Oysters (Crassostrea talienwhanensis) contain large amounts of protein and exhibit many biological activities. This study was aimed at preparing oyster protein hydrolysates (OPH) and evaluating the OPH based on a spatial learning and memory capacity. A response surface methodology was employed to optimize hydrolysis conditions to determine the OPH with the highest AChE inhibitory activity, and the optimum extraction conditions were as follows: enzyme concentration of 1444.88 U g−1, pH of 7.38, extraction temperature of 45 °C, extraction time of 5.56 h and a water/material ratio of 2.45 : 1, and the minimum acetylcholinesterase (AChE) activity was 0.069 mM min−1. The spatial memory and learning abilities and passive avoidance in mice were determined by using the Morris water maze test and a dark/light avoidance test. Furthermore, the OPH group could relieve oxidative stress, reduce AChE levels, increase choline acetyltransferase (ChAT) levels and alleviate inflammatory reaction through reduction of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) levels. Additionally, up-regulated expressions of brain-derived neurotrophic factor (BDNF) and neural cell adhesion molecules (NCAM) were observed in mice treated with OPH. These findings suggested that OPH could be a functional food candidate to improve the learning and memory ability associated with oxidative stress and inflammatory reactions.Oyster protein hydrolysate could be a functional food candidate to improve learning and memory ability.相似文献
Therapeutic vaccines for nicotine addiction show pre-clinical efficacy. Yet, clinical evaluation of the first-generation nicotine vaccines did not meet expectations because only a subset of immunized subjects achieved effective serum antibody levels. Recent studies suggest that vaccine design affects B cell activation, and that the frequency of the hapten-specific B cell subsets contributes to vaccine efficacy against drugs of abuse. To extend this hypothesis to nicotine immunogens, we synthesized a novel hapten containing a carboxymethylureido group at the 2-position of the nicotine structure (2CMUNic) and compared its efficacy to the previously characterized 6CMUNic hapten. Haptens were conjugated to the keyhole limpet hemocyanin (KLH) carrier protein, and evaluated for efficacy against nicotine in mice using the clinically approved alum adjuvant. Using a novel fluorescent antigen-based magnetic enrichment strategy paired with multicolor flow cytometry analysis, polyclonal hapten-specific B cell subsets were measured in mice immunized with either 6CMUNic-KLH or 2CMUNic-KLH. The 6CMUNic-KLH showed significantly greater efficacy than 2CMUNic-KLH on nicotine distribution to serum and to the brain. The 6CMUNic-KLH elicited higher anti-nicotine serum antibody titers, and greater expansion of hapten-specific B cells than 2CMUNic-KLH. Within the splenic polyclonal B cell population, a higher number of hapten-specific IgMhigh and germinal centre B cells predicted greater vaccine efficacy against nicotine distribution. These early pre-clinical findings suggest that hapten structure affects activation of B cells, and that variations in the frequency of early-activated hapten-specific B cell subsets underlie individual differences in vaccine efficacy. 相似文献
Background and aimsType 2 diabetes mellitus (T2DM) has high risk of developing cardiac dysfunction, increasing of either cardiovascular death or hospitalization for heart failure. MicroRNAs (miRNA) affect cardiac function of T2DM. The aim of this study was to investigate the relationships between five miRNA single nucleotide polymorphisms (SNP) and diastolic and systolic function of T2DM.Methods and resultsThree hundred untreated T2DM subjects were included. Each subject underwent SNP genotyping, conventional echocardiography, tissue doppler imaging, and speckle tracking imaging. The effects of miRNA SNPs on diastolic and systolic function were evaluated. The diastolic function of T2DM subjects with miR-133a-1-rs8089787 wild genotype or let-7f-rs10877887 variant genotype was lower than those with miR-133a-1-rs8089787 variant genotype or let-7f-rs10877887 wild genotype, manifesting as higher left atrial volume index, lower mean E′, and higher E/E’ (P < 0.05). There were no significant effects of miR-133a-2-rs13040413, let-7a-1-rs13293512 and miR-27a-rs895819 on the diastolic function of T2DM subjects (P > 0.05). These five miRNA SNPs had no effect on the systolic function of T2DM subjects (P > 0.05).ConclusionsMiRNA-133a-1-rs8089787 and let-7f-rs10877887 were associated with impaired cardiac diastolic function in T2DM. The findings may be a promising therapeutic targets for preventing diastolic dysfunction in T2DM. 相似文献
Background and aimsAssociations of alanine aminotransferase (ALT) and serum uric acid (SUA) with metabolic syndrome (MetS) remain controversial. We aimed to explore individual and combined effects of ALT and SUA on MetS in community residents.Methods and resultsA population-based cross-sectional survey involving randomly selected Chinese adults aged 35–74 years was conducted in 2009 in Qingdao, China, and 4642 participants were included in the current study. Based on a combination of SUA and ALT levels in the tertile, subjects were grouped into Group 1-9. The individual and combined relations of SUA and ALT to MetS were analyzed by logistic regression models. The prevalence of MetS was 28.50% in males and 22.30% in females. ALT and SUA were independently associated with MetS and ORs (95% CIs) were 1.55 (1.42–1.70) and 1.92 (1.72–2.14), respectively, after adjusting for potential confounders. With the elevation of ALT and SUA levels, the risk of developing MetS increased. Compared to Group 1, ORs (95% CIs) of combined ALT and SUA for MetS were 2.21 (1.70–2.88), 4.02 (3.10–5.21), 2.19 (1.62–2.97), 2.53 (1.91–3.34), 4.69 (3.60–6.12), 1.76 (1.17–2.64), 3.65 (2.63–5.06) and 7.15 (5.41–9.46) in Group 2–9, respectively.ConclusionsALT and SUA were both related to MetS independently. Combined elevation of ALT and SUA levels could increase the risk of MetS and its components than an elevation in SUA and ALT alone. Therefore, measures should be taken to lower SUA and ALT levels to reduce the risk of having MetS. 相似文献
Clinical Rheumatology - Idiopathic inflammatory myopathies (IIM) are a group of chronic rheumatic diseases that can affect multiple systems; the risk of ischemic stroke in patients with IIM remains... 相似文献
To evaluate the association of the different degrees of insomnia symptoms with subsequent incidence of type 2 diabetes mellitus (T2DM).
Methods
The data were extracted from Health and Retirement Study 2006–2014 waves. The association of insomnia symptoms with T2DM incidence was evaluated by the competing risk model with cumulative incidence function (death was considered a competing event) and Cox proportional hazard model with the Kaplan–Meier method. Population attributable fraction (PAF) was calculated. All analyses related to our study were conducted between November 2020 and January 2021.
Results
A total of 14,112 patients were included in this study, with an average follow-up of 6.4 years, and the incidence density was 17.9 per 1000 person-years. Insomnia symptoms were positively associated with T2DM incidence compared with those with no insomnia symptoms, regardless of competing risk model (≥?1 symptoms: sub-distribution hazard ratio (SHR) 1.13; 95% confidence interval (CI) 1.02–1.26; P-trend?=?0.012) and Cox proportional hazard model (≥?1 symptoms: hazard ratio (HR) 1.13; 95% CI 1.02–1.26; P-trend?=?0.013). The cumulative incidence function (Gray’s test, p?<?0.001) and Kaplan–Meier estimate (log-rank test, p?<?0.001) also presented this positive relationship. This positive association was more apparent in women and participants with ages from 50 to 65 years. The PAF was 4.1% with 95% CI (0.7–7.9%).
Conclusions
Insomnia symptoms may be an important risk factor for the development of T2DM, which is unbiased by the death competing risk. These findings suggest that management of sleep problems may be an important part of strategies to prevent T2DM.
Stroke is a leading cause of morbidity and mortality worldwide. Although the majority of strokes affect the elderly, the incidence of stroke in young patients is on the rise. Prompt recognition of stroke symptoms and time critical therapies play a key role in management and prognosis of this condition. This is especially critical in young stroke patients, for whom delays in early recognition and treatment can result in many years of disability with associated social and financial burden. Misdiagnosis and unwarranted variation in treatment of stroke in young patients is problematic. Clinician implicit bias, the unconscious and unintentional process of judgement in healthcare decision-making, is a contributor to the short-falls in outcomes in this population. Interventions in this process have been shown to improve clinical outcomes in young stroke patients and represent an active area of study. 相似文献