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1.
Eur J Pharm Sci ; 144: 105214, 2020 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-31935464

RESUMO

There are many kinds of potentially undesirable teeth. At present, surgical extraction is the most efficient way to eliminate these teeth, but it's very complex and invasive. In this study, we investigated the effects of bleomycin (BLM) on dental follicle and tooth eruption as a potential conservative therapy for undesirable teeth. Our data showed that local injection of 0.2 U/kg BLM had no significant effects on tooth eruption compared to the control group in Wistar rats. With higher dose of BLM (0.5 or 2 U/kg), the eruption of treated teeth was interrupted and their root formation failed until 4 weeks postnatal without significant systemic toxicity. Additionally, those effects were not depending on the toxicity of overdose evidenced by TUNEL assay. In summary, injecting BLM into dental follicle at an early stage could interrupt tooth development and eruption, and may prevent the potentially clinical problems resulting from undesirable teeth instead of surgical removal.

2.
J Hazard Mater ; 387: 122018, 2020 Apr 05.
Artigo em Inglês | MEDLINE | ID: mdl-31927260

RESUMO

Graphene-based materials have been demonstrated to facilitate electron extracellular transfer (EET) of Shewanella. In this study, compared to group lacking graphene oxide (GO)-based materials, GO films-added group and graphene oxide/polyvinyl alcohol (GO/PVA) film-added group delivered 2.67- and 3.13-fold increases in the Cr(VI) reduction by Shewanella xiamenensis, respectively. The whole reduction process could be divided into three stages, including microbial Cr(VI) reduction and GO reduction stage, microbial GO reduction stage and microbial Cr(VI) reduction mediated by reduced graphene oxide (rGO) stage. Moreover, gene analysis revealed that addition of GO and GO/PVA films stimulated overexpression of several c-type cytochrome (c-Cyts) genes, including mtrA, mtrB, mtrC, mtrD, mtrE, mtrF, omcA, petC and SO-4047. Specifically, appreciable Cr(VI) reduction by the strains that overexpressed mtrA, mtrB, mtrC, mtrD, mtrE, mtrF and omcA further confirmed that overexpression of c-Cyts genes indeed enhanced the efficiency of Cr(VI) reduction. Based on these results, the specific function of every c-Cyt was clearly found in Cr(VI) reduction by the induction of GO-based materials. Our finding has disclosed a synergetic mechanism stimulated by GO-based materials to enhance Cr(VI) bioreduction that was not only mediated through the modification of material but also upregulated the expression of functional genes.

3.
EBioMedicine ; 51: 102605, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31901865

RESUMO

BACKGROUND: Metabolic modulation is capable of maintaining cell potency, regulating niche homeostasis, or determining cell fate. However, little is known regarding the metabolic landscape during early adipogenesis or whether metabolic modulation could be a potential approach for obesity treatment. METHODS: The metabolic footprint during adipocyte commitment was evaluated by metabolomics analysis in mouse embryonic fibroblasts (MEFs). The role of apoptosis induced by ceramide and how ceramide is regulated were evaluated by omics analysis in vitro, human database and the adipocyte-specific Sirt1 knockout mouse. FINDINGS: The metabolic footprint showed that a complicated diversity of metabolism was enriched as early as 3 h and tended to fluctuate throughout differentiation. Subsequently, the scale of these perturbed metabolic patterns was reduced to reach a balanced state. Of high relevance is the presence of apoptosis induced by ceramide accumulation, which is associated with metabolic dynamics. Interestingly, apoptotic cells were not merely a byproduct of adipogenesis but rather promoted the release of lipid components to facilitate adipogenesis. Mechanistically, ceramide accumulation stemming from hydrolysis and the de novo pathway during early adipogenesis is regulated by Sirt1 upon epigenetic alterations of constitutive Histone H3K4 methylation and H3K9 acetylation. INTERPRETATION: The metabolic footprint during adipocyte commitment highlights that apoptosis induced by ceramide is essential for adipogenesis, which is reversed by suppression of Sirt1. Therefore, Sirt1 may constitute a target to treat obesity or other ceramide-associated metabolic syndromes. FUNDING: This project was supported by grants from the University of Macau (SRG2015-00008-FHS, MYRG2016-00054-FHS and MYRG2017-00096-FHS to RHW; CPG2019-00019-FHS to CXD) and from the National Natural Science Foundation of China (81672603 and 81401978) to QC.

4.
Autophagy ; : 1-16, 2020 Jan 19.
Artigo em Inglês | MEDLINE | ID: mdl-31941401

RESUMO

Macroautophagy (autophagy) is driven by the coordinated actions of core autophagy-related (Atg) proteins. Atg8, the core Atg protein generally considered acting most downstream, has recently been shown to interact with other core Atg proteins via their Atg8-family-interacting motifs (AIMs). However, the extent, functional consequence, and evolutionary conservation of such interactions remain inadequately understood. Here, we show that, in the fission yeast Schizosaccharomyces pombe, Atg38, a subunit of the phosphatidylinositol 3-kinase (PtdIns3K) complex I, interacts with Atg8 via an AIM, which is highly conserved in Atg38 proteins of fission yeast species, but not conserved in Atg38 proteins of other species. This interaction recruits Atg38 to Atg8 on the phagophore assembly site (PAS) and consequently enhances PAS accumulation of the PtdIns3K complex I and Atg proteins acting downstream of the PtdIns3K complex I, including Atg8. The disruption of the Atg38-Atg8 interaction leads to the reduction of autophagosome size and autophagic flux. Remarkably, the loss of this interaction can be compensated by an artificial Atg14-Atg8 interaction. Our findings demonstrate that the Atg38-Atg8 interaction in fission yeast establishes a positive feedback loop between Atg8 and the PtdIns3K complex I to promote efficient autophagosome formation, underscore the prevalence and diversity of AIM-mediated connections within the autophagic machinery, and reveal unforeseen flexibility of such connections.Abbreviations: AIM: Atg8-family-interacting motif; AP-MS: affinity purification coupled with mass spectrometry; Atg: autophagy-related; FLIP: fluorescence loss in photobleaching; PAS: phagophore assembly site; PB: piggyBac; PE: phosphatidylethanolamine; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol 3-phosphate.

5.
Cell Death Differ ; 2020 Jan 20.
Artigo em Inglês | MEDLINE | ID: mdl-31959915

RESUMO

The identification of viability-associated long noncoding RNAs (lncRNAs) is a means of uncovering therapeutic approaches for hepatocellular carcinoma (HCC). In addition, aberrant genome-wide hypomethylation has been implicated in HCC initiation and progression. However, the relationship between lncRNA dysregulation and genome-wide hypomethylation in hepatocarcinogenesis has not been fully elucidated. A novel lncRNA named LINC00662 was previously demonstrated to play a role in gastrointestinal cancer. In this study, we demonstrated that this lncRNA was correlated with survival and exhibited oncogenic properties, both in vitro and in vivo. Moreover, we determined that LINC00662 could lead to genome-wide hypomethylation and alter the genomic methylation profile by synchronously reducing the S-adenosylmethionine (SAM) level and enhancing the S-adenosylhomocysteine (SAH) level. Mechanistically, LINC00662 was determined to regulate the key enzymes influencing SAM and SAH levels, namely, methionine adenosyltransferase 1A (MAT1A) and S-adenosylhomocysteine hydrolase (AHCY), by RNA-RNA and RNA-protein interactions. In addition, we demonstrated that some SAM-dependent HCC-promoting genes could be regulated by LINC00662 by altering the methylation status of their promoters via the LINC00662-coupled axes of MAT1A/SAM and AHCY/SAH. Taken together, the results of this this study indicate that LINC00662 could be a potential biomarker for HCC therapy. More importantly, we proposed a new role of lncRNA in regulating genomic methylation to promote oncogene activation.

6.
J Cell Physiol ; 2020 Jan 13.
Artigo em Inglês | MEDLINE | ID: mdl-31943198

RESUMO

Our previous studies have indicated that long noncoding RNA (lncRNA) SPRY4 intronic transcript 1 (SPRY4-IT1) was highly expressed in hepatocellular carcinoma (HCC). However, it still remained unclear how SPRY4-IT1 worked in tumorgenesis in HCC. In this study, we tested the overexpression of SPRY4-IT1 in HCC tissues and cells through a quantitative real-time polymerase chain reaction. Statistical analyses showed that the upregulation had an association with the tumor node metastasis stage, thrombin time, and alkaline phosphatase. Furthermore, SPRY4-IT1 could be involved in cell proliferation, metastasis, and the epithelial-to-mesenchymal transition (EMT) process in HCC in vitro and in vivo. RNA-sequencing and transcriptome analysis were carried out to explore the mechanism of SPRY4-IT1 in HCC. With SPRY4-IT1 being knocked down or overexpressed, the level of proteins in the tumor necrosis factor (TNF) signaling pathway changed. We detected the RNA binding protein heterogeneous nuclear ribonucleoprotein L (HNRNPL) as a SPRY4-IT1 interacting protein through RNA pull-down assay and liquid chromatography-mass spectrometry, then verified through RNA immunoprecipitation. Downregulation of HNRNPL induced the change of proteins observed on SPRY4-IT1 downregulation revealing the SPRY4-IT1: HNRNPL complex in the TNF signaling pathway and EMT process in HCC. In general, our experimental data and analysis demonstrated the role of SPRY4-IT1 in promoting progress and metastasis of HCC by the TNF signaling pathway.

7.
Br J Pharmacol ; 2020 Jan 23.
Artigo em Inglês | MEDLINE | ID: mdl-31972868

RESUMO

BACKGROUND AND PURPOSE: Roflupram (ROF) improves cognition and limits neuroinflammation in the brain. However, the beneficial effects of ROF in ameliorating Parkinson's disease (PD) remain unknown. Therefore, we aimed to elucidate the pharmacological effects and mechanisms of action of ROF in experimental models of PD. EXPERIMENTAL APPROACH: We utilized SH-SY5Y cells exposed to 1-methyl-4-phenylpyridinium iodide (MPP+ ) as an in vitro PD model. Cell viability and apoptosis were analyzed via the MTT assay and flow cytometry. Mitochondrial morphology, mitochondrial respiratory capacity and ROS were measured by a mitochondrial tracker, a Seahorse analyzer and a MitoSOX-Red dye. For in vivo PD model, behavioral tests, Nissl staining and immunohistochemistry were used to evaluate the protection of ROF. The levels of tyrosine hydroxylase (TH), cAMP response element-binding protein (CREB) and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) were analyzed by Western blotting. KEY RESULTS: ROF decreased MPP+ -induced apoptosis in SH-SY5Y cells and human dopaminergic neurons. ROF also increased mitochondrial respiratory capacity, decreased ROS production and restored mitochondrial morphology. ROF reversed the MPP+ -induced reductions of phosphorylated CREB, PGC-1α, and TH, while the protective effects were blocked by the PKA inhibitor H-89 and via PGC-1α siRNA. In mice treated with MPTP, ROF significantly improved motor functions. Importantly, ROF prevented both dopaminergic neuronal loss and the reduction of phosphorylated CREB and PGC-1α in the substantia nigra and striatum. CONCLUSION AND IMPLICATIONS: ROF protects dopaminergic neurons from apoptosis via the CREB/PGC-1α pathway in PD models. Hence, ROF has potential as a protective drug for the treatment of PD.

8.
Phys Chem Chem Phys ; 22(4): 2399-2404, 2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-31938793

RESUMO

ZnO has broad applications in optoelectronic devices, including ultraviolet light emitters and photodetectors. Herein we report the impact of MoO3 surface functionalization on the photoresponse of epitaxially grown ZnO. Under illumination with 350 nm UV light, the photocurrent of ZnO is found to be enhanced by 2.87 times after the deposition of 0.2 nm MoO3. As corroborated by in situ ultraviolet photoelectron spectroscopy and X-ray photoelectron spectroscopy results, the enhanced photoresponse derives from MoO3 related gap states within the band gap of ZnO and larger upward band bending at the interface, which is attributed to the strong electron transfer from ZnO to MoO3. Moreover, photoluminescence results reveal that the recombination probability of the photo-generated charge carriers in ZnO is reduced after MoO3 surface functionalization.

9.
J Colloid Interface Sci ; 561: 829-837, 2020 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-31767397

RESUMO

The exploration of an efficient nonprecious electrocatalyst for oxygen reduction reaction (ORR) is critical to the commercialization of various electrochemical energy-conversion devices. Herein, a cobalt-gluconate-derived nitrogen and sulfur dual-doped micro/mesoporous carbon sphere (Co9S8/N, S-MCS) with encapsulated high-density cobalt sulfide (Co9S8) nanocrystals is developed by annealing and subsequent high-temperature vulcanization. Particularly, the vulcanization temperature has a critical impact on the formation of high-density Co9S8 nanocrystals. Benefiting from the favorable material characteristics of large surface area, abundant micro/mesopores and high graphitic nanostructures, as well as the synergistic effects between high-density Co9S8 nanocrystals and N, S-dual doped graphitic carbon shells, the resulting catalyst demonstrates superior ORR catalytic activity and durability compared to platinum/carbon (Pt/C) catalyst. More notably, the proposed approach can be extended potentially to fabricate other transition metal sulfide (or oxide, carbide) based electrocatalysts.

10.
Pain ; 161(2): 416-428, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31651582

RESUMO

Chronic pain and anxiety symptoms are frequently encountered clinically, but the neural circuit mechanisms underlying the comorbid anxiety symptoms in pain (CASP) in context of chronic pain remain unclear. Using viral neuronal tracing in mice, we identified a previously unknown pathway whereby glutamatergic neurons from layer 5 of the hindlimb primary somatosensory cortex (S1) (Glu), a well-known brain region involved in pain processing, project to GABAergic neurons in the caudal dorsolateral striatum (GABA). In a persistent inflammatory pain model induced by complete Freund's adjuvant injection, enhanced excitation of the Glu→GABA pathway was found in mice exhibiting CASP. Reversing this pathway using chemogenetic or optogenetic approaches alleviated CASP. In addition, the optical activation of Glu terminals in the cDLS produced anxiety-like behaviors in naive mice. Overall, the current study demonstrates the putative importance of a novel Glu→GABA pathway in controlling at least some aspects of CASP.

11.
Nanoscale ; 12(2): 832-842, 2020 Jan 02.
Artigo em Inglês | MEDLINE | ID: mdl-31830188

RESUMO

Spectrally rich but geometrically simple plasmonic metallic nanoparticles are highly favored in nanophotonics. However, they remain elusive owing to the symmetry-induced mode degeneracy and interband transition-induced plasmonic damping. Hence, most nanoparticles exhibit a single major extinction peak originating from the lowest-order dipole resonance. In this study, we uncover that even a simple tetrahedral nanoparticle supports rich spectral features due to symmetry breaking. This discovery runs counter to the reported gold tetrahedral nanoparticles, where only a single extinction peak was observed. We find that, in the case of a tetrahedral nanoparticle, the plasmonic quadrupole vertex mode becomes a bright mode and hybridizes with the dipole vertex mode, which splits the extinction peak and contributes to spectral diversity and tunability. The peak splitting is also found to be sensitively dependent on the roundness of vertices and edges. Furthermore, the tetrahedral depolarization factors are determined using the previously generalized absorption coefficient. We envision that this work will not only help fill the gap in understanding the optical properties enriched by symmetry breaking but also guide the superior probe design by combining spectral tunability with geometric simplicity of the nanoparticle.

12.
Adv Mater ; 32(3): e1806843, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31074916

RESUMO

Recently, 3D graphene-based macrostructures (3D GBMs) have gained increased attention due to their immense application potential in water treatment. The unique structural features (e.g., large surface area and physically interconnected porous network) as well as fascinating properties (e.g., high electrical conductivity, excellent chemical/thermal stability, ultralightness, and high solar-to-thermal conversion efficiency) render 3D GBMs as promising materials for water purification through adsorption, capacitive deionization, and solar distillation. Moreover, 3D GBMs can serve as scaffolds to immobilize powder nanomaterials to build monolithic adsorbents and photo-/electrocatalysts, which significantly broadens their potential applications in water treatment. Here, recent advances in their synthesis and application toward water purification are highlighted. Remaining challenges and future perspectives are elaborated to highlight future research directions.

13.
Nat Prod Res ; 34(2): 204-209, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30580617

RESUMO

A new oleanane triterpenoid, 2α,3ß,6ß,23,29-pentahydroxyolean-12-en-28- oic acid (1), was isolated from the roots of Rhodomyrtus tomentosa, together with four known oleanane triterpenoids (2-5) and two known ursane triterpenoids (6-7). The structure of compound 1 was determined by extensive NMR and HR-ESI-MS data analysis. Compounds 4-5 showed cytotoxicity against PC12 cell lines at a concentration of 50 µM, and compound 1 exhibited moderate neuroprotective activity against corticosterone induced PC12 cell death at the same concentration.

14.
Redox Biol ; 28: 101342, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31639651

RESUMO

Inhibition of phosphodiesterase 4 (PDE4) produces neuroprotective effects against cerebral ischemia. However, the involved mechanism remains unclear. Augmentation of endoplasmic reticulum (ER) stress promotes neuronal apoptosis, and excessive oxidative stress is an inducer of ER stress. The present study aimed to determine whether suppression of ER stress is involved in the protective effects of PDE4 inhibition against cerebral ischemia. We found that exposing HT-22 cells to oxygen-glucose deprivation (OGD) significantly activated ER stress, as evidenced by increased expression of the 78-kDa glucose-regulated protein (GRP78), phosphorylated eukaryotic translation-initiation factor 2α (eIF2α), and C/EBP-homologous protein (CHOP). Overexpression of PDE4B increased ER stress, while knocking down PDE4B or treatment with the PDE4 inhibitor, FCPR03, prevented OGD-induced ER stress in HT-22 cells. Furthermore, FCPR03 promoted the translocation of nuclear factor erythroid 2-related factor 2 (Nrf-2) from the cytoplasm to the nucleus. Importantly, the Nrf-2 inhibitor, ML385, blocked the inhibitory role of FCPR03 on OGD-induced ER stress. ML385 also abolished the protective role of FCPR03 in HT-22 cells subjected to OGD. Knocking down heme oxygenase-1 (HO-1), which is a target of Nrf-2, also blocked the protective role of FCPR03, enhanced the level of reactive oxygen species (ROS), and increased ER stress and cell death. We then found that FCPR03 or the antioxidant, N-Acetyl-l-cysteine, reduced oxidative stress in cells exposed to OGD. This effect was accompanied by increased cell viability and decreased ER stress. In primary cultured neurons, we found that FCPR03 reduced OGD-induced production of ROS and phosphorylation of eIF2α. The neuroprotective effect of FCPR03 against OGD in neurons was blocked by ML385. These results demonstrate that inhibition of PDE4 activates Nrf-2/HO-1, attenuates the production of ROS, and thereby attenuates ER stress in neurons exposed to OGD. Additionally, we conclude that FCPR03 may represent a promising therapeutic agent for the treatment of ER stress-related disorders.

15.
Cell Death Differ ; 2019 Dec 11.
Artigo em Inglês | MEDLINE | ID: mdl-31827236

RESUMO

Acetaminophen (APAP) is the leading cause of drug-induced acute liver failure. Sphingosine-1-phosphate (S1P), whose formation is catalyzed by sphingosine kinase (SPHK)-1 or -2, is a bioactive lipid implicated in human health and disease. Here, we show that APAP-treated sphK1-deficient (sphK1-/-) mice exhibited markedly less liver damage and reduced inflammation compared with the wild-type mice. SPHK1 deficiency alleviated APAP-induced endoplasmic reticulum (ER) stress by affecting the phosphorylation of inositol-requiring enzyme 1α (IRE1α) and protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK)-eukaryotic translation initiation factor 2α (eIF2α), levels of activating transcription factor 4 (ATF4), and activation of activating transcription factor 6 (ATF6). SPHK1 deficiency also inhibited mitochondrial permeability transition (MPT), as evidenced by the impaired phosphorylation of JNK, apoptosis signal-regulated kinase 1 (ASK1), and glycogen synthase kinase 3ß (GSK3ß). In addition, SPHK1 deficiency reduced the levels of histone deacetylase and promoted the acetylation of p65 and STAT1, thereby impairing the transcription of inflammatory genes. Supplementation with exogenous S1P significantly reversed the activation of the PERK-eIF2α-ATF4 pathway and ATF6 during ER stress as well as the activation of GSK3ß, ASK1, and JNK during MPT. Both FTY720, a functional S1P receptor antagonist, and PF543, an SPHK1 inhibitor, significantly ameliorated APAP-induced liver injury and improved animal survival. Our study reveals a critical role for SPHK1 in mediating APAP-induced hepatotoxicity by promoting ER stress and MPT.

16.
Artigo em Inglês | MEDLINE | ID: mdl-31799795

RESUMO

Defects are ubiquitous in nanomaterials, which often bring new properties that are absent in their pristine counterparts. To date, most studies have focused on the effect of single defect while ignoring the synergy (electronic or other effect) of multifold defects. Herein, a model of photocatalytic molecular oxygen (O2 ) activation is selected to unravel the role of dual defects by decorating bismuth oxide with surface O vacancy and bulk O substitution simultaneously. Results show that introducing dual defects plays a spatial and electronic synergistic process: (i) the O substitution can induce a local electric field in the bulk of BiO2-x , which can promote bulk separation of electrons and holes immediately after their generation; (ii) the O vacancy can efficiently lower the conduction band, serve as the capture center for electrons, thus facilitate the adsorption and activation of O2 . Notably, this effect is greatly promoted by the co-existence of bulk O substitution, and DFT calculations show that only O substitution nearby O vacancy can play this role. This work is expected to inspire more brilliant studies on the versatility of defects engineering in various fields.

17.
Sci Rep ; 9(1): 18660, 2019 Dec 04.
Artigo em Inglês | MEDLINE | ID: mdl-31796858

RESUMO

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

18.
Nan Fang Yi Ke Da Xue Xue Bao ; 39(11): 1293-1297, 2019 Nov 30.
Artigo em Chinês | MEDLINE | ID: mdl-31852647

RESUMO

OBJECTIVE: To investigate the predictive value of body mass index (BMI) combined with waist circumference (WC) for new-onset nonalcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes mellitus (T2DM). METHODS: This community-based prospective cohort study was conducted among 3501 T2DM patients without NAFLD recruited from the staff of Kailuan Company, who underwent routine physical examination in the year 2006 and 2007, and a total of 2920 subjects were included in the final analysis. According to the baseline BMI and WC, the subjects were divided into group A (with normal BMI and WC), group B (with normal BMI but elevated WC), group C (with elevated BMI but a normal WC) and group D (with elevated BMI and WC). The subjects in the 4 groups were followed for the occurrence of NAFLD by reviewing their reports of physical examinations during the periods of 2008-2009, 2010-2011, 2012-2013, 2014-2015 and 2016-2017. The cumulative incidence of NAFLD was compared across the 4 groups and Cox regression analysis was used to test the correlation of BMI and WC with new onset of NAFLD. RESULTS: The cumulative incidence of NAFLD increased progressively in the 4 groups (50%, 66%, 68% and 77%, respectively). Cox regression analysis showed that compared with group A, groups B, C and D had increased risks of NAFLD after adjusting for age, gender and other risk factors, with HR values of 1.62, 1.98 and 2.47, respectively. CONCLUSIONS: Elevated BMI and WC are both independent risk factors for NAFLD in type 2 diabetic patients, and the combination of BMI and WC has a greater predictive value for NAFLD than either of them alone.


Assuntos
Diabetes Mellitus Tipo 2 , Hepatopatia Gordurosa não Alcoólica , Índice de Massa Corporal , Diabetes Mellitus Tipo 2/complicações , Humanos , Hepatopatia Gordurosa não Alcoólica/complicações , Obesidade , Estudos Prospectivos , Fatores de Risco , Circunferência da Cintura
19.
J Sci Food Agric ; 2019 Dec 17.
Artigo em Inglês | MEDLINE | ID: mdl-31846075

RESUMO

BACKGROUND: In this study, low-field nuclear magnetic resonance (LF-NMR) and magnetic resonance imaging (MRI) were used to investigated the moisture migration of beef during refrigeration storage, and its relationships to some physicochemical quality indicators were analyzed using partial least squares regression. RESULTS: Three water components ascribed to bound water, immobilized water and free water in beef matrix were revealed by LF-NMR relaxation results. The transverse relaxation time and peak area of immobilized water declined as storage proceeded, as a result of disruption to the microstructure revealed by scanning electron microscope images. MRI images found obvious water migration of beef during refrigeration storage, and scanning electron microscopy images revealed that the integrity of the muscle fiber bundle was destroyed. In addition, increased storage time also led to increases in pH, total volatile basic nitrogen, TBARS (thiobarbituric acid reactive substances) value, weight loss, cooking loss and b* value, and to decreases in water holding capacity (WHC), L* and a* values, and textural properties. CONCLUSION: The strong correlations between water migration and the physicochemical quality changes suggested the possibility of LF-NMR as a rapid and non-invasive method to evaluate beef quality. © 2019 Society of Chemical Industry.

20.
Cell Rep ; 29(12): 3847-3858.e5, 2019 Dec 17.
Artigo em Inglês | MEDLINE | ID: mdl-31851918

RESUMO

While comorbid pain in depression (CP) occurs at a high rate worldwide, the neural connections underlying the core symptoms of CP have yet to be elucidated. Here, we define a pathway whereby GABAergic neurons from the central nucleus of the amygdala (GABACeA) project to glutamatergic neurons in the parafascicular nucleus (GluPF). These GluPF neurons relay directly to neurons in the second somatosensory cortex (S2), a well-known area involved in pain signal processing. Enhanced inhibition of the GABACeA→GluPF→S2 pathway is found in mice exhibiting CP symptoms. Reversing this pathway using chemogenetic or optogenetic approaches alleviates CP symptoms. Together, the current study demonstrates the putative importance of the GABACeA→GluPF→S2 pathway in controlling at least some aspects of CP.

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