- Sodium and Potassium Intake: Effects on Chronic Disease Outcomes and Risks [BOOK]
- BOOKAgency for Healthcare Research and Quality (US): Rockville (MD)
- CONCLUSIONS: Reducing sodium intake, increasing potassium intake, and use of potassium-containing salt substitutes in the diet significantly decrease BP, particularly among those with hypertension. Limited evidence also suggests that sodium intake is associated with risk for all-cause mortality, and that reducing sodium intake may decrease the risk for CVD morbidity and mortality.
- Ulinastatin attenuates liver injury and inflammation in a cecal ligation and puncture induced sepsis mouse model. [Journal Article]
- JCJ Cell Biochem 2018 Aug 20
- Sepsis is a syndrome of life-threatening multiorgan dysfunction caused by host response dysregulation to infection. Ulinastatin (UTI), a serine protease inhibitor, possesses anti-inflammatory propert...
Sepsis is a syndrome of life-threatening multiorgan dysfunction caused by host response dysregulation to infection. Ulinastatin (UTI), a serine protease inhibitor, possesses anti-inflammatory properties and has been suggested to modulate lipopolysaccharide-induced sepsis. However, little is known about the mechanism underlying its effects on sepsis. In the current study, we investigated the protective effect of UTI on liver injury in a cecal ligation and puncture (CLP)-induced sepsis of C57BL/6 mouse model and explored the possible mechanisms. Mice underwent CLP as sepsis models and were randomized into five groups including the sham group, UTI group, CLP group, UTI-L group, and UTI-H group. UTI was intraperitoneally administered at doses of UTI 1500 U/100 g (UTI-L group) or 3000 U/100 g (UTI-H group), before CLP. The mice were killed, and immunohistochemical changes, cytokine levels, and antioxidant enzyme activities were detected. Our results showed that UTI ameliorated CLP-mediated increases in serum aspartate aminotransferase and alanine aminotransferase activities, histological activity index, degenerative region ratio, and infiltrated inflammatory cell numbers. Moreover, UTI also decreased nitrotyrosine and 4-hydroxynonenal, activated caspase-3, and activated poly (ADP-ribose) polymerase (PARP) levels and inhibited the mitogen-activated protein kinase pathway activation in liver tissues. Our results indicated that UTI could inhibit CLP-induced liver injury by suppressing inflammation and oxidation. Our results indicated that UTI may serve as a potential therapeutic agent for sepsis.
- Male gender, active smoking and previous intestinal resection are risk factors of post-operative endoscopic recurrence in Crohn's disease: results from a prospective cohort study. [Journal Article]
- APAliment Pharmacol Ther 2018 Aug 20
- CONCLUSIONS: Male gender, active smoking at surgery and previous intestinal resection are associated with a higher risk of endoscopic post-operative recurrence, while post-operative anti-TNF treatment is associated with a lower risk.
- High and Low Dose Oral Immunotherapy Similarly Suppress Pro-Allergic Cytokines and Basophil Activation in Young Children. [Journal Article]
- CEClin Exp Allergy 2018 Aug 20
- CONCLUSIONS: Peanut OIT leads to decreases in pro-allergic cytokines, including IL-5, IL-13, and IL-9, and decreased basophil activation. No differences in T cell or basophil responses were found between subjects on low or high dose maintenance OIT, which has implications for clinical dosing strategies. This article is protected by copyright. All rights reserved.
- Meltdown! Local Heating by Decaying Excited Host Positive Polarons Triggers Aggregation Quenching in Blue PhOLEDs. [Journal Article]
- CChemphyschem 2018 Aug 20
- Exciton-polaron induced aggregation (EPIA) in organic host materials for blue Phosphorescent Organic Light Emitting Diodes (PhOLEDs) is driven by a non-radiative decay of electronically excited posit...
Exciton-polaron induced aggregation (EPIA) in organic host materials for blue Phosphorescent Organic Light Emitting Diodes (PhOLEDs) is driven by a non-radiative decay of electronically excited positive polarons resulting in a local heating of the amourphous host matrix. The released heat triggers morphological changes, i.e. molecular aggregation between neighboring host molecules. The resulting aggregates, which our calculations identify as carbazolyl dimers, lead to decreased PhOLED efficiency. Statistical assessment of some host-only morphologies reveals a structure-dependent propensity for molecular aggregation corroborating the identified EPIA mechanism. Our findings provide a fresh look at established molecular design rules and will help to improve blue PhOLED host materials to enhance blue PhOLED device lifetimes.
- Decreased vesicular acetylcholine transporter related to memory deficits in epilepsy: A [18 F] VAT positron emission tomography brain imaging study. [Journal Article]
- EEpilepsia 2018 Aug 20
- CONCLUSIONS: [18 F] VAT PET is a promising method to test the level of VAChT as a valuable biomarker for memory deficits in pilocarpine-induced chronic epileptic rats.
- FAAH variant Pro129Thr modulates subjective effects produced by cocaine administration. [Journal Article]
- AJAm J Addict 2018 Aug 20
- CONCLUSIONS: These results add to existing evidence that this variant of the FAAH genotype may be over-represented among those who have CUD, and this over-representation may result from greater subjective responses to cocaine administration. (Am J Addict 2018;XX:1-7).
- Emicizumab-mediated haemostatic function in patients with haemophilia A is down-regulated by activated protein C through inactivation of activated factor V. [Journal Article]
- BJBr J Haematol 2018 Aug 20
- Activated protein C (APC) inactivates activated factor V (FVa) and moderates FVIIIa by restricting FV cofactor function. Emicizumab is a humanized anti-FIXa/FX bispecific monoclonal antibody that mim...
Activated protein C (APC) inactivates activated factor V (FVa) and moderates FVIIIa by restricting FV cofactor function. Emicizumab is a humanized anti-FIXa/FX bispecific monoclonal antibody that mimicks FVIIIa cofactor function. In recent clinical trials in haemophilia A patients, once-weekly subcutaneous administration of emicizumab was remarkably effective in preventing bleeding events, but the mechanisms controlling the regulation of emicizumab-mediated haemostasis remain to be explored. We investigated the role of APC-mediated reactions in these circumstances. APC dose-dependently depressed thrombin generation (TG) initiated by emicizumab in FVIII-deficient plasmas, and in normal plasmas preincubated with an anti-FVIII antibody (FVIII-depleted). FVIIIa-independent FXa generation with emicizumab was not affected by the presence of APC, protein S and FV. The results suggested that APC-induced down-regulation of emicizumab-dependent TG was accomplished by direct inactivation of FVa. The addition of APC to emicizumab mixed with FVIII-depleted FV-deficient plasma in the presence of various concentrations of exogenous FV demonstrated similar attenuation of TG, irrespective of specific FV concentrations. Emicizumab-related TG in FVIII-depleted FVLeiden plasma was decreased by APC more than that observed with native FVLeiden plasma. The findings indicated that emicizumab-driven haemostasis was down regulated by APC-mediated FVa inactivation in plasma from haemophilia A patients without or with FV defects.
- Forkhead box p3 controls progression of oral lichen planus by regulating microRNA-146a. [Journal Article]
- JCJ Cell Biochem 2018 Aug 20
- Oral lichen planus (OLP) is a severe T cell-mediated disorder of the mucosa, which causes chronic inflammation. Forkhead box P3 (Foxp3) regulates the immune response and plays an important role in im...
Oral lichen planus (OLP) is a severe T cell-mediated disorder of the mucosa, which causes chronic inflammation. Forkhead box P3 (Foxp3) regulates the immune response and plays an important role in immunological diseases. The current study aimed to determine the role of Foxp3 and microRNA (miR)-146a in OLP. Western blot analysis and a quantitative real-time polymerase chain reaction assay showed that the expression of Foxp3 and miR-146a was upregulated in OLP tissues and in lipopolysaccharide (LPS)-incubated HaCaT cells, compared with controls. Foxp3 inhibition significantly decreased miR-146a expression, ameliorated LPS stimulation by decreased cell proliferation, and apoptosis in LPS-incubated HaCaT cells as compared with the LPS group. Cotransfection of Foxp3 small interfering RNA and miR-146a mimics elevated cell proliferation and apoptosis compared with the Foxp3 small interfering RNA group. In addition, miR-146a overexpression upregulated, whereas miR-146a inhibition downregulated, the proliferation and apoptosis of LPS-incubated HaCaT cells. The target gene of miR--146a, tumor necrosis factor receptor-associated factor 6 (TRAF6), was predicted by bioinformatics software and identified by the luciferase reporter assay. Furthermore, Foxp3/miR-146a elevated T regulatory cells and regulated TRAF6 expression in CD4+ T cells that were isolated from peripheral blood of patients with OLP. In conclusion, our study suggests that Foxp3 and miR-146a regulate the progression of OLP by negatively regulating TRAF6, which may provide a promising therapeutic target for OLP treatment.
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- The Polyphenol Rsesveratrol Promotes Skeletal Growth in Mice Through a SirT1-BMP2 Longevity Axis. [Journal Article]
- BJBr J Pharmacol 2018 Aug 20
- CONCLUSIONS: These findings suggest a new mechanism of action in bone remodeling and the ageing skeleton, where RSV positively impacts bone homeostasis via SirT1 activation of BMP2.