = -0.52∼-0.16]) were reduced at the 2-week follow-up, but there was no significant change in the NLRP1 inflammasome compared to the pre-test and control group after immersion in water at 20-30°C. Both the NLRP1 inflammasome (β = -0.48 [95% CI = -0.63∼-0.34]); water 0.01) and urate levels (β = -0.11 [95% CI = -0.24∼-0.03]; p < 0.01) had partial indirect (mediating) effects on the link between immersion in water at 20-30°C and pain at the 4-week follow-up.
Immersion in water at 20-30°C significantly decreased pain and increased the quality of life. Immersion in water at 20-30°C mediated NLRP1 and urate levels to decrease pain, although it had no significant effect on the NLRP1 inflammasome concentration after 4 weeks of follow-up and reduced urate levels only at 2 weeks after immersion in water at 20-30°C.

OBJECTIVE: Detecting the distribution and intensity of NLRP3, NLRP1 and AIM2 expression in different types of periodontitis gingival tissues.
METHODS: A total of 65 gingival tissues were collected from clinic and been divided into three groups: patients with chronic periodontitis (CP), patients with generalized aggressive periodontitis (G-AgP) and healthy control subjects. Real-time polymerase chain reaction (RT-PCR) was performed to detect mRNA expression of NLRP3, NLRP1 and AIM2 in full-thickness tissue. In the meanwhile, immunohistochemistry was used to detect distribution of NLRP3, NLRP1 and AIM2 in the periodontal epithelium and in the connective tissue cells.
RESULTS: The overall intensity of NLRP3 expression was significantly higher in CP or G-AgP than healthy tissue. A more significant difference was observed in the periodontal epithelium layer. NLRP1 was barely expressed in the healthy and periodontitis gingival tissues, whereas AIM2 was expressed at a higher level in the chronic periodontitis group than others.
CONCLUSIONS: The NLRP3, NLRP1 and AIM2 proteins were differentially expressed in gingival tissues from patients with CP and G-AgP and may play vital roles in the progression of periodontal inflammation to different degrees. Our studies may provide a new direction for personalized periodontal treatment.