Thermal-to-Electrical Conversion Based on Salinity Gradient Driven by Evaporation.

Constructing concentration differences between anions and cations at the ends of an ionic conductor is an effective strategy in electricity generation for powering wearable devices. Temperature gradient or salinity gradient is the driving force behind such devices. But their corresponding power generation devices are greatly limited in actual application due to their complex structure and harsh application conditions. In this study, a novel ionic concentration gradient electric generator based on the evaporation difference of the electrolyte is proposed. The device can be constructed without the need for semipermeable membranes, and operation does not need to build a temperature difference. As a demonstration, a PVA-Na ionic hydrogel is prepared as an electrolyte for the device and achieved a thermovoltage of more than 200 mV and an energy density of 77.94 J m-2 at 323 K. Besides, the device exhibits the capability to sustain a continuous voltage output for a duration exceeding 1500 min, as well as enabling charging and discharging cycles for 100 iterations. For practical applications, a module comprising 16 sub-cells is constructed and successfully utilized to directly power a light-emitting diode. Wearable devices and their corresponding cell modules are also developed to recycle body heat.

Early administration of nifedipine protects against angiotensin II-induced cardiomyocyte hypertrophy through regulating CaMKII-SERCA2a pathway and apoptosis in rat cardiomyocytes.

The calcium channel blocker (CCB), nifedipine, is a more effective treatment for early- than late-stage cardiac hypertrophy. We investigated the effects of early- and late-stage nifedipine administration on calcium homeostasis, CaMKII (Ca(2+) /calmodulin-dependent protein kinase II) activity and apoptosis of cardiomyocytes under hypertrophic stimulation with angiotensin II (AngII). Primary rat cardiomyocytes were divided into five treatment groups: AK, AngII plus the CaMKII inhibitor, KN-93; AN-1 (early-stage), AngII plus nifedipine × 48 h; AN-2 (late-stage), AngII × 48 h, then AngII plus nifedipine × 48 h; C, untreated; and A, AngII × 48 h. The t1/2ß [time required for intracellular Ca(2+) concentration ([Ca(2+) ]i) to decline to one half of the peak value] decreased; however, CaMKII and SERCA2a (sarcoplasmic reticulum Ca(2+) -ATPase 2a) activities increased in the AN-1 group compared with the AK group. In the AN-2 group compared with the AN-1 group, CaMKII activity, t1/2α [time required for [Ca(2+) ]i to increase from the bottom to one half of peak value], t1/2ß, and apoptosis increased. These results indicate that the timing of CCB administration affects the calcium concentration and apoptosis of hypertrophic cardiomyocytes through the CaMKII-SERCA2a signalling pathway, thereby influencing the drug's protective activity against cardiomyocyte hypertrophy.

Association between human cartilage glycoprotein 39 (YKL-40) and arterial stiffness in essential hypertension.

BACKGROUND: YKL-40, a proposed marker of inflammation and endothelial dysfunction, is associated with atherosclerosis and an increased cardiovascular mortality in the general population. However, the relationship between YKL-40 and arterial stiffness in hypertensive patients has not been adequately assessed. METHODS: The relationship between serum levels of YKL-40 and arterial stiffness was evaluated in 93 essential hypertensive subjects and 80 normal subjects. Essential hypertensive subjects were divided into two groups based upon urinary albumin-to-creatinine ratio (ACR): nonmicroalbuminuric group, (ACR <30 mg/g, n = 50) and microalbuminuric group (ACR ≥ 30 mg/g, n = 43). Large artery wall stiffness was assessed by measuring femoral arterial stiffness and carotid-femoral pulse wave velocity (cf-PWV). Serum levels of YKL-40 were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: The study demonstrated that YKL-40,cf-PWV and femoral arterial stiffness were increased significantly (P<0.05) in the hypertensive group compared with normal controls. These measurements were also increased significantly ( P<0.05) in the microalbuminuric group compared with the nonmicroalbuminuric group. YKL-40 was positively correlated with cf-PWV( r = 0.44, P = 0.000) and femoral arterial stiffness ( r = 0.42, P =0.001). Multiple linear stepwise regression analysis showed that YKL-40 was the impact factor of arterial stiffness ( P<0.05). CONCLUSION: YKL-40 levels are elevated in essential hypertension subjects with an independent association between increasing YKL-40 levels and increasing arterial stiffness. The study suggests it played a positive role of YKL-40 in the progressing vascular complications in patients with essential hypertension.

Plasma lipoprotein-associated phospholipase A2 in patients with metabolic syndrome and carotid atherosclerosis.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a recently identified and potentially useful plasma biomarker for cardiovascular and atherosclerotic diseases. However, the correlation between the Lp-PLA2 activity and carotid atherosclerosis remains poorly investigated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the potential role of Lp-PLA2 as a comprehensive marker of metabolic syndrome in individuals with and without carotid atherosclerosis. METHODS: We documented 118 consecutive patients with MetS and 70 age- and sex-matched healthy subjects served as controls. The patients were further divided into two groups: 39 with carotid plaques and 79 without carotid plaques to elucidate the influence of Lp-PLA2 on carotid atherosclerosis. The plasma Lp-PLA2 activity was measured by using ELISA method and carotid intimal-media thickness (IMT) was performed by ultrasound in all participants. RESULTS: Lp-PLA2 activity was significantly increased in MetS subgroups when compared with controls, and was higher in patients with carotid plaques than those without plaques (P < 0.05). Furthermore, we found that significant difference in Lp-PLA2 was obtained between patients with three and four disorders of metabolic syndrome (P < 0.01). Age (ß = 0.183, P = 0.029), LDL-cholesterol (ß = 0.401, P = 0.000) and waist-hip ratio (ß = 0.410, P = 0.000) emerged as significant and independent determinants of Lp-PLA2 activity. Multiple stepwise regression analysis revealed that LDL-cholesterol (ß = 0.309, P = 0.000), systolic blood pressure (ß = 0.322, P = 0.002) and age (ß = 0.235, P = 0.007) significantly correlated with max IMT, and Lp-PLA2 was not an independent predictor for carotid IMT. CONCLUSIONS: Lp-PLA2 may be a modulating factor for carotid IMT via age and LDL-cholesterol, not independent predictor in the pathophysiological process of carotid atherosclerosis in patients with MetS.

[The correlation of human serum Lp-PLA2 and hs-CRP and stability of coronary atherosclerotic plaques].

OBJECTIVE: To explore the relationship of serum lipoprotein-associated phospholipase A2 and high sensitive C-reactive protein in vulnerable coronary atherosclerotic plaques. METHODS: Patients undergoing coronary angiography (CAG) were examined for CAD with intravascular ultrasound (IVUS). According to the findings of CAG and IVUS, all the patients were divided into three groups: a control group without plaque, stable plaque group and vulnerable plaque group. The total serum Lp-PLA2 and hs-CRP were measured before angiography and they were valued with T test and Pearson's correlation analysis. RESULTS: (1) Lp-PLA2 level in stable plaque group and vulnerable plaque group was higher than that in control group (P < 0.05). (2) Lp-PLA2 level in the vulnerable plaque group was higher than that in stable plaque group (P < 0.05). (3) hs-CRP level in the vulnerable plaque group is higher than that in the stable plaque group and control group (P < 0.05) and there was significant difference between them. (4) To discriminate vulnerable plaque, the specificity of serum Lp-PLA2 was stronger than that of hs-CRP. CONCLUSIONS: Serum Lp-PLA2 level has higher sensitivity in predicting the vulnerability of the coronary atherosclerotic plaque than hs-CRP. In combination with hs-CRP, we can use Lp-PLA2 as a new biomarker to predict the presence of vulnerable plaque.

Predictive value of fasting blood glucose for serious coronary atherosclerosis in non-diabetic patients.

OBJECTIVE: To determine if high fasting blood glucose (FBG) level is an independent predictor of serious coronary lesions in patients with coronary artery disease (CAD). METHODS: We enrolled 64 patients who had symptoms of chest discomfort and who underwent coronary angiography. FBG was determined from blood samples and the extent of coronary artery lesions was analyzed according to Gensini score. We examined the relationships among diabetes, FBG, and coronary artery severity. RESULTS: Diabetes and FBG were significantly and positively related to Gensini score. Diabetes, but not FBG, was independently correlated with the occurrence of a Gensini score >41. However, FBG was significantly associated with Gensini score >41 in non-diabetic patients. CONCLUSION: Hyperglycemia is an independent predictor of severe CAD in non-diabetic patients. Clinicians should be aware of this and should carry out appropriate early interventions.

Increased plasma osteoprotegerin levels are associated with the presence and severity of acute coronary syndrome.

OBJECTIVE: The objective of this study was to explore the relationship between increased plasma osteoprotegerin (OPG) levels and acute coronary syndrome (ACS). METHODS: Plasma OPG levels from 85 subjects undergoing coronary artery angiography in three different groups, including ACS (n=45), stable angia pectoris (SAP) (n=20) and normal coronary artery (NCA) (n=20), were detected by ELISA. Twenty-two ascending aorta specimens were surgically taken from 8 ACS, 7 SAP and 7 NCA patients, and OPG mRNA expression in the specimens was detected by RT-PCR. In addition, 10 coronary artery sections each were selected from autopsy archives for the presence of vulnerable atherosclerosis plaques (VP), stable plaques (SP) or no plaques (NP) and OPG protein expression in the sections was detected by immunohistochemistry. RESULTS: Plasma OPG concentrations in the ACS group were significantly higher than those in the SAP or NCA group.The levels of plasma OPG in the 1-, 2- and 3-vessel disease subgroups of ACS were increasingly higher (P < 0.05 or 0.01). Multiple logistic regression analyses revealed a significant independent relation between plasma OPG concentration and the presence of ACS (P = 0.032, odd ratio = 1.006).Ascending aorta specimens from the ACS group had a greater OPG mRNA expression than those from the NCA or SAP group (P < 0.01). Sections with VP had a markedly higher OPG expression than sections with SP or NP (P < 0.05 and P < 0.01, respectively). CONCLUSIONS: Increased plasma osteoprotegerin levels are associated with the presence and severity of acute coronary syndrome.

[Study on the association of thrombin activatable fibrinolysis inhibitor and the Thr325Ile and Thr147Ala polymorphisms of its encoding gene CPB2 in patients with coronary heart disease].

OBJECTIVE: To investigate the association of thrombin activatable fibrinolysis inhibitor (TAFI) and its encoding gene CPB2 polymorphism in patients with coronary heart disease (CHD). METHODS: The CPB2 gene polymorphisms of Thr325Ile and Thr147Ala were analyzed with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in patients of acute myocardial infarction (n=100), acute angina pectoris (n=110) and a control group (n=190). The antigen (Ag) and activity (Act) of the TAFI were determined by sandwich enzyme link immunosorbent assay specific for human TAFI and chromogenic assay for activated human TAFI in plasma, respectively. The relationship between Thr325Ile and Thr147Ala gene polymorphism and TAFI Ag and Act were also analyzed. RESULTS: Plasma TAFI Act and TAFI Ag in acute myocardial infarction group and acute angina pectoris group (CHD patients group) were both significantly higher than those of the control group. The genotype frequencies of Thr325Ile (C1040T) and Thr147Ala (G505A) were as the following: C1040C (Thr325Thr) 67 (31.9%) and 64 (33.6%); C1040T (Thr325Ile) 109 (51.9%) and 92 (48.4%); T1040T (Ile325Ile) 34 (16.2%) and 34(17.8%); G505G (Ala147 Ala) 75 (35.7%) and 72 (37.8%); G505A(Thr147Ala) 112 (53.3%) and 96 (50.5%); A505A(Thr147Thr)23 (10.9%) and 22 (11.7%), in the CHD patients and control respectively. Chi-square analysis showed no significant difference in the Thr325Ile and Thr147Ala polymorphism distributions (P > 0.05). In addition, at the 325 position, the TAFI antigen of the Thr325Thr was higher than that of the other genotypes (Thr325Ile and Ile325Ile, P < 0.05). There was no statistical significance between the TAFI antigen of the Thr325Ile and Ile325Ile (P > 0.05). No significant correlation was found between the TAFI Act and the Thr325Ile polymorphism. At the position 147, significant correlation between the polymorphism of the Thr147Ala and TAFI Ag and Act was not found. CONCLUSION: TAFI plays an important role in anti-fibrinolysis. It might be a risk factor for acute myocardial infarction and acute angina pectoris. The Thr325Ile polymorphism had obvious effect on TAFI antigen levels, but the Thr325Ile and Thr147Ala polymorphism had no association with coronary heart disease.

Ulinastatin attenuates diabetes-induced cardiac dysfunction by the inhibition of inflammation and apoptosis.

Ulinastatin exhibits anti-inflammatory activity and protects the heart from ischemia/reperfusion injury. However, whether ulinastatin has a protective effect in diabetic cardiomyopathy is yet to be elucidated. The aim of the present study was to investigate the protective effects of ulinastatin against diabetic cardiomyopathy and its underlying mechanisms. A C57/BL6J mice model of diabetic cardiomyopathy was used and mice were randomly assigned to three groups: Control group, diabetes mellitus (DM) group and DM + ulinastatin treatment group. Cardiac function was assessed using echocardiography and the level of inflammatory cytokine high mobility group box 1 (HMGB1) expression was measured using histopathological examination and reverse transcription-quantitative polymerase chain reaction. The levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 were measured using western blotting and ELISA. The apoptosis rate in the myocardium was assessed by TUNEL assay. Caspase-3 activation, expression of B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated × (Bax) were measured using western blotting, as was the activity of the mitogen activated protein kinase (MAPK) signaling pathway. The results indicated that ulinastatin significantly improved cardiac function in mice with DM. Ulinastatin treatment significantly downregulated HMGB1, TNF-α and IL-6 expression (P<0.05) and significantly reduced the percentage of apoptotic cardiomyocytes (P<0.05) via reduction of caspase-3 activation and the ratio of Bax/Bcl-2 in diabetic hearts (P<0.05). In addition, ulinastatin attenuated the activation of the MAPK signaling pathway. In conclusion, ulinastatin had a protective effect against DM-induced cardiac dysfunction in a mouse model. This protective effect may be associated with the anti-inflammatory and anti-apoptotic abilities of ulinastatin via the MAPK signaling pathway.

[Plasma activated coagulation factor VII and Msp I polymorphism in elderly patients with coronary heart disease].

OBJECTIVE: To investigate the association of activated coagulation factor VII(F7a) and its gene Msp I polymorphism with coronary heart disease in elderly patients. METHODS: This was a case-control study, and the method of candidate gene was adopted. F7 genotypes were identified with polymerase chain reaction amplified genomic deoxyribonulieic acid (DNA) and Msp I restriction fragment length polymorphism analysis, and the level of plasma F7a was detected with recombinant tissue factor method for 108 elderly patients with coronary heart disease and 120 sex- and age-matched healthy control subjects. RESULTS: (1) Plasma F7a levels was significantly higher in elderly patients with coronary heart disease than in healthy control subjects (2.88 +/- 0.62 vs 2.58 +/- 0.60 microg/L, P < 0.05), and was significantly higher in old myocardial infarction than in stable angina pectoris (3.12 +/- 0.62 vs 2.76 +/- 0.60, P < 0.05). F7a was shown to be a risk factor for coronary heart disease in elderly patients by Logistic regression analysis (OR=1.21 P < 0.05). (2) The allelic frequencies were in accordance with Hardy-Weinberg equilibrium. The results suggested that the distribution of genotype and allelic frequencies in the groups displayed no significant difference, and there was no difference between the subgroups of coronary heart disease in elderly patients, either (P > 0.05). (3) F7a level was significantly higher in RR genotype than in Q allele carriers (2.72 +/- 0.60 vs 1.98 +/- 0.59 microg/L, P < 0.05) and was associated with F7 gene polymorphism. CONCLUSION: Plasma F7a level may be an independent risk factor of coronary heart disease in elderly patients, and it may be influenced by the Msp I polymorphism of F7 gene.