Dihydrolipoic Acid Induces Cytotoxicity in Mouse Blastocysts through Apoptosis Processes

α-Lipoic acid (LA) is a thiol with antioxidant properties that protects against oxidative stress-induced apoptosis. LA is absorbed from the diet, taken up by cells and tissues, and subsequently reduced to dihydrolipoic acid (DHLA). In view of the recent application of DHLA as a hydrophilic nanomaterial preparation, determination of its biosafety profile is essential. In the current study, we examined the cytotoxic effects of DHLA on mouse embryos at the blastocyst stage, subsequent embryonic attachment and outgrowth in vitro, in vivo implantation by embryo transfer, and early embryonic development in an animal model. Blastocysts treated with 50 μM DHLA exhibited significantly increased apoptosis and a corresponding decrease in total cell number. Notably, the implantation success rates of blastocysts pretreated with DHLA were lower than that of their control counterparts. Moreover, in vitro treatment with 50 μM DHLA was associated with increased resorption of post-implantation embryos and decreased fetal weight. Data obtained using an in vivo mouse model further disclosed that consumption of drinking water containing 100 μM DHLA led to decreased early embryo development, specifically, inhibition of development to the blastocyst stage. However, it appears that concentrations of DHLA lower than 50 μM do not exert a hazardous effect on embryonic development. Our results collectively indicate that in vitro and in vivo exposure to concentrations of DHLA higher than 50 μM DHLA induces apoptosis and retards early pre- and post-implantation development, and support the potential of DHLA to induce embryonic cytotoxicity

Atomistic nucleation sites of Pt nanoparticles on N-doped carbon nanotubes

[[abstract]]The atomistic nucleation sites of Pt nanoparticles (Pt NPs) on N-doped carbon nanotubes (N-CNTs) were investigated using C and N K-edge and Pt L3-edge X-ray absorption near-edge structure (XANES)/extended X-ray absorption fine structure (EXAFS) spectroscopy. Transmission electron microscopy and XANES/EXAFS results revealed that the self-organized Pt NPs on N-CNTs are uniformly distributed because of the relatively high binding energies of the adsorbed Pt atoms at the imperfect sites. During the atomistic nucleation process of Pt NPs on N-CNTs, stable Pt–C and Pt–N bonds are presumably formed, and charge transfer occurs at the surface/interface of the N-CNTs. The findings in this study were consistent with density functional theory calculations performed using cluster models for the undoped, substitutional-N-doped and pyridine-like-N-doped CNTs.[[journaltype]]國外[[incitationindex]]SCI[[booktype]]紙本[[countrycodes]]GB

MST3 Involvement in Na⁺ and K⁺ Homeostasis with Increasing Dietary Potassium Intake

K+ loading inhibits NKCC2 (Na-K-Cl cotransporter) and NCC (Na-Cl cotransporter) in the early distal tubules, resulting in Na+ delivery to the late distal convoluted tubules (DCTs). In the DCTs, Na+ entry through ENaC (epithelial Na channel) drives K+ secretion through ROMK (renal outer medullary potassium channel). WNK4 (with-no-lysine 4) regulates the NCC/NKCC2 through SAPK (Ste20-related proline-alanine-rich kinase)/OSR1 (oxidative stress responsive). K+ loading increases intracellular Cl−, which binds to the WNK4, thereby inhibiting autophosphorylation and downstream signals. Acute K+ loading-deactivated NCC was not observed in Cl−-insensitive WNK4 mice, indicating that WNK4 was involved in K+ loading-inhibited NCC activity. However, chronic K+ loading deactivated NCC in Cl−-insensitive WNK4 mice, indicating that other mechanisms may be involved. We previously reported that mammalian Ste20-like protein kinase 3 (MST3/STK24) was expressed mainly in the medullary TAL (thick ascending tubule) and at lower levels in the DCTs. MST3−/− mice exhibited higher ENaC activity, causing hypernatremia and hypertension. To investigate MST3 function in maintaining Na+/K+ homeostasis in kidneys, mice were fed diets containing various concentrations of Na+ and K+. The 2% KCl diets induced less MST3 expression in MST3−/− mice than that in wild-type (WT) mice. The MST3−/− mice had higher WNK4, NKCC2-S130 phosphorylation, and ENaC expression, resulting in lower urinary Na+ and K+ excretion than those of WT mice. Lower urinary Na+ excretion was associated with elevated plasma [Na+] and hypertension. These results suggest that MST3 maintains Na+/K+ homeostasis in response to K+ loading by regulation of WNK4 expression and NKCC2 and ENaC activity

Comparisons of Viral Etiology and Outcomes of Hepatocellular Carcinoma Undergoing Liver Resection between Taiwan and Vietnam

Epidemiologic data have suggested that etiologic variations of hepatocellular carcinoma (HCC) exist in different geographic areas, and might be associated with different outcomes. We compared the viral etiology, clinicopathological characteristics and surgical outcomes between 706 Taiwanese and 1704 Vietnamese patients with HCC undergoing liver resection. Vietnamese patients had a significantly higher ratio of hepatitis B virus (HBV) (p < 0.001) and a lower ratio of hepatitis C virus (HCV) (p < 0.001) and non-B non-C than Taiwanese patients. Among patients with HBV or non-B non-C, the mean age was younger in Vietnam than in Taiwan (p < 0.001, p = 0.001, respectively). The HCC patients in Vietnam had significantly higher serum alpha-fetoprotein (AFP) levels (p < 0.001), larger tumors (p < 0.001), and a higher ratio of macrovascular invasion (p < 0.001) and extrahepatic metastasis (p < 0.001), compared to those in Taiwan. Patients treated in Vietnam had a higher tumor recurrent rate (p < 0.001), but no difference in overall survival was found between both groups. In subgroup analysis, the recurrent rate of HCC was the highest in patients with dual HBV/HCV, followed by HCV or HBV, and non-B non-C (p < 0.001). In conclusion, although the viral etiology and clinicopathological characteristics of HCC differed, postoperative overall survival was comparable between patients in Taiwan and Vietnam

花卉及農產品分流條碼辨識系統

一種花卉及農產品分流條碼辨視系統,尤特指在主流道兩側設有互相對應的複數個子流道與分流機構,主流道到各個子流道之前設有感應裝置、轉向輔助裝置及條碼機,由感應裝置判別產品通過,並通知轉向輔助裝置作動,使產品略為轉向,以便條碼機掃讀,且通知分流機構作動,進行分貨之動作,非所屬子流道之產品,直接通過分流機構,殘貨則流至主流道終端,子流道上還設有防傾裝置,由感應裝置判別產品種類,箱型產品直接通過,立式產品由防傾裝置輔助不傾倒,分貨結束,得標人直接到所屬子流道取貨,達到分貨處理自動化,為其特徵者

Anti-Inflammatory Effects of Siegesbeckia orientalis Ethanol Extract in In Vitro and In Vivo Models

This study aims to investigate the anti-inflammatory responses and mechanisms of Siegesbeckia orientalis ethanol extract (SOE). In cell culture experiments, RAW264.7 cells were pretreated with SOE and stimulated with lipopolysaccharide (LPS) for inflammatory mediators assay. In animal experiments, mice were tube-fed with SOE for 1 week, and s.c. injected with λ-carrageenan or i.p. injected with LPS to simulate inflammation. The degree of paw edema was assessed, and cytokine profile in sera and mouse survival were recorded. Data showed that SOE significantly reduced NO, IL-6, and TNF-α production in LPS-stimulated RAW264.7 cells. In vivo studies demonstrated that mice supplemented with 32 mg SOE/kg BW/day significantly lowered sera IL-6 level and resulted a higher survival rate compared to the control group (P=0.019). Furthermore, SOE inhibited LPS-induced NF-κB activation by blocking the degradation of IκB-α. The SOE also reduced significantly the phosphorylation of ERK1/2, p38, and JNK in a dose-dependent manner. In summary, the in vitro and in vivo evidence indicate that SOE can attenuate acute inflammation by inhibiting inflammatory mediators via suppression of MAPKs- and NF-κB-dependent pathways

Plasma visfatin levels are associated with major adverse cardiovascular events in patients with acute ST-elevation myocardial infarction

Purpose: Circulating levels of visfatin, a ubiquitous adipokine, may reflect both the severity of plaque as well as degree of plaque stabilization in acute myocardial injury. The purpose of this study was to test whether the level of visfatin is associated with the occurrence of major adverse cardiovascular events (MACEs) in patients with acute ST-elevation myocardial infarction (STEMI). Methods: Consecutive patients (n=185) with acute STEMI were prospectively enrolled in the study. ELISA was used to measure plasma visfatin concentrations. Composite MACEs included death, recurrent myocardial infarction, target lesion revascularization or re-advanced heart failure. Results: Plasma visfatin levels were significantly higher in composite MACE patients than in non-MACE patients. A multivariate Cox hazard regression model revealed that the predictive independent risk factors for the occurrence of composite MACEs were visfatin level (relative risk = 1.04) and age (relative risk = 6.05). When patients were grouped according to their plasma visfatin levels, composite MACEs occurred more frequently in patients presenting with high visfatin levels. Moreover, Kaplan-Meier analysis revealed that high visfatin levels were significantly associated with the occurrence of composite MACEs. Conclusions: The level of plasma visfatin may be associated with risk of composite MACEs in STEMI patients, and may be useful for risk stratification

Glossogyne Tenuifolia Enhances Posttranslational S-Nitrosylation of Proteins in Vascular Endothelial Cells

Glossogyne tenuifolia (GT) is a traditional Chinese herb that possesses strong antioxidant activity and protects against endothelial cell (EC) injury by inhibition of free reactive oxygen species (ROS). The aim of this study was to elucidate the mechanisms by which GT prevents endothelial injury using a proteomics approach. We used a sensitive method to analyze the S- nitrosoproteins utilizing a modified biotin-switch method in order to detect the possible effects of GT on protein posttranslational modification. After treatment of vascular ECs with GT, two proteins HspA9 (IS1), beta-actin (IS2) were observed to have increased posttranslational S-nitrosylation, whereas seven proteins, vimentin (DS2, DS3 and DS5), tropomyosin 3, 4 (DS6 and DS7) and oxidative phosphorylation protein such as ATP synthase, F1 complex (DS1) and 80K-H protein (DS4), were found to have decreased posttranslational S-nitrosylation. Due to S-nitrosylation of HspA9 causing the reduction of intracellular ROS and S-nitrosylation of ATP synthase interfering with ATP production and ROS formation, our study may indicate a novel mechanism in which GT protects EC injury by the inhibition of oxidative reaction