Consumer price indices - 1. quarter of 2016

Total consumer price level, quarter-on-quarter and year-on-year comparison, consumer price index breakdown

Additional file 3: Figure S2. of The impact of “early” versus “late” initiation of renal replacement therapy in critical care patients with acute kidney injury: a systematic review and evidence synthesis

Article selection process. (PDF 86 kb

Additional file 4: Figure S3. of The impact of “early” versus “late” initiation of renal replacement therapy in critical care patients with acute kidney injury: a systematic review and evidence synthesis

a Mortality forest plot of subgroup analysis of high-quality studies according to post-surgical ICU admission type (n = 3). b Mortality forest plot of subgroup analysis of high-quality studies according to medical ICU admission type (n = 6). (ZIP 120 kb

Additional file 2: Table S1. of The impact of “early” versus “late” initiation of renal replacement therapy in critical care patients with acute kidney injury: a systematic review and evidence synthesis

Search terms used during literature review. (DOCX 15 kb

Additional file 1: Figure S1. of The impact of “early” versus “late” initiation of renal replacement therapy in critical care patients with acute kidney injury: a systematic review and evidence synthesis

Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) checklist. (PDF 51 kb

Inhibition of the NLRP3 inflammasome with glyburide (Glyb) prevents caspase-1 activation and IL-1β production by LPS-challenged cardiac fibroblasts (CFs).

<p>CFs were pretreated with either vehicle or glyburide (50 µM or 200 µM) 30 min before the LPS (1 µg/ml) challenge. Twenty-four hrs after LPS stimulation, the cells were harvested and processed for the measurement (Western blot) of intracellular NLRP3 (A), pro-caspase-1 (B), activated caspase-1 p10 (C), pro-IL-1β (D), and mature IL-1β (E). The supernatants were harvested for the detection of released IL-1β with ELISA (F). The basal levels of the various components of the NLRP3 inflammasome/IL-1β axis were not affected by glyburide. For A through E, representative blots and densitometric analyses are shown. n = 3 for all experiments (A–F). *p<0.05 compared with controls; #p<0.05 compared with LPS treatment alone.</p

Treatment of cardiac fibroblasts (CFs) with LPS activates the NLRP3 inflammasome and results in the maturation (activation) and release of IL-1β.

<p>Mouse CFs were challenged with LPS (1 µg/ml) or saline (control). At the times indicated, the CFs were collected, lysed, and processed for the measurement (Western blot) of intracellular NLRP3 (A), pro-caspase-1 (B), activated caspase-1 p10 (C), pro-IL-1β (D), and IL-1β (E). Released IL-1β was also assessed by ELISA of the supernatants (F). For A through E, representative blots and densitometric analyses are shown. n = 3 for all experiments (A–F), *p<0.05, compared with control.</p

Sepsis-induced increases in myocardial and circulating IL-1β is reduced by inhibition of the NLRP3 inflammasome.

<p>Polymicrobial sepsis (FIP) was induced by i.p. injection of 0.5 ml of fecal material (30 mg/ml). Myocardial tissue was harvested for measurement (Western blot) of NLRP3, pro-caspase-1, activated caspase-1 p10, and pro-IL-1β. Representative Westerns are shown in panel A and densitometric analyses in panels B-E. Mature (activated) IL-1β in myocardial homogenates and plasma assessed with ELISA, panels F and G, respectively. n = 5 for all experiments; *p<0.05 compared with sham, #p<0.05 compared with FIP.</p

Inhibition of the NLRP3 inflammasome prevents LPS-induced increase in myocardial and circulating IL-1β in mice.

<p>Mice were injected (i.p.) with saline (sham), LPS (10 mg/kg), LPS with glyburide (1 mg/Kg), or glyburide alone. Eight hours later, myocardial tissue was harvested for measurement (Western blot) of NLRP3, pro-caspase-1, activated caspase-1p10, pro-IL-1β and IL-1β. Representative Westerns shown in panel A and densitometric analyses in panels B–F. Mature (activated) Il-1β in myocardial homogenates and plasma assessed with ELISA, panels F and G, respectively. n = 5 for all experiments; *p<0.05 compared with sham, #p<0.05 compared with LPS.</p

Sepsis-induced lethality is diminished by inhibition of the NLRP3 inflammasome.

<p>Polymicrobial sepsis (FIP) was induced by i.p. injection of 0.5 ml of fecal material (30 mg/ml) in 20 mice; 10 of these mice also received glyburide (1 mg/Kg, i.p. daily). The mice were monitored hourly for up to 72 hrs, and the survival rate was calculated. The survival rate of the two groups was compared with the Kaplan–Meier test, p = 0.024.</p