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A quantitative determination method of N-acetyl-D-glucosamine (GlcNAc) and N,N'-diacetylchitobiose (GlcNAc)2 is proposed using a proton nuclear magnetic resonance experiment. N-acetyl groups of GlcNAc and (GlcNAc)2 are chosen as target signals, and the deconvolution technique is used to determine the concentration of the corresponding compound. Compared to the HPLC method, 1H-NMR spectroscopy is simple and fast. The method can be used for the analysis of chitin hydrolyzed products with real-time analysis, and for quantifying the content of products using internal standards without calibration curves. This method can be used to quickly evaluate chitinase activity. The temperature dependence of 1H-NMR spectra (VT-NMR) is studied to monitor the chemical shift variation of acetyl peak. The acetyl groups of products are involved in intramolecular H-bonding with the OH group on anomeric sites. The rotation of the acetyl group is closely related to the intramolecular hydrogen bonding pattern, as suggested by the theoretical data (molecular modeling).

A quantitative determination method of N-acetyl-d-glucosamine (GlcNAc) and N,N'-diacetylchitobiose (GlcNAc)(2) is proposed using a proton nuclear magnetic resonance experiment. N-acetyl groups of GlcNAc and (GlcNAc)(2) are chosen as target signals, and the deconvolution technique is used to determine the concentration of the corresponding compound. Compared to the HPLC method, (1)H-NMR spectroscopy is simple and fast. The method can be used for the analysis of chitin hydrolyzed products with real-time analysis, and for quantifying the content of products using internal standards without calibration curves. This method can be used to quickly evaluate chitinase activity. The temperature dependence of (1)H-NMR spectra (VT-NMR) is studied to monitor the chemical shift variation of acetyl peak. The acetyl groups of products are involved in intramolecular H-bonding with the OH group on anomeric sites. The rotation of the acetyl group is closely related to the intramolecular hydrogen bonding pattern, as suggested by the theoretical data (molecular modeling).

The current literature focusing on the effect of obesity and overweight on lung function and fraction of exhaled nitric oxide (FeNO) in children, particularly among healthy children of non-European descent, remains controversial. Furthermore, whether the relationship of obesity and overweight with lung function and FeNO in children is modified by atopy is unclear. The objective of this study was to examine the effect of excess weight on lung function parameters and FeNO among Asian children, with a particular focus on exploring the potential effect modification by atopy. We investigated the effect of excess weight on lung function and FeNO in a population sample of 1,717 children aged 5 to 18 years and explored the potential modifying effect of atopy. There were positive associations of body mass index (BMI) z-score with forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), peak expiratory flow (PEF), and forced expiratory flow at 25-75% (FEF25-75) (all P<0.001), after controlling for confounders. The beta coefficient for FEV1 (0.084) was smaller than that for FVC (0.111). In contrast, a negative association was found between BMI z-score and FEV1/FVC ratio (P<0.001) and FeNO (P = 0.03). A consistent pattern of association for lung function variables was observed when stratifying by atopy. There was a negative association of BMI z-score with FeNO in atopic subjects (P = 0.006), but not in non-atopic subjects (P = 0.46). Excess weight disproportionately impacts lung volumes and airflow in children from the general population, independent of atopic status. Excess weight inversely affects FeNO in atopic but not in non-atopic children.

Among orthopedic surgery materials, poly (methyl methacrylate) (PMMA) is most commonly used for its excellent mechanical properties and rapid self-setting time. However, PMMA bone cement has been reported to cause thermal necrosis and to have poor bioactivity, which must be improved. In contrast, tricalcium silicate (TCS), the most significant component of Portland Cement and the most effective bone cement material, might not always meet the needs of the cement due to its poor mechanical properties and elevated pH levels during hydration. We hypothesize that the benefits of both PMMA and TCS can be harnessed by mixing them together in different proportions. This would represent a better solution for the issues faced when using them alone. We, therefore, prepared a novel organic-inorganic PMMA/TCS composite bone cement mixing PMMA and different amounts of TCS and tested its effect on the biophysical properties. The addition of 30% TCS reduced the exothermic temperature and pH variation during cement setting and hydration processes. However, the mechanical and handling properties of the bioactive PMMA/TCS composite were not affected. The in vitro study also revealed that the composite materials had higher cell viability than pure PMMA and TCS. Also, the in vivo study on animals indicated that the composite materials were more capable of forming bone, which further reinforced the biocompatibility of the proposed PMMA/TCS bone cement. By combining the advantages of each component, it could be possible to construct a more effective composite bone cement material. This would meet the needs of implantation material for orthopedic surgeries or a possible bone filler.

Reduced-representation sequencing (RRS) has made it possible to identify hundreds to thousands of genetic markers for phylogenomic analysis for the testing of phylogenetic hypotheses in non-model taxa. The use of customized probes to capture genetic markers (i.e., ultraconserved element (UCE) approach) has further boosted the efficiency of collecting genetic markers. Three UCE probe sets pertaining to spiders (Araneae) have been published, including one for the suborder Mesothelae (an early diverged spider group), one for Araneae, and one for Arachnida. In the current study, we developed a probe set specifically for the superfamily Araneoidea in spiders. We then combined the three probe sets for Araneoidea, Araneae, and Arachnid into a fourth probe set. In testing the effectiveness of the 4 probe sets, we used the captured loci of the 15 spider genomes in silico (6 from Araneoidea). The combined probe set outperformed all other probe sets in terms of the number of captured loci. The Araneoidea probe set outperformed the Araneae and Arachnid probe sets in most of the included Araneoidea species. The reconstruction of phylogenomic trees using the loci captured from the four probe sets and the data matrices generated from 50% and 75% occupancies indicated that the node linked to the Stegodyphus + RTA (retrolateral tibial apophysis) clade has unstable nodal supports in the bootstrap values, gCFs, and sCFs. Our results strongly indicate that developing ad hoc probe sets for sub-lineages is important in the cases where the origins of a lineage are ancient (e.g., spiders ~380 MYA).

Pharmaceutical drugs targeting dyslipidemia and cardiovascular disease (CVD) may increase the risk of fatty liver disease and other metabolic disorders. To identify potential novel CVD drug targets without these adverse effects, we perform genome-wide analyses of participants in the HUNT Study in Norway (n = 69,479) to search for protein-altering variants with beneficial impact on quantitative blood traits related to cardiovascular disease, but without detrimental impact on liver function. We identify 76 (11 previously unreported) presumed causal protein-altering variants associated with one or more CVD- or liver-related blood traits. Nine of the variants are predicted to result in loss-of-function of the protein. This includes ZNF529 :p.K405X, which is associated with decreased low-density-lipoprotein (LDL) cholesterol (P = 1.3 × 10 −8 ) without being associated with liver enzymes or non-fasting blood glucose. Silencing of ZNF529 in human hepatoma cells results in upregulation of LDL receptor and increased LDL uptake in the cells. This suggests that inhibition of ZNF529 or its gene product should be prioritized as a novel candidate drug target for treating dyslipidemia and associated CVD. Drugs targeting cardiovascular disease (CVD) can have negative consequences for liver function. Here, the authors combine genome wide analyses on 69,479 individuals to identify loss-of-function variants with beneficial effects on CVD-related traits without negative impacts on liver function.

Effect of sertraline, an antidepressant, on cytosolic free Ca2+ levels ([Ca2+]i) in human cancer cells is unclear. This study examined if sertraline altered basal [Ca2+]i levels in suspended OC2 human oral cancer by using fura-2 as a Ca2+-sensitive fluorescent probe. At concentrations of 10−100 μM, sertraline induced a [Ca2+]i rise in a concentration-dependent fashion. The Ca2+ signal was reduced partly by removing extracellular Ca2+ indicating that Ca2+ entry and release both contributed to the [Ca2+]i rise. Sertraline induced Mn2+ influx, leading to quench of fura-2 fluorescence suggesting Ca2+ influx. This Ca2+ influx was inhibited by suppression of phospholipase A2, inhibition of store-operated Ca2+ channels or by modulation of protein kinase C activity. In Ca2+-free medium, pretreatment with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin or 2,5-di-(t-butyl)-1,4-hydroquinone (BHQ) nearly abolished sertraline-induced Ca2+ release. Conversely, pretreatment with sertraline greatly reduced the inhibitor-induced [Ca2+]i rise, suggesting that sertraline released Ca2+ from the endoplasmic reticulum. Inhibition of phospholipase C did not change sertraline-induced [Ca2+]i rise. Together, in human oral cancer cells, sertraline induced [Ca2+]i rises by causing phospholipase C-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via store-operated Ca2+ channels.

The effect of diindolylmethane, a natural compound derived from indole-3-carbinol in cruciferous vegetables, on cytosolic Ca(2+) concentrations ([Ca(2+)](i)) and viability in HA59T human hepatoma cells is unclear. This study explored whether diindolylmethane changed [Ca(2+)](i) in HA59T cells. The Ca(2+)-sensitive fluorescent dye fura-2 was applied to measure [Ca(2+)](i). Diindolylmethane at concentrations of 1-50 μM evoked a [Ca(2+)](i) rise in a concentration-dependent manner. The signal was reduced by removing Ca(2+). Diindolylmethane-induced Ca(2+) influx was not inhibited by nifedipine, econazole, SK&F96365, and protein kinase C modulators but was inhibited by aristolochic acid. In Ca(2+)-free medium, treatment with the endoplasmic reticulum Ca(2+) pump inhibitors thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) inhibited or abolished diindolylmethane-induced [Ca(2+)](i) rise. Incubation with diindolylmethane inhibited thapsigargin or BHQ-induced [Ca(2+)](i) rise. Inhibition of phospholipase C with U73122 reduced diindolylmethane-induced [Ca(2+)](i) rise. At concentrations of 10-75 μM, diindolylmethane killed cells in a concentration-dependent manner. The cytotoxic effect of diindolylmethane was not reversed by chelating cytosolic Ca(2+) with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid. Propidium iodide staining data suggest that diindolylmethane (25-50 μM) induced apoptosis in a concentration-dependent manner. Collectively, in HA59T cells, diindolylmethane induced a [Ca(2+)](i) rise by causing phospholipase C-dependent Ca(2+) release from the endoplasmic reticulum and Ca(2+) influx via phospholipase A(2)-sensitive channels. Diindolylmethane induced cell death that may involve apoptosis.

The effect of diindolylmethane, a natural compound derived from indole-3-carbinol in cruciferous vegetables, on cytosolic Ca 2+ concentrations ([Ca 2+ ] i ) and viability in HA59T human hepatoma cells is unclear. This study explored whether diindolylmethane changed [Ca 2+ ] i in HA59T cells. The Ca 2+ -sensitive fluorescent dye fura-2 was applied to measure [Ca 2+ ] i . Diindolylmethane at concentrations of 1–50 μM evoked a [Ca 2+ ] i rise in a concentration-dependent manner. The signal was reduced by removing Ca 2+ . Diindolylmethane-induced Ca 2+ influx was not inhibited by nifedipine, econazole, SK&F96365, and protein kinase C modulators but was inhibited by aristolochic acid. In Ca 2+ -free medium, treatment with the endoplasmic reticulum Ca 2+ pump inhibitors thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) inhibited or abolished diindolylmethane-induced [Ca 2+ ] i rise. Incubation with diindolylmethane inhibited thapsigargin or BHQ-induced [Ca 2+ ] i rise. Inhibition of phospholipase C with U73122 reduced diindolylmethane-induced [Ca 2+ ] i rise. At concentrations of 10–75 μM, diindolylmethane killed cells in a concentration-dependent manner. The cytotoxic effect of diindolylmethane was not reversed by chelating cytosolic Ca 2+ with 1,2-bis(2-aminophenoxy)ethane- N , N , N ′, N ′-tetraacetic acid. Propidium iodide staining data suggest that diindolylmethane (25–50 μM) induced apoptosis in a concentration-dependent manner. Collectively, in HA59T cells, diindolylmethane induced a [Ca 2+ ] i rise by causing phospholipase C-dependent Ca 2+ release from the endoplasmic reticulum and Ca 2+ influx via phospholipase A 2 -sensitive channels. Diindolylmethane induced cell death that may involve apoptosis.

The effect of diindolylmethane, a natural compound derived from indole-3-carbinol in cruciferous vegetables, on cytosolic Ca super(2+) concentrations ([Ca super(2+)] sub(i)) and viability in HA59T human hepatoma cells is unclear. This study explored whether diindolylmethane changed [Ca super(2+)] sub(i) in HA59T cells. The Ca super(2+)-sensitive fluorescent dye fura-2 was applied to measure [Ca super(2+)] sub(i). Diindolylmethane at concentrations of 1-50 mu M evoked a [Ca super(2+)] sub(i) rise in a concentration-dependent manner. The signal was reduced by removing Ca super(2+). Diindolylmethane-induced Ca super(2+) influx was not inhibited by nifedipine, econazole, SK&F96365, and protein kinase C modulators but was inhibited by aristolochic acid. In Ca super(2+)-free medium, treatment with the endoplasmic reticulum Ca super(2+) pump inhibitors thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) inhibited or abolished diindolylmethane-induced [Ca super(2+)] sub(i) rise. Incubation with diindolylmethane inhibited thapsigargin or BHQ-induced [Ca super(2+)] sub(i) rise. Inhibition of phospholipase C with U73122 reduced diindolylmethane-induced [Ca super(2+)] sub(i) rise. At concentrations of 10-75 mu M, diindolylmethane killed cells in a concentration-dependent manner. The cytotoxic effect of diindolylmethane was not reversed by chelating cytosolic Ca super(2+) with 1,2-bis(2-aminophenoxy)ethane-N,N ,N',N'-tetraacetic acid. Propidium iodide staining data suggest that diindolylmethane (25-50 mu M) induced apoptosis in a concentration-dependent manner. Collectively, in HA59T cells, diindolylmethane induced a [Ca super(2+)] sub(i) rise by causing phospholipase C-dependent Ca super(2+) release from the endoplasmic reticulum and Ca super(2+) influx via phospholipase A sub(2)-sensitive channels. Diindolylmethane induced cell death that may involve apoptosis.