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BACKGROUND: Increased exposure to ambient air pollution, especially fine particulate matter [less than or equal to]2.5 [micro]m ([PM.sub.2.5]) is associated with poorer brain health and increased risk for Alzheimer's disease (AD) and related dementias. The locus coeruleus (LC), located in the brainstem, is one of the earliest regions affected by tau pathology seen in AD. Its diffuse projections throughout the brain include afferents to olfactory areas that are hypothesized conduits of cerebral particle deposition. Additionally, extensive contact of the LC with the cerebrovascular system may present an additional route of exposure to environmental toxicants. OBJECTIVE: Our aim was to investigate if exposure to [PM.sub.2.5] was associated with LC integrity in a nationwide sample of men in early old age, potentially representing one pathway through which air pollution can contribute to increased risk for AD dementia. METHODS: We examined the relationship between [PM.sub.2.5] and in vivo magnetic resonance imaging (MRI) estimates of LC structural integrity indexed by contrast to noise ratio ([LC.sub.CNR]) in 381 men [mean age = 67.3; standard deviation (SD) = 2.6] from the Vietnam Era Twin Study of Aging (VETSA). Exposure to [PM.sub.2.5] was taken as a 3-year average over the most recent period for which data were available (average of 5.6 years prior to the MRI scan). We focused on [LC.sub.CNR] in the rostral-middle portion of LC due to its stronger associations with aging and AD than the caudal LC. Associations between [PM.sub.2.5] exposures and LC integrity were tested using linear mixed effects models adjusted for age, scanner, education, household income, and interval between exposure and MRI. A co-twin control analysis was also performed to investigate whether associations remained after controlling for genetic confounding and rearing environment. RESULTS: Multiple linear regressions revealed a significant association between [PM.sub.2.5] and rostral-middle [LC.sub.CNR] (b = -0.16; p = 0.02), whereby higher exposure to [PM.sub.2.5] was associated with lower [LC.sub.CNR]. A co-twin control analysis found that, within monozygotic pairs, individuals with higher [PM.sub.2.5] exposure showed lower [LC.sub.CNR] (b = - 0.11; p = 0.02), indicating associations were not driven by genetic or shared environmental confounds. There were no associations between [PM.sub.2.5] and caudal [LC.sub.CNR] or hippocampal volume, suggesting a degree of specificity to the rostral-middle portion of the LC. DISCUSSION: Given previous findings that loss of LC integrity is associated with increased accumulation of AD-related amyloid and tau pathology, impacts on LC integrity may represent a potential pathway through which exposure to air pollution increases AD risk. https://doi.org/10.1289/EHP14344, Introduction Neuropathological studies indicate that abnormal tau may first appear in the locus coeruleus (LC) starting early in life, (1,2) with substantial accumulation occurring during the course of Alzheimer's disease [...]

Objective To investigate the improvement effect of adding heparin sodium saline at different time points on the occurrence of severe dialyzer coagulation in maintenance hemodialysis (MHD) patients during dialysis. Methods Patients who underwent MHD treatment at the dialysis center of Xiyuan Hospital from November 2021 to November 2022 and experienced severe coagulation with dialyzers within 2 hours of treatment were included in the study. Electronic medical records were consulted to collect baseline data, data on various dialysis parameters, and relevant case records. According to the time point of adding heparin sodium, it was divided into two groups: the treatment group and the control group. Both groups were treated with 200 mL of physiological saline first, while the treatment group was treated with 1 mL of 625 U/mL (5 mg/mL) heparin sodium saline added to the dialysis machine heparin pump before re infusion of blood, and a maintenance dose of 1 mL/h was given until the dialysis was stopped 30 minutes before the end of dialysis; The control group received the same dose of heparin sodium salt solution added by the same method after re inducing blood. Compare the improvement effect of two sets of processes on severe coagulation dialyzers. Results A total of 12 MHD patients were included in this study. The treatment group consisted of 6 patients who completed 4 hours of normal dialysis treatment, while the control group consisted of 4 patients who completed normal treatment, and 2 patients who returned to the machine early due to severe coagulation in the dialyzer and vascular system. After dismounting, the coagulation level was evaluated. In the treatment group, 4 patients with no coagulation were classified as 0 level; Two patients had grade 1 coagulation on the dialyzer. In the control group, two dialyzers showed grade 3 coagulation, and there were small amounts of clots in both the arterial and venous ampulla; Three dialyzers showed grade 2 coagulation; One dialyzer showed grade 1 coagulation. There was a statistically significant difference (P＜0. 05) in the evaluation of coagulation grade between the two groups. Conclusion The method of adding heparin sodium saline before re infusion of blood can effectively alleviate the severe coagulation condition of the dialyzer, restore the function of dialyzer, and avoid blood loss, which is better than the method of adding heparin sodium saline after re infusion of blood to start extracorporeal circulation. (目的 探究不同时间点追加肝素钠盐水对维持性血液透析(MHD)患者透析中发生透析器重度凝血的改善作用。方法 纳入2021年11—至2022年11月中国中医科学院西苑医院透析中心进行MHD治疗, 在治疗开始2 h内发生透析器重度凝血的患者, 查阅电子病历收集患者基线资料、透析中各参数资料、相关病例记录。根据追加肝素钠的时间点分为治疗组和对照组两组。两组均采用先回冲200 mL生理盐水, 治疗组采用再次引血前通过透析机肝素泵追加浓度为625 U/mL(5 mg/mL)的肝素钠盐水1 mL并给予维持量1 mL/h, 直至透析结束前30min停止; 对照组采用再次引血后通过同种方法追加相同剂量肝素钠盐水。比较两组流程对重度凝血透析器的改善作用。结果 本研究共纳入12例MHD患者, 治疗组6例患者均完成4 h正常透析治疗, 对照组中4例完成正常治疗, 2例因透析器及血管路重度凝血提前回血下机。下机后凝血等级评估, 治疗组中, 4例患者无凝血为0级; 2例患者透析器1级凝血。对照组中, 2例透析器为3级凝血, 动脉壶、静脉壶均存在少量凝血块; 3例透析器为2级凝血; 1例透析器为1级凝血。凝血等级评估经比较两组存在统计学差异(P＜0. 05)。结论 于再次引血前追加肝素钠盐水的方法, 可以有效缓解透析器重度凝血的状况, 恢复透析器的功能, 避免血液丢失, 优于再次引血开始体外循环后再追加的方式。)

We propose the hypothesis that small high-density lipoprotein (HDL) particles reduce the risk of Alzheimers disease (AD) by virtue of their capacity to exchange lipids, affecting neuronal membrane composition and vascular and synaptic functions. Concentrations of small HDLs in cerebrospinal fluid (CSF) and plasma were measured in 180 individuals ≥60 years of age using ion mobility methodology. Small HDL concentrations in CSF were positively associated with performance in three domains of cognitive function independent of apolipoprotein E (APOE) ε4 status, age, sex, and years of education. Moreover, there was a significant correlation between levels of small HDLs in CSF and plasma. Further studies will be aimed at determining whether specific components of small HDL exchange across the blood, brain, and CSF barriers, and developing approaches to exploit small HDLs for therapeutic purposes.

Most actions targeting children's health behaviors have limited involvement of children in the development, potentially contributing to disappointing effectiveness. Therefore, in the 3-year "Kids in Action" study, 9- to 12-year-old children from a lower-socioeconomic neighborhood were involved as coresearchers in the development, implementation, and evaluation of actions targeting health behaviors. The current study describes the controlled trial that evaluated the effects on children's energy balance-related behaviors, physical fitness, and self-rated health, as well as experienced challenges and recommendations for future evaluations. Primary school children from the three highest grades of four intervention and four control schools were eligible for participation. Outcome measures assessed at baseline, and at 1- and 2-year follow-up were as follows: motor fitness by the MOPER test (N = 656, N = 485, N = 608, respectively), physical activity and sedentary behavior by accelerometry (N = 223, N = 149, N = 164, respectively), and consumption of sugar sweetened beverages and snacks and self-rated health by a questionnaire (N = 322, N = 281, N = 275, respectively). Mixed-model analyses were performed adjusted for clustering within schools and relevant confounders. Significant beneficial intervention effects were found on self-reported consumption of energy/sports drinks at T2 versus T0, and on total time and [greater than or equal to]5-minute bouts of moderate-to-vigorous physical activity at T1 versus T0. Significant adverse effects were found on "speed and agility" and "coordination and upper-limb speed." No other significant effects were found. The inconsistent intervention effects may be explained by the dynamic cohort and suboptimal outcome measures. We advise future studies with a similar approach to apply alternative evaluation designs, such as the delayed baseline design.

In this study, headspace solid phase microextraction-gas chromatography-mass spectrometry (HS-SPME-GC-MS) and gas chromatography-olfactory (GC-O) were applied to identify and analyze the volatile aroma compounds of the ethanol extract of figs. Its key characteristic flavor compounds were analyzed by odor activity (OAV) and aroma recombination and omission tests. The results showed that a total of 40 volatile aroma components were identified, of which 18 compounds, such as isobutyrate, γ-butyl lactone, aromatic camphor, nonaldehyde, vanillin and furfural, were important aroma components in the fig extract (OAV > 1). The aroma recombination experiments showed that the sensory properties of the recombined samples, which had typical aroma characteristics such as fruity, sweet, baked and burnt sweet with slight sour, ointment-like and milky, were similar to those of the fig extract. Furthermore, the aroma omission experiments identified gamma-hexanoate, ethyl palmitate, phenmethanol, aromatic camphor, vanillin, benzaldehyde, 4-hydroxy-2,5-dimethyl-3 (2H)-furan, 5-hydroxymyfuran, and methyl cyclopentanolone as key characteristic flavor compounds of the fig extract. The findings of this study provide a theoretical basis for the development and quality control of fig characteristic flavorings.

Exposures to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) have been associated with the emergence of depressive symptoms in older adulthood, although most studies used cross-sectional outcome measures. Elucidating the brain structures mediating the adverse effects can strengthen the causal role between air pollution and increasing depressive symptoms. We evaluated whether smaller volumes of brain structures implicated in late-life depression mediate associations between ambient air pollution exposure and changes in depressive symptoms. This prospective study included 764 community-dwelling older women (aged 81.6 ± 3.6 in 2008-2010) from the Women's Health Initiative Memory Study (WHIMS) Magnetic Resonance Imaging study (WHIMS-MRI; 2005-06) and WHIMS-Epidemiology of Cognitive Health Outcomes (WHIMS-ECHO; 2008-16). Three-year average annual mean concentrations (scaled by interquartile range [IQR]) of ambient PM2.5 (in μg/m3; IQR = 3.14 μg/m3) and NO2 (in ppb; IQR = 7.80 ppb) before WHIMS-MRI were estimated at participants' addresses via spatiotemporal models. Mediators included structural brain MRI-derived grey matter volumes of the prefrontal cortex and structures of the limbic-cortical-striatal-pallidal-thalamic circuit. Depressive symptoms were assessed annually by the 15-item Geriatric Depression Scale. Structural equation models were constructed to estimate associations between exposure, structural brain volumes, and depressive symptoms. Increased exposures (by each IQR) were associated with greater annual increases in depressive symptoms (βPM2.5 = 0.022; 95% Confidence Interval (CI) = 0.003, 0.042; βNO2 = 0.019; 95% CI = 0.001, 0.037). The smaller volume of prefrontal cortex associated with exposures partially mediated the associations of increased depressive symptoms with NO2 (8%) and PM2.5 (13%), and smaller insula volume associated with NO2 contributed modestly (13%) to the subsequent increase in depressive symptoms. We demonstrate the first evidence that the smaller volumes of the prefrontal cortex and insula may mediate the subsequent increases in depressive symptoms associated with late-life exposures to NO2 and PM2.5.

BackgroundWhether racial/ethnic disparities in Alzheimer's disease (AD) risk may be explained by ambient fine particles (PM2.5) has not been studied.MethodWe conducted a prospective, population-based study on a cohort of Black (n = 481) and White (n = 6 004) older women (aged 65-79) without dementia at enrollment (1995-1998). Cox models accounting for competing risk were used to estimate the hazard ratio (HR) for racial/ethnic disparities in AD (1996-2010) defined by Diagnostic and Statistical Manual of Mental Disorders, 4th edition and the association with time-varying annual average PM2.5 (1999-2010) estimated by spatiotemporal model.ResultsOver an average follow-up of 8.3 (±3.5) years with 158 incident cases (21 in Black women), the racial disparities in AD risk (range of adjusted HRBlack women = 1.85-2.41) observed in various models could not be explained by geographic region, age, socioeconomic characteristics, lifestyle factors, cardiovascular risk factors, and hormone therapy assignment. Estimated PM2.5 exposure was higher in Black (14.38 ± 2.21 µg/m3) than in White (12.55 ± 2.76 µg/m3) women, and further adjustment for the association between PM2.5 and AD (adjusted HRPM2.5 = 1.18-1.28) slightly reduced the racial disparities by 2%-6% (HRBlack women = 1.81-2.26). The observed association between PM2.5 and AD risk was ~2 times greater in Black (HRPM2.5 = 2.10-2.60) than in White (HRPM2.5 = 1.07-1.15) women (range of interaction ps: