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BACKGROUND: Increased lipoprotein (a) [lp (a)] has proinflammatory effects, which increase the risk of coronary artery disease. However, the association between lp (a) variability and follow-up C-reactive protein (CRP) level in patients undergoing percutaneous coronary intervention (PCI) has not been investigated. AIM: To explore the association between lp (a) variability and mean CRP levels within the 1st year post-PCI. METHODS: Results of lp (a) and CRP measurements from at least three follow-up visits of patients who had received PCI were retrospectively analyzed. Standard deviation (SD), coefficient of variation (CV), and variability independent of the mean (VIM) are presented for the variability for lp (a) and linear regression analysis was conducted to correlate lp (a) variability and mean follow-up CRP level. The relationship of lp (a) variability and inflammation status was analyzed by restricted cubic spline analysis. Finally, exploratory analysis was performed to test the consistency of results in different populations. RESULTS: A total of 2712 patients were enrolled. Patients with higher variability of lp (a) had a higher level of mean follow-up CRP (P < 0.001). lp (a) variability was positively correlated with the mean follow-up CRP (SD: ß = 0.023, P < 0.001; CV: ß = 0.929, P < 0.001; VIM: ß = 1.648, P < 0.001) by multivariable linear regression analysis. Exploratory analysis showed that the positive association remained consistent in most subpopulations. CONCLUSION: Lp (a) variability correlated with mean follow-up CRP level and high variability could be considered an independent risk factor for increased post-PCI CRP level.
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Adaptive intervention(AI)is a methodology which dynamically evaluates adaptive variables at decision points and timely adjusts and develops tailored strategies to meet individual needs.The study reviewed the origin and development and elaborated the core elements(including intervention outcomes,intervention options,decision points,tailoring variables,and decision rules)and the classification of AI.Based on the literature,the key points of the design and implementation of AI were prospected,which can provide evidence for the research and development of health behavior intervention.
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Gentimilegenins A, B (1, 2), (6R, 8R)-6-hydroxy swerimuslactone A (3), (6R, 8S)-6-hydroxy swerimuslactone A (4), 4-hydroxy roburic acid methyl ester (5), (±) 3'-hydroxy gentioxepine (6), N-heptacosanoyl anthranilic acid (7a), N-nonacosanoyl anthranilic acid (7b), together with 40 known compounds were isolated from the roots of Gentiana macrophylla Pall. Their structures were elucidated on the basis of comprehensive analysis of HRESIMS, IR, 1D-, 2D-NMR and X-ray diffraction. The anti-inflammatory effects of selected compounds were also evaluated through the detection of their inhibitory effects on NO production in LPS-induced RAW264.7 macrophage cells.
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Gentiana/química , Raíces de Plantas/química , Animales , Medicamentos Herbarios Chinos/química , Medicamentos Herbarios Chinos/farmacología , Lipopolisacáridos/toxicidad , Ratones , Modelos Moleculares , Estructura Molecular , Óxido Nítrico/biosíntesis , Células RAW 264.7RESUMEN
There are presently no miracle drugs for non-alcoholic fatty liver disease (NAFLD). This study investigates the synergistic effect of Silibinin combined with Pu-erh tea extract (PTE) against NAFLD and explores the suggested mechanism of action. Ob/ob mice were fed a high fat diet along with the oral administration of Silibinin (86 mg per kg per day), PTE (250 mg per kg per day) or their combination for 6 weeks. Their lean littermates who were fed with standard chow diet were used as the control group. The blood biochemical index and histopathological evaluation were analyzed. The expression of genes involved in the lipogenesis pathway and cholesterol metabolism were evaluated. When compared with that of the NAFLD group, the body weight and blood lipid of the mice from the PTE group or combination group were significantly reduced. To some degree, fat metabolism and the inflammatory response were ameliorated by Silibinin and PTE used alone or in combination. It was notable that the combination group had a stronger efficacy in adjusting fat metabolism and inhibiting oxidative stress than that of Silibinin or PTE used alone. Silibinin and PTE inhibited fat synthesis by regulating the mRNA expression of CRTC2, SREBP-1c, and SCD-1. Moreover, the cholesterol homeostasis was improved in the treatment groups via regulating the mRNA expression of ABCA1 and ApoB100. The improvement of the combination group was superior to each drug used alone. In conclusion, Silibinin in combination with PTE can prevent NAFLD with greater potential than Silibinin or PTE used alone and may be a new therapeutic strategy.
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Camellia sinensis/química , Enfermedad del Hígado Graso no Alcohólico/prevención & control , Extractos Vegetales/administración & dosificación , Silimarina/administración & dosificación , Animales , Modelos Animales de Enfermedad , Humanos , Metabolismo de los Lípidos/efectos de los fármacos , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Obesos , Enfermedad del Hígado Graso no Alcohólico/genética , Enfermedad del Hígado Graso no Alcohólico/metabolismo , Estrés Oxidativo/efectos de los fármacos , Silibina , Proteína 1 de Unión a los Elementos Reguladores de Esteroles/genética , Proteína 1 de Unión a los Elementos Reguladores de Esteroles/metabolismo , Té/química , Factores de Transcripción/genética , Factores de Transcripción/metabolismoRESUMEN
The brain of a human neonate is more vulnerable to hypoglycemia than that of pediatric and adult patients. Repetitive and profound hypoglycemia during the neonatal period (RPHN) causes brain damage and leads to severe neurologic sequelae. Ex vivo high-resolution (1)H nuclear magnetic resonance (NMR) spectroscopy was carried out in the present study to detect metabolite alterations in newborn and adolescent rats and investigate the effects of RPHN on their occipital cortex and hippocampus. Results showed that RPHN induces significant changes in a number of cerebral metabolites, and such changes are region-specific. Among the 16 metabolites detected by ex vivo (1)H NMR, RPHN significantly increased the levels of creatine, glutamate, glutamine, γ-aminobutyric acid, and aspartate, as well as other metabolites, including succine, taurine, and myo-inositol, in the occipital cortex of neonatal rats compared with the control. By contrast, changes in these neurochemicals were not significant in the hippocampus of neonatal rats. When the rats had developed into adolescence, the changes above were maintained and the levels of other metabolites, including lactate, N-acetyl aspartate, alanine, choline, glycine, acetate, and ascorbate, increased in the occipital cortex. By contrast, most of these metabolites were reduced in the hippocampus. These metabolic changes suggest that complementary mechanisms exist between these two brain areas. RPHN appears to affect occipital cortex and hippocampal activities, neurotransmitter transition, energy metabolism, and other metabolic equilibria in newborn rats; these effects are further aggravated when the newborn rats develop into adolescence. Changes in the metabolism of neurotransmitter system may be an adaptive measure of the central nervous system in response to RPHN.