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Background: Pulmonary surfactant dysfunction is an important pathological factor in acute respiratory distress syndrome (ARDS) and pulmonary fibrosis (PF). Objective: In this study, the characteristics of recombinant mature surfactant protein B (SP-B) and reteplase (rPA) fusion protein maintaining good pulmonary surface activity and rPA fibrinolytic activity in acute lung injury cell model were studied. Methods: We studied the characteristics of SP-B fusion expression, cloned rPA gene and N-terminal rPA/C-terminal SP-B co-expression gene, and constructed them into eukaryotic expression vector pEZ-M03 to obtain recombinant plasmids pEZ-rPA and pEZ-rPA/SP-B. The recombinant plasmids was transfected into Chinese hamster ovary (CHO) K1 cells and the expression products were analyzed by Western Blot. Lipopolysaccharide (LPS) was used to induce CCL149 (an alveolar epithelial cell line) cell injury model. Fluorescence staining of rPA and rPA/SP-B was carried out with the enhanced green fluorescent protein (eGFP) that comes with pEZ-M03; the cell Raman spectroscopy technique was used to analyze the interaction between rPA/SP-B fusion protein and the phospholipid structure of cell membrane in CCL149 cells. The enzyme activity of rPA in the fusion protein was determined by fibrin-agarose plate method. Results: The rPA/SP-B fusion protein was successfully expressed. In the CCL149 cell model of acute lung injury (ALI), the green fluorescence of rPA/SP-B is mainly distributed on the CCL149 cell membrane. The rPA/SP-B fusion protein can reduce the disorder of phospholipid molecules and reduce cell membrane damage. The enzyme activity of rPA/SP-B fusion protein was 3.42, and the fusion protein still had good enzyme activity. Conclusion: The recombinant eukaryotic plasmid pEZ-rPA/SP-B is constructed and can be expressed in the eukaryotic system. Studies have shown that rPA/SP-B fusion protein maintains good SP-B lung surface activity and rPA enzyme activity in acute lung injury cell model.

Nuclear factor-erythroid 2 related factor 2 (Nrf2) plays critical roles in attenuating various inflammation- and oxidative stress-induced diseases, including acute lung injury (ALI). Bardoxolone (Bard), a synthetic triterpenoid based on natural product oleanolic acid, is one of the most potent Nrf2 activator. However, if Bard could prevent lipopolysaccharide (LPS)-induced ALI by inducing Nrf2 activation and its down-streaming signals, is still poorly understood. In this study, we attempted to explore the protective effect of Bard on ALI and the underlying molecular mechanisms. The results indicated that Bard significantly attenuated ALI through reducing the lung wet/dry weight ratio and protein concentration, neutrophil infiltration, malondialdehyde (MDA) and myeloperoxidase (MPO) levels, and improving superoxide dismutase (SOD) and glutathione (GSH) activities. In addition, Bard effectively ameliorated histopathological alterations, reactive oxygen species (ROS) production, pro-inflammatory cytokines release, and the expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX2) and high mobility group box 1 (HMGB1). Moreover, the inhibitory role of Bard in inflammation was also attributed to its suppression of nuclear factor-κB (NF-κB) signaling. Furthermore, the activation of mitogen-activated protein kinases (MAPKs) signaling, including p38, extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK), induced by LPS was substantially ameliorated by Bard. The beneficial effects of Bard on ALI were confirmed in LPS-incubated cells in vitro. Meanwhile, the in vitro studies also demonstrated that Bard-improved ALI was largely due to its role in inducing Nrf2 signaling through a dose-dependent manner. Importantly, we found that Bard-attenuated histological changes, inflammation, ROS production, NF-κB and MAPKs signaling in Nrf2+/+ mice were significantly abolished in mice with Nrf2 knockout. Therefore, our study for the first time provided evidence that Bard could effectively ameliorate LPS-induced ALI by reducing oxidative stress and inflammation mainly through the activation of Nrf2 signaling.

Esophageal squamous cell carcinoma (ESCC) is a common malignancy without effective therapy. Histone deacetylase inhibitors (HDACIs) have been demonstrated as an emerging class of anticancer drugs for a range of haematological and solid tumours. However, the effect of HDACIs has not yet been investigated on ESCC cells. In this study, HDACIs were initially considered to have anticancer activity for ESCC, due to the high expression of HDAC genes in ESCC cell lines by analysing expression data of 27 ESCC cell lines from the Broad-Novartis Cancer Cell Line Encyclopedia. Next, we used five ESCC cell lines and one normal immortalized esophageal epithelial cell line to screen three HDACIs, panobinostat (LBH589), vorinostat (SAHA), and trichostatin A (TSA), for the ability to inhibit growth. Here, we report that LBH589 more effectively suppressed cell proliferation of ESCC cell lines, in a dose-dependent manner, than TSA and SAHA, as well as had lower toxicity against the SHEE normal immortalized esophageal epithelial cell line. Further experiments indicated that LBH589 treatment significantly inhibited TP53 (mutated TP53) expression, both at the mRNA and protein level, and simultaneously increased p21 and decreased cyclin D1 expression. Taken together, we propose that LBH589 inhibits ESCC cell proliferation mainly through inducing cell cycle arrest by increasing p21 and decreasing cyclin D1 in a p53-independent manner. SIGNIFICANCE OF THE STUDY: In this study, the antitumor activity of HDACIs LBH589, SAHA, and TSA on ESCC was characterized, with LBH589 displaying the most potent anti-proliferative activity while not harming normal immortalized esophageal epithelial cells. Furthermore, we propose that LBH589 exerts its anti-proliferative effect by inducing cell cycle arrest. The ability to specifically target cancer cells indicates therapeutic potential for use of LBH589 in the treatment of ESCC.

Restoring immune balance by targeting macrophage polarization is a potentially valuable therapeutic strategy for ulcerative colitis (UC). Dioscin is a steroidal saponin with potent anti-inflammatory, immunoregulatory, and hypolipidemic effects. This study examined the protective effect of Dioscin on UC in mice and explored the underlying mechanisms. Mice were induced colitis by dextran sulfate sodium (DSS) and concurrently treated with Dioscin oral administration. RAW264.7 cells were skewed to M1 macrophage polarization by lipopolysaccharide (LPS) and interferon-γ (INF-γ) in vitro, and received Dioscin treatment. The results showed that Dioscin ameliorated colitis in mice, reduced macrophage M1 polarization, but markedly promoted M2 polarization in mice colon. Dioscin inhibited mammalian target rapamycin complex 1 (mTORC1)/hypoxia-inducible factor-1α (HIF-1α) signaling and restrained glycolysis in RAW264.7; however, it activated mammalian target rapamycin complex 2 (mTORC2)/peroxisome proliferator-activated receptor-γ (PPAR-γ) signal and facilitated fatty acid oxidation (FAO). The modulation of mTORs signaling may inhibit M1, but promote M2 polarization. Furthermore, the effect of Dioscin on M2 polarization was neutralized by the FAO inhibitor Etomoxir and the mTORC2 inhibitor JR-AB2-011. In parallel, the inhibitory effect of Dioscin on M1 polarization was mitigated by the mTORC1 agonist L -leucine. Both JR-AB2-011 and L -leucine blocked the therapeutic effect of Dioscin in mice with UC. Therefore, Dioscin ameliorated UC in mice, possibly by restraining M1, while skewing M2 polarization of macrophages. Regulation of mTORC1/HIF-1α and mTORC2/PPAR-γ signals is a possible mechanism by which Dioscin inhibited aerobic glycolysis and promoted FAO of macrophages. In summary, Dioscin protected mice against DSS-induced UC by regulating mTOR signaling, thereby adjusting macrophage metabolism and polarization.

In a recent experimental research, the formation of naphthalene has been demonstrated by La-mediated acetylene bicyclo-oligomerization in the gas phase, and this is the first report of metal-activated acetylene bicyclo-oligomerization to form the naphthalene. In this work, the complete reaction mechanism has been systematically analyzed on the doublet potential energy surface by employing density functional theory (DFT), the results showed that the computational results were consistent with experimental dates. Among them, two possible reaction pathways were identified: (1) LaC4H2 is formed by a second addition of acetylene molecule to LaC2H2 followed by dehydrogenation (path (a)). (2) First, dehydrogenation of LaC2H2, followed by the addition of a second acetylene molecule (path (b)), we found that the optimum pathway was path (a). According to the thermodynamic point of view, the reaction is highly exothermic and favorable. In addition, sequential acetylene additions coupled with dehydrogenation showed that the bicycle-oligomerization reaction can occur. For further analysis of the observed kinetic behavior, the energetic span model was utilized and confirmed the TOF-determining transition state (TDTS) and TOF-determining intermediate (TDI) of the overall reaction. Finally, the optimum path was found and demonstrated.

Despite the increased morbidity of ulcerative colitis (UC) in recent years, available treatments remain unsatisfactory. Pogostemon cablin has been widely applied to treat a variety of gastrointestinal disorders in clinic for centuries, in which patchouli alcohol (PA, C15H26O) has been identified as the major active component. This study attempted to determine the bioactivity of PA on dextran sulfate sodium (DSS)-induced mice colitis and clarify the mechanism of action. Acute colitis was induced in mice by 3% DSS for 7 days. The mice were then given PA (10, 20 and 40mg/kg) or sulfasalazine (SASP, 200mg/kg) as positive control via oral administration for 7 days. At the end of study, animals were sacrificed and samples were collected for pathological and other analysis. In addition, a metabolite profiling and a targeted metabolite analysis, based on the Ultra-Performance Liquid Chromatography coupled with mass spectrometry (UPLC-MS) approach, were performed to characterize the metabolic changes in plasma. The results revealed that PA significantly reduced the disease activity index (DAI) and ameliorated the colonic injury of DSS mice. The levels of colonic MPO and cytokines involving TNF-α, IFN-γ, IL-1β, IL-6, IL-4 and IL-10 also declined. Furthermore, PA improved the intestinal epithelial barrier by enhancing the level of colonic expression of the tight junction (TJ) proteins, for instance ZO-1, ZO-2, claudin-1 and occludin, and by elevating the levels of mucin-1 and mucin-2 mRNA. The study also demonstrated that PA inhibited the DSS-induced cell death signaling by modulating the apoptosis related Bax and Bcl-2 proteins and down-regulating the necroptosis related RIP3 and MLKL proteins. By comparison, up-regulation of IDO-1 and TPH-1 protein expression in DSS group was suppressed by PA, which was in line with the declined levels of kynurenine (Kyn) and 5-hydroxytryptophan (5-HTP) in plasma. The therapeutic effect of PA was evidently reduced when Kyn was given to mice. In summary, the study successfully demonstrated that PA ameliorated DSS-induced mice acute colitis by suppressing inflammation, maintaining the integrity of intestinal epithelial barrier, inhibiting cell death signaling, and suppressing tryptophan catabolism. The results provided valuable information and guidance for using PA in treatment of UC.

The influences of rolling reduction and aluminum sheet initial thickness (AIT) on the thickness fluctuation of aluminum layer (TFA) of embedded aluminum–steel composite sheet produced by cold roll bonding were investigated, the formation mechanism of TFA was analyzed and method to improve the thickness uniformity of the aluminum layer was proposed. The results showed that when the reduction increased, TFA increased gradually. When the reduction was lower than 40%, AIT had negligible effect on the TFA, while TFA increased with the decrease of AIT when the reduction was higher than 40%. The non-uniformities of the steel surface deformation and the interfacial bonding extent caused by the work-hardened steel surface layer, were the main reasons for the formation of TFA. Adopting an appropriate surface treatment can help to decrease the hardening extent of the steel surface for improving the deformation uniformity during cold roll bonding process, which effectively improved the aluminum thickness uniformity of the embedded aluminum/steel composite sheets.

The Ordovician fracture-cavity carbonate rocks in Tahe Oilfield are highly heterogeneous. The development of reservoirs is not controlled by sedimentary facies, but is determined by tectonic karst. Therefore, conventional reservoir modeling ideas and the method is not applicable. In view of the strong heterogeneity of carbonate fracture-cavity reservoirs in the No.4 Block of Tahe Oilfield, the geological, drilling, logging and seismic data are fully integrated, and the traditional “phase-control modeling” idea is taken into account. Based on the karst development model of the Ordovician in the No.4 Block of Tahe Oilfield, the multi-point statistical reservoir modeling method is used to assign the meaning of the phase to the reservoir. According to the relationship between the seismic attributes and the fracture cavity, the “training image” of the “reservoir facies” is established from the seismic attributes, and the Sensim algorithm is used to simulate and establish a three-dimensional geological model of the reservoir facies. The results show that the use of reservoir phase control modeling based on the multi-point statistics not only reduces the uncertainty of stochastic modeling of fracture-cavity carbonate reservoirs, but also significantly improves the accuracy of the model, which can accurately reflect the heterogeneity of fracture-cavity reservoirs.

Livistona chinensis fruit is a traditional Chinese medicine widely used for treating hepatitis, but its protective effect against hepatitis remains unknown. This study investigated the hepatoprotective effect and mechanism of flavonoids from Livistona chinensis fruit (FLCF). Mice received FLCF pre-treatment for 7 days and induced liver injury with LPS+D-GalN. RAW264.7 cells were triggered inflammation by LPS and received FLCF for 24 h. The result showed that FLCF ameliorated the liver pathology in mice, decreased the levels of AST, ALT, MDA, but increased SOD and GSH. Moreover, FLCF inhibited TLR4/NF-κB signaling, while activated Nrf2/HO-1 signaling in LPS+D-GalN mice. These effects were consistent with the in vitro data revealing that FLCF suppressed TLR4/NF-κB signaling, while promoting Nrf2/HO-1 signaling in RAW264.7 cell. The effects of FLCF were neutralized by Nrf2 siRNA. Taken together, these results demonstrated that FLCF has a protective role against acute liver injury and supports its use as a dietotherapy.

Triptolide (TP) is the major active component of Tripterygium wilfordii Hook F (TWHF) and possesses multiple pharmacological effects. However, hepatotoxicity of TP which is one of the toxic properties slows its progression in clinical application. 18β-Glycyrrhetinic acid (GA) is the main bioactive ingredient of Licorice (Glycyrrhiza glabra L.), a herbal medicine famous for its detoxification. This study aims to investigate whether GA possesses protective effect against TP-induced hepatotoxicity in rats. TP interference markedly elevated serum levels of ALT, AST, and ALP, caused evident liver histopathological changes, and elevated hepatic TNF-α, IL-6, IL-1β, and IFN-γ as well as nuclear translocation of NF-κB. TP also significantly elevated liver MDA and declined hepatic activities of SOD, CAT, and GSH-Px. Assay of TUNEL and apoptosis proteins (Bax, Bcl-2, and active caspase-3) showed that TP induced severe hepatocellular apoptosis. In contrast, low-dose GA (50 mg/kg) significantly reversed TP-induced changes above. However, high-dose GA (100 mg/kg) had no such effect. Overall, these findings indicated that low-dose GA but not high-dose GA exhibited a protective effect against TP-induced hepatotoxicity in rats by anti-inflammation, antioxidation, and antiapoptosis, which suggests that the doses of GA/Licorice should be carefully considered when used together with TWHF or TWHF preparations.

Forsterite insulating materials were prepared by molten salt method using forsterite powder, pulp waste, NaCl and Na2CO3 as raw material. The pore size distribution and pore structural parameters of the sample were studied by nitrogen adsorption-desorption method. The fractal dimension of pore was obtained based on FHH (Frenkel-Halsey-Hill) equation. The results showed that adsorption-desorption isotherm of the sample was identified as type II due to the long-narrow pore with narrow openings. The pore size and fractal dimension decreased with the temperature increased. The maximum pore size was about 2 nm in the sample heated at 1100°C in the condition of different content of molten salt. And optimal thermal insulation performance of the sample were obtained in the sample contained 30 wt% Na2CO3 and heat treated at 1100°C.

Starting from different sizes of magnesia and bauxitewith sodium hexametaphosphate as anchoring agent, specimens obtained by suppression were sintered at 1500°C and 1550°C and heat preservation for 3h in the electric hearth furnace, respectively. The effect of particle size distribution of magnesia and bauxite on the properties of magnesia-alumina refractory materials was investigated. The composition of magnesia-alumina refractory which consists of various particle size distributions was determined, according to Andreasen packing model, with distribution coefficient (q) of 0.15, 0.20, 0.25, 0.30, 0.35, 0.40 and 0.50. The fractographs of the specimen were observed by scanning electron microscopy. The linear rate of change, apparent porosity, bulk density and crushing strength of these specimens were studied. The results showed: a crushing strength of 52.39 MPa, an apparent porosity value of 15.55% and a bulk density value of 2.91 g/cm3 were obtained via a particle size distribution coefficient of 0.30 at 1550°C. Simultaneously, the refractory materials had small linear rate of change.

Activation of NLRP3 inflammasomes is crucial in the pathological process of Ulcerative colitis (UC), which could be negatively regulated by PINK1/Parkin-driven mitophagy. Palmatine is a herb derived isoquinoline alkaloid with potent anti-inflammatory and anti-bacteria activities. In present study, we evaluated the effect of palmatine on dextran sulfate sodium (DSS)-induced mice colitis and examined whether its effect is exerted by promoting mitophagy-mediated NLRP3 inflammasome inactivation. The result showed that palmatine (40, 100 mg/kg) significantly prevented bodyweight loss and colonic shortening in DSS mice, and reduced the disease activity index and histopathologic score. The levels of MPO, IL-1β, TNF-α and the number of F4/80+ cells in colon of DSS mice were remarkably decreased by palmatine. Moreover, palmatine suppressed NLRP3 inflammasomes activation, but enhanced the expression of the mitophagy-related proteins involving LC3, PINK1 and Parkin in colonic tissue of DSS mice. These effects was consistent with the in vitro data revealing that palmatine inhibited the activation of NLRP3 inflammasomes, while promoted the expression and mitochondrial recruitment of PINK1 and Parkin in THP-1 cell differentiated macrophages. Furthermore, the effect of palmatine on THP-1 cells was neutralized by a mitophagy inhibitor Cyclosporin A (CsA) and PINK1-siRNA. In parallel, CsA significantly attenuated the therapeutic effect of palmatine in DSS mice, illustrating that the anti-colitis effect of palmatine is closely related to mitophagy. Taken together, the current results demonstrated that palmatine protected mice against DSS-induced colitis by facilitating PINK1/Parkin-driven mitophagy and thus inactivating NLRP3 inflammasomes in macrophage.

Mitofusin 2 (Mfn2) is expressed in numerous human tissues and serves a pivotal role in cell proliferation. However, Mfn2 is considered as an anti-tumor gene, and is silenced in human malignant tumors, including those of breast cancer. However, the mechanisms contributing to Mfn2 silencing and the mechanism of its anti-tumor function in breast cancer remain unclear. In the present study, hypoexpression of Mfn2, and hypermethylation of its promoter, was confirmed in human breast cancer cells and in breast cancer tissues by reverse transcription-quantitative polymerase chain reaction (PCR) and methylation specific PCR, respectively. Chemical demethylation treatment with 5-aza-2'-deoxycytidine upregulated the mRNA expression level of Mfn2 in MCF-7 cells in a dose-dependent manner. In addition, overexpression of Mfn2 repressed the proliferation, migration and invasion of MCF-7 cells, mediated by inhibition of the Ras-extracellular signal-regulated kinase (ERK)1/2 signaling pathway. However, overexpression of Mfn2 with deletion of the p21Ras motif (Mfn2ΔRas) and protein kinase A (PKA) phosphorylation site (Mfn2ΔPKA) partially reduced the anti-tumor function of Mfn2, and inhibited the Ras-ERK1/2 signaling pathway. Taken together, the present study confirmed the anti-tumor effects of Mfn2 in human breast cancer and clarified that the mechanism of its anti-tumor functions includes promoter DNA methylation, the P21Ras binding site and PKA phosphorylation.

The effects of amino acid supply and insulin infusion on skin protein kinetics (fractional synthesis rate (FSR), fractional breakdown rate (FBR), and net balance (NB)) in pigs were investigated. Four-month-old pigs were divided into four groups as follows: control, insulin (INS), amino acid (AA), and INS + AA groups based on the nutritional and hormonal conditions. l-[ring-(13)C6]Phenylalanine was infused. FBR was estimated from the enrichment ratio of arterial phenylalanine to intracellular free phenylalanine. Plasma INS was increased (p < 0.05) in the INS and INS + AA groups. Plasma glucose was maintained by infusion of glucose in the groups receiving INS. The interventions did not change the NB of skin protein. However, the interventions affected the FSR and FBR differently. An infusion of INS significantly increased both FSR and FBR, although AA infusion did not. When an AA infusion was added to the infusion of insulin (INS + AA group), FSR and FBR were both lower when compared with the INS group. Our data demonstrate that in anesthetized pigs INS infusion did not exert an anabolic effect, but rather it increased AA cycling into and out of skin protein. Because co-infusion of AAs with INS ameliorated this effect, it is likely that the increased AA cycling during INS infusion was related to AA supply. Although protein kinetics were affected by both INS and AAs, none of the interventions affected the skin protein deposition. Thus, skin protein content is closely regulated under normal circumstances and is not subject to transient changes in AAs or hormonal concentrations.

The liver plays a central role in regulating fat metabolism; however, it is not clear how the liver distributes the synthesized triglycerides (TGs) to storage and to the plasma.We have measured the relative distribution of TGs produced in the liver to storage and the plasma by means of U-(13)C(16)-palmitate infusion in anesthetized rabbits after an overnight fast.The fractional synthesis rates of TGs stored in the liver and secreted into the plasma were not significantly different (stored vs. secreted: 31.9 ± 0.8 vs. 27.7 ± 2.6%∙h(-1), p0.05). However, the absolute synthesis rates of hepatic stored and secreted TGs were 543 ± 158 and 27 ± 7 nmol∙kg(-1)∙min(-1) respectively, indicating that in fasting rabbits the TGs produced in the liver were predominately stored (92 ± 3%) rather than secreted (8 ± 3%) into the plasma. This large difference was mainly due to the larger pool size of the hepatic TGs which was 21 ± 9-fold that of plasma TGs. Plasma free fatty acids (FFAs) contributed 47 ± 1% of the FA precursor for hepatic TG synthesis, and the remaining 53 ± 1% was derived from hepatic lipid breakdown and possibly plasma TGs depending on the activity of hepatic lipase. Plasma palmitate concentration significantly correlated with hepatic palmitoyl-CoA and TG synthesis.In rabbits, after an overnight fast, the absolute synthesis rate of hepatic stored TGs was significantly higher than that of secreted due to the larger pool size of hepatic TGs. The net synthesis rate of TG was approximately half the absolute rate. Plasma FFA is a major determinant of hepatic TG synthesis, and therefore hepatic TG storage.

Porous composite insulating scaffolds were prepared from mixtures of forsterite, salt (Na2CO3), and phenolic resin by sintering at 900 to 1 100 °C for 10 h, and the sintering behaviour and mechanical properties were examined. The results show that the changes in temperature did not significantly affect the phases present in the samples. However, changing the Na2CO3 content of a sample will change its phase composition. When the Na2CO3 content was 40 wt.% and sintering undertaken at 1 000 °C, the apparent porosity of the sample was 57 %, and its strength was 3.1 MPa. The large number of pores in the samples had diameters of approximately one micron, while the mesopores had diameters concentrated over the interval of 3 to 5 nm.

Ethnopharmacological relevance Pogostemon cablin has been widely used in traditional Chinese medicine for the treatment of many diseases, including skin disorders. In the skin beauty and care prescriptions, Pogostemon cablin is one of the top ten frequently used traditional Chinese medicines. Aim of the study The present study was aimed to investigate the protective effects of the essential oil of Pogostemon cablin (patchouli oil, PO) against UV-induced skin photoaging in mice. Materials and methods To ensure the quality of PO, the chemical compositions of PO were identified, and the content of its chemical marker patchouli alcohol was determined, which was around 28.2% (g/g) in PO. During the experiment period, the dorsal depilated skin of mice was treated with PO for two hours prior to UV irradiation. Then the protective effects of PO on UV-induced skin photoaging were determined by macroscopic and histological evaluations, skin elastic test, collagen content determination and biochemical assays of malondiaidehyde (MDA) content, activities of anti-oxidative indicators including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT). Results Compared to UV exposure groups, present results showed that topical administration of PO, especially at dose of 6 mg/mouse and 9 mg/mouse, significantly inhibited the increase in skin wrinkle formation, alleviated the reduction in skin elasticity and increased the collagen content by about 21.9% and 26.3%, respectively. We also found that application of 6–9 mg/mouse PO could not only decrease the epidermal thickness by about 32.6%, but also prevent the UV-induced disruption of collagen fibers and elastic fibers. Furthermore, the content of MDA was decreased by almost 26.5% and activities of SOD, GSH-Px and CAT were significantly up-regulated after the treatment of PO. Conclusion Results of present study revealed that PO was capable of maintaining skin structural integrity caused by UV irradiation and it was useful in preventing photoaging. These protective effects of PO were possibly due to its anti-oxidative property. Therefore, we suggested that PO should be viewed as a potential therapeutic agent for preventing photoaging.

Silicon carbide nanowires were synthesized on the surface of graphite by partially reacting with silicon powders in NaF–NaCl based salt at 1150–1400 °C in argon. The effects of temperature and time of heat treatment as well as Si/graphite ratio on synthesis of SiC nanowires were studied. The results showed that the formation of SiC nanowires started at about 1200 °C, and the amounts of SiC nanowires increased in the resultant powders with increasing temperature. Their morphologies were characterized by scanning electron microscopy and high-resolution transmission electron microscopy. It was found that β-SiC nanowires with diameter of 10–50 nm and various lengths grew along their preferred direction perpendicular to (111). The zeta potential of graphite was also increased after coating with silicon carbide nanowires. SiC nanowires that formed on the graphite surface acted as an anti-oxidant to a certain extent, and they protected the inner graphite from oxidation.

In this paper, the phase compositions and microstructure of MgO-C samples containing Si powder in N2sintered at 1350-1500°C were investigated by X-ray diffraction (XRD) and scanning electron microscope (SEM). The α-Si3N4, β-Si3N4, MgSiN2and SiC phases have formed together with MgO and C phases in the sintered samples. The morphologies of β-Si3N4crystals were almost in the shape of rod-like through the α-β phase transformation of Si3N4by Mg-Si-O-N and silicon liquid. The morphologies of α-Si3N4crystals were in the shape of equiaxed. The morphology of MgSiN2crystals was in the shape of polyhedron with the size of 5 μm.

Using the natural forsterite and Na2CO3 as a raw material, the forsterite lightweight material was prepared in Na2CO3 molten salt. The reaction between forsterite and Na2CO3 and sintering mechanism of forsterite were studied in the paper. The sintering temperature was 1000 °C, 1100 °C, and the holding time was 1 h, 3 h, 5 h, 7 h, 10 h, respectively. The sintered samples were characterized by XRD and SEM for their microstructure and phase composition analysis which determined the mechanism of the chemical reaction and sintering in the sintering process. The product of Na2MgSiO4 phase in In earlier period of the reactions promoted the rearrangement of particles of forsterite in the initial stage of sintering process. The sintering mechanism was mainly controlled by the diffusion mechanism.

The supercritical-carbon dioxide fluid extract ofChrysanthemum indicumLinné. (CFE) has been demonstrated to be effective in suppressing inflammation. The aim of this study is to investigate the preventive action and underlying mechanisms of CFE on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. ALI was induced by intratracheal instillation of LPS into lung, and dexamethasone was used as a positive control. Results revealed that pretreatment with CFE abated LPS-induced lung histopathologic changes, reduced the wet/dry ratio and proinflammatory cytokines productions (TNF-α, IL-1β, and IL-6), inhibited inflammatory cells migrations and protein leakages, suppressed the levels of MPO and MDA, and upregulated the abilities of antioxidative enzymes (SOD, CAT, and GPx). Furthermore, the pretreatment with CFE downregulated the activations of NF-κB and the expressions of TLR4/MyD88. These results suggested that CFE exerted potential protective effects against LPS-induced ALI in mice and was a potential therapeutic drug for ALI. Its mechanisms were at least partially associated with the modulations of TLR4 signaling pathways.

The therapeutic effect of corilagin (1) was evaluated in an acute colitis model induced by dextran sulfate sodium (DSS) in mice, and the mechanism of action was investigated in this study. Animals were challenged with 2% DSS drinking water for 5 consecutive days and then intraperitoneally treated with 1 (7.5, 15, and 30 mg/kg) daily for 7 days. It was found that 1 significantly decreased the disease activity index, inhibited the shortening of colon length, reduced colon tissue damage, and suppressed myeloperoxidase activity. Moreover, 1 greatly suppressed the secretion of TNF-α, IL-6, and IL-1β, inhibited the degradation of IκB α, and down-regulated expression of cleaved caspase-3 and cleaved caspase-9 in colon tissues of DSS-treated mice. These findings demonstrated that 1 exerts a protective effect on DSS-induced colitis, and its underlying mechanisms are associated with inhibition of the NF-κB pathway that mitigates colon inflammatory responses and apoptosis of intestinal epithelial cells.

The measurement of the fractional breakdown rate (FBR) of muscle proteins during physiological non-steady state of amino acids (AAs) presents some challenges. Therefore, the goal of the present experiment was to modify the bolus stable isotope tracer injection approach to determine both fractional synthesis rate (FSR) and FBR of leg muscle protein during a physiological non-steady state of AAs. The approach uses the traditional precursor-product principle but is modified with the assumption that inward transport of AAs is proportional to their plasma concentrations. The FBR value calculated from the threonine tracer served as a reference to evaluate the validity of the FBR measurement from the phenylalanine tracer, which was under a non-steady-state condition due to the concomitant injection of unlabeled phenylalanine. Plasma phenylalanine concentration increased more than fourfold after the bolus injection, and thereafter it decreased exponentially, whereas the threonine concentration remained stable. FBR values were similar with the two tracers [0.133 ± 0.003 and 0.148 ± 0.003%/h (means ± SE) for the phenylalanine and threonine tracers, respectively, P > 0.05]. In addition, FSR values for the two tracers were similar (0.069 ± 0.002 and 0.067 ± 0.001%/h for the phenylalanine and threonine tracers, respectively, P > 0.05), indicating that the traditional FSR approach can also be used in the non-steady state. Accordingly, net balance (NB) values were similar (−0.065 ± 0.002 and −0.081 ± 0.002%/h for the phenylalanine and threonine tracers, respectively, P > 0.05). This new method of measuring muscle protein FBR during physiological non-steady state gives reliable results and allows simultaneous measurement of muscle protein FSR and thus a calculation of NB.

The aim of this study was to investigate the anti-inflammatory property of the ethanol extract of the root and rhizome ofPogostemon cablin(ERP). The anti-inflammatory effect was evaluated using four animal models including xylene-induced mouse ear edema, acetic acid-induced mouse vascular permeability, carrageenan-induced mouse pleurisy, and carrageenan-induced mouse hind paw edema. Results indicated that oral administration of ERP (120, 240, and 480 mg/kg) significantly attenuated xylene-induced ear edema, decreased acetic acid-induced capillary permeability, inhibited carrageenan-induced neutrophils recruitment, and reduced carrageenan-induced paw edema, in a dose-dependent manner. Histopathologically, ERP (480 mg/kg) abated inflammatory response of the edema paw. Preliminary mechanism studies demonstrated that ERP decreased the level of MPO and MDA, increased the activities of anti-oxidant enzymes (SOD, GPx, and GRd), attenuated the productions of TNF-α, IL-1β, IL-6, PGE2and NO, and suppressed the activities of COX-2 and iNOS. This work demonstrates that ERP has considerable anti-inflammatory potential, which provided experimental evidences for the traditional application of the root and rhizome ofPogostemon cablinin inflammatory diseases.

Cathode material of spent lithium-ion batteries was refined to obtain high value-added cobalt and lithium products based on the chemical behaviors of metal in different oxidation states. The active substances separated from the cathode of spent lithium-ion batteries were dissolved in H2SO4 and H2O2 solution, and precipitated as CoC2O4·2H2O microparticles by addition of (NH4)2C2O4. After collection of the CoC2O4·2H2O product by filtration, the Li2CO3 precipitates were obtained by addition of Na2CO3 in the left filtrate. The experimental study shows that 96.3% of Co (mass fraction) and 87.5% of Li can be dissolved in the solution of 2 mol/L H2SO4 and 2.0% H2O2 (volume fraction), and 94.7% of Co and 71.0% of Li can be recovered respectively in the form of CoC2O4·2H2O and Li2CO3.

MoS2 nanoparticles with fullerene-like (IF-MoS2) structure were successfully obtained at heating temperature higher than 840 °C by chemical vapor deposition method in a three-tube furnace using MoO3 and S (sulfur) powders as raw materials. The synthesized samples were characterized by X-ray diffraction, field emission scanning electron microscopy, transmission electron microscopy, and energy dispersion X-ray spectrometerrespectively. IF-MoS2 nanoparticles can be obtained only in the narrow temperature range of 840 °C-870 °C, and the diameter of IF-MoS2 nanoparticles increases with temperature. A gradual formation mechanism of IF-MoS2 nanoparticles was discussed in detail.

The incidence of inflammatory bowel disease, a relapsing intestinal condition whose precise etiology is still unclear, has continually increased over recent years. Metabolic profiling is an effective method with high sample throughput that can detect and identify potential biomarkers, and thus may be useful in investigating the pathogenesis of inflammatory bowel disease. In this study, using a metabonomics approach, a pilot study based on ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight mass spectrometry (UPLC-ESI-QTOF-MS) was performed to characterize the metabolic profile of plasma and urine samples of rats with experimental colitis induced by 2,4,6-trinitrobenzene sulfonic acid. Acquired metabolic profile data were processed by multivariate data analysis for differentiation and screening of potential biomarkers. Five metabolites were identified in urine: two tryptophan metabolites [4-(2-aminophenyl)-2,4-dioxobutanoic acid and 4,6-cihydroxyquinoline], two gut microbial metabolites (phenyl-acetylglycine and p-cresol glucuronide), and the bile acid 12α-hydroxy-3-oxocholadienic acid. Seven metabolites were identified in plasma: three members of the bile acid/alcohol group (cholic acid, 12α-hydroxy-3-oxocholadienic acid and cholestane-3,7,12,24,25-pentol) and four lysophosphatidylcholines [LysoPC(20:4), LysoPC(16:0), LysoPC(18:1) and LysoPC(18:0)]. These metabolites are associated with damage of the intestinal barrier function, microbiota homeostasis, immune modulation and the inflammatory response, and play important roles in the pathogenesis of inflammatory bowel disease. Our results positively support application of the metabonomic approach in study of the pathophysiological mechanism of inflammatory bowel disease.

Severe burn-induced liver damage and dysfunction is associated with endoplasmic reticulum (ER) stress. ER stress has been shown to regulate global protein synthesis. In the current study, we induced ER stress in vitro and estimated the effect of ER stress on hepatic protein synthesis. The aim was two-fold: (1) to establish an in vitro model to isotopically measure hepatic protein synthesis and (2) to evaluate protein fractional synthetic rate (FSR) in response to ER stress. Human hepatocellular carcinoma cells (HepG2) were cultured in medium supplemented with stable isotopes 1,2-(13)C(2)-glycine and L-[ring-(13)C(6)]phenylalanine. ER stress was induced by exposing the cells to 100 nM of thapsigargin (TG). Cell content was collected from day 0 to 14. Alterations in cytosolic calcium were measured by calcium imaging and ER stress markers were confirmed by Western blotting. The precursor and product enrichments were detected by GC-MS analysis for FSR calculation. We found that the hepatic protein FSR were 0.97 ± 0.02 and 0.99 ± 0.05%/hr calculated from 1,2-(13)C(2)-glycine and L-[ring-(13)C(6)]phenylalanine, respectively. TG depleted ER calcium stores and induced ER stress by upregulating p-IRE-1 and Bip. FSR dramatically decreased to 0.68 ± 0.03 and 0.60 ± 0.06%/hr in the TG treatment group (p0.05, vs. control). TG-induced ER stress inhibited hepatic protein synthesis. The stable isotope tracer incorporation technique is a useful method for studying the effects of ER stress on hepatic protein synthesis.

Metabolomics, the exponentially developing technique, could provide a systemic mapping in toxicology by directly measuring small molecular metabolites. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was found to be neurotoxic in mammalian animals. In this study, we employed liquid chromatography/quadrupole time-of-flight mass spectrometry for non-targeted analysis of metabolic profiling in hippocampal sample sets of the rats exposed to TCDD. Hippocampal metabolome from different ages of the healthy rats (4-week, 12-week and 20-week) was also deciphered. The relationship between the two tested cases was unlocked to delineate TCDD toxicity associated with ageing. Tandem mass spectrometry fragmentation in conjunction with metabolic database searching and compared to authentic standards was utilized for metabolite identification. As a consequence, the reduced levels of phenylalanine and leucine/isoleucine as well as the up-regulation of inosine and hypoxanthine were highlighted for understanding of TCDD toxicity related to age in rats and the trajectory was depicted by principal components analysis.

Insulin has been demonstrated to accelerate skin wound healing; however, its effects on wound metabolism have not been adequately studied.Adult rabbits were prepared by creation of skin donor site wound on the back, catheterization of the carotid artery and jugular vein, and placement of a nasogastric feeding tube under general anesthesia. The rabbits were given total enteral nutrition thereafter. On day 5 stable isotope tracers were infused to measure the kinetics of protein (reflecting tissue repair) and DNA (reflecting cell proliferation) in the wound. During the isotope tracer infusion, regular human insulin was infused at 2.5 mU/kg per min with concomitant glucose infusion for euglycemia in an insulin group but not in a control group.Plasma insulin concentration was 140±26 μU/mL in the insulin group (n=8), greater (P0.001) than that of 16±3 μU/mL in the control group (N=8). In the insulin group the fractional synthetic rates of wound protein and DNA were 9.0±1.2 and 5.4±0.5%/day, greater (Por=0.05) than those of 6.4±0.5 and 4.0±0.6%/day in the control group, respectively. Wound protein fractional breakdown rates were not significantly (P =0.2) different; net protein deposition rate was ~50% greater in the insulin than in the control group, although the difference was not statistically different (P=0.2).Insulin infusion increased wound protein and DNA synthesis, which are anticipated to promote tissue repair and reepithelialization.

3-Hydroxybutyrate methyl ester (HBME) was prepared from hydrolysis of bacterial poly-3-hydroxybutyrate (PHB) using methanol as an esterification agent in the presence of sulfuric acid. Physicochemical and fuel related properties of HBME were studied for the possibility of using HBME as a gasoline additive. When HBME was blended with 97# gasoline in volume ratios of 5%, 8.5%, 10%, 15% and 20%, respectively, it was found that HBME had similar or better properties as a fuel additive compared with ethanol in terms of oxygen content, dynamic viscosity, flash point and boiling point. The blending of HBME and gasoline showed only little difference compared with the 97# gasoline in terms of octane number (RON) and distillation ranges, especially for the HBME 8.5% and 10% blends, which demonstrated an over 93% combustion heat of gasoline with less than 5% reduction in RON.

Ulcerative colitis (UC) is a chronic relapsing disease without satisfactory treatments, in which intestinal inflammation and disrupted intestinal epithelial barrier are two main pathogeneses triggering UC. Berberrubine (BB) is deemed as one of the major active metabolite of berberine (BBR), a naturally-occurring isoquinoline alkaloid with appreciable anti-UC effect. This study aimed to comparatively investigate the therapeutic effects of BB and BBR on dextran sodium sulfate (DSS)-induced mouse colitis model, and explore the potential underlying mechanism. Results revealed that BB (20 mg/kg) produced a comparable therapeutic effect as BBR (50 mg/kg) and positive control sulfasalazine (200 mg/kg) by significantly reducing the disease activity index (DAI) with prolonged colon length and increased bodyweight as compared with the DSS group. BB treatment was shown to significantly ameliorate the DSS-induced colonic pathological alternations and decreased histological scores. In addition, BB markedly attenuated colonic inflammation by alleviating inflammatory cell infiltration and inhibiting myeloperoxidase (MPO) and cytokines (TNF-α, IFN-γ, IL-1β, IL-6, IL-4 and IL-10) productions in DSS mice. Furthermore, BB treatment substantially upregulated the expression of tight junction (TJ) proteins (zonula occludens-1, zonula occludens-2, claudin-1, occludin) and mRNA expression of mucins (mucin-1 and mucin-2), and decreased the Bax/Bcl-2 ratio. In summary, BB exerted similar effect to its analogue BBR and positive control in attenuating DSS-induced UC with much lower dosage and similar mechanism. The protective effect observed may be intimately associated with maintaining the integrity of the intestinal mucosal barrier and mitigating intestinal inflammation, which were mediated at least partially, via favorable modulation of TJ proteins and mucins and inhibition of inflammatory mediators productions in the colonic tissue. This is the first report to demonstrate that BB possesses pronounced anti-UC effect similar to BBR and sulfasalazine with much smaller dosage. BB might have the potential to be further developed into a promising therapeutic option in the treatment of UC.

Fat is a major energy source for skeletal muscle, and disruption of normal trafficking of fatty acids in muscle is linked to insulin resistance. We quantified muscle triglyceride (TG) and phospholipid (PL) synthesis in lean and obese rabbits by means of l-[U-(13)C(16)]palmitate infusion. Intramyocellular palmitoyl-coenzyme A was used as the precursor for rates of TG and PL synthesis, which were compared with the rates calculated using plasma nonesterified palmitate as the precursor. The muscle of obese rabbits had a greater (P < .05) combined pool of fatty acyl-coenzyme A plus fatty acyl-carnitine than lean rabbits (40.9 +/- 3.7 vs 28.6 +/- 5.3 nmol/g). Although the fractional synthetic rates of muscle TG were almost identical (0.095%/h +/- 0.016%/h vs 0.092%/h +/- 0.019%/h), the absolute synthetic rates were greater (P < .01) in the obese than in lean rabbits (39.7 +/- 9.5 vs 10.1 +/- 2.5 nmol g(-1) h(-1)) because of greater TG content in the muscle of obese rabbits. Plasma nonesterified fatty acids and TG accounted for 51% to 55% of the true precursor pool for muscle lipid synthesis in both groups, and the rest was derived from fatty acids recycled within the muscle. In contrast, the fractional and absolute synthetic rates of muscle PL as well as PL contents were comparable in the 2 groups. In conclusion, the content and synthetic rate of muscle TG rather than PL were increased in obese rabbits, which might be linked to insulin resistance. Plasma lipids and muscle lipolysis were the 2 predominate contributors to the intramyocellular fatty acyl-coenzyme A pool for lipid synthesis.

This study presented a capillary zone electrophoresis (CZE) method for the analysis of trace amount of neurotransmitters glutamate (Glu) and aspartate (Asp) in the microdialysates of rat periaqueductal gray matter (PAG). Glu and Asp were derivatized with the fluorescent agent 5-carboxyfluorescein N-succinimidyl ester (CFSE) for the first time and detected by laser-induced fluorescence (LIF) after separation by CZE. The concentration detection limits (S/N=2) were 6.9x10(-10)M and 8.1x10(-10)M for Glu and Asp, respectively. The repeatability (expressed as RSD) of the migration times of CFSE-amino acid were better than 0.5%, and not higher than 1.5% even over the period of 1 month. This method was applied to quantify Glu and Asp in rat PAG microdialysates with the treatment of formalin injection, and the measured basal concentrations of Glu and Asp were (22.4+/-1.6)x10(-6)M and (0.9+/-0.1)x10(-6)M, respectively.

Microbial polyhydroxyalkanoates (PHA) were proposed for the first time as a new type of biofuel. In this paper, poly-R-3-hydroxybutyrate (PHB) and medium chain length PHA (mcl PHA) were, respectively, esterified to become R-3-hydroxybutyrate methyl ester (3HBME) and medium chain length hydroxyalkanoate methyl ester (3HAME) via acid-catalyzed hydrolysis. The recovery percentages of 3HBME and 3HAME were 52 and 65%, respectively. The purities of 3HBME and 3HAME were 97 and 96%, respectively. Combustion heats of 3HBME, 3HAME, ethanol, n-propanol, n-butanol, 0(#) diesel, 90(#) gasoline, and 3HBME-based and 3HAME-based blended fuels were investigated and compared, respectively. It was found that 3HBME and 3HAME had combustion heats valuing 20 and 30 KJ/g, respectively. Ethanol has a combustion heat of 27 KJ/g, while addition of 10% 3HBME or 3HAME enhanced the combustion heat of ethanol to 30 and 35 KJ/g, respectively. The addition of 3HBME or 3HAME into n-propanol and n-butanol led to a slight reduction of their combustion heats. Combustion heats of blended fuels 3HBME/diesel or 3HBME/gasoline and of 3HAME/diesel or 3HAME/gasoline were lower than that of the pure diesel or gasoline. It was roughly estimated that the production cost of PHA-based biofuels should be around US$1200 per ton.

Reactive oxygen species (ROS) play a major role in recruiting and activating inflammatory cells, inducing angiogenesis, fibroblast proliferation, and collagen synthesis, all processes essential to wound healing. However, the same mediators have been implicated in pulmonary and hepatic fibrosis, vascular occlusion, and necrotic tissue damage. We have previously shown that hyperbaric oxygen caused a prolonged elevation of VEGF and delayed wound healing in a rat model of tissue ischemia. In this study we examine the effect of the ROS scavenger, n-acetylcysteine (NAC), on ischemic wound healing. NAC is a virtually nontoxic free radical scavenger that has been used in many experimental studies to block ROS-mediated signaling. Methods: Male Sprague-Dawley rats underwent creation of the ischemic flap previously validated by this laboratory. This model provides two ischemic and two nonischemic excisional wounds. Rats were treated daily with HBO for 90 minutes at 2.4 atm, HBO plus 150 mg/kg NAC intraperitoneal, or control (neither HBO nor NAC). Wounds were analyzed for surface area, lactate, and VEGF. Results: The HBO/NAC-treated animals had markedly impaired healing of their ischemic wounds at day 7 (0.105 ± .005 cm vs. 0.068 ± .002 cm for ctl and 0.064 ± .006 for HBO) and a twofold elevation of VEGF (120 pg/mg protein vs. 60 pg/mg protein). Lactate levels were not altered by NAC treatment and non-ischemic wounds showed no difference in healing, lactate, or VEGF. Conclusion: Reactive oxygen species are required for wound healing. Our initial hypothesis was that the delay in wound closure with HBO treatment was due to excess ROS and that NAC would improve healing. The finding of elevated VEGF and delayed wound healing in the presence of a potent free radical scavenger suggests that blocking ROS signaling prevents the normal mitogenic response to VEGF. Additional studies to examine the VEGF receptor and tyrosine kinase activation will further elucidate the mechanism of ROS signaling in response to HBO treatment.

We have previously reported that local injection of small doses of long-acting insulin-zinc suspension maintained sufficiently high insulin concentration in the wound fluid and accelerated the healing. The present experiment was to measure the rates of cell proliferation (reflected by DNA synthesis) and protein metabolism in the wound. These are the underlying metabolic processes responsible for the healing. Partial thickness skin donor wound was created on the back and indwelling catheters were placed in the carotid artery and jugular vein in adult rabbits under general anesthesia. The wound was covered with Aquaphor gauze, OpSite membrane, and surgical gauze. On day 7 after wounding, the wound was either injected with 0.2 units of insulin-Zn, Zn alone, or no injection; stable isotopes were infused into the jugular vein catheter in conscious rabbits for measurement of DNA synthesis, protein synthesis and breakdown in the wound. The local insulin-Zn injection raised wound insulin concentration to 168 ± 39 μU/ml. In contrast, in the control and Zn groups wound insulin concentrations were below the detectable level. The local injection of insulin-Zn suspension increased (p = 0.03) DNA synthesis in the wound with minor changes in blood glucose concentration which did not require exogenous glucose replacement. In the Zn group, whereas the rate of DNA synthesis tended to increase (p = 0.051 vs. control), the protein net balance (synthesis – breakdown) was lower (p

Whereas nutrition supply is known to be beneficial to wound healing, the role of folate in wound healing is not clear.The experiment consisted of a surgery on day 0 and a tracer infusion on day 5 after surgery. During the surgery a donor wound was created on the back and indwelling catheters were inserted in the carotid artery and jugular vein in rabbits under general anesthesia. A pharyngostomy feeding tube was also inserted in a group receiving enteral feeding after injury (TEN group, n = 6), but not in other two groups receiving rabbit chow after injury and intravenous amino acids with or without folate during tracer infusion (IVAA and IVAA-folate groups, n = 6 each). On day 5 stable isotope tracers were infused in conscious rabbits to determine the fractional synthetic rate (FSR) of wound DNA, and FSR and fractional breakdown rate (FBR) of wound protein. In the IVAA-folate group 5-methyltetrahydrofolate (the active form of folate) was infused at 0.1 mg/h during the tracer infusion.Serum folate concentration in the IVAA-folate group (380 +/- 78 ng/mL) was greater (P0.001) than those in the TEN (20 +/- 6 ng/mL) and IVAA (33 +/- 22 ng/mL) groups. DNA FSRs in the IVAA-folate group (5.02 +/- 1.26%/d) and in the TEN group (4.51 +/- 0.98%/d) were greater (P0.01-0.05) than that in the IVAA group (2.87 +/- 0.61%/d). In the IVAA and IVAA-folate groups net protein deposition (FSR-FBR) was correlated with chow intake (P0.001-0.002).Folate supplementation has a stimulatory effect on wound DNA synthesis, which would be expected to accelerate wound healing. Nutrition intake is essential for tissue repair by a mechanism that increases net protein deposition in the wound.

Whereas diet-induced obese rabbits have been used to study various aspects of obesity, alterations of lipid metabolism in this model have not been clarified. This study aimed to compare plasma nonesterified fatty acid (NEFA) and triglyceride (TG) kinetics in obese and lean rabbits by means of U-(13)C16-palmitate infusion. Young female rabbits consumed either a high-fat diet (49% energy from fat) ad libitum to develop obesity (n = 6) or a normal diet (7.9% energy from fat) as lean control (n = 5). After 10 wk of feeding, the body weight of obese rabbits (5.33 +/- 0.05 kg) was greater (P < 0.001) than that of lean rabbits (3.89 +/- 0.07 kg). The obese rabbits had higher concentrations of plasma NEFA and TG and a greater rate of fatty acid (FA) turnover. Whereas the fractional secretion rates of hepatic TG did not differ, 100% of hepatic secretory TG was synthesized from plasma NEFA in the lean rabbits compared to 59% in the obese rabbits (P < 0.001). In the lean rabbits, hepatic lipase-mediated hydrolysis of lipoprotein TG did not contribute to the FA pool for synthesis of secretory TG, consistent with the naturally occurring deficit in hepatic lipase in this species. We conclude that lipid metabolism in diet-induced obese rabbits is similar to that in obese humans. The deficiency in hepatic lipase in rabbits simplifies the quantitation of hepatic lipid kinetics.

Summary Background Circulating acyl-carnitines (acyl-CNTs) are associated with insulin resistance (IR) and type 2 diabetes (T2D) in both rodents and humans. However, the mechanisms whereby circulating acyl-CNTs are increased in these conditions and their role in whole-body metabolism remains unknown. The purpose of this study was to determine if, in humans, blood cells contribute in production of circulating acyl-CNTs and associate with whole-body fat metabolism. Methods and results Eight non-diabetic healthy women (age: 47 ± 19 y; BMI: 26 ± 1 kg·m −2 ) underwent stable isotope tracer infusion and hyperinsulinemic-euglycemic clamp study to determine in vivo whole-body fatty acid flux and insulin sensitivity. Blood samples collected at baseline (0 min) and after 3 h of clamp were used to determine the synthesis rate of palmitoyl-carnitine (palmitoyl-CNT) in vitro . The fractional synthesis rate of palmitoyl-CNT was significantly higher during hyperinsulinemia (0.788 ± 0.084 vs . 0.318 ± 0.012%·hr −1 , p = 0.001); however, the absolute synthesis rate (ASR) did not differ between the periods ( p = 0.809) due to ∼30% decrease in blood palmitoyl-CNT concentration ( p = 0.189) during hyperinsulinemia. The ASR of palmitoyl-CNT significantly correlated with the concentration of acyl-CNTs in basal ( r = 0.992, p r = 0.919, p = 0.001) periods; and the basal ASR significantly correlated with plasma palmitate oxidation ( r = 0.764, p = 0.027). Conclusion In women, blood cells contribute to plasma acyl-CNT levels and the acyl-CNT production is linked to plasma palmitate oxidation, a marker of whole-body fat metabolism. Future studies are needed to confirm the role of blood cells in acyl-CNT and lipid metabolism under different physiological (i.e., in response to meal) and pathological (i.e., hyperlipidemia, IR and T2D) conditions.

In order to optimize the conditions of construction BAC library, the transformation efficiency of E. coli DH10B was studied in this paper. Our data prove much higher competence of electroporation (reaches 2.19 x 10(10) cfu/microg pUC19 DNA) when harvesting the cells between an OD550 of 0.7 - 0.8. Five different electric field strength (from 9 kV/cm to 25 kV/cm) and three different sized plasmid vector DNAs including pUC19 DNA, pECBAC1 DNA and pCLD04541 DNA, as well as three bacterial artificial chromosomes (BACs) ranging from 40 to 190 kb and their mixture were used to discover the transformation efficiency changes under various conditions. Our data show maximum transformation efficiency and optimal electric field strength of plasmid DNAs drop dramatically with increasing size of the DNA. Molecules of 190 kb transform more than 50-fold less well, on a molar basis, than molecules of 40 kb. And the optimal voltage gradient is strongly dependent on the different sized molecules, for instance, pUC19 reaches the highest transformation efficiency at 21 kV/cm, while the 180 kb BAC DNA gets its best efficiency at 13 kV/cm. This paper demonstrates that conditions may be selected which increase the average size of BAC clones generated by electroporation and could be widely applied in large-insert genome library construction.

Millettiae speciosae Champ. Leguminosae (MSC), is a well-known Chinese herb traditionally used as food material and medicine for enhancing physical strength. Our preliminary study found that the aqueous extract of this herb (MSE) had an anti-fatigue effect. In this paper, we further separated MSE into total polysaccharides (MSP) and supernatant (MSS) by alcohol precipitation, and explored which fraction was active for its anti-fatigue effect. Mice were orally administered with MSP or MSS at the doses of 200, 400, and 800 mg/kg for 20 days and the anti-fatigue effect was assessed by exhaustive swimming exercise (ESE). The biochemical parameters related to fatigue after ESE and the in vitro antioxidant activity of active fraction were determined. Our results showed that MSP, instead of MSS, significantly extended the swimming time to exhaustion (p &lt, 0.05), indicating that MSP is responsible for the anti-fatigue effect of MSE. In addition, MSP treatment increased the levels of glucose (Glu) and muscle glycogen, whereas it decreased the accumulations of blood urea nitrogen (BUN) and lactic acid (Lac). Moreover, ESE increased the levels of creatine phosphokinase (CK), lactic dehydrogenase (LDH), and malondialdehyde (MDA) but reduced superoxide dismutase (SOD) and glutathione (GSH) in plasma. In contrast, MSP inhibited all the above changes relating to fatigue. Furthermore, an in vitro antioxidant test revealed that MSP dose-dependently scavenged ·OH and DPPH free radicals. Taken together, these findings strongly suggested that MSP was able to alleviate physical fatigue by increasing energy resources and decreasing accumulation of detrimental metabolites. The antioxidant activity may crucially contribute to the observed anti-fatigue effect of MSP.

Background Qing-dai powder (QDP), comprising Indigo naturalis (Qing-dai) and dried alum (Ku-fan), was used in Chinese medicine to treat the conditions associated with mucosal hemorrhage, such as ulcerative colitis (UC). This study aims to investigate the effects and potential mechanism of QDP on dextran sulfate sodium (DSS)-induced acute colitis in mice and to examine the regulatory effects of QDP on macrophages. Methods Seven- to eight-week-old male C57BL/6 mice were challenged with 2.0 % DSS in drinking water for 5 days and then the colitic mice were arbitrarily allocated into five groups (n = 10 for each group). QDP (0.77, 1.54 and 3.08 g/kg) and sulfasalazine (SASP) (0.20 g/kg) were orally administered for 7 days. The disease activity index was determined by scores of body weight loss, diarrhea and rectal bleeding; histological signs of damage was analyzed by H&E staining; myeloperoxidase activity was measured by colorimetric method, levels of proinflammatory cytokines were determined by ELISA; changes in macrophages in the colon were analyzed by immunohistochemistry (IHC) and flow cytometry. Lipopolysaccharide (LPS)-induced RAW264.7 cells were treated with or without QDP, then the production of TNF-α and IL-6 were measured by ELISA; and protein molecules such as COX-2, iNOS, IкB-α were determined by Western blot. Results Oral administration of QDP at dosages of 1.54 and 3.08 g/kg significantly reduced disease activity index on day 12 (P

The incidence of inflammatory bowel disease (IBD), characterized by chronic, relapsing intestinal inflammation, has continually increased in recent years. A previous study by our group identified five potential metabolic markers possibly associated with the pathology of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced IBD in rats. The present study aimed to examine the potential therapeutic effects of the essential oil of Pogostemon cablin (also known as patchouli; PO) on TNBS-induced rats and investigate the concomitant metabolic changes by targeting the previously identified potential markers. Pogostemon cablin is widely used to treat gastrointestinal diseases, including IBD, in China. The results of the present study showed that PO (270 mg/kg, rectal instillation) significantly alleviated colonic damage and reduced disease activity indicators and colonic myeloperoxidase in TNBS-induced rats. In addition, a targeted metabolic profiling study identified that four metabolites were elevated in the urine of the animals in the TNBS group, which were significantly inhibited by treatment with PO: Two tryptophan metabolites [4-(2-aminophenyl)-2,4-dioxobutanoic acid and 4,6-cihydroxyquinoline] and two gut microbial metabolites (phenylacetylglycine and p-cresol glucuronide). Taken together, these findings suggested that PO ameliorated the symptoms of TNBS-induced IBD and reversed the metabolic changes potentially associated with TNBS-induced IBD in rats.

Caffeic acid phenyl ester (CAPE) is a potent anti-inflammatory agent and it can eliminate the free radicals. This study aimed to investigate the radioprotective effects of CAPE on X-ray irradiation induced intestinal injury in rats. Rats were intragastrically administered with 10 μmol/kg/d CAPE for 7 consecutive days before exposing them to a single dose of X-ray irradiation (9Gy) to abdomen. Rats were sacrificed 72 h after exposure to radiation. We found that pretreatment with CAPE effectively attenuated intestinal pathology changes, apoptosis, oxidative stress, bacterial translocation, the content of nitric oxide and myeloperoxidase as well as the concentration of plasma tumor necrosis factor-α. Pretreatment with CAPE also reversed the activation of p38MAPK and the increased expression of intercellular cell adhesion molecule-1 induced by radiation in intestinal mucosa. Taken together, these results suggest that pretreatment with CAPE could be a promising candidate for treating radiation-induced intestinal injury.

Whereas Sulfamylon is effective in treatment of burn wound infection, controversy exists regarding its effect on the healing process.A partial thickness skin donor site wound was created on the back and indwelling catheters were placed in the carotid artery and jugular vein in rabbits under general anesthesia. Sulfamylon cream (8.5%, BERTEK Pharmaceuticals Inc., Morgantown, W Va) was applied on the wound, with either open or occlusive dressing. The control wound was covered with dressings only. On day 7 after injury, stable isotope tracers were infused to determine the fractional synthetic rate (FSR) of DNA, and FSR and fractional breakdown rate (FBR) of protein in the wound.In the Sulfamylon-open dressing group, the DNA FSR was 1.3 +/- 0.6%/day, the protein FSR was 8.0 +/- 3.5%/day, and the net protein deposition (FSR - FBR) was -0.3 +/- 3.7%/day. These values were lower (P.01 to .05) than the corresponding values in the control group (DNA FSR: 2.9 +/- 0.9%/day; protein FSR: 20.5 +/- 8.4%/day; net protein deposition: 7.9 +/- 6.0%/day). Sulfamylon cream selectively inhibited DNA FSR from the de novo base synthesis pathway (2.3 +/- 1.2 vs 0.8 +/- 0.5%/day, P.05 vs control). With the occlusive dressing Sulfamylon cream did not decrease wound DNA FSR due to a stimulation of the base salvage pathway, but still decreased protein FSR (11.5 +/- 5.1%/day, P.05 vs control). Histologic slides indicated that Sulfamylon cream inhibited re-epithelialization, collagen formation, and angiogenesis in the wound.Topical Sulfamylon cream application inhibited DNA and protein synthesis in the wound, which would be expected to retard the healing process.

The structures and energies of formation and migration of the mono- and di-vacancy in Cu crystal have been described and calculated with modified analytical embedded atom method (MAEAM). The lattice relaxation is considered with molecular dynamics (MD) method at T=0 K. The results show the FN di-vacancy is the most stable and likely occurs in practice from the energy minimization. Compared with the mono-vacancy, the formation energy of the FN di-vacancy is higher than that of a mono-vacancy, but lower than that of two isolated mono-vacancy. The preferred migration mechanism of the FN di-vacancy is multi-jump of either vacancy (rotating the di-vacancy). The calculated migration energy of the FN di-vacancy is lower than that of a mono-vacancy, so the FN di-vacancy is easier to migrate. All of the calculated results are in good agreement with the experimental values.