Spatially resolved Spectro-photometry of M81: Age, Metallicity and Reddening Maps

In this paper, we present a multi-color photometric study of the nearby spiral galaxy M81, using images obtained with the Beijing Astronomical Observatory 60/90 cm Schmidt Telescope in 13 intermediate-band filters from 3800 to 10000{\AA}. The observations cover the whole area of M81 with a total integration of 51 hours from February 1995 to February 1997. This provides a multi-color map of M81 in pixels of 1\arcsec.7 \times 1\arcsec.7. Using theoretical stellar population synthesis models, we demonstrate that some BATC colors and color indices can be used to disentangle the age and metallicity effect. We compare in detail the observed properties of M81 with the predictions from population synthesis models and quantify the relative chemical abundance, age and reddening distributions for different components of M81. We find that the metallicity of M81 is about $Z=0.03$ with no significant difference over the whole galaxy. In contrast, an age gradient is found between stellar populations of the central regions and of the bulge and disk regions of M81: the stellar population in its central regions is older than 8 Gyr while the disk stars are considerably younger, $\sim 2$ Gyr. We also give the reddening distribution in M81. Some dust lanes are found in the galaxy bulge region and the reddening in the outer disk is higher than that in the central regions.Comment: Accepted for publication in AJ (May 2000 issue). 27 pages including 6 figures. Uses AASTeX aasms4 styl

Intermediate-band Surface Photometry of the Edge-on Galaxy: NGC 4565

We present a deep, 42.79 hr image of the nearby, edge-on galaxy NGC 4565 in the Beijing-Arizona-Taipei-Connecticut (BATC) 6660A band using the large-format CCD system on the 0.6m Schmidt telescope at the Xinglong Station of the National Astronomical Observatories of China (NAOC). we obtain a final image that is calibrated to an accuracy of 0.02 mag in zero point, and for which we can measure galaxy surface brightness to an accuracy of 0.25 mag at a surface brightness at 27.5 mag arcsec^-2 at 6660A, corresponding to a distance of 22 kpc from the center of the disk. The integrated magnitude of NGC4565 in our filter is m6660=8.99 (R magnitude of 9.1) to a surface brightness of 28 mag arcsec-2. We analyze the faint outer parts of this galaxy using a two-dimensional model comprised of three components: an exponential thin disk, an exponential thick disk, and a power-law halo. A total of 12 parameters are included in our model. We determine the best values of our model parameters via 10,000 random initial values, 3,700 of which converge to final values. The thin disk and thick disk parameters we determine here are consistent with those of previous studies of this galaxy. However, our very deep image permits a better determination of the power law fit to the halo, constraining this power law to be between r^-3.2 and r^-4.0, with a best fit value of r^-3.88. We find the axis ratio of the halo to be 0.44 and its core radius to be 14.4 kpc (for an adopted distance of 14.5 Mpc).Comment: 34 pages, 11 figures, will appear in March 2002 of A

The effects of distinct fatty acids on central leptin sensitivity, hypothalamic inflammation, and central-regulated hepatic metabolism

Consumption of a fat-rich diet is implicated in the development of central leptin resistance and obesity in modern societies. Epidemiological evidence suggests that saturated fatty acids (SFA) and n-6 polyunsaturated fatty acids (n-6 PUFA), highly consumed in Western diets, induce potent inflammation and impair leptin signalling in the hypothalamus, leading to the dysregulation of central leptin on body energy homeostasis and peripheral metabolism. However, n-3 PUFA and n-3 PUFA derivatives have well-known anti-inflammatory properties, and exert anti-obesity effects by improving central leptin sensitivity and its metabolic action in peripheral tissues. However, the role and mechanism of distinct fatty acids, especially directly act on central nervous system, regulate central leptin sensitivity, hypothalamic leptin signalling pathways, and hepatic energy homeostasis remain largely undiscovered. The present thesis aims to determine the effect of intracerebroventricular (icv) injection of distinct fatty acids on central leptin sensitivity in C57BL/6J male mice. Body energy homeostasis, hypothalamic leptin signalling, and centrally regulated hepatic glucose and lipid metabolism in response to distinct fatty acids will be characterised. The contribution of hypothalamic inflammatory effects induced by different fatty acids will also be investigated. The fatty acids to be examined are SFA palmitic acid (PA), n-6 PUFA arachidonic acid (ARA), n-3 PUFA docosahexaenoic acid (DHA), and n-3 PUFA derivative α-ethyl DHA ethyl ester. We demonstrate that the icv administration of PA and ARA induces central leptin resistance, evidenced by the inhibition of central leptin\u27s suppression on food intake and body weight gain. In addition to central leptin resistance, the hypothalamic leptin JAK2- STAT3 and PI3K-Akt signalling pathways were impaired, with the down-regulation of leptin signalling mediators pSTAT3, pJAK2, pAkt, and pFOXO1. Furthermore, the central administration of PA and ARA blunted the leptin-induced decrease of hepatic gluconeogenesis, glucose transportation, lipogenesis, cholesterol synthesis, and increase in hepatic β-oxidation. PA and ARA induced potent hypothalamic pro-inflammatory effects and increased pro-inflammatory cytokines and inflammatory mediators, as well as increased leptin signalling negative regulator SOCS3. On the other hand, central injection of DHA and DHA derivative exerted an anorexigenic effect by reducing energy intake and body weight gain in high-fat diet (HFD) mice. Both DHA and DHA derivative improved leptin JAK2-STAT3 and PI3K-Akt signalling in the hypothalamus, and consequently restored central leptin-mediated hepatic glucose and lipid metabolism. In addition, we also demonstrate that PA and ARA can inhibit, while DHA can improve central leptin action in mediating hypothalamic sympathetic activity, which may associated with the impaired or promoted hepatic energy metabolism. In summary, elevated central PA and ARA concentrations induce leptin resistance and pro-inflammatory response in the central nervous system, which is associated with the dysregulation of the central leptin effect on energy homeostasis and hepatic metabolism. DHA and DHA derivative reverse HFD-induced adiposity, and decrease hypothalamic inflammation, which contributes to an increased central leptin sensitivity and improved regulation of hepatic metabolism. Thus, the administration of distinct fatty acids may provide realistic and alternative therapeutic strategies for the treatment of obesity and associated metabolic disturbances

Arachidonic acid impairs hypothalamic leptin signaling and hepatic energy homeostasis in mice

Epidemiological evidence suggests that the consumption of a diet high in n-6 polyunsaturated fatty acids (PUFA) is associated with the development of leptin resistance and obesity. We aim to examine the central effect of n-6 PUFA, arachidonic acid (ARA) on leptin sensitivity and leptin-regulated hepatic glucose and lipid metabolism. We found that intracerebroventricular injection of ARA (25 nmol/day) for 2.5 days reversed the effect of central leptin on hypothalamic JAK2, pSTAT3, pAkt, and pFOXO1 protein levels, which was concomitant with a pro-inflammatory response in the hypothalamus. ARA also attenuated the effect of central leptin on hepatic glucose and lipid metabolism by reversing the mRNA expression of the genes involved in gluconeogenesis (G6Pase, PEPCK), glucose transportation (GLUT2), lipogenesis (FAS, SCD1), and cholesterol synthesis (HMG-CoA reductase). These results indicate that an increased exposure to central n-6 PUFA induces central cellular leptin resistance with concomitant defective JAK2-STAT3 and PI3K-Akt signaling

Palmitic acid induces central leptin resistance and impairs hepatic glucose and lipid metabolism in male mice

The consumption of diets rich in saturated fat largely contributes to the development of obesity in modern societies. A diet high in saturated fats can induce inflammation and impair leptin signaling in the hypothalamus. However, the role of saturated fatty acids on hypothalamic leptin signaling, and hepatic glucose and lipid metabolism remains largely undiscovered. In this study, we investigated the effects of intracerebroventricular (icv) administration of a saturated fatty acid, palmitic acid (PA, C16:0), on central leptin sensitivity, hypothalamic leptin signaling, inflammatory molecules and hepatic energy metabolism in C57BL/6 J male mice. We found that the icv administration of PA led to central leptin resistance, evidenced by the inhibition of central leptin\u27s suppression of food intake. Central leptin resistance was concomitant with impaired hypothalamic leptin signaling (JAK2-STAT3, PKB/Akt-FOXO1) and a pro-inflammatory response (TNF-α, IL1-β, IL-6 and pIκBa) in the mediobasal hypothalamus and paraventricular hypothalamic nuclei. Furthermore, the pre-administration of icv PA blunted the effect of leptin-induced decreases in mRNA expression related to gluconeogenesis (G6Pase and PEPCK), glucose transportation (GLUT2) and lipogenesis (FAS and SCD1) in the liver of mice. Therefore, elevated central PA concentrations can induce pro-inflammatory responses and leptin resistance, which are associated with disorders of energy homeostasis in the liver as a result of diet-induced obesity

Bardoxolone methyl prevents insulin resistance and the development of hepatic steatosis in mice fed a high-fat diet

High-fat (HF) diet-induced obesity is a major risk factor for the development of insulin resistance and hepatic steatosis. We examined the hypothesis that bardoxolone methyl (BM) would prevent the development of insulin resistance and hepatic steatosis in mice fed a HF diet. C57BL/6J male mice were fed a lab chow (LC), HF (40% fat), or HF diet supplemented with 10 mg/kg/day BM orally for 21 weeks. Glucose metabolism was assessed using a glucose tolerance test (GTT) and insulin sensitivity test (IST). Signalling molecules involved in insulin resistance, inflammation, and lipid metabolism were examined in liver tissue via western blotting and RT-PCR. BM prevented HF diet-induced insulin resistance and alterations in the protein levels of protein tyrosine phosphatase 1B (PTP1B), forkhead box protein O1 (FOXO1) and BDNF, and expression of the insulin receptor (IR), IRS-1 and glucose-6-phosphatase (G6Pase) genes. Furthermore, BM prevented fat accumulation in the liver and decreases in the β-oxidation gene, peroxisomal acyl-coenzyme A oxidase 1 (ACOX) in mice fed a HF diet. In the livers of HF fed mice, BM administration prevented HF diet-induced macrophage infiltration, inflammation as indicated by reduced IL-6 and signal transducer and activator of transcription 3 (STAT3) protein levels and TNFα mRNA expression, and increased nuclear factor-like 2 (Nrf2) mRNA expression and nuclear protein levels. These findings suggest that BM prevents HF diet induced insulin resistance and the development of hepatic steatosis in mice fed a chronic HF diet through modulation of molecules involved in insulin signalling, lipid metabolism and inflammation in the liver

DHA reduces hypothalamic inflammation and improves central leptin signaling in mice

Aims: Anti-obesity effects and improved leptin sensitivity from n-3 polyunsaturated fatty acids (n-3 PUFAs) have been reported in diet-induced obese animals. This study sought to determine the beneficial central effects and mechanism of docosahexaenoic acid (DHA, 22:6 n-3) in high-fat (HF) diet fed mice. Main methods: Male C57BL/6J mice were given HF diet with or without intracerebroventricular (icv) injection of docosahexaenoic acid (DHA, 22:6 n-3) for two days. Central leptin sensitivity, hypothalamic inflammation, leptin signaling molecules and tyrosine hydroxylase (TH) were examined by central leptin sensitivity test and Western blot. Furthermore, the expression of hepatic genes involved in lipid metabolism was examined by RT-PCR. Key findings: We found that icv administration of DHA not only reduced energy intake and body weight gain but also corrected the HF diet-induced hypothalamic inflammation. DHA decreased leptin signaling inhibitor SOCS3 and improved the leptin JAK2-Akt signaling pathways in the hypothalamus. Furthermore, icv administration of DHA improved the effects of leptin in the regulation of mRNA expression of enzymes related to lipogenesis, fatty acid β-oxidation, and cholesterol synthesis in the liver. DHA increased leptin-induced activation of TH in the hypothalamus. Significance: Therefore, increasing central DHA concentration may prevent the deficit of hypothalamic regulation, which is associated with disorders of energy homeostasis in the liver as a result of a high-fat diet

EmotionNAS: Two-stream Architecture Search for Speech Emotion Recognition

Speech emotion recognition (SER) is a crucial research topic in human-computer interactions. Existing works are mainly based on manually designed models. Despite their great success, these methods heavily rely on historical experience, which are time-consuming but cannot exhaust all possible structures. To address this problem, we propose a neural architecture search (NAS) based framework for SER, called "EmotionNAS". We take spectrogram and wav2vec features as the inputs, followed with NAS to optimize the network structure for these features separately. We further incorporate complementary information in these features through decision-level fusion. Experimental results on IEMOCAP demonstrate that our method succeeds over existing state-of-the-art strategies on SER.Comment: Submitted to Interspeech 202