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Objective. Pulse pressure waves contain information about human physiology. There is a need for a simple, accurate way to know cardiovascular health in the clinic, so as to realize the implementation of convenient and effective early health monitoring for patients with arteriosclerosis. Approach. This study proposes an arteriosclerosis assessment method based on fitting a lognormal function, along with improving a conventional electronic sphygmomanometer. During the deflation phase of blood pressure measurement, the cuff pressure was kept constant (40 mmHg) and an additional 10 s of pulse signal was acquired. To derive the pulse pressure waveforms for a single cycle, the acquired pulse data of 101 cases were preprocessed in this study, including filtering for noise removal, onset point identification, removal of baseline drift, and normalization. In this study, an improved pulse resolution algorithm is proposed for the multimodal problem of the pulse wave, combining waveform matching and threshold setting, and finally obtaining the resolution parameters of the lognormal function with an average error less than 1.5%. Main results. According to the correlation analysis, the resolved parameters A 1, W 2, C 2, W 3, and C 3 were significantly correlated with brachial-ankle Pulse Wave Velocity, and the absolute correlation range in 0.17–0.53, which can be used as a reference index for arteriosclerosis. An arteriosclerosis assessment model was constructed based on the support vector mechanism, and the prediction accuracy was 91.1%. Significance. This study provides a new solution idea for the arteriosclerosis assessment method as well as the pulse resolution algorithm, which has a greater reference value. [ABSTRACT FROM AUTHOR]

There are comorbidities and complications in atopic dermatitis and psoriasis that often occur after the appearance of skin inflammation. Statistically, data show that patients with psoriasis and atopic dermatitis have a shorter life expectancy than patients without psoriatic dermatitis, due to the occurrence of arteriosclerosis, myocardial infarction, and cerebral infarction. Many types of skin inflammation are treated with various antibody preparations, and marked improvement in patients' quality of life can be achieved. The next theme is to understand the pathogenesis of arteriosclerosis, myocardial infarction, stroke, and other complications associated with dermatitis and to find treatments and drugs to reduce their occurrence. The skin, a crucial immune organ, generates large amounts of inflammatory cytokines in response to various stimuli, leading to systemic inflammation and potential damage to internal organs. The link between inflammatory skin conditions like psoriasis and atopic dermatitis with serious health complications such as vascular disorders and systemic amyloidosis has been increasingly recognized. In psoriasis, biological treatments targeting Interleukin (IL)-17A, a key cytokine, have shown promise in reducing cardiovascular risks. Recent developments include treatments that target both IL-17A and IL-17F in the psoriasis field, though each cytokine's impact on internal organ damage is still under debate. Among visceral complications secondary to dermatitis, systemic amyloidosis and atherosclerosis have been reported to be controlled by suppressing IL-17 in the early stages of dermatitis. Still, it remains unclear whether suppressing IL-17 prevents organ damage in the late stages of persistent severe dermatitis. A study using a long-lasting dermatitis mouse model that overexpressed human caspase-1 in keratinocytes (Kcasp1Tg) investigated the effects of deleting IL-17A and IL-17F on visceral complications. Cross-mating Kcasp1Tg with IL-17A-, IL-17F-, and IL-17AF-deficient mice assessed the skin and visceral organs histologically, and RT-PCR analysis of aortic sclerosis markers was performed. Despite less improvement in dermatitis, deletion of IL-17A in Kcasp1Tg mice showed promising results in reducing multiple organ amyloidosis. On the other hand, the effect was observed in both IL-17A and IL-17F deleted mice for aortic sclerosis. The inhibition of IL-17A and IL-17F was suggested to reduce the risk of developing comorbidities in internal organs. IL-17A and IL-17F were found to act similarly or produce very different results, depending on the organ. [ABSTRACT FROM AUTHOR]

Background: Coronary artery disease (CAD) significantly contributes to global fatalities. Recent studies have demonstrated the crucial roles of sortilin1 (SORT1) and sestrin1 (SESN1) in lipid metabolism, as well as their involvement in the development of CAD. The aberrant expression or activity of SORT1 can consequently lead to metabolic and vascular diseases. Sestrins, including SESN1, play a crucial role in helping cells survive by maintaining metabolic balance while also reducing oxidative stress (OS). OS contributes to the progression of atherosclerosis-related diseases, such as CAD. The study aimed to compare the gene expression of SORT1 and SESN1 in peripheral blood mononuclear cells (PBMCs), alongside serum OS markers, in CAD patients and controls. Materials: The case-control study included 49 CAD patients and 40 controls. The expression of the SORT1 and SESN1 genes was quantified using qRT-PCR, and the expression of the SORT1 protein was evaluated by western blotting. OS markers, including total oxidation status (TOS), total antioxidant capacity (TAC), and malondialdehyde (MDA), were measured using spectrophotometric and fluorometric methods. Results: SORT1 gene and protein expressions were similar between groups. CAD patients had a non-significant decrease in SESN1 gene expression. MDA levels were significantly higher in CAD patients, whereas TOS and TAC levels did not differ significantly. Conclusion: For atherosclerosis-related disorders like CAD, MDA shows potential as a non-invasive, easy-to-use, affordable, and stable biomarker. Further research is needed to elucidate the precise roles of SORT1 and SESN1 in CAD pathogenesis. [ABSTRACT FROM AUTHOR]

Aim To study the causal relationship between coffee consumption and atherosclerosis risk. Methods Based on the public genome database IEU Open GWAS project website, relevant data were obtained, and instrumental variables closely related to exposure and outcome were screened. Mendelian randomization analysis was performed using the inverse variance weighted method, weighted median method, and MR Egger method to assess the causal relationship between coffee consumption and arteriosclerosis (including coronary atherosclerosis, peripheral atherosclerosis, cerebral atherosclerosis, and other atherosclerosis). In addition, the Egger intercept method was used to detect the level of pleiotropy, the Cochran Q test was used to assess the heterogeneity, and the leave one out method was used to perform sensitivity analysis, so as to ensure the robustness of the results. Results The study showed that the F-values of the instrumental variables included in the study were all greater than 10, and there was no weak instrumental variables bias. Coffee consumption was positively correlated with the risk of coronary atherosclerosis (OR=1. 535 5, 95%CI=1. 108 4 ~ 2. 127 2, P =0. 009 9), peripheral atherosclerosis (OR=2. 098 6, 95%CI=1. 182 2 ~3. 725 7, P =0. 011 4), and other atherosclerosis (OR=1.864 7,95%CI=1.052 9 ~3.302 4, P =0. 032 6), but not with the risk of cerebral atherosclerosis. Heterogeneity test Q_pval>0. 05, level pleiotropy test interval P>0. 05. Conclusions The single nucleotide polymorphisms selected in the study are all strong instrumental variables, and there is no heterogeneity or horizontal pleiotropy, indicating reliable results. The research shows that coffee consumption increases the risk of coronary atherosclerosis, peripheral atherosclerosis and other atherosclerosis, and has no significant correlation with the risk of cerebral atherosclerosis. The health management of atherosclerosis patients should reduce coffee consumption. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of Osteoporosis Self-Assessment Tool for Asia (OSTA) index on brachial ankle pulse wave velocity (baPWV) and its predictive value for peripheral atherosclerosis in menopausal women. Methods A total of 1 138 menopausal women who underwent physical examination at our hospital from January 2022 to December 2022 were enrolled in the study. General clinical data were collected, the OSTA index was calculated, and baPWV was measured. Patients were divided into the control group (n=539) and the peripheral atherosclerosis group (n=599) according to the baPWV values (peripheral atherosclerosis occurs with baPWV ≥1 400 cm/s). Linear regression and Logistic regression were used to analyze the effect of OSTA index on baPWV in menopausal women. The predictive value of peripheral atherosclerosis was evaluated using the receiver operating characteristic (ROC) curve. Results The OSTA index was lower in the peripheral atherosclerosis group than that in the control group [-0.40 (-2.20, 1.00) vs. 0.40 (-0.60, 1.40), P＜0.05]. Univariate linear regression analysis was used to conclude that the OSTA index was an influencing factor of baPWV, and after correcting for risk factors, multivariate linear regression analysis indicated that OSTA index still affected the value of baPWV (P＜0.05). The linear regression equation was baPWV= -27.911-39.752×OSTA+6.444×SBP+7.008×DBP+11.506×HCY+27.942×Hs-CRP. Logistic regression analysis suggested that increased OSTA index was a protective factor for peripheral atherosclerosis (OR= 0.664, 95%CI: 0.535-0.823, P＜0.001). ROC curve analysis suggested that OSTA index was -1.25 as the optimal cutoff point, which predicted peripheral atherosclerosis with an area under the curve of 0.619, a sensitivity of 36.2% and a specificity of 86.3%. Conclusion In menopausal women, OSTA index is an influential factor for baPWV, and increased OSTA index is a protective factor against peripheral atherosclerosis, which can be used to predict baPWV value. [ABSTRACT FROM AUTHOR]

The article examines the prevalence of atherosclerosis in ancient mummified humans, revealing that nearly 40 percent of subjects exhibited vascular calcium across various cultures and eras. Topics discussed include the incidence of atherosclerosis in both elite and non-elite populations, the vascular territories commonly affected, and the implications of these findings for understanding the disease's historical context.

Cerebral microhemorrhages (CMHs, also known as cerebral microbleeds) are a critical but frequently underestimated aspect of cerebral small vessel disease (CSVD), bearing substantial clinical consequences. Detectable through sensitive neuroimaging techniques, CMHs reveal an extensive pathological landscape. They are prevalent in the aging population, with multiple CMHs often being observed in a given individual. CMHs are closely associated with accelerated cognitive decline and are increasingly recognized as key contributors to the pathogenesis of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). This review paper delves into the hypothesis that atherosclerosis, a prevalent age-related large vessel disease, extends its pathological influence into the cerebral microcirculation, thereby contributing to the development and progression of CSVD, with a specific focus on CMHs. We explore the concept of vascular aging as a continuum, bridging macrovascular pathologies like atherosclerosis with microvascular abnormalities characteristic of CSVD. We posit that the same risk factors precipitating accelerated aging in large vessels (i.e., atherogenesis), primarily through oxidative stress and inflammatory pathways, similarly instigate accelerated microvascular aging. Accelerated microvascular aging leads to increased microvascular fragility, which in turn predisposes to the formation of CMHs. The presence of hypertension and amyloid pathology further intensifies this process. We comprehensively overview the current body of evidence supporting this interconnected vascular hypothesis. Our review includes an examination of epidemiological data, which provides insights into the prevalence and impact of CMHs in the context of atherosclerosis and CSVD. Furthermore, we explore the shared mechanisms between large vessel aging, atherogenesis, microvascular aging, and CSVD, particularly focusing on how these intertwined processes contribute to the genesis of CMHs. By highlighting the role of vascular aging in the pathophysiology of CMHs, this review seeks to enhance the understanding of CSVD and its links to systemic vascular disorders. Our aim is to provide insights that could inform future therapeutic approaches and research directions in the realm of neurovascular health. [ABSTRACT FROM AUTHOR]

(1) Objective: To optimize the preparation process of hyaluronic acid-modified ginsenoside Rb1 self-assembled nanoparticles (HA@GRb1@CS NPs), characterize and evaluate them in vitro, and investigate the mechanism of action of HA@GRb1@CS NPs in treating cardiovascular diseases (CVDs) associated with inflammation and oxidative stress. (2) Methods: The optimal preparation process was screened through Plackett–Burman and Box–Behnken designs. Physical characterization of HA@GRb1@CS NPs was conducted using transmission electron microscopy, Fourier-transform infrared spectroscopy, X-ray diffraction, and differential scanning calorimetry. Stability experiments, in vitro drug release studies, and lyophilisate selection were performed to evaluate the in vitro performance of HA@GRb1@CS NPs. The anti-inflammatory and antioxidant capabilities of HA@GRb1@CS NPs were assessed using H9c2 and RAW264.7 cells. Additionally, bioinformatics tools were employed to explore the mechanism of action of HA@GRb1@CS NPs in the treatment of CVDs associated with inflammation and oxidative stress. (3) Results: The optimal preparation process for HA@GRb1@CS NPs was achieved with a CS concentration of 2 mg/mL, a TPP concentration of 2.3 mg/mL, and a CS to TPP mass concentration ratio of 1.5:1, resulting in a particle size of 126.4 nm, a zeta potential of 36.8 mV, and a PDI of 0.243. Characterization studies confirmed successful encapsulation of the drug within the carrier, indicating successful preparation of HA@GRb1@CS NPs. In vitro evaluations demonstrated that HA@GRb1@CS NPs exhibited sustained-release effects, leading to reduced MDA (Malondialdehyde) content and increased SOD (Superoxide Dismutase) content in oxidatively damaged H9c2 cells. Furthermore, it showed enhanced DPPH (2,2-Diphenyl-1-picrylhydrazyl) and ABTS+ [2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)] free radical scavenging rates and inhibited the release of inflammatory factors NO (Nitric Oxide) and IL-6 (Interleukin-6) from RAW264.7 cells. (4) Conclusions: The HA@GRb1@CS NPs prepared in this study exhibit favorable properties with stable quality and significant anti-inflammatory and antioxidant capabilities. The mechanisms underlying their therapeutic effects on CVDs may involve targeting STAT3, JUN, EGFR, CASP3, and other pathways regulating cell apoptosis, autophagy, anti-lipid, and arterial sclerosis signaling pathways. [ABSTRACT FROM AUTHOR]

Introduction: Increasing evidence has indicated a connection between bipolar disorder (BD) and arteriosclerosis (AS), yet the specific molecular mechanisms remain unclear. This study aims to investigate the hub genes and molecular pathways for BD with AS. Methods: BD-related dataset GSE12649 were downloaded from the Gene Expression Omnibus database and differentially expressed genes (DEGs) and key module genes derived from Limma and weighted gene co-expression network analyses (WGCNA) were identified. AS-related genes were sourced from the DisGeNET database, and the overlapping genes between DEGs and AS-related genes were characterized as differentially expressed arteriosclerosis-related genes (DE-ASRGs). The functional enrichment analysis, protein-protein interaction (PPI) network and three machine learning algorithms were performed to explore the hub genes, which were validated with two external validation sets. Additionally, immune infiltration was performed in BD. Results: Overall, 67 DE-ASRGs were found to be overlapping between the DEGs and AS-related genes. Functional enrichment analysis highlighted the cancer pathways between BD and AS. We identified seven candidate hub genes (CTSD, IRF3, NPEPPS, ST6GAL1, HIF1A, SOX9 and CX3CR1). Eventually, two hub genes (CX3CR1 and ST6GAL1) were identified as BD and AS co-biomarkers by using machine learning algorithms. Immune infiltration had revealed the disorder of immunocytes. Discussion: This study identified the hub genes CX3CR1 and ST6GAL1 in BD and AS, providing new insights for further research on the bioinformatic mechanisms of BD with AS and contributing to the diagnosis and prevention of AS in psychiatric clinical practice. [ABSTRACT FROM AUTHOR]

Introduction: Coronary sclerosis is a risk factor for the progression to obstructive coronary artery disease (CAD). However, understanding its impact on the outcomes of patients with myocardial infarction and non-obstructive coronary arteries is limited. This study aimed to explore the prognostic influence of coronary sclerosis on in- and out-of-hospital events in troponin-positive patients with non-obstructive coronary arteries. Methods: This study was a retrospective cohort analysis based on prospectively collected data. A total of 24,775 patients who underwent coronary angiography from 2010 to 2021 in a German university hospital were screened, resulting in a final study cohort of 373 troponin-positive patients with non-obstructive coronary arteries and a follow-up period of 6.2 ± 3.1 years. Coronary sclerosis was defined as coronary plaques without angiographically detectable stenotic lesions of 50% or more in the large epicardial coronary arteries. The primary study endpoint was the occurrence of in-hospital events. Secondary endpoints included events during follow-up. Results: Patients with coronary sclerosis were significantly older (70 ± 12 vs. 58 ± 16 years, p < 0.001), had ST-segment elevation less frequently on electrocardiogram (9.4% vs. 18.7%, p = 0.013), and suffered more often from diabetes mellitus (23.3% vs. 13.1%, p = 0.009), arterial hypertension (79.6% vs. 59.8%, p < 0.001), chronic obstructive pulmonary disease (17.1% vs. 9.4%, p = 0.028), chronic kidney disease (22.2% vs. 8.4%, p < 0.001), atrial fibrillation (19.8% vs. 12.2%, p = 0.045), and valvular diseases than patients without CAD. Patients with coronary sclerosis were more likely to receive medication for primary/secondary prevention on admission and at discharge. The incidence of in- and out-of-hospital events was significantly higher in patients with coronary sclerosis (in-hospital: 42.8% vs. 29.9%, p = 0.010; out-of-hospital: 46.0% vs. 26.1%, p < 0.001). Mortality rates tended to be higher in the coronary sclerosis group (29.4% vs. 20.0%, p = 0.066). Conclusion: Patients diagnosed with coronary sclerosis presented a higher incidence of comorbidities and increased medication use, and experienced higher rates of both in-hospital and out-of-hospital events, primarily due to the clustering of cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

There is limited published data regarding cardiovascular disease in nondomestic felid populations. To address this knowledge gap, necropsy cases of tigers and lions with representative myocardial samples submitted to a diagnostic laboratory were histologically assessed with hematoxylin and eosin and Sirius red stains. A total of 32 submissions (15 tigers, 17 lions) were identified in a 4-year period. All tigers and lions had some degree of coronary artery lesions in the left ventricle and/or interventricular septum. Major findings included moderate to marked arteriosclerosis in 8 tigers (53%) and 4 lions (24%) and moderate to marked perivascular fibrosis in 10 tigers (67%) and 9 lions (53%). Moreover, 10 tigers (67%) and 8 lions (47%) had coronary artery lesions with variable degrees of perivascular cardiomyocyte degeneration and/or loss. To our knowledge, this is the first report describing coronary artery pathology in captive tigers and lions. [ABSTRACT FROM AUTHOR]

BACKGROUND: Apolipoprotein E ε4 allele (APOE-ε4) is the main genetic risk factor for late-onset Alzheimers disease (AD) and may impact cognitive function also via other neuropathological lesions. However, there is limited evidence available from diverse populations, as APOE associations with dementia seem to differ by race. Therefore, we aimed to evaluate the pathways linking APOE-ε4 to cognitive abilities through AD and non-AD neuropathology in an autopsy study with an admixed sample. METHODS: Neuropathological lesions were evaluated following international criteria using immunohistochemistry. Participants were classified into APOE-ε4 carriers (at least one ε4 allele) and non-carriers. Cognitive abilities were evaluated by the Clinical Dementia Rating Scale sum of boxes. Mediation analyses were conducted to assess the indirect association of APOE-ε4 with cognition through AD-pathology, lacunar infarcts, hyaline arteriosclerosis, cerebral amyloid angiopathy (CAA), Lewy body disease (LBD), and TAR DNA-binding protein 43 (TDP-43). RESULTS: We included 648 participants (mean age 75 ± 12 years old, mean education 4.4 ± 3.7 years, 52% women, 69% White, and 28% APOE-ε4 carriers). The association between APOE-ε4 and cognitive abilities was mediated by neurofibrillary tangles (β = 0.88, 95% CI = 0.45; 1.38, p

Abstract Background Coronary artery disease (CAD) significantly contributes to global fatalities. Recent studies have demonstrated the crucial roles of sortilin1 (SORT1) and sestrin1 (SESN1) in lipid metabolism, as well as their involvement in the development of CAD. The aberrant expression or activity of SORT1 can consequently lead to metabolic and vascular diseases. Sestrins, including SESN1, play a crucial role in helping cells survive by maintaining metabolic balance while also reducing oxidative stress (OS). OS contributes to the progression of atherosclerosis-related diseases, such as CAD. The study aimed to compare the gene expression of SORT1 and SESN1 in peripheral blood mononuclear cells (PBMCs), alongside serum OS markers, in CAD patients and controls. Materials The case-control study included 49 CAD patients and 40 controls. The expression of the SORT1 and SESN1 genes was quantified using qRT-PCR, and the expression of the SORT1 protein was evaluated by western blotting. OS markers, including total oxidation status (TOS), total antioxidant capacity (TAC), and malondialdehyde (MDA), were measured using spectrophotometric and fluorometric methods. Results SORT1 gene and protein expressions were similar between groups. CAD patients had a non-significant decrease in SESN1 gene expression. MDA levels were significantly higher in CAD patients, whereas TOS and TAC levels did not differ significantly. Conclusion For atherosclerosis-related disorders like CAD, MDA shows potential as a non-invasive, easy-to-use, affordable, and stable biomarker. Further research is needed to elucidate the precise roles of SORT1 and SESN1 in CAD pathogenesis.

Background In the field of cardiovascular risk assessment, aortic stiffness is considered a key predictive indicator, and carotid-femoral pulse wave velocity (cfPWV) is recognized as the gold standard for non-invasive assessment of atherosclerotic risk in the aorta. Due to challenges such as technical difficulty, cfPWV testing has not been widely implemented in China. Objective This study aimed to develop and validate a screening model for early atherosclerotic risk in the aorta based on cardiovascular risk factors, with the intention of replacing the complex measurement process of cfPWV and reducing reliance on traditional measurement methods. Methods A total of 878 participants recruited from the Health Checkup Center of the First Affiliated Hospital of Anhui Medical University between May and November 2023 were selected as research subjects, randomly divided into a model-building group (n=703) and a validation group (n=175) in an 8∶2 ratio. Patient general information, laboratory test results, and cfPWV were collected. Based on the cfPWV examination results and relevant guidelines, participants in the model-building group were divided into those without atherosclerotic risk in the aorta (n=503) and those with atherosclerotic risk in the aorta (n=200). Multifactorial Logistic regression analysis was used to screen variables and establish a nomogram assessment model. The receiver operating characteristic curve (ROC curve) for predicting the risk of atherosclerosis in the aorta was plotted for the model, and the model's discriminative ability and calibration were assessed using the area under the ROC curve (AUC) and the Hosmer-Lemeshow test, respectively. The Delong test was used to compare the AUCs of different models, and decision curve analysis (DCA) was used to assess the clinical utility of the model. Internal validation of the model was performed using the bootstrap method with 1 000 resampling iterations. Results Participants with atherosclerotic risk in the model-building group were older, had higher BMI, systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), urea, fasting blood glucose (FBG), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), total cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), hemoglobin (Hb), and a higher proportion of alcohol consumption, dyslipidemia, and diabetes than those without atherosclerotic risk in the aorta. The glomerular filtration rate (GFR) and platelet count (PLT) were lower in those with atherosclerotic risk (P0.05). A nomogram model was constructed using age, MAP, FBG, and Hb as predictive factors, with an AUC of 0.941 (95%CI=0.920-0.962) for the training set, sensitivity of 0.832, and specificity of 0.917. The AUC for the validation set was 0.961 (95%CI=0.914-1.000), with sensitivity of 0.872 and specificity of 0.964. DCA results indicated that the use of the early atherosclerosis screening model could benefit participants in clinical practice. Conclusion Based on four simple indexes of age, mean arterial pressure, hemoglobin and fasting blood glucose, a screening model for early aortic sclerosis risk was established, which provides a convenient and efficient method for early vascular function screening.

Weiyong Xu,1,2 Zhenchang Wang,3 Huaqing Yao,1,2 Zifeng Zeng,1,2 Xinping Lan1,2 1Center for Cardiovascular Diseases, Meizhou People’s Hospital, Meizhou, People’s Republic of China; 2Guangdong Provincial Engineering and Technology Research Center for Molecular Diagnostics of Cardiovascular Diseases, Meizhou People’s Hospital, Meizhou, People’s Republic of China; 3Department of Emergency Medicine, Meizhou People’s Hospital, Meizhou, People’s Republic of ChinaCorrespondence: Xinping Lan, Center for Cardiovascular Diseases, Meizhou People’s Hospital, Meizhou Academy of Medical Sciences, Meizhou, People’s Republic of China, Email lan-xinping@163.comObjective: To investigate the distribution of arteriosclerotic vessels of arteriosclerosis, differential serum lipid profiles, and differences in the proportion of dyslipidaemia between patients with single-site arteriosclerosis and multi-site arteriosclerosis (significant hardening of ≥ 2 arteries).Methods: The data of 6581 single-site arteriosclerosis patients and 5940 multi-site arteriosclerosis patients were extracted from the hospital medical record system. Serum total cholesterol (TC), triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein (Apo) A1, ApoB concentrations and C-reactive protein (CRP) between patients with single-site arteriosclerosis and multi-site arteriosclerosis were collected and analyzed.Results: The most diseased arteries were coronary arteries (n=7099, 33.7%), limb arteries (n=6546, 31.1%), and carotid arteries (n=5279, 25.1%). TC, LDL-C, TC/HDL-C, and LDL-C/HDL-C levels were higher and CRP level was lower in multi-site arteriosclerosis patients than those in single-site arteriosclerosis patients. The TC, LDL-C levels in non-elderly (< 65 years old) female patients were higher and TG/HDL-C, TC/HDL-C, LDL-C/HDL-C levels were lower than those in non-elderly male patients, while the TG, TC, LDL-C, and TG/HDL-C levels in elderly (≥ 65 years old) female patients were higher and LDL-C/HDL-C level was lower than those in elderly male patients. The proportion of dyslipidemia in descending order was as follows: low HDL-C (31.9%), elevated TG (16.9%), elevated TC (9.0%), and elevated LDL-C (4.2%). The levels of TC, LDL-C, TC/HDL-C, and LDL-C/HDL-C in patients with peripheral arteriosclerosis were higher than those in patients with cardio-cerebrovascular arteriosclerosis.Conclusion: There were differences in serum lipid levels in patients with arteriosclerosis with different age, gender and distribution of arteriosclerotic vessels.Keywords: arteriosclerosis, arteriosclerotic vessels, dyslipidemia, serum lipid, CRP

IntroductionThe extent to which the Big Five personality traits and subjective well-being (SWB) are discriminatory predictors of clinical manifestation of dementia versus dementia-related neuropathology is unclear.MethodsUsing data from eight independent studies (Ntotal = 44,531; Ndementia = 1703; baseline Mage = 49 to 81 years, 26 to 61% female; Mfollow-up range = 3.53 to 21.00 years), Bayesian multilevel models tested whether personality traits and SWB differentially predicted neuropsychological and neuropathological characteristics of dementia.ResultsSynthesized and individual study results indicate that high neuroticism and negative affect and low conscientiousness, extraversion, and positive affect were associated with increased risk of long-term dementia diagnosis. There were no consistent associations with neuropathology.DiscussionThis multistudy project provides robust, conceptually replicated and extended evidence that psychosocial factors are strong predictors of dementia diagnosis but not consistently associated with neuropathology at autopsy.HighlightsN(+), C(-), E(-), PA(-), and NA(+) were associated with incident diagnosis. Results were consistent despite self-report versus clinical diagnosis of dementia. Psychological factors were not associated with neuropathology at autopsy. Individuals with higher conscientiousness and no diagnosis had less neuropathology. High C individuals may withstand neuropathology for longer before death.