Ellagic acid protects against angiotensin II-induced hypertrophic responses through ROS-mediated MAPK pathway in H9c2 cells.

The early myocardial response of hypertension is an elevation of angiotensin-II (Ang-II) concentration, leading to heart failure and cardiac hypertrophy. This hypertrophic event of the heart is mediated by the interaction of Ang type 1 receptors (AT-R1), thereby modulating NADPH oxidase activity in cardiomyocytes, which alters redox status in cardiomyocytes. Ellagic acid (EA) has anti-inflammatory and anti-oxidative capacities. Thus, EA has potential preventive effects on cardiovascular diseases and diabetes. In the last decades, because the protective effect of EA on Ang-II-induced hypertrophic responses is unclear, this study aims to investigate the protective effect of EA in cardiomyocytes. H9c2 cells were treated to Ang-II 1 µM for 24 h to induce cellular damage. We found that EA protected against Ang-II-increased cell surface area and pro-hypertrophic gene expression in H9c2. EA reduced Ang-II-caused AT-R1 upregulation, thereby inhibiting oxidative stress NADPH oxidase activation. EA mitigated Ang-II-enhanced p38 and extracellular-signal-regulated kinase (ERK) phosphorylation. Moreover, EA treatment under Ang-II stimulation also reversed NF-κB activity and iNOS expression. This study shows that EA protects against Ang-II-induced myocardial hypertrophy and attenuates oxidative stress through reactive oxygen species-mediated mitogen-activated protein kinase signaling pathways in H9c2 cells. Thus, EA may be an effective compound for preventing Ang-II-induced myocardial hypertrophy.

Rhodiola and Salidroside Attenuate Oxidative Stress-Triggered H9c2 Cardiomyoblast Apoptosis Through IGF1R-Induced ERK1/2 Activation.

Oxidative stress is a pivotal factor in the pathogenesis of various cardiovascular diseases. Rhodiola, a traditional Chinese medicine, is recognized for its potent antioxidant properties. Salidroside, a phenylpropanoid glycoside derived from Rhodiola rosea, has shown remarkable antioxidant capabilities. This study aimed to elucidate the potential protective mechanisms of Rhodiola and salidroside against H2O2-induced cardiac apoptosis in H9c2 cardiomyoblast cells. H9c2 cells were exposed to H2O2 for 4 h, and subsequently treated with Rhodiola or salidroside for 24 h. Cell viability and apoptotic pathways were assessed. The involvement of insulin-like growth factor 1 receptor (IGF1R) and the activation of extracellular regulated protein kinases 1/2 (ERK1/2) were investigated. H2O2 (100 µM) exposure significantly induced cardiac apoptosis in H9c2 cells. However, treatment with Rhodiola (12.5, 25, and 50 µg/mL) and salidroside (0.1, 1, and 10 nM) effectively attenuated H2O2-induced cytotoxicity and apoptosis. This protective effect was associated with IGF1R-activated phosphorylation of ERK1/2, leading to the inhibition of Fas-dependent proteins, HIF-1α, Bax, and Bak expression in H9c2 cells. The images from hematoxylin and eosin staining and immunofluorescence assays also revealed the protective effects of Rhodiola and salidroside in H9c2 cells against oxidative damage. Our findings suggest that Rhodiola and salidroside possess antioxidative properties that mitigate H2O2-induced apoptosis in H9c2 cells. The protective mechanisms involve the activation of IGF1R and subsequent phosphorylation of ERK1/2. These results propose Rhodiola and salidroside as potential therapeutic agents for cardiomyocyte cytotoxicity and apoptosis induced by oxidative stress in heart diseases. Future studies may explore their clinical applications in cardiac health.

Sesamin suppresses angiotensin-II-enhanced oxidative stress and hypertrophic markers in H9c2 cells.

Myocardial hypertrophy plays a crucial role in cardiovascular disease (CVD) development. Myocardial hypertrophy is an adaptive response by myocardial cells to stress after cardiac injury to maintain cardiac output and function. Angiotensin II (Ang-II) regulates CVD through the renin-angiotensin-aldosterone system, and its signaling in cardiac myocytes leads to excessive reactive oxygen species (ROS) production, oxidative stress, and inflammation. Sesamin (SA), a natural compound in sesame seeds, has anti-inflammatory and anti-apoptotic effects. This study investigated whether SA could attenuate hypertrophic damage and oxidative injuries in H9c2 cells under Ang-II stimulation. We found that SA decreased the cell surface area. Furthermore, Ang-II treatment reduced Ang-II-increased ANP, BNP, and ß-MHC expression. Ang-II enhanced NADPH oxidase activity, ROS formation, and decreased Superoxide Dismutase (SOD) activity. SA treatment reduces Ang-II-caused oxidative injuries. We also found that SA mitigates Ang-II-induced apoptosis and pro-inflammatory responses. In conclusion, SA could attenuate Ang-II-induced cardiac hypertrophic injuries by inhibiting oxidative stress, apoptosis, and inflammation in H9c2 cells. Therefore, SA might be a potential supplement for CVD management.

Angiotensin II receptor blocker irbesartan attenuates sleep apnea-induced cardiac apoptosis and enhances cardiac survival and Sirtuin 1 upregulation.

BACKGROUND: The purpose of this study was to investigate whether or not angiotensin II type 1 receptor blocker irbesartan (ARB) with a partial agonist of PPAR-γ could protect against chronic nocturnal intermittent hypoxia (CIH)-induced cardiac Fas/FasL-mediated to mitochondria-mediated apoptosis. METHODS: Sprague-Dawley rats were in a normoxic control group (CON-G), or rats were in a chronic nocturnal intermittent hypoxia group (HP-G, from 3 to 7% oxygen versus 21% oxygen per forty seconds cycle, nocturnally 8 h per day for 1 month), or rats were in a chronic nocturnal intermittent hypoxia group pretreated with ARB (50 mg/kg/day, S.C.) (ARB-HP-G). Echocardiography, H&E staining, TUNEL staining, and Western blotting were measured in the left ventricle. RESULTS: Hypoxia-induced SIRT1 degradation, Fas receptors, FADD, active caspase-8 and caspase-3 (Fas/FasL apoptotic pathway) and Bax, tBid, active caspase-9 and -3 (mitochondrial apoptotic pathway) and TUNEL-positive apoptosis were reduced in ARB-HP-G when compared with HP-G. IGF-I, IGF1 receptor, p-PI3k, p-Akt, Bcl2, and Bcl-XL (IGF1/PI3K/AKT pro-survival pathway) were increased in ARB-HP-G compared to HP-G. CONCLUSIONS: Our findings suggest that the ARB may prevent cardiac Fas/FasL to mitochondrial apoptotic pathways and enhance cardiac IGF1/PI3K/AKT pro-survival pathway in the sleep apnea model associated with JNK de-activation and SIRT1 upregulation. ARB prevents chronic sleep apnea-enhanced cardiac apoptosis via enhancing survival pathways.

Exercise Training Enhances BDNF/TrkB Signaling Pathway and Inhibits Apoptosis in Diabetic Cerebral Cortex.

This study aimed to clarify the therapeutic effects of exercise training on neural BDNF/TrkB signaling and apoptotic pathways in diabetic cerebral cortex. Thirty-six male C57BL/6JNarl mice were randomly divided into three groups: control (CON-G), diabetic group (DM-G, 100 mg/kg streptozotocin, i.p.), and diabetic with exercise training group (DMEX-G, Swim training for 30 min/day, 5 days/week). After 12 weeks, H&E staining, TUNEL staining, and Western blotting were performed to detect the morphological changes, neural apoptosis, and protein levels in the cerebral cortex. The Bcl2, BclxL, and pBad were significant decreased in DM-G compared with CON-G, whereas they (excluded the Ras and pRaf1) were increased in DMEX-G. In addition, interstitial space and TUNEL(+) apoptotic cells found increased in DM-G with increases in Fas/FasL-mediated (FasL, Fas, FADD, cleaved-caspase-8, and cleaved-caspase-3) and mitochondria-initiated (tBid, Bax/Bcl2, Bak/BclxL, Bad, Apaf1, cytochrome c, and cleaved-caspase-9) apoptotic pathways. However, diabetes-induced neural apoptosis was less in DMEX-G than DM-G with observed raises in the BDNF/TrkB signaling pathway as well as decreases in Fas/FasL-mediated and mitochondria-initiated pathways. In conclusion, exercise training provided neuroprotective effects via enhanced neural BDNF/TrkB signaling pathway and prevent Fas/FasL-mediated and mitochondria-initiated apoptotic pathways in diabetic cerebral cortex.

Cardiovascular Disease and Possible Ways in Which Lycopene Acts as an Efficient Cardio-Protectant against Different Cardiovascular Risk Factors.

Foods rich in antioxidants such as lycopene have a major role in maintaining cardiac health. Lycopene, 80% of which can be obtained by consuming a common vegetable such as tomato, can prevent the disturbances that contribute to cardiovascular disease (CVD). The present work begins with a brief introduction to CVD and lycopene and its various properties such as bioavailability, pharmacokinetics, etc. In this review, the potential cardio-protective effects of lycopene that reduce the progression of CVD and thrombotic complications are detailed. Further, the protective effects of lycopene including in vitro, in vivo and clinical trials conducted on lycopene for CVD protective effects are explained. Finally, the controversial aspect of lycopene as a protective agent against CVD and toxicity are also mentioned.

Confounded by obesity and modulated by urinary uric acid excretion, sleep-disordered breathing indirectly relates to hyperuricaemia in males: A structural equation model.

Sleep-disordered breathing (SDB) causes hypoxic stress and can trigger uric acid (UA) overproduction. We comprehensively investigated whether SDB, interacting with components of metabolic syndrome, hepatic and renal dysfunctions, low physical fitness, sedentary lifestyle, disrupted sleep, and chronic systemic inflammation (CSI), is directly associated with hyperuricaemia. In 528 community-based males (mean [SD] age 46.2 [7.4] years), we cross-sectionally analysed measures of anthropometry; self-reported lifestyle habits; overnight sleep polysomnography data; cardiopulmonary exercise tests; and biomarkers of cardiometabolic, hepatic, and renal functions; and CSI, using structural equation modelling. Objective disrupted sleep, C-reactive protein, low physical fitness, and sedentary lifestyle were not related to UA levels in univariate analysis and were excluded. The latent variables (with corresponding manifest variables) obesity (body mass index, waist-hip ratio), hypertension (post-sleep systolic, diastolic blood pressure), dyslipidaemia (total cholesterol, triglyceride/high-density lipoprotein cholesterol), hepatic dysfunction (alanine aminotransferase, aspartate transaminase), and renal dysfunction (blood urea nitrogen, serum creatinine) were positively; and hyperglycaemia (fasting glucose, glycated haemoglobin) was negatively associated with hyperuricaemia (serum UA), except for SDB (Apnea-Hypopnea Index, percentage of oxygen saturation <90% period against total sleep time, oxygen desaturation index) in the one-stage influence model. In the two-stage model, SDB, closely interacting with obesity, was positively indirectly associated with hyperuricaemia through directly linked renal dysfunction and obesity-linked hypertension, inverse hyperglycaemia, dyslipidaemia, and hepatic dysfunction. In conclusion, structural equation modelling reveals that SDB closely interacts with obesity and is positively but indirectly related to hyperuricaemia in males. This suggests that urinary UA excretion modulates and obesity confounds the SDB-hyperuricaemia relationship.

Anti-apoptotic and pro-survival effects of longan flower extracts on rat hearts with fructose-induced metabolic syndrome.

The aim of this study was to investigate the effects of longan flower (LF) water extract on cardiac apoptotic and survival pathways in rat models of fructose-induced metabolic syndrome. The study findings revealed that the levels of glucose, insulin, triglyceride, and cholesterol and TUNEL-positive apoptotic cells were significantly increased in the HF group compared with the control group; whereas, the levels were decreased in the HFLF group. The expressions of Fas, FADD, and activated caspases 8 and 3, as well as the expressions of Bax, Bak, Bax/Bcl-2, Bak/Bcl-xL, cytosolic cytochrome c, and activated caspases 9 and 3 were increased in the HF group were significantly reversed in HFLF administrated group. Furthermore, LF extract increased IGF-1R, p-PI3K, p-Akt, Bcl-2, and Bcl-xL expression compared to HF group. Taken together, the present findings help identify LF as a potential cardioprotective agent that can be effectively used in treating fructose-induced metabolic syndrome.

Possible Neuroprotective Mechanisms of Physical Exercise in Neurodegeneration.

Physical exercise (PE) improves physical performance, mental status, general health, and well-being. It does so by affecting many mechanisms at the cellular and molecular level. PE is beneficial for people suffering from neuro-degenerative diseases because it improves the production of neurotrophic factors, neurotransmitters, and hormones. PE promotes neuronal survival and neuroplasticity and also optimizes neuroendocrine and physiological responses to psychosocial and physical stress. PE sensitizes the parasympathetic nervous system (PNS), Autonomic Nervous System (ANS) and central nervous system (CNS) by promoting many processes such as synaptic plasticity, neurogenesis, angiogenesis, and autophagy. Overall, it carries out many protective and preventive activities such as improvements in memory, cognition, sleep and mood; growth of new blood vessels in nervous system; and the reduction of stress, anxiety, neuro-inflammation, and insulin resistance. In the present work, the protective effects of PE were overviewed. Suitable examples from the current research work in this context are also given in the article.

Objective Sleep Measures in Inpatients With Subacute Stroke Associated With Levels and Improvements in Activities of Daily Living.

OBJECTIVE: To investigate whether objective polysomnographic measures of prevalent sleep problems such as sleep-disordered-breathing (SDB) and insomnia are associated with activities of daily living levels in inpatients at rehabilitation units. DESIGN: Retrospective and observational study. SETTING: Single rehabilitation center. PARTICIPANTS: Inpatients with subacute stroke (N=123) (61.6±13.1 years; 23.8±3.4 kg/m2; 33% women; 90.5±36.7 days post-stroke) underwent a 1-night polysomnographic study and a 1-month inpatient rehabilitation program. MAIN OUTCOME MEASURES: Admission and discharge Barthel Index (BI) scores and its change scores. RESULTS: One hundred three (92%) patients had moderate-to-severe SDB (46.7±25.1 events/h in the apnea-hypopnea index), and 24 (19.5%) patients had acceptable continuous positive airway pressure adherence. Diverse values were found for total sleep time (259±71 min), sleep efficiency (69.5%±19.3%), sleep latency (24.3±30.9 min), and wakefulness after sleep onset (93.1±74.2 min). Admission BI scores and the BI change scores were 33.8±23.2 and 10.1±9.2, respectively. The National Institutes of Health Stroke Scale (NIHSS, 10.2±5.6), available in 57 (46%) patients, was negatively associated with admission levels and gains in BI change scores (P<.001, =0.002, respectively) in a univariate analysis. In regression models with backward selection, excluding NIHSS score, both age (P=.025) and wakefulness after sleep onset (P<.001) were negatively associated (adjusted R2=0.260) with admission BI scores. Comorbidity of hypertension; sleep latency percentage of stage 1, non-rapid eye movement sleep; and desaturation events ≥4% (P<.001, 0.001, 0.021, and 0.043, respectively; adjusted R2=0.252) were negatively associated with BI score gains. CONCLUSIONS: Based on objective sleep measures, insomnia rather than SDB in inpatients with subacute stroke was associated negatively with admission levels of activity of daily living and its improvement after a 1-month rehabilitation course.

Cardiovascular Benefits of Exercise Training in Postmenopausal Hypertension.

Exercise training is often considered the cornerstone of nonpharmacological therapy for postmenopausal hypertension while aerobic exercise is the mainstay of life style modification for antihypertension. Moderate-intensity aerobic exercise is well tolerated on most days of the week by most people with postmenopausal hypertension and is not suspected to detract from exercise adherence. That being said, moderate aerobic exercise may be superior for eliciting cardiovascular benefits in hypertensive postmenopausal women and resistance exercise may offer desirable benefits. The beneficial outcomes of exercise training for hypertensive postmenopausal women include improvements in blood pressure, autonomic tone, baroreflex sensitivity, oxidative stress, nitric oxide (NO), bioavailability, and lipid profiles, as well as cardiovascular function and cardiorespiratory fitness. This partly explains the fact that exercise training programs have a positive effect for cardiovascular disease in hypertensive postmenopausal women. This review is to collect and present the literature of exercise training in postmenopausal hypertension. Our review may provide the current understanding of beneficial effects and mechanisms of exercise intervention for prevention and treatment of stage 1 to 2 hypertensive postmenopausal women.

Anti-Renal Fibrotic Effect of Exercise Training in Hypertension.

The purpose of this study was to evaluate the effects of exercise training on renal fibrosis in hypertensive rats. Masson's trichrome staining and Western blotting were performed on the excised renal cortex from sixteen male spontaneously hypertensive rats (SHR), which were randomly divided into either a sedentary hypertensive group (SHR) or exercise hypertensive group (SHR-EX, running on an exercise treadmill for 60 min/day, 5 sessions/week, for 12 weeks), and from eight male Wistar-Kyoto rats which served as a sedentary normotensive group (WKY). The systolic blood pressure (SBP) and renal fibrosis in hypertensive rats improved after exercise training. The inflammatory-related protein levels of interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2), as well as the fibrotic-related protein levels of transforming growth factor-beta (TGF-ß), phospho-Smad2/3 (p-Smad2/3), connective tissue growth factor (CTGF), matrix metalloproteinase-9 (MMP-9), and matrix metalloproteinase-2 (MMP-2) were decreased in the SHR-EX group when compared with the SHR group. Exercise training suppressed the hypertension-induced renal cortical inflammatory and fibrotic pathways in hypertensive rat models. These findings might indicate a new therapeutic effect for exercise training to prevent renal fibrosis in hypertensive nephropathy.

Scaling exponent values as an ordinary function of the ratio of very low frequency to high frequency powers in heart rate variability over various sleep stages.

PURPOSE: To assess the physiological meanings of the detrended fluctuation analysis (DFA) slope α and its relationship to spectral measures in heart rate variability, this study investigated changes of α and its corresponding spectral measures over various night-sleep stages. METHODS: The overall DFA α and natural-logarithm-transformed power values of the spectral parameters ln[high-frequency (HF)], ln[low-frequency (LF)], and ln[very-low-frequency (VLF)], and their relationship from one 5-min proper electrocardiography segment in each of pre-sleep-wakefulness (AWK), non-rapid eye movement stage 2 (N2), slow-wave (N3), the first and the latest rapid-eye movement sleep (REM1, and REM2), were computed in 93 otherwise healthy males (44.1 ± 7.7 years.) with wide-ranged apnea-hypopnea, periodic-limb movement and arousal indices (19.0 ± 20.9, 4.7 ± 9.9, and 10.7 ± 18.2 h, respectively). RESULTS: While ln(HF) dipped from AWK, N2, and N3 to REM1 then rebounded to the origin level at REM2, ln(VLF) dipped from AWK to N2, N3 trough, and then surged to levels surpassing AWKs and N2s at REM1 and REM2. ln(LF/HF), ln(VLF/HF), and α dipped from AWK and N2 to N3 trough, surged to levels surpassing AWKs, and N2s at REM1 then became attenuated at REM2. By general linear modeling, the relationship between α and the corresponding spectral values can be seen over various stages as α = b 0 + 0.147 × ln(VLF/HF) (R (2) = 0.766), regardless of age and sleep-sympathoexcitatory episodes. CONCLUSION: The REM sleep attenuations appeared in ln(HF) and its derivatives, such as ln(LF/HF), ln(VLF/HF), and the overall DFA slope α values. The quantitative function of ln(VLF/HF) describes the α values constantly for overnight sleep stages, and it is not affected by age, LF, PLM, and AHI. Our findings therefore suggest that in sleep studies with spectral HRV measures, ln(VLF/HF) as a surrogate of the overall DFA slope α should be calculated at the same time.

The Coexistence of Hypertension and Ovariectomy Additively Increases Cardiac Apoptosis.

To investigate whether the coexistence of hypertension and ovariectomy will increase cardiac Fas receptor and mitochondrial-dependent apoptotic pathways, histopathological analysis, the TUNEL assay and Western blotting were performed on the excised hearts from three groups of female spontaneously hypertensive rats (SHR), which were divided into a sham-operated group (SHR-Sham), bilaterally ovariectomized group (SHR-OVX) and normotensive Wistar Kyoto rats (WKY). Compared with the WKY group, the SHR-Sham group exhibited decreased protein levels of ERα, ERß, p-Akt/Akt, Bcl-2, Bcl-xL and p-Bad and decreased further in the SHR-OVX group, as well as protein levels of t-Bid, Bak, Bad, Bax, cytochrome c, activated caspase-9 and activated caspase-3 (mitochondria-dependent apoptosis) increased in the SHR-Sham group and increased further in the SHR-OVX group. Compared with the WKY group, protein levels of Fas ligand, TNF-α, Fas death receptors, TNFR1, FADD and activated caspase-8 (Fas receptor-dependent apoptosis) increased in the SHR-Sham group, but did not increase in the SHR-OVX group, except Fas ligand and TNF-α. The coexistence of hypertension and ovariectomy attenuated the estrogen receptor survival pathway and appeared to additively increase the cardiac mitochondria-dependent, but not the Fas receptor-dependent apoptosis pathway, which might provide one possible mechanism for the development of cardiac abnormalities in hypertensive postmenopausal women.

Obstructive sleep apnea rather than diabetes or obesity associated with proteinuria in late mid-aged male workers: a decision tree analysis.

BACKGROUND: Both proteinuria and obstructive sleep apnea (OSA) are associated with cardiovascular events and consequent mortality. To examine whether age, OSA, diabetes, and obesity are potential predictors of proteinuria, a data-driven analysis was performed to delineate a potential categorical classification algorithm. METHODS: In this cross-sectional community-based cohort study, demographic data, blood pressure, serum biochemical analyses, proteinuria via single dipstick urinalysis, and overnight polysomnographies were measured in 300 males with sedentary work styles. RESULTS: Sixty-one (20.3 %) of all these participants had proteinuria. Logistic regression analysis showed that glycated hemoglobin (HbA1c), duration of arterial oxygen saturation <90 %, age, and log high-sensitivity C-reactive protein, but not apnea-hypopnea index (AHI), were responsible for 16.7 % of the variance of proteinuria's presence. A decision tree analysis showed that subjects over 49 years old had a higher risk for proteinuria than those subjects of 49 years old, or less. In the over 49-year-old group, subjects with an AHI >21 events/h had a higher risk for proteinuria; whereas in the 49-year-old and less group, subjects with HbA1c >7 %, or with HbA1c ≤7, and body mass index (BMI) >27.4 kg/m(2) had a higher risk for proteinuria than their counterparts. CONCLUSIONS: AHI was the major determinant responsible for the presence of proteinuria in late mid-aged male workers, while HbA1c and BMI were found in the junior subgroup. By algorithmic analysis, this study provides a comprehensive hierarchical model for better understanding of the correlates of proteinuria and sleep apnea.

Effects of rhodiola crenulata on mice hearts under severe sleep apnea.

BACKGROUND: The goal of this study is to determine if Rhodiola Crenulata (RC) has protective effects on mice hearts with severe sleep apnea model. METHODS: Sixty-four C57BL/6 J mice 5-6 months old were distributed into 4 groups i.e. Control group (21% O2, 24 h per day, 8 weeks, n=16); Hypoxia group (Hypoxia: 7% O2 60 s, 20% O2 alternating 60 s, 8 h per day, 8 weeks, n=16); Hypoxia+90RC and Hypoxia+270RC group (Hypoxia for 1st 4 weeks and hypoxia pretreated 90 mg/Kg and 270 mg/Kg Rhodiola Crenulata by oral gavage per day for 2nd 4 weeks, each n=16). Excised hearts from 4 groups of mice were analyzed for heart weight index changes using H&E staining, TUNEL-positive assays and Western Blotting protein. RESULTS: Cardiac widely dispersed TUNEL-positive apoptotic cells in mice hearts were less in Hypoxia+RC90 and Hypoxia+RC270 than those in Hypoxia. Compared with Hypoxia, the protein levels of Fas ligand, Fas death receptors, Fas-Associated Death Domain (FADD), activated caspase 8, and activated caspase 3 (Fas dependent apoptotic pathways) were decreased in Hypoxia+RC90, Hypoxia+RC270. The protein levels of Bad, Bax, t-Bid, activated caspase 9, activated caspase 3 (mitochondria dependent apoptotic pathway) were less in Hypoxia+RC90, Hypoxia+RC270 than those in hypoxia. The protein levels of Bcl2, Bcl-xL, p-Bad (Bcl2-realted anti-apoptotic pathway) and VEGF, p-PI3k, p-AKT (VEGF-related pro-survival pathway) were higher in Hypoxia+RC90, Hypoxia+RC270 than those in hypoxia. CONCLUSIONS: Our findings suggest that Rhodiola Crenulata have protective effects on chronic intermittent hypoxia-induced cardiac widely dispersed apoptosis via Fas-dependent and mitochondria-dependent apoptotic and VEGF-related pro-survival pathway.

Effects of audio-visual aids on foreign language test anxiety, reading and listening comprehension, and retention in EFL learners.

This study examined the effects of audio-visual aids on anxiety, comprehension test scores, and retention in reading and listening to short stories in English as a Foreign Language (EFL) classrooms. Reading and listening tests, general and test anxiety, and retention were measured in English-major college students in an experimental group with audio-visual aids (n=83) and a control group without audio-visual aids (n=94) with similar general English proficiency. Lower reading test anxiety, unchanged reading comprehension scores, and better reading short-term and long-term retention after four weeks were evident in the audiovisual group relative to the control group. In addition, lower listening test anxiety, higher listening comprehension scores, and unchanged short-term and long-term retention were found in the audiovisual group relative to the control group after the intervention. Audio-visual aids may help to reduce EFL learners' listening test anxiety and enhance their listening comprehension scores without facilitating retention of such materials. Although audio-visual aids did not increase reading comprehension scores, they helped reduce EFL learners' reading test anxiety and facilitated retention of reading materials.

Activated apoptotic and anti-survival effects on rat hearts with fructose induced metabolic syndrome.

Consumption of fructose has been linked to the development of metabolic syndrome, whereas the cardiomyopathic changes and cardiac apoptosis of dietary high-fructose intake have not yet been clarified. The purpose of this study was to evaluate the effects of high-fructose on cardiac apoptotic and survival pathways. Thirty-two Wistar rats were randomly divided into a control group (CON), which received a standard chow diet, and a fructose-induced metabolic syndrome group (FIMS), which received a 50% fructose-content diet for 13 weeks. Histopathological analysis, TUNEL assays and Western blotting were performed on the excised hearts from both groups. The blood pressure, glucose, insulin, triglyceride and cholesterol levels were significantly increased in the FIMS group, compared with the CON group. The abnormal myocardial architecture, enlarged interstitial space and increased cardiac TUNEL-positive apoptotic cells were observed in the FIMS group. The TNF-α, TNF receptor 1, Fas ligand, Fas receptor, FADD, and activated caspase-3 and 8 protein levels (Fas pathway) and the Bax, Bak, Bax/Bcl-2, Bak/Bcl-xL, cytosolic cytochrome c, and activated caspase-3 and nine protein levels (mitochondria pathway) were increased in the FIMS group compared with those in the CON group. The IGFI, IGFI-R, p-PI3K, p-Akt, Bcl-2 and Bcl-xL protein levels (survival pathway) were all significantly decreased in the FIMS group compared with those in the CON group. High-fructose intake elevated blood pressure and glucose levels; moreover, high-fructose diet activated cardiac Fas-dependent and mitochondria-dependent apoptotic pathways and suppressed the survival pathway, which might provide one possible mechanism for developing heart failure in patients with metabolic syndrome.

Cardiac hypertrophy-related pathways in obesity.

Obesity is often associated with the development of cardiac hypertrophy but the hypertrophy-related pathways in obesity remain unknown. The purpose of this study was to evaluate cardiac hypertrophy-related markers, atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), tumor necrosis factor-alpha (TNFα) and hypertrophy-related pathways, interleukin (IL)-6-STAT3, IL-6-MEK5-ERK5 and calcineurin-nuclear factor of activated T-cells (NFAT)3 in the excised hearts from obese rats. Twelve obese Zucker rats were studied at 5-6 months of age and twelve age-matched lean Zucker rats served as the control group. The cardiac characteristics, myocardial architecture, ANP, BNP, TNFα levels, IL-6, STAT3, p-STAT3, MEK5, ERK-5, p-ERK-5, calcineurin and NFAT3 in the left ventricle from the rats were measured by heart weight index, echocardiography, vertical cross section, histological analysis, reverse transcription polymerase chain reaction and western blotting. Compared with the lean control, the whole heart weight, the left ventricule weight, the ratio of the whole heart weight to tibia length, echocardiographic interventricular septum, left ventricular posterior wall thickness, myocardial morphological changes and systolic blood pressure were found to increase in the obese rats. The protein levels of ANP, BNP, TNFα, IL-6, STAT3, p-STAT3, MEK-5, ERK-5, p-ERK 5, calcineurin and NFAT3 were also significantly increased in the hearts of the obese rats. The results showed that the hypertrophy-related markers, ANP, BNP and TNFα, the hypertrophy-related pathways IL-6-STAT3 and IL-6-MEK5-ERK5, and the calcineurin-NFAT3 hypertrophy-related pathways were more active in obese Zucker rats, which may provide possible hypertrophic mechanisms for developing cardiac hypertrophy and pathological changes in obesity.

Evaluation of candidate measures for home-based screening of sleep disordered breathing in Taiwanese bus drivers.

BACKGROUND: Sleepiness-at-the-wheel has been identified as a major cause of highway accidents. The aim of our study is identifying the candidate measures for home-based screening of sleep disordered breathing in Taiwanese bus drivers, instead of polysomnography. METHODS: Overnight polysomnography accompanied with simultaneous measurements of alternative screening devices (pulse oximetry, ApneaLink, and Actigraphy), heart rate variability, wake-up systolic blood pressure and questionnaires were completed by 151 eligible participants who were long-haul bus drivers with a duty period of more than 12 h a day and duty shifting. RESULTS: 63.6% of professional bus drivers were diagnosed as having sleep disordered breathing and had a higher body mass index, neck circumference, systolic blood pressure, arousal index and desaturation index than those professional bus drivers without evidence of sleep disordered breathing. Simple home-based candidate measures: (1) Pulse oximetry, oxygen-desaturation indices by ≥3% and 4% (r = 0.87~0.92); (2) Pulse oximetry, pulse-rising indices by ≥7% and 8% from a baseline (r = 0.61~0.89); and (3) ApneaLink airflow detection, apnea-hypopnea indices (r = 0.70~0.70), based on recording-time or Actigraphy-corrected total sleep time were all significantly correlated with, and had high agreement with, corresponding polysomnographic apnea-hypopnea indices [(1) 94.5%~96.6%, (2) 93.8%~97.2%, (3) 91.1%~91.3%, respectively]. Conversely, no validities of SDB screening were found in the multi-variables apnea prediction questionnaire, Epworth Sleepiness Scale, night-sleep heart rate variability, wake-up systolic blood pressure and anthropometric variables. CONCLUSIONS: The indices of pulse oximetry and apnea flow detection are eligible criteria for home-based screening of sleep disordered breathing, specifically for professional drivers.