Metal Sulfide S-Scheme Homojunction for Photocatalytic Selective Phenylcarbinol Oxidation.

Metal sulfide-based homojunction photocatalysts are extensively explored with improved photocatalytic performance. However, the construction of metal sulfide-based S-scheme homojunction remains a challenge. Herein, the fabrication of 2D CdIn2S4 nanosheets coated 3D CdIn2S4 octahedra (referred to as 2D/3D n-CIS/o-CIS) S-scheme homojunction photocatalyst is reported by simply adjustment of polyvinyl pyrrolidone amount during the solvothermal synthesis. The formation of S-scheme homojunction within n-CIS/o-CIS is systematically investigated via a series of characterizations, which can generate an internal electric field to facilitate the separation and migration of photogenerated electron-hole pairs. The 2D/3D n-CIS/o-CIS composite exhibits significantly improved photocatalytic activity and stability in the selective oxidation of phenylcarbinol (PhCH2OH) to benzaldehyde (PhCHO) when compared to pure n-CIS and o-CIS samples under visible light irradiation. It is hoped that this work can contribute novel insights into the development of metal sulfides S-scheme homojunction photocatalysts for solar energy conversion.

Photoredox Coupling of CO2 Reduction with Benzyl Alcohol Oxidation over Ternary Metal Chalcogenides (ZnmIn2S3+m, m = 1-5) with Regulable Products Selectivity.

Integrating photocatalytic CO2 reduction with selective benzyl alcohol (BA) oxidation in one photoredox reaction system is a promising way for the simultaneous utilization of photogenerated electrons and holes. Herein, ZnmIn2S3+m (m = 1-5) semiconductors (ZnIn2S4, Zn2In2S5, Zn3In2S6, Zn4In2S7, and Zn5In2S8) with various composition faults were synthesized via a simple hydrothermal method and used for effective selective dehydrocoupling of benzyl alcohol into high-value C-C coupling products and reduction of CO2 into syngas under visible light. The absorption edge of ZnmIn2S3+m samples shifted to shorter wavelengths as the atomic ratio of Zn/In was increased. The conduction band and valence band position can be adjusted by changing the Zn/In ratio, resulting in controllable photoredox ability for selective BA oxidation and CO2 reduction. For example, the selectivity of benzaldehyde (BAD) product was reduced from 76% (ZnIn2S4, ZIS1) to 27% (Zn4In2S7, ZIS4), while the selectivity of hydrobenzoin (HB) was increased from 22% to 56%. Additionally, the H2 formation rate on ZIS1 (1.6 mmol/g/h) was 1.6 times higher than that of ZIS4 (1.0 mmol/g/h), and the CO formation rate on ZIS4 (0.32 mmol/g/h) was three times higher than that of ZIS1 (0.13 mmol/g/h), demonstrating that syngas with different H2/CO ratios can be obtained by controlling the Zn/In ratio in ZnmIn2S3+m. This study provides new insights into unveiling the relationship of structure-property of ZnmIn2S3+m layered crystals, which are valuable for implementation in a wide range of environment and energy applications.

Erythropoietin modulates imbalance of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 in doxorubicin-induced cardiotoxicity.

BACKGROUND: Doxorubicin (DOX) is a highly effective anti-cancer drug with limited clinical use due to its serious cardiotoxicity. Recent studies reported that erythropoietin (EPO) could exert a cardioprotective effect by non-erythropoietic effects. This study was to investigate fibrosis of DOX-induced cardiotoxicity and determine mechanisms of EPO against extracellular matrix (ECM) remodelling. METHODS: Rats were grouped as the control group, the DOX group and the DOX+EPO group. DOX (2.5 mg/kg/dose, six doses for two weeks) was administered to induce cardiotoxicity by intraperitoneal injections in the DOX group and the DOX+EPO group, and EPO (2500U/kg/dose, six doses for two weeks) was administered simultaneously in the DOX+EPO group. Two weeks after the last administration, rats were killed with cardiac tissues used for histological analyses and immunological detections for matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2). RESULTS: Rats treated with DOX showed degenerative changes with cardiac fibrosis. Compared to the control group, the expression of MMP-2 was up-regulated whereas that of TIMP-2 was down-regulated in the DOX group. EPO administration improved cardiac fibrosis, decreased MMP-2 expression, increased TIMP-2 expression and ameliorated imbalance of MMP-2/TIMP-2 ratio. CONCLUSIONS: The present study suggests that EPO can exert a cardioprotective effect on DOX-induced cardiotoxicity which may be associated with improving MMP-2/TIMP-2 imbalance.

Preventive cardioprotection of erythropoietin against doxorubicin-induced cardiomyopathy.

INTRODUCTION: Doxorubicin (DOX) is a highly effective chemotherapeutic agent related to dose-dependent cardiomyopathy. Recent evidence suggests that erythropoietin (EPO) can play a protective role in cardiovascular diseases by non-erythropoietic effects. In the present study, we tested the hypothesis that EPO may protect against DOX-induced cardiomyopathy through anti-apoptotic mechanisms both in vitro and in vivo. MATERIALS AND METHODS: Isolated neonatal Wistar rat cardiomyocytes were treated with vehicle, DOX with or without EPO, or EPO. Twenty-four hours later, the cells were used to determine cardiomyocyte apoptosis (TUNEL assay). Cardiomyopathy was induced in Wistar rats by intraperitoneal injections (IP) of DOX (2.5 mg/kg, six times for 2 weeks). EPO (2,500 U/kg, six times for 2 weeks) was administered simultaneously in the DOX+EPO group and the EPO group. Two weeks after the last administration, cardiac function was evaluated by echocardiography and invasive haemodynamic measurements. Rats were then sacrificed for histological and TUNEL analyses, with immunological detection for cardiac Troponin-T (cTnT), alpha-actinin, Bax and Bcl-2. RESULTS: EPO significantly ameliorated DOX-induced apoptosis of cultured cardiomyocytes as demonstrated by TUNEL assay. In the rat model, cardiac function significantly decreased in the DOX group. In contrast, the DOX+EPO group showed considerable improvement in cardiac function, inhibition of cardiomyocyte apoptosis, reduction of fibrosis, as well as up-regulation of Bcl-2 protein expression. CONCLUSIONS: Our results suggest that EPO exerts preventive cardioprotective effects on DOX-induced cardiomyopathy via anti-apoptotic pathways. The up-regulation of Bcl-2 protein expression may contribute to this.

Association of 4G/5G polymorphism in PAI1 promoter with PAI1 level in deep vein thrombosis.

OBJECTIVE: To reveal the association of 4G/5G polymorphism in the promoter region of the plasminogen activator inhibitor 1 gene (PAI1) with plasma PAI1 level in deep vein thrombosis (DVT) in Chinese Han ethnic group. METHODS: One hundred and twenty Chinese DVT patients and 120 healthy controls were recruited. The PAI1 promoter 4G/5G polymorphism was detected using polymerase chain reaction (PCR). The antigen of tissue-type plasminogen activator (tPA) or PAI1 was quantified by a commercially available enzyme-linked immunosorbent assay (ELISA) in DVT cases and health controlsì respectively. RESULTS: Neither in the distribution of PAI1 promoter 4G/5G polymorphism nor in the frequencies of 4G and 5G allele was there a difference between two groups. The levels of PAI1 antigen in the carriers of the 4G/4G genotype were significantly higher than those either in the 4G/5G genotype or in the 5G/5G genotype; In the 4G/5G genotype or in the 5G/5G genotype the TG levels are an independently determinant factor of PAI1 antigen levels. CONCLUSION: There is a close relationship of the PAI1 4G/5G polymorphism to its plasma level in deep vein thrombosis in Chinese Han ethnic group, although lack of association between this genetic variation and risk of DVT suggest no major cause-effect pathogenic role of this polymorphism by itself.

[Inhibitory effect of ardipusilloside-I on Lewis pulmonary carcinoma and hepatocarcinoma SMMC-7721].

OBJECTIVE: To study the antitumor effect of ardipusilloside-I (ADS-I) on Lewis pulmonary carcinoma and hepatocarcinoma SMMC-7721. METHODS: Lewis pulmonary metastasizing model was made by Sc. diluted 3-time 20 microl cancer cells in the right sole of C57BL/6 mice, after we treated the mice 14 days with ADS-I orally, cut the neoplasia-foot and weighed, we calculated the inhibitory rate in situ, then put the mice to death after being administrated 11 days continuously, counted the lung medtastasis colony and calculated the metastasis inhibitory rate; Human being hepatocarcinoma model was made by sc. in the back 5 x 10(6)/ml SMMC-7721 cells per BALB/c/nu nude mice, after we treated them orally 16 days with ADS-I continuously, measured the volume of tumor growth and body weight, and drew the growth curve, we detached the tumor and calculated the inhibitory rate of tumor growth in the end. RESULTS: Lewis pulmonary carcinoma inhibitory rate in situ and lung transfer inhibitory rate of ADS-I (25 mg/kg - 100 mg/kg) were between 40.5% and 54.0%, 45.4% and 69.1% respectively; Inhibitory rate of hepatocarcinoma SMMC-7721 was between 45.6% and 56.3%. CONCLUSIONS: ADS-I has inhibitory effect on Lewis pulmonary metastasis carcinoma and hepatocarcinoma SMMC-7721 carcinoma.

[Intravascular ultrasound study of coronary remodeling and determination of matrix metalloproteinase and hypersensitive C-reactive protein].

OBJECTIVE: To investigate remodeling characteristics of coronary lesions in patients with acute coronary syndromes (ACS) versus stable angina pectoris (SA) using intravascular ultrasound (IVUS), and to explore the relationship between arterial remodeling and clinical presentation or matrix metalloproteinase (MMPs) or hyper-sensitive C-reactive protein (hs-CRP). METHODS: We studied culprit lesions of 38 patients with ACS and 18 patients with SA using IVUS before coronary intervention. The lesion site and a proximal or distal reference site including the external elastic membrane (EEM) area and lumen area were analyzed. Plaque area and remodeling index (RI) were calculated, and directions of arterial remodeling were determined. Positive remodeling was defined as RI > 1.05 and negative remodeling as RI < 0.95. We analyzed the culprit lesion qualitatively, identified high risk plaque and compared them in each group. The blood level of MMP-2, MMP-9 and hs-CRP in each group were also determined. RESULTS: The plaque area at culprit lesions in patients with ACS was significantly larger (11.94 +/- 4.90 versus 9.17 +/- 3.36 mm2; P = 0.035), and also the RI in ACS group was significantly greater than that of patients with SA (0.972 +/- 0.222 versus 0.796 +/- 0.130; P = 0.003). The distribution of remodeling in these two groups was different: positive remodeling was more frequent in ACS group than in SA group (34.2% versus 5.6%, P = 0.047), whereas negative remodeling was more frequent in SA group (52.6% versus 88.9%, P = 0.003). There was higher incidence of high risk plaque in ACS group compared to SA (76.3% versus 50.0%, P = 0.040). The level of serum MMP-2 in ACS group was higher than that of SA group (250.65 +/- 47.97 microg/L versus 214.21 +/- 47.20 microg/L, P = 0.029). The same applied for plasma MMP-9 (84.26 +/- 9.78 microg/L versus 68.46 +/- 22.82 microg/L, P = 0.038) and serum hs-CRP (3.62 +/- 3.37 mg/L versus 1.48 +/- 1.52 mg/L, P = 0.041). CONCLUSIONS: Positive remodeling, larger plaque area and higher incidence of high risk plaque are associated with ACS, whereas negative remodeling is more common in patients with SA. This association between the extent of remodeling and clinical presentation may reflect a greater tendency that plaques with positive remodeling can cause ACS. The change of level of MMP-2, MMP-9 and hs-CRP in ACS patients may be helpful in investigating vulnerable plaques.

[Changes of angiotensin II and its receptor during the development of chronic intermittent hypoxia-induced hypertension in rats].

OBJECTIVE: To observe the changes of angiotensin II (ATII) and ATII type-1 receptor (AT1R) during the development of chronic intermittent hypoxia (CIHO)-induced hypertension in rats, and the effect in the mechanism of CIHO-induced hypertension. METHODS: Seventy-two male Wistar rats were divided into three groups:intermittent hypoxia group (IH), sham control group (SC) and control group (UC). By using supply of nitrogen (30 s each cycle) followed by compressed air (30 s each cycle) into the exposure chambers (4% - 6% nadir ambient oxygen with return to 21%), IH rats were subjected to intermittent hypoxia every 60 s for 8 h/d during the diurnal sleep period. SC rats were similarly treated but received compressed air instead of nitrogen. UC rats were not treated. Mean arterial pressure (MAP), the levels of ATII and renin activity (RA) in plasma as well as the expression of AT1R mRNA in tissue were measured on day 7, 21 and 42 after experiment. RESULTS: MAP was significantly elevated in IH rats [(102.2 +/- 6.2) mm Hg, 1 mm Hg = 0.133 kPa] compared with initial MAP [(94.1 +/- 4.3) mm Hg, P < 0.01] and compared with that in SC [(95.7 +/- 3.6) mm Hg], UC [(97.2 +/- 3.6) mm Hg, all P < 0.05] on day 42. The levels of ATII and RA in plasma in IH rats increased gradually over time, and RA started to increase significantly on day 7 [(3.86 +/- 1.25) ng.ml(-1).h(-1)] compared with that in SC [(2.73 +/- 0.98) ng.ml(-1).h(-1)], UC [(2.55 +/- 0.87) ng.ml(-1).h(-1), all P < 0.05], and ATII started to increase significantly on day 21 [(214 +/- 41) ng/L] compared with that in SC [(124 +/- 21) ng/L], UC [(121 +/- 18) ng/L, all P < 0.01]. The RA and ATII levels in plasma showed positive correlation with MAP (r = 0.529, P = 0.008; r = 0.475, P = 0.019 respectively). The expression of AT1R mRNA in heart, kidney and aorta in IH rats showed no differences compared with that in SC and UC group (all P > 0.05). All indices were not different between SC and UC rats at any time point (all P > 0.05). CONCLUSION: CIHO can cause the levels of circulating RA and ATII to increase, but has no effects on AT1R mRNA expression in tissue, which suggests that activated renin-angiotensin system may contribute to the pathogenesis of CIHO-induced hypertension.

[Level of tissue plasminogen activator protein in pulmonary artery in acute pulmonary thromboembolism in rabbit].

OBJECTIVE: To study the changes in tissue plasminogen activator(t-PA) protein in pulmonary artery and its clinical significance after acute pulmonary thromboembolism (PTE). METHODS: Thirty rabbits were randomly divided into four groups after replicating a model of acute PTE in rabbit by thrombi occlusion method. Specimens were obtained from both normal and morbid pulmonary artery 3, 8 and 24 hours after APE, and protein contents of t-PA were determined using immunohistochemical method. RESULTS: A few endothelial cells and smooth muscle cells of the normal pulmonary artery were positive for t-PA. After 3 hours of PTE, there was no significant changes in t-PA positive stain among embolismic, non-embolismic and normal pulmonary artery. After 8 and 24 hours of PTE, strong positive staining was found in the residual endothelial cells and a part of smooth muscle cells (all P<0.01). CONCLUSION: There is significantly strong positive staining for t-PA in the pulmonary artery wall after pulmonary embolism, implying that the local fibrinolysis activity was enhanced, and it might be helpful for lysis of the embolus.