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Cerebral ischemia results in increased oxidative stress in the affected brain. Accumulating evidence suggests that quercetin possesses anti-oxidant and anti-inflammatory properties. The essential elements magnesium (Mg), zinc (Zn), selenium (Se), and transition metal iron (Fe), copper (Cu), and antioxidants superoxide dismutase (SOD) and catalase (CAT) are required for brain functions. This study investigates whether the neuroprotective effects of quercetin on the ipsilateral brain cortex involve altered levels of essential trace metals, the Cu/Zn ratio, and antioxidant activity. Rats were intraperitoneally administered quercetin (20 mg/kg) once daily for 10 days before ischemic surgery. Cerebral ischemia was induced by ligation of the right middle cerebral artery and the right common carotid artery for 1 h. The ipsilateral brain cortex was homogenized and the supernatant was collected for biochemical analysis. Results show that rats pretreated with quercetin before ischemia significantly increased Mg, Zn, Se, SOD, and CAT levels, while the malondialdehyde, Fe, Cu, and the Cu/Zn ratio clearly decreased as compared to the untreated ligation subject. Taken together, our findings suggest that the mechanisms underlying the neuroprotective effects of quercetin during cerebral ischemic injury involve the modulation of essential elements, transition metals, Cu/Zn ratio, and antioxidant activity.

In this study, near-infrared (NIR) technology was utilized to develop a low-cost real-time near infrared (NIR) guiding device for cannulation. A portable device that can be used by medical practitioners and also by students for their skills development training in performing cannulation. Methods. First, is the development of a reflectance type optical vein finder using three (3) light emitting diode (LED) lights with 960 nm wavelength, complementary metal-oxide-semiconductor-infrared (CMOS-IR) sensor camera with 1920 × 1080 UXGA (1080P), IR filter set for the given wavelength, and an open-source image processing software. Second, is the actual in-vitro human testing in two sites: the arm and dorsal hand of 242 subjects. The following parameters were included, such as gender, age, mass index (BMI), and skin tone. In order to maximize the assessment process towards the device, the researchers included the arm circumference. This augmented subcutaneous vein imaging study using the develop vein finder device compared the difference in the captured vein images through visual and digital imaging approaches. The human testing was performed in accordance with the ethical standards of the Trinity University of Asia—Institutional Ethics Review Committee (TUA—IERC). Results. The NIR imaging system of the developed vein finder in this study showed its capability as an efficient guiding device through real-time vein pattern recognition, for both sites. Improved captured vein images were observed, having 100% visibility of vein patterns on the dorsal hand site. Fourteen (5.79%) out of 242 subjects reported non-visible peripheral subcutaneous veins in the arm sites. Conclusions. The developed vein finder device with the NIR technology and reflected light principle with low-energy consumption was efficient for real-time peripheral subcutaneous vein imaging without the application of a tourniquet. This might be utilized as a guiding device in locating the vein for the purpose of cannulation, at a very low cost as compared to the commercially available vein finders. Moreover, it may be used as an instructional device for student training in performing cannulation.

Cerebral ischemia causes increased oxidative stress due to the overproduction of reactive oxygen species. The polyphenol compound resveratrol exerts neuroprotective effects through its antioxidant and anti-inflammatory abilities. The trace elements magnesium (Mg), zinc (Zn), and selenium (Se) also exert antioxidant properties. This study mainly investigates whether the neuroprotective effect of resveratrol during cerebral ischemia is related to its modulation of the concentrations of trace element and toxic metal lead (Pb). Experimental rats were administered resveratrol (20 mg/kg) once daily for 10 consecutive days. Cerebral ischemia was surgically induced via ligation of the right middle cerebral artery and right common carotid artery for 1 h. Brain cortex tissues were homogenized, and the supernatants were harvested for biochemical analysis. Experimental results showed that rats pretreated with resveratrol before cerebral ischemia had significantly higher trace element concentrations of Mg, Zn, and Se and higher antioxidant activity (superoxide dismutase and catalase) in the brain cortex as compared to untreated cerebral ischemia rats. Conversely, resveratrol pretreatment markedly attenuated lipid peroxidation and concentrations of the toxic metal Pb as compared to untreated cerebral ischemic rats. Altogether, the findings of this study highlight that the mechanism underlying the neuroprotective effect of resveratrol involves modulation of the brain levels of trace elements, toxic metal lead, lipid peroxidation, and antioxidant activity.

Curcumin, a popular yellow pigment of the dietary spice turmeric, has been reported to inhibit cell growth and to induce apoptosis in a wide variety of cancer cells. Although numerous studies have investigated anticancer effects of curcumin, the precise molecular mechanism of action remains unidentified. Whereas curcumin mediates cell survival and apoptosis through mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling cascades, its impact on the upstream regulation of MAPK is unclear. The leucine-zipper and sterile-α motif kinase alpha (ZAKα), a mitogen-activated protein kinase kinase kinase (MAP3K), activates the c-Jun N-terminal kinase (JNK) and NF-κB pathway. This paper investigated the prospective involvement of ZAKα in curcumin-induced effects on cancer cells. Our results suggest that the antitumor activity of curcumin is mediated via a mechanism involving inhibition of ZAKα activity.

Calcium silicate cement has attracted much attention for bone defect repair and regeneration due to its osteogenic properties. Biomaterial-associated infections and washout have become a common clinical problem. In order to enhance the antibacterial and washout performance of calcium silicate cement to meet clinical needs, different types of chitosan, including chitosan polysaccharide (CTS), quaternary ammonium chitosan (QTS), and chitosan oligosaccharide (COS), as a liquid phase were added to the calcium silicate powder. The physicochemical properties, in vitro bioactivity, antibacterial efficacy, and osteogenic effects (MG63 cells) of the cement were evaluated. Antibacterial activity was conducted with Gram-negative Escherichia coli (E. coli) and a Gram-positive Staphylococcus aureus (S. aureus) bacteria. The amount of intracellular reactive oxygen species (ROS) produced in the bacteria cultured with the chitosan solution was also detected. The experimental results showed that the chitosan additive did not affect the crystalline phase of calcium silicate cement, but increased the setting time and strength of the cement in a concentration-dependent manner. Within the scope of this study, CTS and QTS solutions with a concentration of not1 wt% improved the washout resistance of the control cement, while the COS solutions failed to strengthen the cement. When soaked in simulated body fluid (SBF) for 1 day, all cement samples formed apatite spherules. As the soaking time increased, the diametral tensile strength of all cements decreased and the porosity increased. The assays of MG63 cell function showed lower osteogenic activity of osteoblastic cells grown on the surfaces of the chitosan-incorporated cements in comparison with the control cement without chitosan. At the same 1% concentration, compared with QTS and COS cement, CTS cement had lower cell attachment, proliferation, differentiation, and mineralization. Conversely, the CTS cement resulted in the highest bacteriostasis ratio among the three hybrid cements against two bacteria. The ROS production followed the order of CTS QTS COS at the same 1% concentration. In conclusion, calcium silicate cement with 1% QTS may be a viable candidate for bone defect repair in view of anti-washout performance, setting time, antibacterial activity, and osteogenic activity shown in this study.

To accelerate GaN adoption, beyond-JEDEC system-level reliability should be done to prove the robustness of GaN in applications. In this paper, a new hard switching test vehicle (half-bridge RC load) was proposed & demonstrated to achieve system-like stress, flexibility of acceleration test, low system power consumption with large sample size, easy setup & control which can meet system-level reliability requirement.

Background: Osteosarcoma is one of the most malignant cancers in children. Naringenin exhibits several cellular functions. Objectives: In this study, we investigate the effects of naringenin on osteosarcoma. Materials and Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to detect the cell viability. Zymography assay and transwell assay were used to measure the matrix metalloproteinase (MMP) activity and migration ability. Western blot analysis was used to determine the expression of migration-related proteins. Results: No overt alternation of cytotoxicity in response to different concentrations of naringenin for 24 h was found by MTT assay. MMP-2 and MMP-9 activities and expression were significantly repressed by naringenin in a dose-dependent manner, as evidenced by zymography and Western blot analysis. Naringenin dose dependently reduced the expression of mesenchymal marker Snail. Conclusion: These results indicate that naringenin exhibited antimigration property through inhibition of MMP-2 and MMP-9 and downregulation of Snail expression. Thus, naringenin may be a potential inhibitor of metastasis of osteosarcoma.

Proliferation/migration of vascular smooth muscle cells (VSMCs) plays vital roles in the pathogenesis of atherosclerosis and restenosis after percutaneous coronary intervention. Water extracts from mulberry fruit can inhibit VSMCs proliferation and migration and thereby atherosclerosis. In the present study, our aim was to identify the functional polyphenols in mulberry polyphenol extracts (MPEs) and confirm their effects on atherosclerosis and its underlying mechanisms. Western blot analysis of the impact of MPEs on inducible nitric oxide synthase (iNOS), adenosine 5′-monophosphate-activated protein kinase (AMPK), and proteins related to cell cycle progression showed that 1) MPEs initially activate iNOS to increase NO release, thereby activating (in succession) AMPK, p53, p21, and p-Rb, which eventually results in cell cycle arrest of VSMCs and 2) inhibitors of iNOS, AMPK, and p53 blunt or reverse the induction of cell cycle arrest. Thus, MPEs inhibit atherosclerosis through inducing NO production and AMPK/p53 activation and thereby cell cycle arrest of VSMCs.

BACKGROUND Previous studies have shown that mulberry polyphenolic compounds have an anti-atherosclerotic effect in rabbits. Apoptosis of vascular smooth muscle cells (VSMCs) is the key determinant of the number of VSMCs in remodeling. To examine the effect of mulberry polyphenol extracts (MPEs) on the apoptosis of VSMCs and thus the prevention of atherosclerosis, this study investigated the ability of MPEs to induce apoptosis in vitro and the underlying mechanism. RESULTS It was found that MPEs initially activated JNK/p38 and p53, which in turn activated both Fas-ligand and mitochondrial pathways, thereby causing mitochondrial translocation of Bax and a reduction in Bcl-2. This then triggered the cleavage of procaspases, finally resulting in apoptosis of VSMCs. CONCLUSION This study shows that MPEs may suppress atherosclerosis through stimulating apoptosis of VSMCs via activating JNK/p38 and p53 signaling. © 2015 Society of Chemical Industry

The aim of this study was to evaluate the pharmacological effect of EGb761 on the dynamic alterations of magnesium (Mg) and energy metabolites including glucose and lactate in brain cortex of gerbil during focal cerebral ischemia. A single dose of EGb761 (...

Atherosclerosis involves the proliferation and migration of vascular smooth muscle cells (VSMCs). The migration of VSMCs from the media into the intima and their subsequent proliferation are important processes in neointima formation in atherosclerosis and restenosis after percutaneous coronary interventions. Acarbose, an alpha-glucosidase inhibitor, has been demonstrated to not affect serum levels of glucose and decrease the progression of intima-media thickening in rabbits fed with a high cholesterol diet (HCD). We previously showed that increased Ras protein levels enhanced the migration of TNF-α treated A7r5 cells. The aim of this study was to determine the inhibitory effects of acarbose on Ras expression in A7r5 cells. Acarbose also inhibited the phosphorylation of focal adhesion kinase (FAK) and Akt, activities of the matrix metalloproteinases (MMPs) MMP-2 and MMP-9, and protein expressions of small G proteins (Ras, Cdc42, RhoA, and Rac1) in a dose-dependent manner. We also found that acarbose could effectively inhibit the proliferation and migration of RasG12V A7r5 cells by blocking small G proteins and phosphoinositide-3-kinase (PI3K)/Akt signaling. These studies demonstrated that acarbose could theoretically decrease atherosclerosis by targeting Ras signaling.

Previous studies have shown that mulberry water extracts (MWEs), which contain polyphenolic compounds, have an antiatherosclerotic effect in vivo and in vitro through stimulating apoptosis of vascular smooth muscle cells (VSMCs). Histological analysis was performed on atherosclerotic lesions from high-cholesterol diet (HCD)-fed rabbits after treatment with 0.5–1% MWEs for 10 weeks. Immunohistochemistry showed that the expressions of SMA, Ras, and matrix metalloproteinase-2 in the VSMCs were dose-dependently inhibited after MWE treatment. The antimigratory effects of MWEs on A7r5 VSMCs were assessed by western blot analysis of migration-related proteins, visualization of F-actin cytoskeleton, and reverse transcription polymerase chain reaction. The results showed that MWEs inhibited VSMC migration through reducing interactions of the integrin-β3/focal adhesion kinase complex, alterations of the cytoskeleton, and downregulation of glycogen synthase kinase 3β/nuclear factor κB signaling. Taken together, MWEs...

Mulberry 1-deoxynojirimycin (DNJ), an inhibitor of α-glucosidase, has been reported to help prevent diabetes mellitus and suppress lipid accumulation. The aim of this study was to determine whether mulberry DNJ has pleiotropic effects on the development of atherosclerosis. The mechanisms by which mulberry DNJ might inhibit migration of A7r5 vascular smooth muscle cells (VSMCs) under hyperglycemic conditions mimicking diabetes were investigated. The antimigratory effects of DNJ on VSMCs were assessed by Western blot analysis of migration-related proteins and by electric cell-substrate impedance sensing (ECIS) and visualization of F-actin cytoskeleton. Two pathways of DNJ-mediated inhibition of VSMC migration were identified. The first involved AMPK activation to inhibit fatty acid synthase (FASN) and Akt activity and then RhoB activation to inhibit nuclear factor-κB (NF-κB) and matrix metalloproteinase-2 (MMP) activity. The second involved inhibition of focal adhesion kinase (FAK), Ras, and RhoA activity leading to inhibition of F-actin activity.

Preventive effects of ellagic acid against doxorubicin-induced cardiac oxidative, inflammatory and apoptotic stress were examined. This agent at 0.25, 0.5 or 1% was added in feed and supplied to mice for 8 weeks, and followed by doxorubicin treatment. Ellagic acid intake increased its deposit in heart. Pre-intake of this compound at 0.5 and 1% significantly attenuated doxorubicin caused increase in plasma creatine phosphokinase activity. Doxorubicin treatment decreased glutathione content, increased reactive oxygen species (ROS), malonyldialdehyde (MDA), interleukin (IL)-6, IL-10, monocyte chemoattractant protein-1 and tumor necrosis factor-alpha levels, declined glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities, and enhanced xanthine oxidases (XO) activity in heart. Ellagic acid intake dose-dependently reserved glutathione content, lowered ROS and MDA levels, and reduced XO activity. This compound at 0.5 and 1% retained GPX and SOD activities, and decreased cytokines in heart. Doxorubicin treatment raised cardiac activity and protein production of caspase-3, nuclear factor kappa B (NF-κB) p50 and p65. Ellagic acid dose-dependently lowered caspase-3 activity and cleaved caspase-3 formation, and at 0.5 and 1% declined activity and protein level of NF-κB. Doxorubicin treatment also up-regulated cardiac expression of p-p38, p-ERK 1/2 and p-JNK, and ellagic acid at 0.5 and 1% suppressed p-p38 expression and at 1% down-regulated p-ERK 1/2 expression. These findings suggest that ellagic acid is a potent cardiac protective agent against doxorubicin.

The protective effects of Houttuynia cordata aqueous extract (HCAE) in mice consuming a high saturated fat diet (HFD) were examined. HCAE, at 0.5, 1, or 2%, was supplied in drinking water for 8 weeks. HCAE was rich in phenolic acids and flavonoids. HCAE intake at 1 and 2% decreased body weight, epididymal fat, insulin resistance, triglyceride and total cholesterol contents in plasma and liver from HFD-treated mice (p < 0.05). HFD enhanced hepatic activity of malic enzyme, fatty acid synthase (FAS) and 3-hydroxy-3-methylglutaryl coenzyme A reductase; and augmented the hepatic level of saturated fatty acids (p < 0.05). HCAE intake at 2% reduced malic enzyme and FAS activities, and lowered saturated fatty acids content in liver (p < 0.05). HCAE suppressed HFD induced oxidative and inflammatory stress in the heart and liver via reducing the malondialdehyde level, retaining glutathione content and glutathione peroxidase activity, decreasing tumor necrosis factor-alpha, interleukin (IL)-1beta and IL-6 production (p < 0.05). These results support that Houttuynia cordata is a potent food against HFD induced obesity, and oxidative and inflammatory injury.

Acarbose, an α-glucosidase inhibitor, is reported to reduce the incidence of silent myocardial infarction and slow the progression of intima-media thickening in patients with glucose intolerance. Here we investigate other impacts of acarbose on atherosclerosis development and the underlying mechanisms of atherosclerosis initiation and progression in vivo and in vitro. Rabbits fed a high cholesterol diet (HCD) were treated with acarbose (2.5–5.0 mg kg−1). Immunohistochemistry was used to assess the expression of inducible nitric oxide synthase (iNOS), Ras, proliferating cell nuclear antigen (PCNA), IL-6, β-galactosidase, and p-AMPK in atherosclerotic lesions. Treatment with acarbose in HCD-fed rabbits was found to significantly reduce the severity of aortic atheroma and neointimal expression of α-actin, PCNA, IL-6, TNF-α, Ras, and β-galactosidase; to significantly increase expression of iNOS and p-AMPK, but not to affect serum levels of glucose, total cholesterol, and LDL. Western blot analysis showed acarbose dose-dependently decreased β-galactosidase and Ras expression and increased p-AMPK expression in TNF-α-treated A7r5 cells. In addition, acarbose restored p-AMPK and iNOS levels in AMPK inhibitor- and iNOS inhibitor-treated A7r5 cells, respectively. In conclusion, acarbose can pleiotropically inhibit rabbit atherosclerosis by reducing inflammation, senescence, and VSMCs proliferation/migration via upregulating AMPK signals.

GaN Cascode performance optimization for high efficient power applications is presented in this paper. Analytical equations of Cascode capacitance network (Ciss, Coss, Cgd) is demonstrated and the equations accuracy is verified through experimental measurement. Analysis shows that Cascode Cgd is determined by HV D-MISFETs Cds, LV Si FETs Cgd/Coss ratio, and extra zener diode capacitance. With low intrinsic capacitance HV D-MISFETs [1-2], proper LV Si FETs selection, and extra zener diode protection, optimization for Cascode switching figure-of-merit (FOM, Ron x Qgd) is well demonstrated. 8.8X lower switching figure-of-merit than commercial best-in-class Si SJ FETs [3] is achieved, double pulse test (DPT) and hard switching PFC system verification result all indicate that GaN Cascode is the promising solution and ready for next generation energy systems.

Mulberry extracts are antidiabetic and antihyperlipidemic, as well as preventive of cardiovascular disease. The current study investigates the protective mechanisms of mulberry water extracts (MWEs) in carbon tetrachloride (CCl 4 )-induced hepatic injury. Oral administration of MWEs significantly reduced the lipid peroxidation triggered by CCl 4 , as shown by the reduced production of thiobarituric acid-reactive substance (TBARS). The levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) were also reduced via cotreatment with MWEs compared with CCl 4 treatment alone. Cotreatment with MWE evidently reduced CCl 4 -induced liver weight and inhibited lipid deposition and fibrogenesis. In a similar manner, cotreatment with silymarin, a well-known liver protective agent, also reversed the CCl 4 -induced effects, such as reduced TBARS formation, decreased serum AST, ALT, and ALP levels, blocked lipid accumulation, and liver fibrosis. Furthermore, MWEs attenuated the proinflammatory genes such as cyclooxygenase 2, nuclear factor kappa B, and inducible nitric oxide synthase expression. The current findings suggest that MWEs such as silymarin exhibit protective and curative effects against CCl 4 -induced liver damage and fibrosis via decreased lipid peroxidation and inhibited proinflammatory gene expression.

1,3,5-Tri-N-alkylcarbamylphloroglucinols (1–4) are synthesized as conformationally constrained analogs of triacylglycerols (TGs) to probe Jenck's proximity effect in the cholesterol esterase inhibition. For the cholesterol esterase inhibition, inhibitors 1–4 are 220–760-fold more potent than 1,2,3-tri-N-alkylcarbamylglycerols (13–15) that are substrate analogs of TG. Comparison of tridentate inhibitors 1–4, bidentate inhibitors 3,5-di-N-n-alkylcarbamyloxyphenols (5–8) and monodentate inhibitors 5-N-n-alkylcarbamyloxyresorcinols (9–12) indicates that inhibitory potencies are as followed: tridentate inhibitor > bidentate inhibitor > monodentate inhibitor. The log ki and pKi values of tridentate inhibitors, bidentate inhibitors, and monodentate inhibitors are linearly correlated with the alkyl chain length indicating a common mechanism in each inhibition. Also, positive slopes of these correlations indicate that the longer chain inhibitors bind more tightly to the enzyme than the shorter ones. Molecular dockings of tridentate 1, bidentate 5, and monodentate 9 into the X-ray crystal structure of cholesterol esterase suggest that one carbamyl group in the cis form of the inhibitor binds to the acyl chain-binding site of the enzyme. The second carbamyl groups in the trans forms of inhibitors 1 and 5 bind to the second acyl chain-binding site of the enzyme. The third carbamyl group in the trans form of inhibitor 1 binds to the third acyl chain-binding site of the enzyme. Moreover, the configuration of the inhibitor in the enzyme-inhibitor complex is the (1,3,5)-(cis, trans, trans)-tricarbamate form that mimics the (+gauche, −gauche)-conformation of TG.

This study analyzed the content of eight triterpenes (oleanolic acid, ursolic acid, arjunolic acid, asiatic acid, boswellic acid, corosolic acid, madecassic acid, and maslinic acid) in ten vegetables and eight fruits. These compounds at 0.5% were supplied to mice for 4 or 8 weeks. The bioavailability, tissue distribution, and antioxidative protection of these triterpenes were examined. Results showed that triterpenes were detected in eight vegetables and six fruits. Basil and brown mustard contained seven test triterpenes, in the range of 14-102 mg/100 g dry weight. The level of each triterpene in plasma, brain, heart, liver, kidney, colon, and bladder increased as the feeding period was increased from 4 weeks to 8 weeks (P0.05). Renal homogenates from mice with triterpene intake had greater antioxidative effects against glucose-induced glutathione loss and malondialdehyde and oxidized glutathione production when compared with those from control groups (P0.05). These data support that these triterpenes were absorbed and deposited in their intact forms, which in turn exerted in vivo antioxidative protection.

Genome-wide association studies have revealed that many single nucleotide polymorphisms (SNPs) are associated with breast cancer, and yet the potential SNP-SNP interactions have not been well addressed to date. This study aims to develop a methodology for the selection of SNP-genotype combinations with a maximum difference between case and control groups. We propose a new chaotic particle swarm optimization (CPSO) algorithm that identifies the best SNP combinations for breast cancer association studies containing seven SNPs. Five scoring functions, that is, the percentage correct, sensitivity/specificity, positive predictive value/negative predictive value, risk ratio, and odds ratio, are provided for evaluating SNP interactions in different SNP combinations. The CPSO algorithm identified the best SNP combinations associated with breast cancer protection. Some SNP interactions in specific SNPs and their corresponding genotypes were revealed. These SNP combinations showed a significant association with breast cancer protection (P0.05). The sensitivity and specificity of the respective best SNP combinations were all higher than 90%. In contrast to the corresponding non-SNP-SNP interaction combinations, the estimated odds ratio and risk ratio of the SNP-SNP interaction in SNP combinations for breast cancer were less than 100%. This suggests that CPSO can successfully identify the best SNP combinations for breast cancer protection. In conclusion, we focus on developing a methodology for the selection of SNP-genotype combinations with a maximum difference between case and control groups. The CPSO method can effectively identify SNP-SNP interactions in complex biological relationships underlying the progression of breast cancer.

(2S,4aR,8aS)-Cis,cis-, (2R,4aS,8aR)-cis,cis-, rac-cis,cis-, and rac-trans,cis-decahydro-2-naphthyl-N-n-butylcarbamates are synthesized from condensation of (2S,4aR,8aS)-cis,cis-, (2R,4aS,8aR)-cis,cis-, rac-cis,cis-, and rac-trans,cisdecahydro- 2-naphthols, respectively, with n-butyl isocyanate in the presence of triethylamine in dichloromethane. Optically pure (2S,4aR,8aS)-(-)- and (2R,4aS,8aR)-(+)-cis,cis-decahydro-2-naphthols are resolved by the porcine pancreatic lipase- catalyzed acetylation of decahydro-2-naphthols with vinyl acetate in t-butyl methyl ether. Absolute configurations of (2S,4aR,8aS)-(-)- and (2R,4aS,8aR)-(+)- cis,cis-decahydro-2-naphthols are determined from the ¹⁹F NMR spectra of their Mosher's ester derivatives. (2S,4aR,8aR)-Trans,cis- and (2R,4aS,8aS)-trans,cis-decahydro-2-naphthols can't be resolved from the porcine pancreatic lipase-catalyzed acetylation of decahydro-2-naphthols with vinyl acetate in t-butyl methyl ether. For the inhibitory potency of Pseudomonas lipase, (2S,4aR,8aS)-cis,cis-decahydro-2-naphthyl-N-n-butylcarbamate is 3.5 times more potent than (2R,4aS,8aR)-cis,cis-decahydro-2-naphthyl-N-n-butylcarbamate; racemic cis,cis-decahydro- 2-naphthyl-N-n-butylcarbamate is about the same with trans,cis-decahydro-2-naphthyl-N-n-butylcarbamate. These inhibitors also show similar effects on porcine pancreatic lipase.

In this study, to change the proportion of 20%、21% RFL solution content, and in which compounds were added 7%, 8% of the IL-6 conditions, in the different EP100, EP200, EP300 fabrics, testing adhesion strength the changes between of fabric and fabric, fabric and rubber, respectively, for different concentrations under the conditions, observed in viscosity variations of the RFL solution. The results indicate that, the viscosity of RFL solution will increase with the ratio improve and the concentration of IL-6 conditions, in 21% RFL solution content and adding 8% of the IL-6 can reach the best results, EP 100 fabric and fabric of the adhesion strength is 21.24kgf, the adhesion strength of fabric and rubber is 28.09 kgf.

Four stereoisomers of 2-norbornyl-N-n-butylcarbamates are characterized as the pseudo substrate inhibitors of cholesterol esterase. Cholesterol esterase shows enantioselective inhibition for enantiomers of exo- and endo-2-norbornyl-N-n-butylcarbamates. For the inhibitions by (R)-(+)- and (S)-(-)-exo-2-norbornyl-N-n-butylcarbamates, the R-enantiomer is 6.8 times more potent than the S-enantiomer. For the inhibitions by (R)-(+)- and (S)-(-)-endo-2-norbornyl-N-n-butyl-carbamates, the S-enantiomer is 4.6 times more potent than the R-enantiomer. The enzyme-inhibitor complex models have been proposed to explain these different enantioselectivities.

Previous investigation has proposed that Antrodia Camphorata possesses beneficial effect mainly on liver protection. To date, the antioxidative effect of Antrodia Camphorata on the tissues of brain, kidney, lung, and liver, however, has not yet clarified. In this current experiment, eighty male Sprague-Dawley rats were randomly divided into control and Antrodia Camphorate-treated subject. Both subjects were intraperitoneally injected with normal saline and Antrodia Camphorata for consecutive 14 days, respectively. On day 15, rats were sacrificed and tissues of brain, kidney, lung, and liver were immediately harvested and homogenate. The malondialdehyde level, an end-product of lipid peroxidation, was measured in different tissues. Experimental result showed that the malondialdehyde levels were significantly (P < 0.05) reduced in all tissues after receiving Antrodia Camphorate as compared with the control subject. Specifically, an obvious decline (12.93%) of the malondialdehyde level was found in the brain as compared to the tissues of kidney, lung, and liver. Accordingly, our present result indicates that Antrodia Camphorate can significantly decline oxidative damage as presented by a reduced malondialdehyde levels in the tissues of brain, kidney, lung, and liver. In addition, it seems likely that the best tissue protective efficacy offered by Antrodia Camphorate in declining oxidative damage is found in the brain tissue.

This study was carried out to investigate the impact of polyphenol-rich extract from mulberry leaf on the proliferation of vascular smooth muscle cell (VSMC) and verify its mechanism in vitro. VSMC proliferation is an important pathophysiological process in the development of atherosclerosis, which is the major cause of coronary artery disease (CAD). Polyphenol-rich foods, such as mulberry leaf, have been reported to reduce the risk of CAD. The effect of mulberry leaf extract (MLE) on cell growth was measured by a growth curve assay, on distribution of cells in the cell cycle by flow cytometry, and on cyclin-dependent kinase (CDK) activity and cell-cycle regulatory proteins by Western blot, immunoblotting, and immunoprecipitation analyses. The results showed that MLE induced phosphorylation of p53, promoted expression of p21 and p27, decreased CDK2/4 activity, inhibited phosphorylation of Rb, and thereby blocked the G1 to S transition in the cell cycle.

Mulberry, the fruit of Morus alba, is commonly used in Chinese medicines because of its many pharmacologic effects. Mulberry leaves contain many phenolic antioxidants that can reduce cardiovascular disease. Atherosclerosis involves proliferation and migration of vascular smooth muscle cell (VSMC). Thus, we investigated the mechanisms by which mulberry leaf extract (MLE) might inhibit migration of VSMC. MLE was rich in polyphenols (44.82%), including gallic acid, protocatechuic acid, catechin, gallocatechin gallate, caffeic acid, epicatechin, rutin, and quercetin. MLE could inhibit the migration of A7r5 cells in a dose- and time-dependent manner. MLE also inhibited the activities of matrix metalloproteinases (MMPs) MMP-2 and MMP-9, protein expressions, and phosphorylation of FAK and Akt, and protein expressions of small guanosine triphosphatases (GTPases: c-Raf, Ras, Rac1, Cdc42, and RhoA) in a dose-dependent manner. NF-kappaB expression was also inhibited by MLE. MLE could effectively inhibit the migration of VSMC by blocking small GTPase and Akt/NF-kappaB signals.

Benzene-1,2-, 1,3-, and 1,4-di-N-substituted carbamates (1–15) are synthesized as the constrained analogs of gauche, eclipsed, and anti conformations, respectively, for the glycerol backbones of triacylglycerol. Carbamates 1–15 are characterized as the pseudo substrate inhibitors of cholesterol esterase. Long chain carbamates are more potent inhibitors than short chain ones. Comparison of different geometries for benzene-di-substituted carbamates, such as benzene-1,2-di-N-octylcarbamate (3) (ortho-3), benzene-1,3-di-N-octylcarbamate (8) (meta-8), and benzene-1,4-di-N-octylcarbamates (13) (para-13), indicates that inhibitory potencies are as followed: meta-8 > para-13 > ortho-3. Therefore, we suggest that the preferable conformation for the C(sn-1)–O/C(sn-2)–O glycerol backbone in the enzyme–triacylgycerol complex is the eclipsed conformation. Meanwhile, kinetic data indicate that among ortho, meta, and para carbamates, meta carbamates most resemble the substrate cholesterol ester.

Aims. This study sought to compare the antihypertensive efficacy and tolerability of a fixed‐dose combination with amlodipine/benazepril with that of amlodipine monotherapy in Chinese hypertensive subjects. Results. This multicenter, double‐blind, 8‐week study randomized 111 patients to fixed‐dose amlodipine besylate/benazepril HCl (2.5/5 mg/day titrated to 5/10 mg/day as needed at week 4 to reach goal blood pressure (BP)

The goal of this work was to determine the reaction mechanism for Pseudomonas species lipase activation by cardiovascular drugs such as lovastatin, simvastatin, amlodipine besylate, nifedipine, and hydralazine hydrochloride based on the results from enzyme kinetics. These drugs are the essential activators of Pseudomonas species lipase in the presence of triton-X 100 or taurochloate in vitro. Moreover, QSAR studies show that the pK A values are correlated with the molecular weights of these drugs.

We describe the formation of stable dithiol-bifunctionalized Ru(II)-terpyridine monolayer onto gold electrode. The coverage-dependent behavior onto gold electrode has been studied by electrochemical technique. The stability, surface charge coverage, and electrontransfer kinetics were assessed by cyclic voltammetry. Functionalized monolayer-protected Au clusters (MPCs) were also prepared. The spectroscopic characterization data of MPCs using UV–Vis and TEM techniques are discussed. TEM images showed that functionalized spherical nanoclusters of 4.7 ± 0.3 and 4.3 ± 0.2 nm were produced. The particle sizes are uniform with a narrow size distribution. The morphology of Au(1 1 1) metal surface modified with MPCs was imaged using atomic force microscopy (AFM). The nanoparticle layer exhibits a distinct surface morphology, irregularly shaped domains with dimensions from 20 to 60 nm and root mean square heights of 2.401 nm. � 2007 Elsevier B.V. All rights reserved.

Benzene-1,2-, -1,3-, and -1,4-di-N-substituted carbamates (1-15) are synthesized as the constrained analogs of gauche, eclipsed, and anti conformations of diesters of ethylene glycol, respectively. Carbamates 1-15 are characterized as the pseudo-substrate inhibitors of Pseudomonas species lipase. Long-chain carbamates are more potent inhibitors than short-chain ones. Different geometries of benzene-di-substituted carbamates, such as benzene-1,2-di-N-octylcarbamate (3) (ortho compound), benzene-1,3-di-N-octylcarbamate (8) (meta compound), and benzene-1,4-di-N-octylcarbamate (13) (para compound), show similar inhibitory potencies for the enzyme. In other words, kinetic data suggest that the enzyme does not discriminate ortho, meta, and para geometries of these constrained analogs.

We describe a synthetic pathway to the formation of stable pyridine-functionalized octanethiolate mixed monolayer-protected Au clusters (MPCs). The spectroscopic characterization data of MPCs using NMR, UV-Vis, TEM, XPS, and thermal-analysis-mass techniques are discussed. TEM analysis showed that spherical nanoclusters of 3-5 nm were produced. Furthermore, the particle sizes are uniform with a narrow size distribution. The pyridine-functionalized MPCs formed 2D superlattices with hexagonal packing covering on the carbon-coated copper grids during the toluene evaporation. For all samples, the S 2p(3/2) and 2p(1/2) components that appeared at approximately 162 and approximately 163 eV, respectively, in the XPS spectra compare very well with the typical value of chemisorbed S species. Thermal analysis mass spectrometer was used to analyze desorption behavior of octanethiolated MPCs or pyridine-functionalized mixed MPCs. The TA-mass spectra have revealed that MCPs exist monomer and dimer desorption behavior from monomeric thiolate adsorbed on the surface.

1,2-Ethylene-di-N-n-propylcarbamate (1) is characterized as an essential activator of Pseudomonas species lipase while 1,2-ethylene-di-N-n-butyl-, t-butyl-, n-heptyl-, and n-octyl-carbamates (2-5) are characterized as the pseudo substrate inhibitors of the enzyme in the presence of the detergent taurocholate or triton X-100. The inhibition and activation reactions are more sensitive in taurocholate than in triton X-100. From CD studies, the enzyme changes conformations in the presence of the detergent and further alters conformations by addition of the carbamate activator or inhibitor into the enzyme-detergent adduct. Therefore, this study suggests that the conformational change of lipase during interfacial activation is a continuous process to expose the active site of the enzyme to substrate. From 600 MHz (1)H NMR studies, the conformations of the alpha- and beta-methylene moieties of the activator 1,2-ethylene-di-N-n-propylcarbamate in the presence of substrate change after adding taurocholate into the mixture, and the conformations of the beta-methylene moieties of the inhibitor 1,2-ethylene-di-N-n-butylcarbamate in the presence of substrate alter after adding taurocholate into the mixture.