ObjectivesThe association between sleep duration and serum lipid profile in the middle-aged and the elderly is unclear. The aim of this study was to investigate and evaluate the relationships between ...sleep duration and levels of serum total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C) and triglycerides in these populations.DesignCross-sectional observational study.SettingCommunity-based investigation in Guishan Township of northern Taiwan.ParticipantsA total of 400 community-dwelling middle-aged and elderly individuals were enrolled. All participants underwent a baseline assessment in 2014, which included anthropometrics, blood samples and self-administered questionnaires. Participants were classified into three groups based on their sleep duration.Outcome measuresMultivariate logistic regression was used to obtain ORs and 95% CIs to assess the relationship between sleep duration and lipid profiles.ResultsParticipant mean age was 64.5 years and 35.3% were men. Subjects with longer (>7 hours) and shorter (<6 hours) nightly sleep duration had a higher prevalence of low HDL-C levels (HDL <40 mg/dL) than those with moderate sleep duration (6–7 hours). Multivariate logistic regression revealed that, compared with individuals with sleep duration of 6–7 hours, the ORs of having low HDL-C were 3.68 (95% CI 1.59 to 8.49) greater for individuals with sleep duration of <6 hours and 2.89 (95% CI 1.10 to 7.61) greater for individuals with sleep duration of >7 hours.ConclusionsThere was a U-shaped relationship between sleep duration and HDL-C levels. Sleep duration >7 hours or <6 hours increased the risk of low serum HDL-C levels.
•VFR and WC were more strongly associated with high CVD risk than BMI among middle-aged and elderly persons.•Abdominal obesity indices like VFR and WC are stronger predictors than BMI of predicting ...high CVD risk.•The cut-off points of VFR and WC indicating high CVD risk are 12.5 and 82.50 cm for male; 7.5 and 80.75 cm for female.
The aim was to investigate the relationships between visceral fat rating scale (VFR), waist circumference (WC), body mass index (BMI) and cardiovascular disease (CVD) risk.
In this cross-sectional, community-based study, participants completed questionnaire that included personal and medical history, and underwent anthropometric measurement and blood sampling. The 2008 general CVD risk model was used to predict CVD risk. Associations between CVD risk and VFR, WC, BMI were evaluated by means of analysis of covariance (ANCOVA) with gender as covariate, Chi-squared test, Pearson’s correlation, Cochran-Armitage test, multivariate logistic regression and receiver operating characteristic curves.
A total of 377 people were enrolled. A significant association was identified between VFR, WC, BMI, and CVD risk, with coefficient of determination (r2) of 0.32 (p < 0.001), 0.18 (p < 0.001) and 0.03 (p = 0.001), respectively. There was a trend toward increasing prevalence of high CVD risk as VFR, WC, and BMI increased (all p values <0.05). Multivariate logistic regression revealed VFR (OR = 1.21; 95%CI = 1.02–1.24), WC (OR = 1.07; 95%CI = 1.04–1.11) and BMI (OR = 1.11; 95%CI = 1.02–1.21) to be independent predictors of high CVD risk. In male, the area under curves of VFR and WC are greater than BMI: 0.641, 0.647 and 0.562. In female, the area under curves of VFR and WC are also greater than BMI: 0.656, 0.688 and 0.601.
VFR and WC were more strongly associated with high CVD risk than BMI among middle-aged and elderly persons in Taiwan.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Background: Both inflammation and chronic kidney disease (CKD) are related to cardiovascular disease. Whether inflammatory biomarkers are associated with impaired glomerular filtration rate (GFR) is ...unclear in hypertensives. Methods:We recruited hypertension patients fromthe cardiovascular clinic of a tertiarymedical center in Taiwan. GFR was calculated using the 7-item Modification of Diet in Renal Disease (MDRD) study equation and impaired GFR (IGFR) was defined as GFR less than 60 ml/min/1.73 m2. High-sensitivity C-reactive protein (hsCRP) kits were used for the measurement of the CRP levels. Results: In our study, 572 consecutive hypertensive patients were enrolled. The range of patient age was 26-91 years (mean 60.5 11.7), and hsCRP and GFR ranged from 0.01 to 9.99 mg/L and 16.6 to 239.6 ml/min//1.73 m2, respectively. HsCRP levels were correlated with GFR (p = 0.01) and the presence of IGFR (p = 0.009). Multivariate regression analysis showed hsCRP (p = 0.03), age (p ＜ 0.001) and urinary albumin-to-creat
Both inflammation and chronic kidney disease (CKD) are related to cardiovascular disease. Whether inflammatory biomarkers are associated with impaired glomerular filtration rate (GFR) is unclear in ...hypertensives.
We recruited hypertension patients from the cardiovascular clinic of a tertiary medical center in Taiwan. GFR was calculated using the 7-item Modification of Diet in Renal Disease (MDRD) study equation and impaired GFR (IGFR) was defined as GFR less than 60 ml/min/1.73 m(2). High-sensitivity C-reactive protein (hsCRP) kits were used for the measurement of the CRP levels.
In our study, 572 consecutive hypertensive patients were enrolled. The range of patient age was 26-91 years (mean 60.5 ± 11.7), and hsCRP and GFR ranged from 0.01 to 9.99 mg/L and 16.6 to 239.6 ml/min//1.73 m(2), respectively. HsCRP levels were correlated with GFR (p = 0.01) and the presence of IGFR (p = 0.009). Multivariate regression analysis showed hsCRP (p = 0.03), age (p < 0.001) and urinary albumin-to-creatinine ratio (UACR) (p = 0.002) are independent factors associated with GFR. Furthermore, hsCRP levels odds ratio (OR) = 1.16, 95% CI = 1.03-1.31, p = 0.02, age (OR = 1.09, 95% CI = 1.07-1.12, p < 0.001), and UACR (OR = 1.02, 95% CI = 1.01-1.04, p < 0.001) independently predicted the presence of IGFR using binary logistic regression analysis.
Information obtained from our study showed that hsCRP is associated with IGFR in hypertensives.
Chronic kidney disease; C-reactive protein; Glomerular filtration rate; Hypertension; Inflammation.
Nonapnea sleep disorders (NASDs) and associated problems, which are highly prevalent in patients with kidney diseases, are associated with unfavorable medical sequelae. Nonetheless, whether NASDs are ...associated with acute kidney injury (AKI) development has not been thoroughly analyzed. We examined the association between NASD and AKI. We conducted a population-based study by using 1,000,000 representative data from the Taiwan National Health Insurance Research Database for the period from January 1, 2000, to December 31, 2010. We studied the incidence and risk of AKI in 9178 newly diagnosed NASD patients compared with 27,534 people without NASD matched according to age, sex, index year, urbanization level, region of residence, and monthly income at a 1:3 ratio. The NASD cohort had an adjusted hazard ratio (hazard ratio HR; 95% confidence interval CI = 1.15-2.63) of subsequent AKI 1.74-fold higher than that of the control cohort. Older age and type 2 diabetes mellitus were significantly associated with an increased risk of AKI (P < 0.05). Among different types of NASDs, patients with insomnia had a 120% increased risk of developing AKI (95% CI = 1.38-3.51; P = 0.001), whereas patients with other sleep disorders had a 127% increased risk of subsequent AKI (95% CI = 1.07-4.80; P = 0.033). Men with NASDs were at a high risk of AKI (P < 0.05). This nationwide population-based cohort study provides evidence that patients with NASDs are at higher risk of developing AKI than people without NASDs.
We screened 26 bisphosphonates against a farnesyl diphosphate synthase from Plasmodium vivax, finding a poor correlation between enzyme and cell growth inhibition (R 2 = 0.06). To better predict cell ...activity data, we then used a combinatorial descriptor search in which pIC50(cell) = a pIC50(enzyme) + bB + cC + d, where B and C are descriptors (such as SlogP), and a−d are coefficients. R 2 increased from 0.01 to 0.74 (for a leave-two-out test set of 26 predictions). The method was then further validated using data for nine other systems, including bacterial, viral, and mammalian cell systems. On average, experimental/predicted cell pIC50 correlations increased from R 2 = 0.28 (for an enzyme-only test set) to 0.70 (for enzyme plus two descriptor test set predictions), while predictions based on scrambled cell activity had no predictive value (R 2 = 0.13). These results are of interest since they represent a general way to predict cell from enzyme inhibition data, with in three cases, R 2 values increasing from ∼0.02 to 0.72.
•ACME could restore fatty acid storage in non-induced HSCs.•ACME inhibited several biomarker of the activated HSC.•Antrodia cinnamomea could use as an functional food for the prevention of liver ...fibrosis.
The direct modulation of Antrodia cinnamomea (AC) on the prominent role of liver fibrosis-hepatic stellate cells (HSCs) in situ remains unclear. Firstly, the administration of A. cinnamomea mycelial extract (ACME) could improve liver morphology and histological changes including collagen formation and GPT activity in the liver of thioacetamide (TAA)-injured rats. The morphology and fatty acid restore of TAA-induced HSCs (THSCs) returned to the non-chemical induced HSCs (NHSCs) type as measured by immunofluorescence and Oil Red O staining. PPARγ was upregulated associated with the lowering of α-SMA protein in NHSC-ACME. ACME inhibited the MMP-2 activity in NHSCs by gelatin Zymography. After LC–MS/MS, the cytoskeleton (tubulin, lamin A) and heat shock protein 8 in NHSC-ACME, and guanylate kinase, brain-specific kinase, SG-II and p55 proteins were downregulated in THSC-ACME. Whereas MHC class II, SMC6 protein, and phospholipase D were upregulated in NHSC-ACME. Furthermore, PKG-1 was downregulated in NHSC-ACME and upregulated in THSC-ACME. SG-II and p55 proteins were downregulated in NHSC-ACME and THSC-ACME by Western blotting. Taken together, the beneficial effect of A. cinnamomea on the induction of HSC cellular proteins is potentially applied as an alternative and complementary medicine for the prevention and amelioration of a liver injury.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
In multiple cervical root transection injuries, motor and sensory recovery has been demonstrated after repairing both dorsal and ventral roots with autologous grafts applied to the dorsal and ventral ...aspects, respectively. However, in clinical situations, autologous grafts may not be sufficient to repair both roots in this situation. In this study, the authors evaluated whether repairing ventral root alone is sufficient for simultaneous sensory and motor function recovery.
In the transected group, the left 6th–8th cervical roots were pulled and transected at the spinal cord junction. In the repair group, the transected root was anastomosed to a single autologous nerve graft, which was inserted into the ventral horn through a pial incision. Acidic fibroblast growth factor mixed with fibrin glue was applied to the surgical area. Motor function, sensory function, cortical somatosensory evoked potentials (SSEPs), axon tracing, and CGRP+ fibers were evaluated.
The repaired rats exhibited simultaneous sensory and motor function recovery. At the 16th weeks, SSEPs reappeared in all animals of the repair group, but not in the transected group. Retrograde axon tracing demonstrated an increased number of sensory neurons in the dorsal root ganglia and regenerating nerve fibers in the dorsal horn. CGRP+ fibers were significantly increased in the repair group and restricted to laminae I and II.
This is the first report that in multiple root avulsions with insufficient grafts, repairing ventral roots alone leads to both sensory recovery and motor recovery. This finding may help patients with multiple cervical root avulsions.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Abstract only Metabolic syndrome-induced cardiomyopathy is a significant risk factor for cardiovascular diseases (CVDs). The proximal tubular cells of the kidney play a crucial role in regulating ...glucose and lipid metabolism. Mitochondrial dysfunction in these cells has been linked to the development of metabolic syndrome-induced cardiac dysfunction. AKT1, a serine/threonine protein kinase, regulates mitochondrial function. In this study, we investigated the effects of renal proximal tubular mitochondrial AKT1 on metabolic syndrome-induced cardiomyopathy in transgenic mice. We generated transgenic mouse lines, KMioxCAKT, with inducible overexpression of mitochondrial AKT1, specifically in renal proximal tubular cells. One line was induced with tamoxifen, while the other was with corn oil. Both lines were fed a high-fat diet (HFD) for 16 weeks to provoke metabolic syndrome. For renal function, although serum BUN ( p= 0.728 ) and creatinine ( p=0.622 ) were not changed, the proteinuria ( p=0.031 ) and the urine KIM-1 ( p=0.012 ) were decreased in tamoxifen-induced KMioxCAKT. The glomerulosclerosis index ( p =0.027), tubulointerstitial fibrosis score ( p =0.032), tubular dilatation score ( p =0.032), tubular vacuolation score ( p =0.031), and tubular casts ( p =0.018) of renal histology were amended in tamoxifen-induced KMioxCAKT. The fasting glucose level ( p =0.015); the 15 to 120 minutes glucose levels ( p =0.020); the fasting insulin level ( p=0.037 ), and insulin resistance measured by Homeostatic Model Assessment for Insulin Resistance ( p=0.005 ) were reduced in metabolic syndrome with augmentation of renal tubular mitochondrial AKT1. In addition, tamoxifen-induced KMioxCAKT mice had significantly attenuated cardiac hypertrophy in the heart compared to corn oil-induced KMioxCAKT. Our results suggest that enhancing renal proximal tubular mitochondrial AKT1 could ameliorate the cardiorenal metabolic syndrome.
The molecular mechanism leading to the transdifferentiation of hepatic stellate cells (HSC) into myofibroblast-like cells following liver injury is not well understood. The state of cultured rat HSCs ...was determined using primarily fluorescence microscopy (UV), immunofluorescence (IF) (Glial fibrillary acidic protein (GFAP), Desmin, alpha-smooth muscle actin (alpha-SMA), F-actin) and immunocytochemistry (ICC) (GFAP, Desmin, alpha-SMA, Fibulin-2). Additionally, tapping-mode atomic force microscopy (TM-AFM) and field-emission scanning electron microscopy (FE-SEM) with low-resistivity indium-tin-oxide (ITO) thin-film were performed to observe the micro-morphological character of cells during HSC differentiation. Quiescent HSCs changed to the activated state were identified via UV, IF, and ICC observations. Normal rat HSCs (NHSCs) and thioacetamide-induced rat HSCs (THSCs) were demonstrated to be UV
−, GFAP
+, Desmin
+, alpha-SMA
+ and Fibulin-2
−. After F-actin staining, lamellipodia and filopodia were found in both NHSCs and THSCs, but membrane ruffles were only seen in THSCs. The micro-structures of lamellipodia and filopodia in both NHSCs and THSCs were confirmed using FE-SEM and TM-AFM with ITO; in contrast, the micro-projection was not found. Moreover, “aerial root” structures were observed for the first time in the filopodia of THSCs using TM-AFM. These results reveal that HSC transdifferentiation to a myofibroblastic-like cell (activated HSC) from thioacetamide-induced rat HSC induces extensive changes in the cytoskeleton.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
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