Shank3 deficiency elicits autistic-like behaviors by activating p38α in hypothalamic AgRP neurons.

BACKGROUND: SH3 and multiple ankyrin repeat domains protein 3 (SHANK3) monogenic mutations or deficiency leads to excessive stereotypic behavior and impaired sociability, which frequently occur in autism cases. To date, the underlying mechanisms by which Shank3 mutation or deletion causes autism and the part of the brain in which Shank3 mutation leads to the autistic phenotypes are understudied. The hypothalamus is associated with stereotypic behavior and sociability. p38α, a mediator of inflammatory responses in the brain, has been postulated as a potential gene for certain cases of autism occurrence. However, it is unclear whether hypothalamus and p38α are involved in the development of autism caused by Shank3 mutations or deficiency. METHODS: Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and immunoblotting were used to assess alternated signaling pathways in the hypothalamus of Shank3 knockout (Shank3-/-) mice. Home-Cage real-time monitoring test was performed to record stereotypic behavior and three-chamber test was used to monitor the sociability of mice. Adeno-associated viruses 9 (AAV9) were used to express p38α in the arcuate nucleus (ARC) or agouti-related peptide (AgRP) neurons. D176A and F327S mutations expressed constitutively active p38α. T180A and Y182F mutations expressed inactive p38α. RESULTS: We found that Shank3 controls stereotypic behavior and sociability by regulating p38α activity in AgRP neurons. Phosphorylated p38 level in hypothalamus is significantly enhanced in Shank3-/- mice. Consistently, overexpression of p38α in ARC or AgRP neurons elicits excessive stereotypic behavior and impairs sociability in wild-type (WT) mice. Notably, activated p38α in AgRP neurons increases stereotypic behavior and impairs sociability. Conversely, inactivated p38α in AgRP neurons significantly ameliorates autistic behaviors of Shank3-/- mice. In contrast, activated p38α in pro-opiomelanocortin (POMC) neurons does not affect stereotypic behavior and sociability in mice. LIMITATIONS: We demonstrated that SHANK3 regulates the phosphorylated p38 level in the hypothalamus and inactivated p38α in AgRP neurons significantly ameliorates autistic behaviors of Shank3-/- mice. However, we did not clarify the biochemical mechanism of SHANK3 inhibiting p38α in AgRP neurons. CONCLUSIONS: These results demonstrate that the Shank3 deficiency caused autistic-like behaviors by activating p38α signaling in AgRP neurons, suggesting that p38α signaling in AgRP neurons is a potential therapeutic target for Shank3 mutant-related autism.

TSHR signaling promotes hippocampal dependent memory formation through modulating Wnt5a/ß-catenin mediated neurogenesis.

Subclinical hyperthyroidism is defined biochemically as a low or undetectable thyroid-stimulating hormone (TSH) with normal thyroid hormone levels. Low TSHR signaling is considered to associate with cognitive impairment. However, the underlying molecular mechanism by which TSHR signaling modulates memory is poorly understood. In this study, we found that Tshr-deficient in the hippocampal neurons impairs the learning and memory abilities of mice, accompanying by a decline in the number of newborn neurons. Notably, Tshr ablation in the hippocampus decreases the expression of Wnt5a, thereby inactivating the ß-catenin signaling pathway to reduce the neurogenesis. Conversely, activating of the Wnt/ß-catenin pathway by the agonist SKL2001 results in an increase in hippocampal neurogenesis, resulting in the amelioration in the deficits of memory caused by Tshr deletion. Understanding how TSHR signaling in the hippocampus regulates memory provides insights into subclinical hyperthyroidism affecting cognitive function and will suggest ways to rationally design interventions for neurocognitive disorders.

Energy deficiency promotes rhythmic foraging behavior by activating neurons in paraventricular hypothalamic nucleus.

Background: Dysregulation of feeding behavior leads to a variety of pathological manifestations ranging from obesity to anorexia. The foraging behavior of animals affected by food deficiency is not fully understood. Methods: Home-Cage system was used to monitor the behaviors. Immunohistochemical staining was used to monitor the trend of neuronal activity. Chemogenetic approach was used to modify neuronal activity. Results: We described here a unique mouse model of foraging behavior and unveiled that food deprivation significantly increases the general activities of mice with a daily rhythmic pattern, particularly foraging behavior. The increased foraging behavior is potentiated by food cues (mouthfeel, odor, size, and shape) and energy deficit, rather than macronutrient protein, carbohydrate, and fat. Notably, energy deficiency increases nocturnal neuronal activity in paraventricular hypothalamic nucleus (PVH), accompanying a similar change in rhythmic foraging behavior. Activating neuronal activity in PVH enhances the amplitude of foraging behavior in mice. Conversely, inactivating neuronal activity in PVH decreases the amplitude of foraging behavior and impairs the rhythm of foraging behavior. Discussion: These results illustrate that energy status and food cues regulate the rhythmic foraging behavior via PVH neuronal activity. Understanding foraging behavior provides insights into the underlying mechanism of eating-related disorders.

The effect of hyperthyroidism on cognitive function, neuroinflammation, and necroptosis in APP/PS1 mice.

BACKGROUND: Increasing evidence has linked the thyroid dysfunction to the pathogenesis of dementia. Evidence from clinical studies has demonstrated that hypothyroidism is related to an increased risk of dementia. But the association of hyperthyroidism with dementia is largely unknown. METHODS: We used the adenovirus containing thyrotropin receptor (TSHR) amino acid residues 1-289 (Ad-TSHR289)-induced Graves' disease (GD) phenotype in Alzheimer's disease (AD) model mice (APP/PS1 mice) to evaluate the effect of hyperthyroidism on the cognitive function and ß-amyloid (Aß) accumulation. RESULTS: GD mice exhibited a stable long-term hyperthyroidism and cognitive deficits. Single Cell RNA-sequencing analysis indicated that microglia function played a critical role in the pathophysiological processes in GD mice. Neuroinflammation and polarization of microglia (M1/M2 phenotype) and activated receptor-interacting serine/threonine protein kinase 3 (RIPK3)/mixed lineage kinase domain-like pseudo-kinase (MLKL)-mediated necroptosis contributed to the pathological process, including Aß deposition and neuronal loss. RIPK3 inhibitor could inhibit GD-mediated Aß accumulation and neuronal loss. CONCLUSIONS: Our findings reveal that GD hyperthyroidism aggravates cognitive deficits in AD mice and induces Aß deposition and neuronal loss by inducing neuroinflammation and RIPK3/MLKL-mediated necroptosis.

p38α in the preoptic area inhibits brown adipose tissue thermogenesis.

OBJECTIVE: Elevation of energy expenditure through an increase of brown adipose tissue (BAT) thermogenesis is regarded as one of the most promising ways to prevent obesity development. The preoptic area (POA) of the hypothalamus is a critical area for control of BAT thermogenesis. However, the intracellular signaling cascades in the POA for regulation of BAT thermogenesis are poorly understood. METHODS: Phosphorylation proteomics (phosphoproteomics) and bioinformatics approaches were used to disclose numerous hypothalamic signaling pathways involved in the regulation of BAT thermogenesis. Conditional manipulation of the p38α gene in mouse POA was performed by stereotaxic injection of adeno-associated virus 9 vector to explore the role of p38α in BAT thermogenesis. RESULTS: Multiple hypothalamic signaling pathways were triggered by cold exposure, especially the mitogen-activated protein kinase (MAPK) signaling pathway. The p38α activation, but not extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun NH2-terminal kinase (JNK), in the hypothalamus was significantly decreased during cold exposure. p38α deficiency in the POA dramatically elevated energy expenditure owing to a marked increase in BAT thermogenesis, resulting in significantly decreased body weight gain and fat mass. Overexpression of p38α in the POA led to a dramatic increase in weight gain. CONCLUSIONS: These results demonstrate that p38α in the POA exacerbates obesity development, at least in part owing to a decrease in BAT thermogenesis.

Single-Cell Sequencing Analysis of the db/db Mouse Hippocampus Reveals Cell-Type-Specific Insights Into the Pathobiology of Diabetes-Associated Cognitive Dysfunction.

Diabetes-associated cognitive decline (DCD), is one of the complications of diabetes, which is characterized by a series of neurophysiological and pathological abnormalities. However, the exact pathogenesis of DCD is still unknown. Single-cell RNA sequencing (scRNA-seq) could discover unusual subpopulations, explore functional heterogeneity and identify signaling pathways and potential markers. The aim of this research was to provide deeper opinion into molecular and cellular changes underlying DCD, identify different cellular types of the diabetic mice hippocampus at single-cell level, and elucidate the factors mediating the pathogenesis of DCD. To elucidate cell specific gene expression changes in the hippocampus of diabetic encephalopathy. Single-cell RNA sequencing of hippocampus from db/m and db/db mice was carried out. Subclustering analysis was performed to further describe microglial cell subpopulations. Interestingly using immunohistochemistry, these findings were confirmed at the protein level. Single cell analysis yielded transcriptome data for 14621 hippocampal cells and defined 11 different cell types. Analysis of differentially expressed genes in the microglia compartments indicated that infection- and immune system process- associated terms, oxidative stress and inflammation play vital roles in the progression of DCD. Compared with db/m mouse, experiments at the protein level supported the activation of microglia, increased expression of inflammatory factors and oxidative stress damage in the hippocampus of db/db mouse. In addition, a major finding of our research was the subpopulation of microglia that express genes related to pro-inflammatory disease-associated microglia (DAM). Our research reveals pathological alterations of inflammation and oxidative stress mediated hippocampal damage in the db/db mice, and may provide potential diagnostic biomarkers and therapeutic interventions for DCD.

[Characteristics and Sources of PM2.5-O3 Compound Pollution in Tianjin].

The characteristics and sources of PM2.5-O3 compound pollution were analyzed based on the high-resolution online monitoring data of PM2.5, O3 and volatile organic compounds(VOCs) observed in Tianjin from 2017 to 2019. The results showed that total PM2.5-O3 compound pollution was 34 days, which only appeared between March and September and slightly increased by year. The peak value of ρ(O3)(301-326 µg·m-3) appeared when ρ(PM2.5) ranged from 75 µg·m-3 to 85 µg·m-3. During PM2.5-O3 compound pollution, the average ρ(VOCs) was 72.59 µg·m-3, and the chemical compositions of VOCs were alkanes, aromatics, alkenes, and alkynes, accounting for 61.51%, 20.38%, 11.54%, and 6.57% of VOCs concentration on average, respectively. The concentration of the top 20 species of VOCs increased, among which the proportion of alkane species such as ethane, n-butane, isobutane, and isopentane increased; the proportion of alkenes and alkynes decreased slightly; and the proportion of benzene and 1,2,3-trimethylbenzene of aromatic hydrocarbons increased slightly. The ozone formation potential(OFP) contribution of alkanes, alkenes, aromatics, and alkynes were 19.68%, 39.99%, 38.08%, and 2.25%, respectively; the contributions of alkanes, alkenes, and aromatics to secondary organic aerosol(SOA) formation potential were 7.94%, 2.17%, and 89.89%, respectively. Compared with that of non-compound pollution, the contribution of alkanes and aromatics to OFP increased 13.8% and 4.3%, and that to SOA formation potential increased 2.3% and 0.2%, respectively. The contribution of alkenes to OFP and SOA formation potential decreased 9.4% and 15.6%, respectively, and the contribution of alkynes to OFP increased 7.7% in compound pollution. The contributions of main species such as 1-pentene, n-butane, methyl cyclopentane, isopentane, 1,2,3-trimethylene, propane, toluene, acetylene, o-xylene, ethylbenzene, m-ethyltoluene, and m/p-xylene to OFP increased, and that of isoprene to OFP decreased. The contribution of benzene, 1,2,3-trimethylbenzene, toluene, and o-xylene to the potential formation of SOA increased during compound pollution. Positive matrix factorization was applied to estimate the contributions of sources to OFP and SOA formation potential in compound pollution, solvent usage, automobile exhaust, petrochemical industrial emission, natural source, liquefied petroleum gas(LPG) evaporation, combustion source, gasoline evaporation, and other industrial process sources were identified as major sources of OFP and SOA formation potential; the contributions of each source to OFP were 21.9%, 16.9%, 16.7%, 12.4%, 8.3%, 7.7%, 2.9%, and 13.2%, respectively, and to SOA formation potentials were 46.8%, 14.4%, 7.1%, 11.9%, 5.9%, 6.6%, 1.6%, and 5.7%, respectively. Solvent usage, automobile exhaust, and petrochemical industrial emissions were main sources for PM2.5-O3 compound pollution.

[Characteristics and Sources of VOCs at Different Ozone Concentration Levels in Tianjin].

To further study the effect of volatile organic compounds (VOCs) on ozone pollution, the characteristics and sources of VOCs at different ozone (O3) concentration levels were analyzed, using high-resolution online monitoring data obtained from Tianjin in the summer of 2019. Results showed that VOCs concentrations were 32.94, 38.10, 42.41, and 47.12 µg ·m-3, when the O3 concentration levels were categorized as excellent, good, light pollution, and moderate pollution, respectively. VOCs were composed of alkanes, alkenes, alkynes and aromatics, which accounted for 61.72%-63.36%, 14.96%-15.51%, 2.73%-4.13%, and 18.53%-19.10%, respectively, of VOCs concentrations at different O3 concentration levels. Among them, the proportion of alkanes was slightly higher when O3 concentration was categorized as good or light pollution, alkenes and alkynes accounted for the highest proportion when O3 concentration was excellent, and the proportion of aromatics was highest during periods of moderate pollution. The main VOCs species were propane, ethane, ethylene, toluent, n-butane, isopentane, m/p-xylene, propylene, acetylene, n-hexane, isobutene, benzene, n-pentane, isoprene, and 1,2,3-trimethylbenzene. The concentration percentage of isopentane, n-pentane, benzene, ethylene, propylene, n-butane, and isobutane increased gradually as O3 concentration increased. Significant increases in isoprene and 1,2,3-trimethylbenzene were observed during periods of light and moderate pollution. Alkenes and aromatics had higher ozone formation potential (OFP), and the contribution of alkenes to OFP declined as the O3 level rose, whereas that of aromatics increased. Ethylene, propylene, m/p-xylene, 1,2,3-trimethylbenzene, toluene, isoprene, trans-2-butene, and cis-2-pentene were the key species for O3 generation, and the contribution ratio of 1,2,3-trimethylbenzene, isoprene, propylene, and ethylene to OFP increased significantly during light or moderate O3 pollution. Positive matrix factorization was applied to estimate the source contributions of VOCs. Automobile exhaust, solvent usage, liquefied petroleum gas (LPG)/gasoline evaporation, combustion, petrochemical industrial emissions, natural sources, and other industrial emissions were identified as major sources of VOCs in summer. As O3 concentration level rose, the contribution percentage of automobile exhaust, LPG/gasoline evaporation, petrochemical industrial emissions, and natural sources increased gradually, whereas the contribution of combustion and other industrial emissions decreased overall. The contribution of solvent usage was lower when O3 levels indicated light or moderate pollution than when it was good.

Berberine improves intralipid-induced insulin resistance in murine.

Insulin resistance (IR) is a major metabolic risk factor even before the onset of hyperglycemia. Recently, berberine (BBR) is found to improve hyperglycemia and IR. In this study, we investigated whether BBR could improve IR independent of hyperglycemia. Acute insulin-resistant state was induced in rats by systemic infusion of intralipid (6.6%). BBR was administered via different delivery routes before or after the beginning of a 2-h euglycemic-hyperinsulinemic clamp. At the end of experiment, rats were sacrificed, gastrocnemius muscle was collected for detecting mitochondrial swelling, phosphorylation of Akt and AMPK, as well as the mitochondrial permeability regulator cyclophilin D (CypD) protein expression. We showed that BBR administration markedly ameliorated intralipid-induced IR without affecting blood glucose, which was accompanied by alleviated mitochondrial swelling in skeletal muscle. We used human skeletal muscle cells (HSMCs), AML12 hepatocytes, human umbilical vein endothelial cells, and CypD knockout mice to investigate metabolic and molecular alternations. In either HSMCs or AML12 hepatocytes, BBR (5 µM) abolished palmitate acid (PA)-induced increase of CypD protein levels. In CypD-deficient mice, intralipid-induced IR was greatly attenuated and the beneficial effect of BBR was diminished. Furthermore, we demonstrated that the inhibitory effect of BBR on intralipid-induced IR was mainly mediated by skeletal muscle, but not by intestine, liver, or microvasculature; BBR administration suppressed intralipid-induced upregulation of CypD expression in skeletal muscle. These results suggest that BBR alleviates intralipid-induced IR, which is related to the inhibition of CypD protein expression in skeletal muscle.

[Characterization and Source Apportionment of Atmospheric VOCs in Tianjin in 2019].

The characterization and source apportionment of atmospheric volatile organic compounds (VOCs) in Tianjin in 2019 were investigated based on high-resolution online monitoring data observed at an urban site in Tianjin. The results showed that the average annual concentration of VOCs was 48.9 µg·m-3, and seasonal concentrations followed with winter (66.9 µg·m-3) > autumn (47.9 µg·m-3) > summer (42.0 µg·m-3) > spring (34.6 µg·m-3). The chemical compositions of the VOCs were alkanes, aromatics, alkenes, and alkynes, which accounted for 65.0%, 17.4%, 14.6%, and 3.0% of the VOCs concentrations on average, respectively. The proportion of alkanes, aromatics, and alkynes was the highest in autumn, summer, and winter, respectively, while a higher alkenes proportion was observed in summer and winter. The ozone formation potential contribution of alkanes, alkenes, aromatics, and alkynes in spring and summer was 16.9%, 48.6%, 33.5%, and 1.0%, respectively, and the species with higher contributions were ethene, propylene, m,p-xylene, 1,2,3-trimethylbenzene, toluene, isoprene, trans-2-butene, cis-2-pentene, o-xylene, and m-ethyltoluene. During autumn and winter, the aromatics contributed as much as 91.5% to the secondary organic aerosol (SOA) formation potential, and o-xylene, toluene, m,p-xylene, ethylbenzene, o-ethyltoluene, and benzene were the main contributing species. Positive matrix factorization was applied to estimate VOCs source contributions, and automobile exhaust, liquefied petroleum gas/natural gas (LPG/NG) and gasoline evaporation, solvent usage, petrochemical industrial emissions, combustion, and natural sources were identified as major sources of VOCs in spring and summer, accounting for 29.2%, 19.9%, 16.4%, 10.3%, 7.3%, and 6.6%, respectively. While in autumn and winter, the contributions of LPG/NG and gasoline evaporation, automobile exhaust, combustion, solvent usage, and petrochemical industrial emissions were 32.4%, 21.9%, 18.5%, 13.3%, and 8.4%, respectively. Compared to the source contributions in spring and summer, a significant increase was observed for LPG/NG and combustion emission of 62.8% and 153.4%, respectively, and other sources decreased by 18.4%-25.0% in autumn and winter. Source composition spectrums showed that the petrochemical industry and solvent usage were the main emission sources of alkenes and aromatics in spring and summer, and combustion and solvent usage were the main emission sources of aromatics in autumn and winter. Thus, focus should be played on the petrochemical industry and solvent usage in spring and summer and on combustion and solvent usage in autumn and winter to further prevent and control ozone and SOA in Tianjin.

Thyrotropin receptor signaling deficiency impairs spatial learning and memory in mice.

Subclinical hyperthyroidism, a condition characterized by decreased thyroid-stimulating hormone (TSH) and normal concentration of thyroid hormone, is associated with an elevated risk for cognitive impairment. TSH is the major endogenous ligand of the TSH receptor (TSHR) and its role is dependent on signal transduction of TSHR. It has not, however, been established whether TSHR signaling is involved in the regulation of cognition. Here, we utilized Tshr knockout mice and found that Tshr deletion led to significantly compromised performance in learning and memory tests. Reduced dendritic spine density and excitatory synaptic density as well as altered synaptic structure in CA1 subfield of the hippocampus were also noted. Furthermore, the synapse-related gene expression was altered in the hippocampus of Tshr -/- mice. These findings suggest that TSHR signaling deficiency impairs spatial learning and memory, which discloses a novel role of TSHR signaling in brain function.

FSH signaling is involved in affective disorders.

Affective disorders are a set of mental disorders and particularly disrupt the mental health of susceptible women during puberty, pregnancy, parturition and menopause transition, which are characterized by dramatic changes in reproductive hormone profiles. The serum FSH level changes significantly during these periods; yet, the role of FSH in mood regulation is poorly understood. In the current study, FSHR knockout (Fshr-/-) mice displayed enhanced affective disorder behaviors in an open field test and a forced swim test, accompanied by altered gene expression profiles. The differentially expressed genes between Fshr-/- mice and Fshr+/+ mice were enriched in multiple neuroendocrine metabolic pathways. FSHR deletion significantly increased/decreased the mRNA and/or protein expression levels of AOX1, RDH12, HTR3a and HTR4 in mood-mediating brain regions, including the hippocampus and prefrontal cortex. These results reveal that FSH signaling is involved in the development of affective disorders.

FSHR ablation induces depression-like behaviors.

Alteration in reproductive hormones profile is associated with the increasing risk of menopausal depression in women. Serum follicle-stimulating hormone (FSH) level is changed during the menopause transition, while the effect of FSH on menopausal depression has remained undefined. In this study we investigated whether or how FSH affected menopausal depression in postmenopausal (ovariectomized) FSHR knockout mice (Fshr-/-). We found that Fshr-/- mice displayed aggravated depression-like behaviors, accompanied by severe oxidative stress in the whole brain, resulted from significantly reduced glutamate cysteine ligase modifier subunit (GCLm) in glutathione synthesis and glucose-6-phosphate dehydrogenase (G6PD) in NADP/NADPH transition. Importantly, administration of ROS scavenger N-acetyl cysteine (NAC, 150 mg · kg-1 · d-1, i.p. for 12 weeks) attenuated the depression-like behaviors of Fshr-/- mice. Consistent with these in vivo experiment results, we found that pretreatment with FSH (50, 100 ng/mL) dose-dependently increased protein levels of GCLm and G6PD, and decreased the ROS production in N2a mouse neuroblastoma cells. These findings demonstrate that FSH signaling is involved in pathogenesis of menopausal depression, and likely to maintain the redox-optimized ROS balance in neurons.

[Secondary Inorganic Pollution Characteristics During Heavy Pollution Episodes of 2017 in Tianjin].

Based on monitoring data collected at the supersite of Tianjin in 2017, seven typical heavy pollution episodes were investigated. The concentrations of air pollutants and secondary inorganic transformation products were analyzed to study the secondary inorganic pollution characteristics during the heavy pollution episodes. Compared to clean weather, concentrations of NO3- and SO42- during the heavy pollution episodes increased at rapid growth rates. These rates were obviously higher than the rate for PM2.5 increases, which indicates that the secondary inorganic reactions had an important influence on PM2.5 pollution during the episodes. The concentrations of PM2.5 and SO2 during the episodes in the latter half of the year were lower than those in the first half of the year probably because a substantial amount of coal use had been controlled. During the heavy pollution episodes, the NO2/SO2 values were 1.5 to 19.6, with higher values in the latter half of the year than the first half of the year suggestive of a greater influence from mobile sources. During most episodes, NO3- concentrations were higher than SO42- concentrations, and SOR values were higher than NOR values, which shows that the secondary transformation of nitrate and sulfate both played important roles during the heavy pollution episodes. When SO2 concentrations decreased significantly, SO42- concentrations did not decrease obviously, thus indicating that besides the secondary inorganic reactions, other factors also had a large impact on the generation of sulfate.

Adiponectin inhibits KISS1 gene transcription through AMPK and specificity protein-1 in the hypothalamic GT1-7 neurons.

Adiponectin secreted from adipose tissues plays a role in the regulation of energy homeostasis, food intake, and reproduction in the hypothalamus. We have previously demonstrated that adiponectin significantly inhibited GNRH secretion from GT1-7 hypothalamic GNRH neuron cells. In this study, we further investigated the effect of adiponectin on hypothalamic KISS1 gene transcription, which is the upstream signal of GNRH. We found that globular adiponectin (gAd) or AICAR, an artificial AMPK activator, decreased KISS1 mRNA transcription and promoter activity. Conversely, inhibition of AMPK by Compound C or AMPKα1-SiRNA augmented KISS1 mRNA transcription and promoter activity. Additionally, gAd and AICAR decreased the translocation of specificity protein-1 (SP1) from cytoplasm to nucleus; however, Compound C and AMPKα1-siRNA played an inverse role. Our experiments in vivo demonstrated that the expression of Kiss1 mRNA was stimulated twofold in the Compound C-treated rats and decreased about 60-70% in gAd- or AICAR-treated rats compared with control group. The numbers of kisspeptin immunopositive neurons in the arcuate nucleus region of Sprague Dawley rats mimicked the same trend seen in Kiss1 mRNA levels in animal groups with different treatments. In conclusion, our results provide the first evidence that adiponectin reduces Kiss1 gene transcription in GT1-7 cells through activation of AMPK and subsequently decreased translocation of SP1.

Spectroscopic studies of dye-surfactant interactions with the co-existence of heavy metal ions for foam fractionation.

The interaction between a cationic dye Methylene Blue (MB) and an anionic surfactant sodium dodecyl sulfate (SDS) with the presence of Cd2+ was investigated spectrophotometrically in a certain concentration range. The spectrophotometric measurements of dye-metal ion-surfactant system were carried out. The results indicated that the SDS concentration had a significant influence on the dye spectrum, while the addition of Cd2+ hardly caused change of the maximum value of absorbance. According to this observation, we concluded that electrostatic and hydrophobic interaction between dye and surfactant occurred up to a certain level, and the homo-ions Cd2+ almost exerted no effect on the dye-surfactant complexation, establishing a theoretical foundation for simultaneous removal of organic dye and heavy metal using foam fractionation. Meanwhile, the effects of their interaction on foam performance were investigated. The results showed that the addition of Cd2+ favored the tendency to ameliorate foam properties just contrary to MB. The feasibility of foam separation for dye and heavy metal removal from simulated wastewater was also confirmed using a continuous foam fractionator. In the simultaneous removal process, with the initial SDS concentration ranging from 0.5 to 5.0 mmol/L, the maximum removal efficiencies of MB and Cd2+ were obtained as 99.69% and 99.61%, respectively. The enrichment ratios were reduced from 24.34 to 7.65 for MB and from 22.01 to 3.35 for Cd2+.

Quantitative evaluation of heavy metals' pollution hazards in liquefaction residues of sewage sludge.

Liquefaction residues (LR) are the main by-products of sewage sludge (SS) liquefaction. This study quantitatively evaluates the potential ecological risk and pollution degrees of heavy metals (Pb, Zn, Cu, Cd, Cr and Ni) in LR versus SS. The leaching rates (R1) of heavy metals in LR were much lower than those in SS, revealing that the mobility/leachability of heavy metals was well suppressed after liquefaction. Geo-accumulation index (Igeo) indicated that the liquefaction process significantly weakened the contamination degrees of heavy metals. Potential ecological risk index (RI) demonstrated that overall risks caused by heavy metals were obviously lowered from 1093.56 (very high risk) in SS to 4.72 and 1.51 (low risk) in LR1 and LR2, respectively. According to the risk assessment code (RAC), each tested heavy metal had no or low risk to the environments after liquefaction. In a word, the pollution hazards of heavy metals in LR were markedly mitigated.