Coffee grounds-derived carbon quantum dots as peroxidase mimetics for colorimetric and fluorometric detection of ascorbic acid.

In this study, we reported the eco-responsible synthesis of iron-doped carbon quantum dots (Fe-CQDs) from waste coffee grounds through a simple hydrothermal method. The Fe-CQDs exhibited high peroxidase-like activity, which could convert 3,3',5,5'-tetramethylbenzidine (TMB) into blue ox-TMB in the presence of H2O2. After adding ascorbic acid (AA) to above system, the blue solution faded. Based on this phenomenon, a colorimetric method for visual monitoring of H2O2 and AA was developed. Meanwhile, the fluorescence of Fe-CQDs can be quenched by the formed ox-TMB via inner filter effect (IFE), followed by the recovery upon the addition of AA. Therefore, Fe-CQDs can be acted as a fluorescent probe to detect H2O2 and AA through the "on-off-on" mode. Furthermore, the dual-recognition methods based on Fe-CQDs were used to measure AA content in beverage samples. Thus, this work would shed much light on converting waste into biomass CQDs and their potential applications in biomolecular detection.

Exploring the evolutionary characteristics between cultivated tea and its wild relatives using complete chloroplast genomes.

BACKGROUND: Cultivated tea is one of the most important economic and ecological trees distributed worldwide. Cultivated tea suffer from long-term targeted selection of traits and overexploitation of habitats by human beings, which may have changed its genetic structure. The chloroplast is an organelle with a conserved cyclic genomic structure, and it can help us better understand the evolutionary relationship of Camellia plants. RESULTS: We conducted comparative and evolutionary analyses on cultivated tea and wild tea, and we detected the evolutionary characteristics of cultivated tea. The chloroplast genome sizes of cultivated tea were slightly different, ranging from 157,025 to 157,100 bp. In addition, the cultivated species were more conserved than the wild species, in terms of the genome length, gene number, gene arrangement and GC content. However, comparing Camellia sinensis var. sinensis and Camellia sinensis var. assamica with their cultivars, the IR length variation was approximately 20 bp and 30 bp, respectively. The nucleotide diversity of 14 sequences in cultivated tea was higher than that in wild tea. Detailed analysis on the genomic variation and evolution of Camellia sinensis var. sinensis cultivars revealed 67 single nucleotide polymorphisms (SNPs), 46 insertions/deletions (indels), and 16 protein coding genes with nucleotide substitutions, while Camellia sinensis var. assamica cultivars revealed 4 indels. In cultivated tea, the most variable gene was ycf1. The largest number of nucleotide substitutions, five amino acids exhibited site-specific selection, and a 9 bp sequence insertion were found in the Camellia sinensis var. sinensis cultivars. In addition, phylogenetic relationship in the ycf1 tree suggested that the ycf1 gene has diverged in cultivated tea. Because C. sinensis var. sinensis and its cultivated species were not tightly clustered. CONCLUSIONS: The cultivated species were more conserved than the wild species in terms of architecture and linear sequence order. The variation of the chloroplast genome in cultivated tea was mainly manifested in the nucleotide polymorphisms and sequence insertions. These results provided evidence regarding the influence of human activities on tea.

Etiologic and treatment conceptualizations of disordered eating symptoms among mainland Chinese therapists.

OBJECTIVE: Reports of disordered eating are increasing in mainland China; however, little is known regarding Chinese psychotherapists' conceptualizations of disordered eating symptomatology. This study explores Chinese psychotherapists' conceptualizations of binge eating (BE)/vomiting symptoms and treatment considerations. METHOD: In-depth, semi-structured interviews were conducted with mainland Chinese psychotherapists (N = 41) in Mandarin. Participants were given a hypothetical case and provided their conceptualization of the patient's BE/vomiting etiology and treatment recommendations. Etiological conceptualizations were coded using directed content analysis, and treatment recommendations were grouped by intervention strategy. RESULTS: Participants described psychosocial risk factors for BE/vomiting including intrapersonal characteristics and the childhood family environment, but rarely discussed genetic and neurobiological factors. Few participants reported that they would prioritize the BE/vomiting symptoms in treatment and their specific treatment recommendations varied widely. DISCUSSION: Most research on BE/vomiting behaviors in the literature is based on Western samples with little attention to mainland Chinese populations. Participants in this study provided conceptualizations of risk factors and treatment recommendations that could generally find evidence in the existing Western literature, even if some theories are no longer supported by updated Western research and the participants focused primarily on psychosocial risks as opposed to genetic/neurobiological factors. It will be important for future research to ascertain mainland Chinese therapists' understanding of these additional types of risk. These findings also suggest a disconnect between clinical findings on neurobiological risks and Chinese therapists' knowledge and/or perceived clinical utility of these risks. Implications for treatment and research dissemination to diverse global communities are discussed.

Association between Physical Exercise and Biomarkers of Oxidative Stress among Middle-Aged and Elderly Community Residents with Essential Hypertension in China.

This study aimed to investigate the role of different types and frequencies of physical exercise in biomarkers of oxidative stress among middle-aged and elderly community residents with essential hypertension in China. A community-based cross-sectional survey was undertaken in 7 subdistricts. Individuals, 45-79 years old, with essential hypertension (n = 402) and without cardiovascular disease (n = 1047) were included. Superoxide dismutase (SOD) activities and plasma levels of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) were determined. Multilevel linear regression was used to estimate the associations between various types of physical exercise and oxidative stress biomarker levels. Participants engaged in high frequency walking/square dancing or taiji/yoga demonstrated decreased systolic blood pressure in both groups; however, diastolic blood pressure decreased only among individuals with hypertension participating in walking/square dancing. In individuals with hypertension, MDA levels decreased in those participating in walking/square dancing, SOD activity increased in those participating in walking/square dancing, and 4-HNE levels decreased in those involved in taiji/yoga. In individuals without cardiovascular disease, MDA levels decreased in those involved in walking/square dancing or taiji/yoga, SOD activity increased in those performing walking/square dancing, and 4-HNE levels decreased in those involved in taiji/yoga. Oxidative stress marker levels also improved in those involved in walking/square dancing or taiji/yoga groups as the exercise frequency increased. Thus, frequent participation in walking/square dancing or taiji/yoga effectively decreases hypertension-related oxidative stress biomarker levels.

HER2 Targeting Peptides Screening and Applications in Tumor Imaging and Drug Delivery.

Herein, computational-aided one-bead-one-compound (OBOC) peptide library design combined with in situ single-bead sequencing microarray methods were successfully applied in screening peptides targeting at human epidermal growth factor receptor-2 (HER2), a biomarker of human breast cancer. As a result, 72 novel peptides clustered into three sequence motifs which are PYL***NP, YYL***NP and PPL***NP were acquired. Particularly one of the peptides, P51, has nanomolar affinity and high specificity for HER2 in ex vivo and in vivo tests. Moreover, doxorubicin (DOX)-loaded liposome nanoparticles were modified with peptide P51 or P25 and demonstrated to improve the targeted delivery against HER2 positive cells. Our study provides an efficient peptide screening method with a combination of techniques and the novel screened peptides with a clear binding site on HER2 can be used as probes for tumor imaging and targeted drug delivery.

[FTIR detection of unregulated emissions from a diesel engine with biodiesel fuel].

Biodiesel, as one of the most promising alternative fuels, has received more attention because of limited fossil fuels. A comparison of biodiesel and petroleum diesel fuel is discussed as regards engine unregulated exhaust emissions. A diesel fuel, a pure biodiesel fuel, and fuel with 20% V/V biodiesel blend ratio were tested without engine modification The present study examines six typical unregulated emissions by Fourier transform infrared spectroscopy (FTIR) method: formaldehyde (HCHO), acetaldehyde (C2 H4 O), acetone (C3 H6 O), toluene (C7 H8), sulfur dioxide (SO2), and carbon dioxide (CO2). The results show addition of biodiesel fuel increases the formaldehyde emission, and B20 fuel has little change, but the formaldehyde emission of pure biodiesel shows a clear trend of addition. Compared with the pure diesel fuel, the acetaldehyde of B20 fuel has a distinct decrease, and the acetaldehyde emission of pure biodiesel is lower than that of the pure diesel fuel at low and middle engine loads, but higher at high engine load. The acetone emission is very low, and increases for B20 and pure biodiesel fuels as compared to diesel fuel. Compared with the diesel fuel, the toluene and sulfur dioxide values of the engine show a distinct decrease with biodiesel blend ratio increasing. It is clear that the biodiesel could reduce aromatic compounds and emissions of diesel engines. The carbon dioxide emission of pure biodiesel has a little lower value than diesel, showing that the biodiesel benefits control of greenhouse gas.

Inhibition of hypothalamic fatty acid synthase triggers rapid activation of fatty acid oxidation in skeletal muscle.

Malonyl-CoA functions as a mediator in the hypothalamic sensing of energy balance and regulates the neural physiology that governs feeding behavior and energy expenditure. The central administration of C75, a potent inhibitor of the fatty acid synthase (FAS), increases malonyl-CoA concentration in the hypothalamus and suppresses food intake while activating fatty acid oxidation in skeletal muscle. Closely correlated with the increase in muscle fatty acid oxidation is the phosphorylation/inactivation of acetyl-CoA carboxylase, which leads to reduced malonyl-CoA concentration. Lowering muscle malonyl-CoA, a potent inhibitor of carnitine/palmitoyl-CoA transferase 1 (CPT1), releases CPT1 from inhibitory constraint, facilitating the entry of fatty acids into mitochondria for beta oxidation. Also correlated with these events are C75-induced increases in the expression of skeletal muscle peroxisome proliferator-activated receptor alpha (PPARalpha), a transcriptional activator of fatty acid oxidizing enzymes, and uncoupling protein 3 (UCP3), a thermogenic mitochondrial uncoupling protein. Phentolamine, an alpha-adrenergic blocking agent, prevents the C75-induced increases of skeletal muscle UCP3 and whole body fatty acid oxidation and C75-induced decrease of skeletal muscle malonyl-CoA. Thus, the sympathetic nervous system is implicated in the transmission of the "malonyl-CoA signal" from brain to skeletal muscle. Consistent with the up-regulation of UCP3 and PPARalpha is the concomitant increase in the expression of PGC1alpha, transcriptional coactivator of the UCP3 and PPARalpha-activated genes. These findings clarify the mechanism by which the hypothalamic malonyl-CoA signal is communicated to metabolic systems in skeletal muscle that regulate fatty acid oxidation and energy expenditure.

A role for hypothalamic malonyl-CoA in the control of food intake.

The cellular level of malonyl-CoA, an intermediate in fatty acid biosynthesis, depends on its rate of synthesis catalyzed by acetyl-CoA carboxylase relative to its rate of utilization and degradation catalyzed by fatty acid synthase and malonyl-CoA decarboxylase, respectively. Recent evidence suggests that hypothalamic malonyl-CoA functions in the regulation of feeding behavior by altering the expression of key orexigenic and anorexigenic neuropeptides. Here we report that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a 5'-AMP kinase activator, rapidly lowers malonyl-CoA both in GT1-7 hypothalamic neurons and in the hypothalami of mice. These effects correlate closely with the phosphorylation of acetyl-CoA carboxylase, an established target of AMP kinase. Intracerebroventricular (i.c.v.) administration of AICAR rapidly lowers hypothalamic [malonyl-CoA] and increases food intake. Expression of an adenoviral cytosolic malonyl-CoA decarboxylase vector (Ad-cMCD) in hypothalamic GT1-7 cells decreases malonyl-CoA. When delivered by bilateral stereotaxic injection into the ventral hypothalamus (encompassing the arcuate nucleus) of mice, Ad-cMCD increases food intake and body weight. Ad-MCD delivered into the ventral hypothalamus also reverses the rapid suppression of food intake caused by i.c.v.-administered C75, a fatty acid synthase inhibitor that increases hypothalamic [malonyl-CoA]. Taken together these findings implicate malonyl-CoA in the hypothalamic regulation of feeding behavior.

Monitoring energy balance: metabolites of fatty acid synthesis as hypothalamic sensors.

Because energy balance is important for survival, a system is required to monitor energy status and to make appropriate adjustments in energy intake and energy expenditure. In higher animals, a centrally located system has evolved to accomplish this task. When caloric intake exceeds expenditure, the surplus is channeled into energy storage pathways, primarily the synthesis of fatty acids, which are converted into fat and stored in adipose tissue. Thus, metabolic flux through the pathway of fatty acid synthesis, located in the lipogenic tissues, reflects the "energy status" of the animal. The enzymatic machinery of this pathway is also expressed in the brain, notably the hypothalamus. In the hypothalamus, intermediates in this pathway appear to serve as energy sensors that signal higher brain centers to produce appropriate responses, e.g., altered food intake and energy expenditure.

Effect of centrally administered C75, a fatty acid synthase inhibitor, on ghrelin secretion and its downstream effects.

The central administration of the fatty acid synthase (FAS) inhibitor, C75, rapidly suppresses the expression of orexigenic neuropeptides [neuropeptide Y (NPY) and agouti-related protein (AgRP)] and activates expression of anorexigenic neuropeptides [proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART)] in the hypothalamus. The combined actions of these changes inhibit food intake and decrease body weight. Intracerebroventricular injection of C75 appears to rapidly inhibit the secretion of ghrelin by hypothalamic explants ex vivo and by the stomach in vivo. Ghrelin administered intracerebroventricularly reverses the anorexic effect of C75, suggesting that C75 acts upstream of ghrelin. Because ghrelin-producing neurons are known to form synapses onto NPY/AgRP neurons, we suggest that the reversal of C75-induced anorexia by ghrelin may be mediated by NPY/AgRP neurons. This hypothesis is supported by the finding that ghrelin reverses the C75-induced inactivation (assessed by c-Fos expression) of neurons in the arcuate nucleus that express NPY (assessed by immunohistochemical costaining). These effects closely correlate with appropriate changes downstream in the expression of the hypothalamic neuropeptides that regulate feeding behavior, i.e., down-regulation of the expression of NPY and AgRP and up-regulation of the expression of proopiomelanocortin/alpha-melanocyte-stimulating hormone, provoked by C75 and reversed by ghrelin. We propose a model in which ghrelin secretion plays an intermediary role between malonyl-CoA, the substrate of fatty acid synthase, and the neural circuitry regulating energy homeostasis.

Long-term effects of a fatty acid synthase inhibitor on obese mice: food intake, hypothalamic neuropeptides, and UCP3.

Short-term treatment of lean and obese mice with the fatty acid synthase (FAS) inhibitor, C75, alters expression of hypothalamic neuropeptides thereby reducing food intake, body weight, and body fat. Here we report the long-term effects of C75 on obese (Ob/Ob) mice. A low dose of C75 administered every third day for 30 days reduced food intake by 62% and body weight by 43% whereas body weight of ad lib-fed controls increased by 11%. Loss of body weight correlated with decreased adipose and liver tissue mass. Decreased food intake correlated with decreased expression of hypothalamic neuropeptide mRNAs for NPY, AgRP, and MCH and an increased expression of neuropeptide mRNAs for alphaMSH (i.e., POMC) and CART. Consistent with increased energy expenditure, C75 treatment caused greater weight loss than pair-fed controls and increased expression of skeletal muscle UCP-3 mRNA. Lowered blood glucose was due largely to restriction of food intake. C75 blocked the normal fasting-induced rise in blood free fatty acids and ketones due either to decreased adipose tissue lipolysis and hepatic ketogenesis or increased fatty acid and ketone utilization by peripheral tissues, notably skeletal muscle.

Hypothalamic malonyl-CoA as a mediator of feeding behavior.

Previous studies showed that i.p. administration of C75, a potent inhibitor of fatty acid synthase (FAS), blocked fasting-induced up-regulation of orexigenic neuropeptides and down-regulation of anorexigenic neuropeptides in the hypothalami of mice. As a result, food intake and body weight were drastically reduced. Here we provide evidence supporting the hypothesis that hypothalamic malonyl-CoA, a substrate of FAS, is an indicator of global energy status and mediates the feeding behavior of mice. We use a sensitive recycling assay to quantify malonyl-CoA to show that the hypothalamic malonyl-CoA level is low in fasted mice and rapidly (< or = 2 h) increases (approximately 5-fold) on refeeding. Intracerebroventricular (i.c.v.) administration of C75 to fasted mice rapidly (< or = 2 h) increased (by 4-fold) hypothalamic malonyl-CoA and blocked feeding when the mice were presented with food. Moreover, prior i.c.v. administration of an acetyl-CoA carboxylase inhibitor, 5-(tetradecyloxy)-2-furoic acid, rapidly (although only partially) prevented the C75-induced rise of hypothalamic malonyl-CoA and prevented the C75-induced decrease of food intake. These effects correlated closely with the rapid (< or = 2 h) and reciprocal effects of i.c.v. C75 on the expression of hypothalamic orexigenic (NPY and AgRP) and anorexigenic (proopiomelanocortin) neuropeptide mRNAs. Previous results showing that C75 administered i.c.v. rapidly activates hypothalamic neurons of the arcuate and paraventricular nuclei are consistent with the results reported in this paper. Together these findings suggest that level of hypothalamic malonyl-CoA, which depends on the relative activities of acetyl-CoA carboxylase and FAS, is an indicator of energy status and mediates feeding behavior.