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1.
World J Clin Cases ; 10(16): 5241-5252, 2022 Jun 06.
Artigo em Inglês | MEDLINE | ID: mdl-35812685

RESUMO

BACKGROUND: In 2016, the Chinese government issued the Healthy China 2030 plan, which also produced the initiative practice for health (IPFH) concept. However, people's knowledge and awareness of the IPFH are unclear. AIM: To investigate awareness of IPFH in the Chinese population and explore the relevant influential factors. METHODS: An internet-based self-designed questionnaire survey was used to collect respondents' demographic characteristics and awareness of health and the IPFH from March 26 to April 18, 2020. IPFH consciousness was assessed by the scores for different related questions. The Student's t test, the Chi-square test, and multiple logistic regression analysis were performed to analyze the differences and influencing factors. RESULTS: A total of 2678 valid questionnaires were collected. Of the respondents, 973 (36.3%) had heard of the IPFH concept. In addition, 89.5% of participants agreed with the view that the IPFH is beneficial to improving quality of life, and over half thought that a regular schedule, a reasonable diet, tobacco and alcohol control, a cheerful mood, specific life goals and plans, taking the initiative to accept health-related education and implement health knowledge, good interpersonal relationships, and regular physical examinations were closely related to the IPFH. The majority of respondents paid attention to their health and usually obtained health-related knowledge via social media and were also willing to promote the IPFH. Most of the participants underestimated the role of hospitals, family doctors, and health managers in promoting the IPFH. Age, monthly income, and medical-related work experience were the influencing factors for IPFH awareness. CONCLUSION: The Chinese population has limited knowledge of the IPFH. People with strong IPFH awareness are older, earn more, and have medical-related work experience.

2.
BMC Oral Health ; 20(1): 59, 2020 02 19.
Artigo em Inglês | MEDLINE | ID: mdl-32075626

RESUMO

BACKGROUND: In this study, we conducted a quantitative analysis of the clinical parameters of crown and gingival morphology (CGM) of the maxillary anterior teeth (MAT). We also analyzed the correlation of these parameters with periodontal biotype (PB), with a view to providing objective standards for PB diagnosis. METHODS: The three-dimensional (3D) maxillary digital models of 56 individuals were obtained using an intra-oral scanner. The following parameters were measured with the SpaceClaim software: gingival angle (GA), papilla width (PW), papilla height (PH), crown length (CL), crown width (CW), crown width/crown length ratio (CW/CL), bucco-lingual width of the crown (BLW), contact surface width (CSW), and contact surface height/crown length ratio (CS/CL). The PB were determined based on the transparency of the periodontal probe through the gingival sulcus. Independent factors influencing PB were analyzed by logistic regression, and the optimal cutoff values for the independent influencing factors were analyzed using receiver operating characteristic curves (ROC curves). RESULTS: There was no significant difference in the parameters of CGM of the MAT at the left and right sides. The thick biotype accounted for 69.6%, and the parameters of GA, PW, PH, CW, CW/CL and CS/CL were significantly correlated with PB (P ≤ 0.2). GA (odds ratio (OR) = 1.206) and PW (OR = 5.048) were identified as independent predictive factors of PB, with areas under the ROC curve (AUC) of 0.807 and 0.881, respectively, and optimal cutoff values of 95.95° and 10.01 mm, respectively. CONCLUSION: The CGMs of the MAT at the left and right side are symmetrical. The thin biotype accounts for a small proportion, and GA and PW are independent influencing factors of PB. GA of 95.95° and PW of 10.01 mm are the optimal cutoff values for categorization of individuals as thick biotype. This indicates that when the GA and PW of the right maxillary central incisor are G ≥ 95.95° and ≥ 10.01 mm, respectively, there is a higher probability that these individuals will be categorized as thick biotype.


Assuntos
Coroas , Gengiva/anatomia & histologia , Incisivo/anatomia & histologia , Humanos , Maxila/anatomia & histologia , Periodontia/instrumentação , Coroa do Dente/anatomia & histologia
3.
J Neurochem ; 151(5): 608-625, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31314916

RESUMO

Glial glutamate transporter 1 (GLT-1) plays a vital role in the induction of brain ischemic tolerance (BIT) by ischemic preconditioning (IPC). However, the mechanism still needs to be further explained. The aim of this study was to investigate whether peroxisome proliferator-activated receptor gamma (PPARγ) participates in regulating GLT-1 during the acquisition of BIT induced by IPC. Initially, cerebral IPC induced BIT and enhanced PPARγ and GLT-1 expression in the CA1 hippocampus in rats. The ratio of nuclear/cytoplasmic PPARγ was also increased. At the same time, the up-regulation of PPARγ expression in astrocytes in the CA1 hippocampus was revealed by double immunofluorescence for PPARγ and glial fibrillary acidic protein. Then, the mechanism by which PPARγ regulates GLT-1 was studied in rat cortical astrocyte-neuron cocultures. We found that IPC [45 min of oxygen glucose deprivation (OGD)] protected neuronal survival after lethal OGD (4 h of OGD), which usually leads to neuronal death. The activation of PPARγ occurred earlier than the up-regulation of GLT-1 in astrocytes after IPC, as determined by western blot and immunofluorescence. Moreover, the preadministration of the PPARγ antagonist T0070907 or PPARγ siRNA significantly attenuated GLT-1 up-regulation and the neuroprotective effects induced by IPC in vitro. Finally, the effect of the PPARγ antagonist on GLT-1 expression and BIT was verified in vivo. We observed that the preadministration of T0070907 by intracerebroventricular injection dose-dependently attenuated the up-regulation of GLT-1 and BIT induced by cerebral IPC in rats. In conclusion, PPARγ participates in regulating GLT-1 during the acquisition of BIT induced by IPC. Cover Image for this issue: doi: 10.1111/jnc.14532. Open Science: This manuscript was awarded with the Open Materials Badge For more information see: https://cos.io/our-services/open-science-badges/.


Assuntos
Encéfalo/irrigação sanguínea , Encéfalo/metabolismo , Transportador 2 de Aminoácido Excitatório/metabolismo , Precondicionamento Isquêmico , PPAR gama/metabolismo , Animais , Isquemia Encefálica/metabolismo , Técnicas In Vitro , Masculino , Neuroglia/metabolismo , Ratos , Ratos Wistar
4.
Mol Neurobiol ; 54(1): 58-71, 2017 01.
Artigo em Inglês | MEDLINE | ID: mdl-26732590

RESUMO

Our previous study has proved that the up-regulation of glial glutamate transporter 1 (GLT-1) played an important role in the acquisition of brain ischemic tolerance after cerebral ischemic preconditioning (CIP) in rats. However, little is known about the mechanism involved in the up-regulation of GLT-1 in the process. The present study investigates whether p38 MAPK, ERK1/2, and/or JNK participates in the up-regulation of GLT-1 during the induction of brain ischemic tolerance by CIP. It was found that CIP significantly enhanced the expression of p-p38 MAPK without altering p-ERK1/2 and p-JNK expression in the CA1 hippocampus. Inhibition of p38 MAPK function by its selective inhibitor SB203580 or knockdown p38 MAPK expression by its antisense oligodeoxynucleotides (AS-ODNs) suppressed the induction of brain ischemic tolerance. Furthermore, p38 MAPK was activated earlier than the up-regulation of GLT-1 in the CA1 hippocampus after CIP. Meanwhile, the expression of p-p38 MAPK by astrocytes was increased, and p38 MAPK AS-ODNs dose-dependently inhibited the up-regulation of GLT-1 after CIP. Taken together, it could be concluded that p38 MAPK participates in the mediation of GLT-1 up-regulation during the induction of brain ischemic tolerance after CIP.


Assuntos
Isquemia Encefálica/metabolismo , Transportador 2 de Aminoácido Excitatório/biossíntese , Hipocampo/metabolismo , Precondicionamento Isquêmico/métodos , Regulação para Cima/fisiologia , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Animais , Isquemia Encefálica/patologia , Hipocampo/patologia , Masculino , Ratos , Ratos Wistar
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