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This short review presents an overview of visible-light-driven asymmetric catalysis by chiral complexes of first-row transition metals. The processes described here include dual catalysis by a chiral complex of copper, nickel, cobalt, or chromium and an additional photoredox or energy-transfer catalyst, and bifunctional catalysis by a single chiral copper or nickel catalyst. These methods allow valuable transformations with high functional group compatibility. They provide stereoselective construction of carbon–carbon or carbon–heteroatom bonds under mild conditions, and produce a diverse range of previously unknown enantioenriched compounds.1 Introduction2 Nickel-Based Photocatalytic Asymmetric Catalysis3 Copper-Based Photocatalytic Asymmetric Catalysis4 Photocatalytic Asymmetric Catalysis by Chiral Complexes of Cobalt or Chromium5 Conclusion

A poly(vinylidene fluoride)/ethyl cellulose and amino-functionalized nano-SiO2 (PVDF-EC-(A-SiO2)) composite coated on polyethylene (PE) is developed as the functional separator of 5 V high-voltage lithium ion batteries with enhanced performance. Compared with the PE separator, the composite membrane has a uniform interconnected structure, an increased melting temperature from 138 °C (PE) to 140.8 °C, a decreased contact angle from 49.5° to 23.2°, and higher ionic conductivity from 0.34 mS cm−1 to 0.79 mS cm−1. In particular, the electrochemical window is raised to 5.3 V (vs. Li/Li+). LiNi0.5Mn1.5O4/Li batteries with this separator display a high discharge capacity of 131.6 mAh g−1 and a superior cycling stability with a capacity retention of 95.7% after 200 cycles at 0.5 C. Those results demonstrate that the PVDF-EC-(A-SiO2)/PE composite separator exhibits a good-performance in cycling stability and thermal stability, implying promising potential application in high-voltage lithium ion batteries.

In this study, glycyrrhetinic acid (GA)-modified D-α-tocopheryl polyethylene glycol 1000 succinate (TPGS) polymeric micelles (TGA PMs) were developed for the delivery of etoposide (ETO) to hepatoma cells. GA was incorporated as a ligand because of its high affinity to the hepatocytes, while TPGS functioned as a P-gp inhibitor to reverse multidrug resistance. ETO-loaded TGA PMs (ETO-TGA PMs) displayed a mean particle size of 133.6±1.2nm with a low poly-dispersity index (0.224±0.013) and negative zeta potential (-16.30mV). The drug loading and entrapment efficiency of ETO-TGA PMs were 10.4% and 79.8%, respectively. ETO-TGA PMs also exhibited faster drug release behavior at pH 5.8 and relatively stable drug release at pH 7.4. Confocal laser scanning microscope (CLSM) observations and in vivo imaging studies revealed that TGA PMs displayed higher cellular uptake and selective accumulation at the tumor site, indicating good tumor targetability. Furthermore, ETO-TGA PMs displayed significant cytotoxicity towards HepG2 cells and higher anti-tumor efficacy (75.96%), compared to the control group. This could be due to TGA-mediated targeted drug delivery to the hepatocytes as well as P-gp inhibition. These findings suggest that TGA PMs have the potential to be used as a targeted drug delivery system for hepatic cancer therapy.

Zein/pectin core-shell nanoparticles with average diameter of about 235 nm and polydispersity index (PDI) of 0.24 were developed to encapsulate, protect and deliver resveratrol. Biopolymer nanoparticles could be formed containing up to 10.2% (w/w) resveratrol, with a particle yield of 91.7% and a resveratrol loading efficiency of 77.9%. The nanoparticles formed were spherical and had good redispersibility in aqueous solutions. The encapsulated resveratrol had a higher in vitro antioxidant activity than free resveratrol as determined by DPPH·, ABTS+ scavenging ability, and iron (III) reducing power. The encapsulated resveratrol also exhibited higher antiproliferative activity when tested using human hepatocarcinoma Bel-7402 cells than free resveratrol, with IC50 values of 17.6 μg/mL (77.2 μM) and 25.6 μg/mL (112.0 μM) respectively. The colloidal form of resveratrol developed in this study may be particularly useful for application in functional foods and beverages, as well as in dietary supplements and pharmaceutical products.

Fused deposition modeling (FDM) is an important process among the available additive manufacturing technologies in various industries. Although there exists many works investigating the effects of FDM process parameters on the mechanical properties of printed materials, there are still several points need to be studied. One is the effects of process parameters on the dynamic mechanical properties of FDM-printed materials, especially in environments where the temperature often changes. The other is the mechanism by which process parameters affect the mechanical properties of printed materials. Aiming at these two points, uniaxial tensile tests and dynamic mechanical analysis are carried out respectively to characterize the tensile properties and dynamic mechanical properties of FDM-printed PLA materials under different FDM process parameters, namely printing angle, layer thickness, fill rate and nozzle temperature. Based on the experimental results explanations are given for the influence of the FDM process parameters on the mechanical properties of the printed materials.

The purpose of this study was to evaluate the antibacterial activity and mechanism of linalool against Pseudomonas aeruginosa. The determination of antibacterial activity was based on the minimum inhibitory concentration (MIC) and the minimum bactericide concentration (MBC). Further, the antibacterial mechanism was explored by a growth curve assay, scanning electron microscopy (SEM), cell membrane permeability, membrane potential and respiratory chain dehydrogenase determination. The MIC and the MBC of linalool were 431 μg/mL and 862 μg/mL, respectively. The growth curve assay showed that the growth of P. aeruginosa was inhibited. The results of SEM revealed that linalool disrupted the normal morphology of the cell. The release of nucleic acids as well as the decrease in the membrane potential proved that the membrane integrity of P. aeruginosa was destroyed. Moreover, the respiratory chain was damaged by respiratory chain dehydrogenase determination as the absorbance at 490 nm decreased. This research suggested that it was possible for linalool to become a preservative of food by destroying the cell membrane, resulting in cell death.

Eisai hyperbilirubinemic rats (EHBR) are mutant Sprague-Dawley rats that exhibit impaired biliary organic anion and reduced glutathione (GSH) secretion. In addition, liver GSH levels are twice that of age- matched controls. The mechanisms for the defect in biliary GSH secretion and the increase in cell GSH are not fully understood. We previously showed that canalicular membrane-enriched vesicles isolated from EHBR livers exhibited normal GSH transport. In the present study, we examined the steady-state rat canalicular reduced glutathione transporter (RcGshT) messenger RNA (mRNA) and protein levels, as well as the mechanisms for the increase in cell GSH. Both Northern and Western blot analyses of EHBR livers showed nearly identical RcGshT mRNA and polypeptide levels, respectively, as compared with controls. Treatment with phenobarbital, which increased steady-state RcGshT mRNA by five- to sixfold, RcGshT polypeptide, and biliary GSH secretion by onefold in controls, had a smaller effect on steady-state RcGshT-mRNA level in EHBR (by 1.5-fold) and did not increase RcGshT polypeptide or biliary GSH secretion. In examining possible mechanisms for increased liver GSH, both cysteine level and gamma-glutamylcysteine synthetase (GCS) activity were significantly higher than controls, while the activity of GSH synthetase was unchanged. Northern and Western blot analyses also showed increased steady-state GCS heavy subunit (GCS-HS) mRNA and polypeptide levels, respectively. In addition to liver, GSH levels in kidney, duodenal, jejunal, and ileal mucosa of EHBR were 200% to 300% of age-matched control rats. GCS activity was also increased in kidney cytosol of EHBR. Thus, the defect in biliary GSH secretion in EHBR most likely is either at the posttranslational level of RcGshT or in the inhibition exerted by retained endogenous organic anions. In addition, there is a widespread up-regulation of GSH synthesis capacity in the tissues of EHBR. (Hepatology 1996 Jul;24(1):253-8)

We have shown previously that plating primary cultures of rat hepatocytes under low density, which stimulates hepatocytes to shift from the G 0 to the G 1 phase of the cell cycle, resulted in increased levels of glutathione (GSH) and cysteine, and increased activity of γ-glutamylcysteine synthetase (GCS), the rate-limiting enzyme in GSH synthesis (Lu et al., Am. J. Physiol. 1992;263:C1181-C1189). In the current work we examined changes in GSH homeostasis after two-thirds partial hepatectomy (PH). Male Sprague-Dawley rats underwent two-thirds PH or sham operation. GSH, oxidized glutathione (GSSG), cysteine, GSH efflux, DNA synthesis, changes in GCS subunit messenger RNA (mRNA), and protein levels were measured 12 and 24 hours after PH. Both liver GSH and cysteine levels were doubled at 12 hours and remained elevated at 24 hours after PH. GSSG levels also increased, but the ratio of GSH to GSSG levels remained unchanged. The increase in GSH and cysteine levels preceded the increase in DNA synthesis. Sinusoidal GSH efflux was unchanged after two-thirds PH, but biliary GSH efflux decreased. However, total GSH efflux was minimally altered after two-thirds PH. The increase in GSH can be largely accounted for by the increase in both cysteine availability and the activity of GCS. The steady-state mRNA and protein levels of the GCS heavy subunit were increased at 12 hours after PH. The mRNA level of the GCS light subunit was unchanged. In summary, early in the course of liver regeneration the steady-state hepatic GSH levels double because of an increase in the biosynthesis of GSH.

gamma-Glutamylcysteine synthetase (GCS) is the rate-limiting enzyme in the biosynthesis of glutathione and is composed of a heavy and a light subunit. Although the heavy subunit is enzymically active alone, the light subunit plays an important regulatory role by making the holoenzyme function more efficiently. In the current study we examined whether conditions which are known to influence gene expression of the heavy subunit also influence that of the light subunit, and the mechanisms involved. Treatment of cultured rat hepatocytes with hormones such as insulin and hydrocortisone, or plating hepatocytes under low cell density increased the steady-state mRNA level of the heavy subunit only. Treatment with diethyl maleate (DEM), buthionine sulphoximine (BSO) and t-butylhydroquinone (TBH) increased the steady state mRNA level and gene transcription rates of both subunits. These treatments share in common their ability to induce oxidative stress and activate nuclear factor kappa B (NF-kappa B). Treatment with protease inhibitors 7-amino-1-chloro-3-tosylamido-2-heptanone (TLCK) or L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK) had no influence on the basal NF-kappa B and GCS subunit mRNA levels, but blocked the activation of NF-kappa B by DEM, BSO and TBH, and the increase in GCS heavy subunit mRNA level by BSO and TBH. On the other hand, the DEM-, BSO- and TBH-induced increase in GCS light-subunit mRNA level was unaffected by TLCK and TPCK. Thus only the heavy subunit is hormonally regulated and growth sensitive, whereas both subunits are regulated by oxidative stress. Signalling through NF-kappa B is involved only in the oxidative-stress-mediated changes in the heavy subunit gene expression.

S-adenosylmethionine synthetase (SAMS) catalyzes the formation of S-adenosylmethionine (SAM) and is essential to normal cell function. There are two forms of SAMS, liver-specific and nonliver-specific (often referred to as "kidney"), which are products of two different genes. SAMS isoenzymes differ greatly in kinetic parameters and sensitivity to inhibition by methionine analogs. The current work studied changes in SAMS and their significance in liver cancer. Northern blot analysis showed that while normal liver expresses only liver-specific SAMS, both HepG2 and HuH-7 cells express only nonliver-specific SAMS. Absence of liver-specific SAMS messenger RNA (mRNA) was not because of gene deletion or rearrangement but complete lack of gene transcription. Reverse-transcription polymerase chain reaction (RT-PCR) with liver- and kidney-specific SAMS primers showed that liver-specific SAMS mRNA was absent with only kidney SAMS mRNA present in HepG2, HuH-7, Hep3B, and HuH-1 cells, and four consecutive hepatocellular carcinoma (HCC) specimens. Normal liver tissues from the same patients express both forms of SAMS mRNA. As a result of the change in SAMS expression, SAMS activity was higher in HepG2 and HuH-7 cells at physiologically relevant methionine concentrations but lower at high (mmol/L) methionine concentrations than rat hepatocytes. Treatment with ethionine and seleno-D,L-ethionine, two inhibitors known to have I50 values 50 to 60 times lower against SAMS purified from Novikoff hepatoma cells as compared with SAMS purified from normal rat liver, resulted in increased cell lysis in HepG2 and HuH-7 cells but not cultured rat hepatocytes. These agents did not affect cellular adenosine triphosphate (ATP) levels but inhibited SAMS activity in HepG2 and HuH-7 cells when added to their protein extracts. In summary, expression of SAMS is altered in human liver cancer. This occurrence may provide a potentially exploitable target for cancer chemotherapy.

Methionine adenosyltransferase (MAT) catalyzes the formation of S-adenosylmethionine (SAM), the principal methyl donor, and is essential to normal cell function. The two forms of MAT, liver-specific and nonliver specific, are products of two different genes, MAT1A and MAT2A, respectively. Mature liver expresses mainly MAT1A. We reported a switch from MAT1A to MAT2A gene expression in human liver cancer cells (Hepatology 24:1090-1097, 1996). We also showed in a cell line model which expresses different types of MAT that expression of MAT2A was associated with more rapid cell growth and DNA synthesis (Gastroenterology 112:A1235, 1997). In the current work we examined the possible mechanisms involved. METHODS: A HUH-7 cell line model which expresses different types of MAT was established by transfection and antisense strategies. Different types of MAT differ greatly in their kinetic properties and in the feedback inhibition exerted by SAM, which strongly inhibits only the product of MAT2A. To see if differences in MAT expression resulted in changes in the steady state levels of SAM, S-adenosylhomocysteine (SAIl) and DNA methylation, these were measured using high performance liquid chromatography. These same parameters were also measured along with cell growth and DNA synthesis in untransfected HUH-7 ceils supplemented with SAM (lmM) for four days. RESULTS: Untransfected HUH-7 cells which express only MAT2A had the lowest SAM level (0.54 ± 0.003 nmol/mg protein) and SAM to SAH ratio (1.36 ± 0.13). Both SAM level and SAM to SAH ratio increased by 50-75% after MAT1A-transfection and by an additional 60-80% after MAT2A-antisense treatment. SAH levels were not significantly influenced by MAT expression. DNA methylation changed in parallel to changes in SAM level and SAM to SAH ratio. Supplementing nntransfected HUH-7 ceils with SAM in the culture medium increased SAM level, SAM to SAH ratio and DNA methylation and decreased cell growth and DNA synthesis. CONCLUSIONS: The steady state SAM level, SAM to SAH ratio and DNA methylation are influenced by the type of MAT expressed. The differences in SAM to SAH ratio and DNA methylation are most likely responsible for the differences in the rate of cell growth observed.