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1.
Artigo em Inglês | MEDLINE | ID: mdl-34636395

RESUMO

BACE1 antisense RNA (BACE1-AS) is implicated in promoting cell proliferation in different types of tumors. However, the function and mechanism of BACE1-AS in hepatocellular carcinoma (HCC) are still unclear. In the present study, we found that the relative expression of BACE1-AS in HCC cell lines, HCC tissues, and serum samples of HCC patients was significantly increased, and its high expression was correlated with the poor prognosis of HCC patients. In addition, overexpression of BACE1 promoted HCC cell proliferation, cell cycle progression, migration, and invasion, but inhibited cell apoptosis, while knockdown of BACE1 exerted the opposite role. Furthermore, BACE1-AS sponged microRNA-214-3p (miR-214-3p) and inhibited its expression, thus promoting Apelin (APLN) expression. Overexpression or knockdown of miR-214-3p could partially reverse the abnormal proliferation, cell cycle progression, migration, invasion, and apoptosis caused by overexpression or knockdown of BACE1. These findings suggest that the BACE1-AS/miR-214-3p/APLN axis is a novel signaling pathway that facilitates HCC.

2.
Oxid Med Cell Longev ; 2021: 3766919, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34664015

RESUMO

Myocardial ischemic/reperfusion (MI/R) is a leading cause of cardiovascular disease with high morbidity and mortality. However, the mechanisms underlying pathological reperfusion remain obscure. In this study, we found that dioscin, a natural product, could be a potential candidate for treating MI/R through modulating cardiac dysfunction. Mechanistically, our work revealed that dioscin could suppress the production of reactive oxygen species (ROS) via repressing the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2) and enhancing the expression of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx). These findings indicate that dioscin may be a potential candidate for therapeutic interventions in MI/R injury.

3.
Br J Ophthalmol ; 2021 Sep 06.
Artigo em Inglês | MEDLINE | ID: mdl-34489339

RESUMO

BACKGROUND/AIMS: Congenital cataracts, which are genetically heterogeneous eye disorders, result in visual loss in childhood around the world. CRYBA1/BA3 serves as an abundant structural protein in the lens, and forms homomers and heteromers to maintain lens transparency. In previous study, we identified a common cataract-causing mutation, ßA3-glycine at codon 91 (G91del) (c.271-273delGAG), which deleted a highly conserved G91del and led to perinuclear zonular cataract. In this study, we aimed to explore the underlying pathogenic mechanism of G91del mutation. METHODS: Protein purification, size-exclusion chromatography, spectroscopy and molecular dynamics simulation assays were used to investigate the effects on the heteromers formation and the protein structural properties of ßA3-crystallin caused by G91del mutation. Intracellular ßA3-G91del overexpression, MTT (3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide) and cell apoptosis were used to investigate the cellular functions of ßA3-G91del. RESULTS: ßA3-crystallin and ßB2-crystallin could form heteromers, which have much more stable structures than ßA3 homomers. Interestingly, ßA3/ßB2 heteromers improved their resistance against the thermal stress and the guanidine hydrochloride treatment. However, the pathogenic mutation ßA3-G91del destroyed the interaction with ßB2, and thereby decreased its structural stability as well as the resistance of thermal or chemical stress. What's more, the ßA3-G91del mutation induced cell apoptosis and escaped from the protection of ßB2-crystallin. CONCLUSIONS: ßA3/ßB2 heteromers play an indispensable role in maintaining lens transparency, while the ßA3-G91del mutation destabilises heteromers formation with ßB2-crystallin, impairs cellular viability and induces cellular apoptosis. These all might contribute to cataract development.

4.
Artigo em Inglês | MEDLINE | ID: mdl-34494284

RESUMO

Previous studies reveal that hydrogen sulphide (H2 S) exerts neuroprotection against neurotoxin-induced Parkinson's disease (PD), but the underlying mechanism remains elusive. The present study was aimed to investigate whether H2 S inhibits neuronal apoptosis of substantia nigra with the involvement of autophagy via promoting leptin signalling in 6-hydroxydopamine (6-OHDA)-induced PD rats. In this study, neuronal apoptosis was analysed by TUNEL staining, the activity of caspase-3 was measured by Caspase-3 fluorometric assay kit, the expressions of Bax, Bcl-2, Beclin-1, LC3II, P62 and leptin were determined by Western blot analysis, and the numbers of autophagosomes and autolysosomes were assessed by transmission electron microscopy. Results showed that NaHS, a donor of exogenous H2 S, mitigates 6-OHDA-induced the increases in the numbers of TUNEL-positive cells, the activity of caspase-3 and the expression of Bax, and attenuates 6-OHDA-induced a decrease in the expression of Bcl-2 in substantia nigra of rats. In addition, 6-OHDA enhanced the expressions of Beclin-1, LC3-II and P62, increased the number of autophagosomes, and decreased the number of autolysosomes in the substantia nigra, which were also blocked by administration of NaHS. Furthermore, NaHS reversed 6-OHDA-induced the down-regulation of leptin expression in the substantia nigra, and treatment with leptin-OBR, a blocking antibody of leptin receptor, attenuated the inhibition of NaHS on neuronal apoptosis and the improvement of NaHS on the blocked autophagic flux in substantia nigra of 6-OHDA-treated rats. Taken together, these results demonstrated that H2 S attenuates neuronal apoptosis of substantia nigra depending on restoring impaired autophagic flux through up-regulating leptin signalling in PD.

5.
Behav Brain Res ; 417: 113562, 2021 Sep 06.
Artigo em Inglês | MEDLINE | ID: mdl-34499939

RESUMO

BACKGROUND: Our previous works demonstrated that ß2-microglobulin (ß2m), a systemic pro-aging factor, induce depressive-like behaviors. Hydrogen sulfide (H2S) is identified as a potential target for treatment of depression. The aim of the present work is to explore whether H2S antagonizes ß2m-induced depressive-like behaviors and the underlying mechanisms. METHODS: The depressive-like behaviors were detected using the novelty suppressed feeding test (NSFT), tail suspension test (TST), forced swimming test (FST) and open field test (OFT). The expressions of Warburg-related proteins, including hexokinase II (HK II), pyruvate kinase M2 (PKM2), Lactate dehydrogenase A (LDHA), pyruvate dehydrogenase (PDH) and pyruvate dehydrogenase kinase 1(PDK1), and synaptic plasticity-related proteins, including postsynaptic density protein 95 (PSD95) and synaptophysin1 (SYN1), were determined by western blotting. RESULT: we found that NaHS (the donor of H2S) attenuated the depressive-like behaviors in the ß2m-exposed rats, as judged by NSFT, TST, FST, and OFT. We also demonstrated that NaHS enhanced the synaptic plasticity, as evidenced by the upregulations of PSD95 and SYN1 expressions in the hippocampus of ß2m-exposed rats. Furthermore, NaHS improved the Warburg effect in the hippocampus of ß2m-exposed rats, as evidenced by the upregulations of HK II, PKM2, LDHA and PDK1 expressions, and the downregulation of PDH expression. CONCLUSION: H2S prevents ß2m-induced depressive-like behaviors, which is involved in improvement of hippocampal synaptic plasticity as a result of enhancement of hippocampal Warburg effect.

7.
Curr Med Sci ; 41(4): 667-672, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34403090

RESUMO

OBJECTIVE: Previous study suggested that estradiol (E2) plays an important role in otolith shedding by regulating the expression of otoconin 90 (OC90). The purpose of this article is to provide further data on the effect and mechanism of E2 on the morphology of otolith. METHODS: The rats receiving bilateral ovariectomy (OVX) were used as animal models. Co-immunoprecipitation was used to observe the relationship between estrogen receptor (ER) and estrogen-related receptor α (ERRα). The morphology of otolith was observed under the scanning electron microscopy. Western blotting and qPCR were used for quantitative analysis of the roles of ER and ERRα in regulating OC90 expression. RESULTS: The looser otoliths were observed in rats receiving bilateral OVX, which could be reversed by supplementation with E2. The level of ERRα was decreased in bilateral OVX rats. ER and ERRα interacted with each other on the regulation of the expression of OC90. CONCLUSION: Our results suggest ER and ERRα are both important downstream receptors involved in regulating OC90 expression in utricles of rats, and ERRα probably functions by interacting with ER. This provides evidence for the mechanism of otolith shedding. And it may be significant for future studies of targeted prevention and therapies for benign paroxysmal positional vertigo.

8.
Artigo em Inglês | MEDLINE | ID: mdl-34406943

RESUMO

Mismatch negativity (MMN) has been consistently found deficit in schizophrenia, which was considered as a promising biomarker for assessing the impairments in pre-attentive auditory processing. However, the functional connectivity between brain regions based on MMN is not clear. This study provides an in-depth investigation in brain functional connectivity during MMN process among patients with first-episode schizophrenia (FESZ), chronic schizophrenia (CSZ) and healthy control (HC). Electroencephalography (EEG) data of 128 channels is recorded during frequency and duration MMN in 40 FESZ, 40 CSZ patients and 40 matched HC subjects. We reconstruct the cortical endogenous electrical activity from EEG recordings using exact low-resolution electromagnetic tomography and build functional brain networks based on source-level EEG data. Then, graph-theoretic features are extracted from the brain networks with the support vector machine (SVM) to classify FESZ, CSZ and HC groups, since the SVM has good generalization ability and robustness as a universally applicable nonlinear classifier. Furthermore, we introduce the graph neural network (GNN) model to directly learn for the network topology of brain network. Compared to HC, the damaged brain areas of CSZ are more extensive than FESZ, and the damaged area involved the auditory cortex. These results demonstrate the heterogeneity of the impacts of schizophrenia for different disease courses and the association between MMN and the auditory cortex. More importantly, the GNN classification results are significantly better than those of SVM, and hence the EEG-based GNN model of brain networks provides an effective method for discriminating among FESZ, CSZ and HC groups.

9.
Int Heart J ; 62(4): 752-755, 2021 Jul 30.
Artigo em Inglês | MEDLINE | ID: mdl-34276017

RESUMO

This study aimed to evaluate the concentration of plasma elabela (ELA) in patients with coronary heart disease (CHD) and its correlation with the disease classification.We enrolled 238 patients diagnosed by coronary angiography as CHD and 86 controls. The CHD group was divided into three subgroups: stable angina (SA), unstable angina (UAP), and acute myocardial infarction (AMI). The plasma levels of ELA were measured in all participants and compared among different groups. The relationship between ELA and CHD classification was analyzed.ELA levels were markedly higher by 10.71% in patients with CHD than in controls (P < 0.05). The concentration of ELA in UAP and AMI subgroups were higher than in controls and SA subgroup. The former difference was significant (P < 0.05), but the latter was not. In addition, the ELA concentration was not correlated with SYNTAX score, left ventricular ejection fraction, and other biochemical variables.The newfound hormone, ELA, significantly increased in patients with UAP and AMI. There is a tendency that ELA levels might be correlated with CHD classification, but not with lesion severity. ELA may play a role in acute coronary syndrome.


Assuntos
Isquemia Miocárdica/sangue , Hormônios Peptídicos/sangue , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Isquemia Miocárdica/classificação
10.
Int J Mol Sci ; 22(14)2021 Jul 19.
Artigo em Inglês | MEDLINE | ID: mdl-34299317

RESUMO

Decidualization is a crucial step for human reproduction, which is a prerequisite for embryo implantation, placentation and pregnancy maintenance. Despite rapid advances over recent years, the molecular mechanism underlying decidualization remains poorly understood. Here, we used the mouse as an animal model and generated a single-cell transcriptomic atlas of a mouse uterus during decidualization. By analyzing the undecidualized inter-implantation site of the uterus as a control, we were able to identify global gene expression changes associated with decidualization in each cell type. Additionally, we identified intercellular crosstalk between decidual cells and niche cells, including immune cells, endothelial cells and trophoblast cells. Our data provide a valuable resource for deciphering the molecular mechanism underlying decidualization.


Assuntos
Decídua/citologia , Decídua/metabolismo , Útero/citologia , Útero/metabolismo , Animais , Comunicação Celular/genética , Comunicação Celular/imunologia , Decídua/imunologia , Implantação do Embrião/genética , Células Endoteliais/citologia , Células Endoteliais/metabolismo , Feminino , Humanos , Camundongos , Modelos Animais , Placentação/genética , Gravidez , Manutenção da Gravidez/genética , RNA-Seq , Análise de Célula Única , Células Estromais/citologia , Células Estromais/metabolismo , Transcriptoma , Trofoblastos/citologia , Trofoblastos/metabolismo , Útero/imunologia
11.
Neural Plast ; 2021: 9912686, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34194489

RESUMO

Microglia-mediated neuroinflammation is one of the most remarkable hallmarks of neurodegenerative diseases (NDDs), including AD, PD, and ALS. Accumulating evidence indicates that microglia play both neuroprotective and detrimental roles in the onset and progression of NDDs. Yet, the specific mechanisms of action surrounding microglia are not clear. Modulation of microglia function and phenotypes appears to be a potential strategy to reverse NDDs. Until recently, research into the epigenetic mechanisms of diseases has been gradually developed, making it possible to elucidate the molecular mechanisms underlying the epigenetic regulation of microglia in NDDs. This review highlights the function and phenotypes of microglia, elucidates the relationship between microglia, epigenetic modifications, and NDDs, as well as the possible mechanisms underlying the epigenetic modulation of microglia in NDDs with a focus on potential intervention strategies.

12.
Korean J Parasitol ; 59(3): 311-317, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-34218604

RESUMO

The present study reports a rare case of Taenia saginata infection, which was initially diagnosed as acute cholecystitis in a Tibetan patient at the Qinghai-Tibetan Plateau pastoral area, China. A 45-year-old female was initially diagnosed with acute cholecystitis at a hospital in China. She had a slight fever, weight loss and constipation and complained of pain in the upper abdomen and left back areas. Increase of monocyte, eosinophil and basophil levels were shown. Taenia sp. eggs were detected in a fecal examination. An adult tapeworm approximately 146 cm in length, whitish-yellow color, was collected from the patient after treatment with traditional Chinese medicine. The adult tapeworm had a scolex and proglottids with genital pores. The scolex was rectangular shape with 4 suckers and rostellum without hooklet. The cox1 gene sequence shared 99.5-99.8% homology with that of T. saginata from other regions in China. The patient was diagnosed finally infected with T. saginata by morphological and molecular charateristics.

13.
Bone ; 153: 116106, 2021 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34252604

RESUMO

Transcriptome-wide association studies (TWAS) systematically investigate the association of genetically predicted gene expression with disease risk, providing an effective approach to identify novel susceptibility genes. Osteoporosis is the most common metabolic bone disease, associated with reduced bone mineral density (BMD) and increased risk of osteoporotic fractures, whereas genetic factors explain approximately 70% of the variance in phenotypes associated with bone. BMD is commonly assessed using dual-energy X-ray absorptiometry (DXA) to obtain measurements (g/cm2) of areal BMD. However, quantitative computed tomography (QCT) measured 3D volumetric BMD (vBMD) (g/cm3) has important advantages compared with DXA since it can evaluate cortical and trabecular microstructural features of bone quality, which can be used to directly predict fracture risk. Here, we performed the first TWAS for volumetric BMD (vBMD) by integrating genome-wide association studies (GWAS) data from two independent cohorts, namely the Framingham Heart Study (FHS, n = 3298) and the Osteoporotic Fractures in Men (MrOS, n = 4641), with tissue-specific gene expression data from the Genotype-Tissue Expression (GTEx) project. We first used stratified linkage disequilibrium (LD) score regression approach to identify 12 vBMD-relevant tissues, for which vBMD heritability is enriched in tissue-specific genes of the given tissue. Focusing on these tissues, we subsequently leveraged GTEx expression reference panels to predict tissue-specific gene expression levels based on the genotype data from FHS and MrOS. The associations between predicted gene expression levels and vBMD variation were then tested by MultiXcan, an innovative TWAS method that integrates information available across multiple tissues. We identified 70 significant genes associated with vBMD, including some previously identified osteoporosis-related genes such as LYRM2 and NME8, as well as some novel loci such as DNAAF2 and SPAG16. Our findings provide novel insights into the pathophysiological mechanisms of osteoporosis and highlight several novel vBMD-associated genes that warrant further investigation.

14.
Phytomedicine ; 90: 153630, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34217968

RESUMO

BACKGROUND: Intracerebral hemorrhage (ICH), the most fatal subtype of stroke, has no disease-modifying treatment. Da-cheng-qi decoction (DCQ), composed of rhubarb, is one of the most commonly used Chinese traditional decoctions in ICH treatment. But the mechanism is not clear. Emodin is an active compound found in rhubarb. PURPOSE: To study the protective effects of DCQ on ICH and its possible mechanisms of action. METHODS: The ICH model was reproduced by injecting collagenase-VII into the left caudate putamen (CPu) of rats. DCQ and emodin were used to treat the ICH rats for 7 days. Behavior tests, proteomic analysis, morphological studies, and western blotting were performed. RESULTS: The neurological deficits in the ICH rats recovered with DCQ and emodin on the 14th day after ICH. The proteomics data revealed that DCQ significantly corrected the pathological signals in the CPu and hippocampus after ICH. The numbers of amoebic microglia in the CPu and M2 microglia in both CPu and hippocampus were significantly increased after DCQ and emodin treatment. The increase in GluN2B-containing NMDA receptor (NR2B) and postsynaptic density protein-95, activation of mitogen-activated protein kinase (MAPK) signals in the CPu, and secondary neurodegeneration (SND) in the hippocampus were significantly recovered in DCQ-treated rats. Inhibition of MAPK p38 (p38) in the hippocampus was observed after DCQ and emodin treatment. CONCLUSION: The protective effects of DCQ on ICH were confirmed in this study, and its mechanism may be related to the inhibition of MAPK and activation of M2 microglia. These results are beneficial to the development of ICH therapeutic targets.


Assuntos
Hemorragia Cerebral , Medicamentos de Ervas Chinesas , Emodina/farmacologia , Hipocampo/efeitos dos fármacos , Animais , Hemorragia Cerebral/tratamento farmacológico , Medicamentos de Ervas Chinesas/farmacologia , Proteômica , Ratos , Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
15.
Menopause ; 28(10): 1143-1149, 2021 07 26.
Artigo em Inglês | MEDLINE | ID: mdl-34313616

RESUMO

OBJECTIVE: To examine the contribution of skeletal mass index (SMI) as a mediator in the relationship between menarcheal age and hip/spine bone mineral density (BMD) in premenopausal women by race/ethnicity. METHODS: The data of 4,329 participants (age ≥ 18; mean age=35.7 ±â€Š9.5) of Whites (n = 2,543), African Americans (n = 1,236), and Asians (n = 550) enrolled from October 2011 to January 2019 from the Louisiana Osteoporosis Study were analyzed. After adjustment for physiological and behavioral factors, multivariable linear regression analyses were conducted to evaluate each component of the proposed mediation models, and mediation was verified by the bootstrapping resampling approach. RESULTS: Premenopausal women with early menarcheal age tended to have higher SMI and BMD than women with normal menarcheal age among all races/ethnicities included. Women with late menarcheal age were, however, more likely to have a lower SMI than their counterparts with normal menarcheal age (r = -0.212, 95% CI = [-0.321 to -0.103] for White women; r = -0.181, 95% CI = [-0.410 to -0.008] for African-American women; r = -0.174, 95% CI = [-0.343 to -0.006] for Asian women). Similar results were found for both spine and hip BMD. SMI fully mediated the difference in BMD due to different menarcheal ages among Whites, African Americans, and Asian women with early menarcheal age; however, no mediating effects were observed for Asian women with late menarcheal age. CONCLUSIONS: SMI, as a full mediator, affected the relationship between menarcheal age and BMD among premenopausal women, and the mediating effects varied by race/ethnicity. To prevent or slow down the loss of hip/spine BMD and the development of osteoporosis, measures aiming at minimizing the risk for muscle mass loss should be recommended, especially for White and African-American women with late menarcheal age.


Assuntos
Densidade Óssea , Osteoporose , Adulto , Grupos Étnicos , Feminino , Humanos , Pessoa de Meia-Idade , Músculo Esquelético , Pré-Menopausa
16.
Zhen Ci Yan Jiu ; 46(5): 391-6, 2021 May 25.
Artigo em Chinês | MEDLINE | ID: mdl-34085462

RESUMO

OBJECTIVE: To observe the effects of electroacupuncture (EA) on the body weight, disease progression and the expression of heat shock protein 70 (HSP70) in lumbar spinal cord of amyotrophic lateral sclerosis (ALS) mice, so as to explore the mechanism of EA on treating ALS. METHODS: Eighteen ALS transgenic SOD1G93A mice were randomly divided into model, EA and medication groups, with 6 mice in each group, and six C57BL/6J mice were used as the normal group. Mice in the EA group received EA at "Quchi"(LI11)-"Hegu"(LI4), "Zusanli"(ST36)- "Sanyinjiao"(SP6), 30 min/time, 5 times/week, for 8 weeks.Mice in the medication group were given riluzole solution (7.6 mg·kg-1·d-1) by gavage for 8 weeks. The body weight of the mice was recorded and the motor function of the hind limbs was evaluated by the neurological function scoring stan-dard of the ALS Therapeutic Development Institute. The expression of HSP70 in lumbar spinal cord was detected by Western blot and immunohistochemistry, respectively. RESULTS: Compared with the normal group, the body weight and the expression of HSP70 in the model group decreased significantly (P<0.05), while no significant difference in the body weight was found among other groups(P>0.05). After intervention and in comparison with the model group, the disease onset time and paralysis time of the EA group and the medication group were significantly delayed (P<0.05, P<0.01), the expression of HSP70 in the EA group and the medicine group was significantly increased (P<0.05, P<0.01).But there was no significant difference in the survival time among all groups(P>0.05). The disease onset time of the EA group was shorter than that in the medication group (P<0.05). CONCLUSION: EA can increase the expression of HSP70 in lumbar spinal cord, thereby delaying the progression of ALS.


Assuntos
Esclerose Amiotrófica Lateral , Eletroacupuntura , Esclerose Amiotrófica Lateral/genética , Esclerose Amiotrófica Lateral/terapia , Animais , Proteínas de Choque Térmico HSP70/genética , Camundongos , Camundongos Endogâmicos C57BL
17.
Aging (Albany NY) ; 13(11): 15078-15099, 2021 05 29.
Artigo em Inglês | MEDLINE | ID: mdl-34051074

RESUMO

Depression is a complex neuropsychiatric disease involved multiple targets and signaling pathways. Systems pharmacology studies could potentially present a comprehensive molecular mechanism to delineate the anti-depressant effect of emodin (EMO). In this study, we investigated the anti-depressant effects of EMO in the chronic unpredictable mild stress (CUMS) rat model of depression and gained insights into the underlying mechanisms using systems pharmacology and molecular simulation analysis. Forty-three potential targets of EMO for treatment of depression were obtained. GO biological process analysis suggested that the biological functions of these targets mainly involve the regulation of reactive oxygen species metabolic process, response to lipopolysaccharide, regulation of inflammatory response, etc. KEGG pathway enrichment analysis showed that the PI3K-Akt signaling pathway, insulin resistance, IL-17 signaling pathway were the most significantly enriched signaling pathways. The molecular docking analysis revealed that EMO might have a strong combination with ESR1, AKT1 and GSK3B. Immunohistochemical staining and Western blotting showed that 2 weeks' EMO treatment (80 mg/kg/day) reduced depression related microglial activation, neuroinflammation and altered PI3K-Akt signaling pathway. Our findings provide a systemic pharmacology basis for the anti-depressant effects of EMO.


Assuntos
Antidepressivos/farmacologia , Emodina/farmacologia , Animais , Antidepressivos/uso terapêutico , Comportamento Animal , Depressão/complicações , Depressão/tratamento farmacológico , Emodina/química , Emodina/uso terapêutico , Ontologia Genética , Genoma , Inflamação/patologia , Masculino , Microglia/patologia , Simulação de Acoplamento Molecular , Neurônios/metabolismo , Neurônios/patologia , Fosfatidilinositol 3-Quinases/metabolismo , Córtex Pré-Frontal/patologia , Mapeamento de Interação de Proteínas , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos Sprague-Dawley , Reprodutibilidade dos Testes , Transdução de Sinais , Estresse Psicológico/complicações , Estresse Psicológico/tratamento farmacológico
18.
Hua Xi Kou Qiang Yi Xue Za Zhi ; 39(3): 274-278, 2021 Jun 01.
Artigo em Inglês, Chinês | MEDLINE | ID: mdl-34041875

RESUMO

OBJECTIVES: The effect of Vps4b gene mutation on the expressions of cytokeratin 14 (CK14) and proliferating cell nuclear antigen (PCNA) in the Hertwig's epithelial root sheath (HERS) is investigated. METHODS: The bilateral mandibular tissues of mouse on postnatal days 5, 9, 11, 15, and 19 were removed. The mandibular first molar tissue sections were obtained after paraffin embedding. The CK14 and PCNA expressions in the epithelial root sheath of the normal mouse and Vps4b knockout mouse were compared through immunohistochemistry. RESULTS: On postnatal day 5, the normal mouse began to form HERS and had a strong positive PCNA expression in the HERS cells; on postnatal day 9, the HERS structure was continuous, and PCNA was positive in the HERS cells; on postnatal day 11, a small portion of HERS began to break, and PCNA was weakly positive in the HERS cells; on postnatal day 15, HERS continued to fracture; PCNA was weakly and positively expressed in the HERS cells on the root surface; on postnatal day 19, the tooth root reached normal physiological length, and PCNA was positively expressed in the HERS cells of the terminal part. Similar to the normal mouse, the gene knockout mouse also formed a HERS structure on postnatal day 5. However, HERS began to break on postnatal day 9. On postnatal day 19, only a few fragments of HERS were found on the root surface, and the root development was immature. Moreover, the expression intensity of PCNA in the gene knockout mouse was decreased. CONCLUSIONS: The Vps4b gene mutation may change the CK14 and PCNA expressions, leading to abnormal root development.


Assuntos
Células Epiteliais , Raiz Dentária , ATPases Associadas a Diversas Atividades Celulares , Animais , Complexos Endossomais de Distribuição Requeridos para Transporte , Queratina-14 , Camundongos , Camundongos Knockout , Antígeno Nuclear de Célula em Proliferação
19.
Water Res ; 199: 117197, 2021 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-33971534

RESUMO

Inhibitory effects of phosphate on zero-valent iron (ZVI) dissolution have been studied mainly focusing on a single chemical system. Little is known about inhibitory effects and the mechanism of phosphate on ZVI dissolution within a bioreactor during long-term operation. This study demonstrates the feasibility of achieving energy recovery from phosphate-containing domestic sewage using an efficient anaerobic reactor with micro-sized or nano-sized ZVI addition. The results indicate that the chemical oxygen demand (COD) removal and methane production are enhanced by ZVI addition. A maximum COD removal efficiency of 89% and methane content of 60% was achieved. However, the strengthening effect of ZVI on methane production is weakened by the presence of phosphate in domestic sewage. Analyzing the variations of Fe2+ ions and phosphate concentrations and characterizing the micro-morphology of corroded ZVI proved that the generated Fe2+ ions reacts with phosphate and forms a passivation layer on the ZVI surface, inhibiting further dissolution of ZVI. As an improved alternative, we chose the double layered core-shell structured ZVI@carbon composite as an excellent candidate to reduce the inhibitory effects of phosphate on ZVI dissolution. In this way, the direct formation of precipitates on the ZVI surface can be avoided due to the protective carbon layer which adjusts the ion transfer. Adding ZVI@carbon composites accelerate the methane content by 16%. To our knowledge, this is the first report on adding ZVI@carbon composites to promote the anaerobic metabolism in studies, which are focusing on reducing the inhibition of ZVI by phosphate.


Assuntos
Ferro , Esgotos , Anaerobiose , Carbono , Metano , Fosfatos , Solubilidade , Eliminação de Resíduos Líquidos
20.
Front Endocrinol (Lausanne) ; 12: 632324, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33868169

RESUMO

Obesity is a prevalent metabolic disease caused by an imbalance in food intake and energy expenditure. Although acupuncture is widely used in the treatment of obesity in a clinical setting, its mechanism has not been adequately elucidated. As the key pivot of appetite signals, the hypothalamus receives afferent and efferent signals from the brainstem and peripheral tissue, leading to the formation of a complex appetite regulation circuit, thereby effectively regulating food intake and energy homeostasis. This review mainly discusses the relationship between the hypothalamic nuclei, related neuropeptides, brainstem, peripheral signals, and obesity, as well as mechanisms of acupuncture on obesity from the perspective of the hypothalamus, exploring the current evidence and therapeutic targets for mechanism of action of acupuncture in obesity.

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