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991.
Shaun Eslick Evan J. Williams Bronwyn S. Berthon Timothy Wright Constantine Karihaloo Mark Gately Lisa G. Wood 《Nutrients》2022,14(4)
Background: Chronic low-grade systemic inflammation is a characteristic of obesity that leads to various non-communicable diseases. Weight loss and SCFAs are potential strategies for attenuating obese systemic inflammation. Methods: Blood samples were collected from 43 obese subjects (BMI ≥ 30 kg/m2) scheduled for laparoscopic bariatric sleeve surgery, 26 obese subjects at follow-up 12–18 months post-surgery and 8 healthy weight subjects (BMI 18.5–24.9 kg/m2). Monocytes were isolated from blood and adipose tissue macrophages from visceral adipose tissue of obese subjects only. Isolated cells stimulated with 1 ng/mL LPS and treated simultaneously with 300 mM of sodium acetate or 30 mM of sodium propionate or butyrate and supernatant were harvested after 15 h incubation. TNF-α and IL-6 cytokines were measured via ELISA and mRNA gene expression of FFAR2 and FFAR3, HDAC1, HDAC2 and HDAC9, RELA and NFKB1 and MAPK1 via RT-qPCR. Results: TNF-α and IL-6 production and NFKB1 and RELA mRNA expression were significantly decreased in follow-up subjects compared to baseline. SCFAs significantly reduced TNF-α and IL-6 and altered FFAR and HDAC mRNA expression in monocytes and macrophages from obese subjects. Conclusion: Weight loss and ex vivo SCFA treatments were successful in combatting systemic inflammation in obesity. Results highlighted molecular changes that occur with weight loss and as a result of SCFA treatment. 相似文献
992.
Benjamin Mason Meier Judith Bueno de Mesquita Gian Luca Burci Danwood Chirwa Stphanie Dagron Mark Eccleston-Turner Lisa Forman Lawrence O Gostin Roojin Habibi Stefania Negri Alexandra Phelan Sharifah Sekalala Allyn Taylor Pedro A Villarreal Alicia Ely Yamin Steven J Hoffman 《Bulletin of the World Health Organization》2022,100(3):178
993.
994.
Hilary A. Seifert Lisa A. Collier Cortney B. Chapman Stanley A. Benkovic Alison E. Willing Keith R. Pennypacker 《Journal of neuroimmune pharmacology》2014,9(5):679-689
The delayed immune response to stroke is responsible for the increased neural injury that continues to occur after the initial ischemic event. This delayed immune response has been linked to the spleen, as splenectomy prior to middle cerebral artery occlusion (MCAO) is neuroprotective. Interferon gamma (IFNγ) is linked to the splenic response, which enhances neural injury following MCAO. IFNγ activates the expression of the inflammatory chemokine interferon-inducible protein 10 (IP-10). This study was designed to determine the role of IFNγ signaling in the inflammatory response following MCAO. Expression of IP-10 increased in the brain and the spleen following MCAO. Splenectomy inhibited the increase of IP-10 in the brain post-MCAO, while recombinant IFNγ administration to splenectomized rats returned IP-10 levels in the brain to levels found in rats after MCAO only. Systemic administration of an IFNγ neutralizing antibody to MCAO-treated rats reduced infarct volume and IP-10 levels in the brain. T cell infiltration was reduced in the MCAO-damaged brains of IFNγ antibody-treated animals relative to those that received isotype control antibodies. Additionally, inhibiting IFNγ signaling with splenectomy or an IFNγ neutralizing antibody blocked the induction of IP-10 expression and decreased neurodegeneration following MCAO. Targeting this pro-inflammatory pathway following stroke could be a promising stroke therapeutic. 相似文献
995.
Role of PPARalpha in mediating the effects of phthalates and metabolites in the liver 总被引:1,自引:0,他引:1
Lapinskas PJ Brown S Leesnitzer LM Blanchard S Swanson C Cattley RC Corton JC 《Toxicology》2005,207(1):149-163
Phthalate esters belong to a large class of compounds known as peroxisome proliferators (PP). PP include chemicals that activate different subtypes of the peroxisome proliferator-activated receptor (PPAR) family. The ability of phthalate esters and their metabolites to activate responses through different PPAR subtypes is not fully characterized. We investigated the ability of two phthalate esters di-(2-ethylhexyl) phthalate (DEHP) and di-n-butyl phthalate (DBP) and selected metabolites to activate PPAR (alpha, beta/delta, gamma) using a transient transfection assay. The monoester of DEHP, mono-(2-ethylhexyl) phthalate (MEHP) activated all three subtypes of PPAR, but preferentially activated PPARalpha. A second metabolite of DEHP, 2-ethylhexanoic acid (2-EHXA) was a weaker activator of all three subtypes. DBP, but not the primary metabolite mono-n-butyl phthalate weakly activated all three PPAR subtypes. MEHP and DBP but not DEHP and MBP interacted directly with human PPARalpha and PPARgamma as determined by scintillation proximity assays. Both DEHP and DBP activated expression of PP-inducible gene products in wild-type but not PPARalpha-null mice suggesting that both of these phthalates exert their effects by activation of PPARalpha in vivo. The preferential activation of PPARalpha by phthalate ester metabolites suggests that these phthalates mediate their toxic effects in rodent liver in a manner indistinguishable from other PP. 相似文献
996.
C. Gopalsami W. Yotis K. Corrigan S. Schade J. Keene L. Simonson 《Oral microbiology and immunology》1993,8(2):121-124
The effect of the outer membrane (outer sheath) of Treponema denticola on bone resorption was studied. Bone resorption was measured by the release of previously incorporated 45 Ca from the shafts of the radii and ulnae of 19-day fetal rats. A treated-over-control ratio (T/C ratio) significantly greater than 1 indicated the stimulation of bone resorption by the test substance. The addition of outer membrane of T. denticola increased the release of 45 Ca from the assay bones. The minimum concentrations required to yield significant 45 Ca release from the assay bones were 15, 22 and 75 μg protein/ml for serovars a, b and c, respectively. These protein values corresponded to estimated lipopolysaccharide contents of 0.6, 0.8 and 2.8 μg/ml, based on 3-deoxy-2- manno -octulosonate analysis. Heat treatment of outer membrane (60° for 30 min) did not change the effect on 45 Ca release. Parathyroid hormone or prostaglandin E2 known to act synergistically with lipopolysaccharides in bone resorption, was also added to the assay system. Neither prostaglandin E2 at 10-7 M nor parathyroid hormone at 40 ng/ml, by itself, increased 45 Ca release. However, in the presence of 10 μg protein/ml of outer membrane of serovar b at 120 h, the T/C ratio was increased to 1.31±0.07 and 1.58±0.118, respectively. These results suggest that a lipopolysaccharide-like material is present in the outer membrane of T. denticola that may be responsible for bone resorption in the in vitro system. 相似文献
997.
998.
The Berlin‐Frankfurt‐Münster protocol for the upfront treatment of aggressive lymphomas: The Bologna experience 下载免费PDF全文
999.
1000.
Genome‐wide association study of a nicotine metabolism biomarker in African American smokers: impact of chromosome 19 genetic influences 下载免费PDF全文
Meghan J. Chenoweth Jennifer J. Ware Andy Z. X. Zhu Christopher B. Cole Lisa Sanderson Cox Nikki Nollen Jasjit S. Ahluwalia Neal L. Benowitz Robert A. Schnoll Larry W. Hawk Jr Paul M. Cinciripini Tony P. George Caryn Lerman Joanne Knight Rachel F. Tyndale 《Addiction (Abingdon, England)》2018,113(3):509-523