Associations of serum carotenoids with visceral adiposity index and lipid accumulation product: a cross-sectional study based on NHANES 2001-2006.

BACKGROUND: Visceral adiposity index (VAI) and lipid accumulation product (LAP) are comprehensive indicators to evaluate visceral fat and determine the metabolic health of individuals. Carotenoids are a group of naturally occurring antioxidants associated with several diseases. The purpose of this investigation was to explore the association between serum carotenoid concentration and VAI or LAP. METHODS: The data were obtained from the National Health and Nutrition Examination Survey between 2001 and 2006. The levels of serum carotenoids were evaluated using high-performance liquid chromatography. Multivariate linear regression models were employed to investigate the relationship between levels of serum carotenoids and VAI or LAP. The potential non-linear relationship was determined using threshold effect analysis and fitted smoothing curves. Stratification analysis was performed to investigate the potential modifying factors. RESULTS: In total, 5,084 participants were included in this population-based investigation. In the multivariate linear regressions, compared to the lowest quartiles of serum carotenoids, the highest quartiles were significantly associated with VAI, and the effect size (ß) and 95% CI was - 0.98 (- 1.34, - 0.62) for α-carotene, - 1.39 (- 1.77, - 1.00) for ß-carotene, - 0.79 (- 1.18, - 0.41) for ß-cryptoxanthin, - 0.68 (- 0.96, - 0.39) for lutein/zeaxanthin, and - 0.88 (- 1.50, - 0.27) for trans-lycopene. Using piece-wise linear regression models, non-linear relationships were found between ß-carotene and trans-lycopene and VAI with an inflection point of 2.44 (log2-transformed, ug/dL) and 3.80 (log2-transformed, ug/dL), respectively. The results indicated that α-carotene, ß-cryptoxanthin, and lutein/zeaxanthin were linearly associated with VAI. An inverse association was also found between serum carotenoids and LAP after complete adjustments. CONCLUSION: This study revealed that several serum carotenoids were associated with VAI or LAP among the general American population. Further large prospective investigations are warranted to support this finding.

A 2,2'-bipyridyl calcium complex: synthesis, structure and reactivity studies.

A 2,2'-bipyridyl calcium complex based on a tridentate ligand [CH3C(N-2,6-iPr2C6H3)CHC(CH3)NCH2CH2N(CH3)2]Ca(bipy)(THF) (1) was prepared by the reduction of {[CH3C(N-2,6-iPr2C6H3)CHC(CH3)NCH2CH2N(CH3)2]CaI(THF)}2 with potassium graphite in the presence of 2,2'-bipyridine (bipy). Complex 1 is a good Ca(I)synthon, as shown by its reactivity with I2, PhCH2SSCH2Ph, PhCH2SeSeCH2Ph and 9-fluorenone, yielding the calcium iodide complex [CH3C(N-2,6-iPr2C6H3)CHC(CH3)NCH2CH2N(CH3)2]CaI(bipy) (2), calcium thiolate [CH3C(N-2,6-iPr2C6H3)CHC(CH3)NCH2CH2N(CH3)2]Ca(SCH2Ph)(bipy) (3), calcium selenolate [CH3C(N-2,6-iPr2C6H3)CHC(CH3)NCH2CH2N(CH3)2]Ca(SeCH2Ph)(bipy) (4), and calcium ketyl complex [CH3C(N-2,6-iPr2C6H3)CHC(CH3)NCH2CH2N(CH3)2]Ca[O-(9-C13H8˙)](bipy)·2THF (5·2THF), respectively. In addition, reactions of complex 5 with CS2, CH2CHCH2Br and PhCH2Br give the corresponding dimeric bis(thiolate) complex {[S2CC(CMe(NAr))C(Me)NCH2CH2NMe2]Ca(DME)}2 (6), dimeric calcium bromide complex {[(9-CH2CHCH2-C13H8-9)-O]CaBr(THF)(bipy)}2 (7) and {[(9-C6H5CH2-C13H8-9)-O]CaBr[O-(9-C13H8)](bipy)}2 (8). These results demonstrated that the calcium ketyl complex 5 can also be employed as a single-electron transfer reagent. All the new compounds were characterized by various spectroscopic methods, and their solid-state structures were further confirmed by single-crystal X-ray diffraction analyses.

Azobenzenyl Calcium Complex: Synthesis and Reactivity Studies of a Ca(I) Synthon.

Attempted preparation of a low-valent Ca(I) complex by reduction of Ca iodide precursor [LCaI(THF)]2 (1) (L = [CH3C(NAr)CHC(CH3)NCH2CH2N(CH3)2]-, Ar = 2,6-iPr2C6H3), with KC8 led to isolation of a dinuclear calcium azaallyl complex {[H2CC(NAr)CHC(CH3)(NCH2CH2N(CH3)2)]Ca(THF)}2 (2). Alternatively, reaction of 1 with KC8 in the presence of azobenzene gives an azobenzenyl calcium complex LCa(PhNNPh)(THF) (3). The electron paramagnetic resonance and UV-vis spectra of complex 3 suggest that the (PhNNPh) moiety should be regarded as a radical anion. Complex 3 can react with Me3SiN3, Me3SiCHN2, CS2, W(CO)6, elemental sulfur, and AgBr, resulting in the formation of the azido complex [LCaN3(THF)]2 (5), isonitril complex {LCa[CNN(Si(CH3)3)]}2 (6), dimeric bis(thiolate) complex {[S2CC(CMe(NAr))C(Me)NCH2CH2NMe2]Ca(DME)}2 (7), metallocyclic carbene complex {[OC(W(CO)5)N(C6H5)]Ca(THF)3}2 (8), bis(thiolate) complex {[S2C(CMe(NAr))C(Me)NCH2CH2NMe2]Ca(THF)}2 (9), and bromide complex [LCaBr(THF)]2 (10). Additional insights on the reaction process resulting in the formation of complex 7 are provided by density-functional theory studies. These results demonstrate that the (PhNNPh)•- radical anion can serve as a very potent one-electron donor, and 3 acts as a low-valent calcium(I) synthon.

Pollen-Mimetic Metal-Organic Frameworks with Tunable Spike-Like Nanostructures That Promote Cell Interactions to Improve Antigen-Specific Humoral Immunity.

The exine capsules of pollen particles exhibit a variety of characteristic surface morphologies that promote their cell interactions; their use as antigen carriers for vaccination has been proposed. However, the allergy-causing substances in pollen particles may not all be removed, even by vigorous chemical treatments. To resolve this issue, this work develops systemic approaches for synthesizing pollen-mimetic metal-organic frameworks (MOFs), which comprise aluminum (Al) ions and an organic linker (2-aminoterephthalic acid), with tunable spike-like nanostructures on their surfaces. The as-synthesized MOFs act not only as a delivery vehicle that carries a model antigen (ovalbumin, OVA) but also as an adjuvant (Al). Scanning and transmission electron microscopies images reveal that the aspect ratio of the nanospikes that are grown on the MOFs can be controlled. A higher aspect ratio of the nanospikes on the MOFs is associated with greater cell attachment and faster and more efficient phagocytosis in cells, which results in greater expressions of pro-inflammatory cytokines. Consequently, a more robust immune response against the antigen of interest is elicited. These findings have broad implications for the rational design of the future antigen/adjuvant-presenting particles for vaccination.

Alcohol aggravates ketamine-induced behavioral, morphological and neurochemical alterations in adolescent rats: The involvement of CREB-related pathways.

Currently, an increasing proportion of adolescent ketamine users simultaneously consume alcohol. However, the potential behavioural and neurological alterations induced by such a drug combination and the underlying mechanisms have not been systematically examined. Therefore, in the present study, the behavioural and morphological changes and the underlying mechanisms were studied in adolescent rats after repeated alcohol and/or ketamine treatment. This study provided the first evidence that co-administration of alcohol (2 and 4 g/kg, i.g.) in adolescent rats significantly potentiated the neurotoxic properties of repeated ketamine (30 mg/kg, i.p.) treatments over 14 days, manifesting as increased locomotor activity, stereotypic behaviour, ataxia and morphological changes. This potentiation was associated with the enhancement by alcohol of ketamine-induced glutamate (Glu) and dopamine (DA) release in the cortex and hippocampus. Further mechanistic study demonstrated that alcohol potentiated ketamine-induced neurotoxicity through down-regulation of Akt (a serine/threonine kinase or protein kinase, PKB), protein kinase A (PKA), calmodulin-dependent kinase IV (CaMK-IV)-mediated cyclic AMP-responsive element binding protein (CREB) pathways and induction of neuronal apoptosis in the cortex and hippocampus of the adolescent rats. As this study provides strong evidence that repeated alcohol and ketamine co-exposure may cause serious neurotoxicity, attention needs to be drawn to the potential risk of this consumption behaviour, especially for adolescents.

Alcohol amplifies ketamine-induced apoptosis in primary cultured cortical neurons and PC12 cells through down-regulating CREB-related signaling pathways.

Recreational use of ketamine (KET) has been increasing worldwide. Previous studies have demonstrated that KET induced neurotoxicity; however, few studies have examined how alcohol (ALC) affects KET-induced neurotoxicity. In light of the fact that some KET abusers combine KET with ALC, the present study was aimed to investigate the effects of ALC on KET-induced neurotoxicity and the underlying mechanism in vitro. Our data revealed that co-treatment with ALC and KET was more detrimental to cell viability than KET single treatment in both PC12 cells and primary cultured rat cortical neurons. Furthermore, ALC exacerbated KET-induced apoptosis characterized by morphological changes and the sub-G1 phase increase, which were mitigated by the pretreatment of CNQX, a known alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/kainite (KA) receptor antagonist. In addition, ALC and KET co-treatment led to intracellular Ca2+ overload, down-regulation of p-Akt, p-CREB, PKA, CaMK-IV, Bcl-2 and BDNF expression and up-regulation of cleaved caspase-3 and Bax expression, which can be attenuated by CNQX pretreatment. These results indicate that the potentiation of ALC on KET-induced neurotoxicity was related to the down-regulation of CREB-related pathways. Our present study also indicates that ALC and KET co-abuse might cause serious neurotoxicity which should be conveyed to the public and drew enough attention.

Baicalin Attenuates Ketamine-Induced Neurotoxicity in the Developing Rats: Involvement of PI3K/Akt and CREB/BDNF/Bcl-2 Pathways.

Ketamine is widely used as an anesthetic in pediatric clinical practice. However, numerous studies have reported that exposure to ketamine during the developmental period induces neurotoxicity. Here we investigate the neuroprotective effects of baicalin, a natural flavonoid compound, against ketamine-induced apoptotic neurotoxicity in the cortex and hippocampus of the Sprague-Dawley postnatal day 7 (PND7) rat pups. Our results revealed that five continuous injections of ketamine (20 mg/kg) at 90-min intervals over 6 h induced obvious morphological damages of neuron by Nissl staining and apoptosis by TUNEL assays in the prefrontal cortex and hippocampus of PND7 rat pups. Baicalin (100 mg/kg) pretreatment alleviated ketamine-induced morphological change and apoptosis. Caspase-3 activity and caspase-3 mRNA expression increase induced by ketamine were also inhibited by baicalin treatment. LY294002, an inhibitor of PI3K, abrogated the effect of baicalin against ketamine-induced caspase-3 activity and caspase-3 mRNA expression increase. In addition, Western blot studies indicated that baicalin not only inhibited ketamine-induced p-Akt and p-GSK-3ß decrease, but also relieved ketamine-induced p-CREB and BDNF expression decrease. Baicalin also attenuated ketamine-induced Bcl-2/Bax decrease and caspase-3 expression increase. Further in vitro experiments proved that baicalin mitigated ketamine-induced cell viability decrease in the MTT assay, morphological change by Rosenfeld's staining, and caspase-3 expression increase by Western blot in the primary neuron-glia mixed cultures. LY294002 abrogated the protective effect of baicalin. These data demonstrate that baicalin exerts neuroprotective effect against ketamine-induced neuronal apoptosis by activating the PI3K/Akt and its downstream CREB/BDNF/Bcl-2 signaling pathways. Therefore, baicalin appears to be a promising agent in preventing or reversing ketamine's apoptotic neurotoxicity at an early developmental stage.