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1.
Artigo em Inglês | MEDLINE | ID: mdl-38791811

RESUMO

BACKGROUND: Achieving high academic success is known to be influenced by many factors including, but not limiting to, physical and mental health. The present study aimed to assess the relationship between physical health, mental health, and university students' success, and to explore the associations between these factors and their academic achievement. METHODS: A cross-sectional, self-administered online survey was used to collect data from college students in three different universities in Lebanon during the Fall 2023 semester. Mental health was evaluated using validated screening tools for depression, anxiety, and stress, specifically the Patient Health Questionnaire (PHQ-9), the General Anxiety Disorder (GAD-7), and Cohen's Perceived Stress Scale (PSS), respectively. Additionally, general questions regarding physical health and lifestyle factors were incorporated into the questionnaire. Academic achievement was measured using students' grade point average (GPA). RESULTS: A total of 261 students completed the self-administered online survey. The results revealed that approximately 42% and 36% of students were experiencing moderate to severe symptoms of depression and anxiety, respectively, and 75.1% of students exhibited symptoms of moderate stress. The majority of participants (99.2%) did not report any physical disability. Chi-square analysis revealed a significant association between mental health status (depression, anxiety, and stress) and GPA level (p = 0.03, p = 0.044, p = 0.015, respectively). Multiple logistic regression models identified eight correlates of GPA and highlighted the relationship between physical health and student success. For instance, students who considered themselves moderately active had lower odds of achieving a higher GPA than those who considered themselves active (OR = 0.41, p = 0.045). CONCLUSIONS: This is the first investigation into Lebanese university students' academic success in relation to lifestyle and mental health profiles. The findings indicate that implementing public health programs and interventions targeting mental health and lifestyle behaviors is essential for enhancing student success.


Assuntos
Ansiedade , Depressão , Nível de Saúde , Saúde Mental , Estudantes , Humanos , Líbano/epidemiologia , Estudos Transversais , Universidades , Estudantes/psicologia , Estudantes/estatística & dados numéricos , Masculino , Feminino , Saúde Mental/estatística & dados numéricos , Adulto Jovem , Adulto , Depressão/epidemiologia , Ansiedade/epidemiologia , Adolescente , Inquéritos e Questionários , Estresse Psicológico/epidemiologia , Sucesso Acadêmico
2.
Biomedicines ; 10(10)2022 Oct 20.
Artigo em Inglês | MEDLINE | ID: mdl-36289914

RESUMO

Non-alcoholic fatty liver disease (NAFLD) is a common liver lesion that is untreatable with medications. Glucagon-like peptide-1 receptor (GLP-1R) agonists have recently emerged as a potential NAFLD pharmacotherapy. However, the molecular mechanisms underlying these drugs' beneficial effects are not fully understood. Using Fourier transform infrared (FTIR) spectroscopy, we sought to investigate the biochemical changes in a steatosis cell model treated or not with the GLP-1R agonist Exendin-4 (Ex-4). HepG2 cells were made steatotic with 400 µM of oleic acid and then treated with 200 nM Ex-4 in order to reduce lipid accumulation. We quantified steatosis using the Oil Red O staining method. We investigated the biochemical alterations induced by steatosis and Ex-4 treatment using Fourier transform infrared (FTIR) spectroscopy and chemometric analyses. Analysis of the Oil Red O staining showed that Ex-4 significantly reduces steatosis. This reduction was confirmed by FTIR analysis, as the phospholipid band (C=O) at 1740 cm-1 in Ex-4 treated cells is significantly decreased compared to steatotic cells. The principal component analysis score plots for both the lipid and protein regions showed that the untreated and Ex-4-treated samples, while still separated, are clustered close to each other, far from the steatotic cells. The biochemical and structural changes induced by OA-induced lipotoxicity are at least partially reversed upon Ex-4 treatment. FTIR and chemometric analyses revealed that Ex-4 significantly reduces OA-induced lipid accumulation, and Ex-4 also restored the lipid and protein biochemical alterations caused by lipotoxicity-induced oxidative stress. In combination with chemometric analyses, FTIR spectroscopy may offer new approaches for investigating the mechanisms underpinning NAFLD.

3.
Dis Markers ; 2020: 8822859, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33133304

RESUMO

Nonalcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide in part due to the concomitant obesity pandemic and insulin resistance (IR). It is increasingly becoming evident that NAFLD is a disease affecting numerous extrahepatic vital organs and regulatory pathways. The molecular mechanisms underlying the nonalcoholic steatosis formation are poorly understood, and little information is available on the pathways that are responsible for the progressive hepatocellular damage that follows lipid accumulation. Recently, much research has focused on the identification of the epigenetic modifications that contribute to NAFLD pathogenesis. Noncoding RNAs (ncRNAs) are one of such epigenetic factors that could be implicated in the NAFLD development and progression. In this review, we summarize the current knowledge of the genetic and epigenetic factors potentially underlying the disease. Particular emphasis will be put on the contribution of microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs) to the pathophysiology of NAFLD as well as their potential use as therapeutic targets or as markers for the prediction and the progression of the disease.


Assuntos
Hepatopatia Gordurosa não Alcoólica/genética , RNA não Traduzido/genética , Biomarcadores , Epigênese Genética , Humanos , Hepatopatia Gordurosa não Alcoólica/diagnóstico , Hepatopatia Gordurosa não Alcoólica/mortalidade , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Prognóstico , RNA não Traduzido/sangue
4.
Artigo em Inglês | MEDLINE | ID: mdl-29589550

RESUMO

BACKGROUND: Previous studies have demonstrated that flagellin, a component of bacterial flagella, engages Toll-Like receptor 5 (TLR-5) causing the activation of the Myeloid Differentiation Factor-88 (MYD-88) pathway that leads to the production of pro-inflammatory cytokines including Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-12 (IL-12). In physiological levels, cytokines can aid in protection against infectious agents. However, excessive production of cytokines can lead to septic shock during sepsis. OBJECTIVE: In this study, we aimed at investigating the effect of denatured flagellin on hindering the effects induced by intact flagellin or flagellated Pseudomonas aeruginosa on the Toll-Like Receptor-5 (TLR-5) in mice. METHODS: Mouse mononuclear cells (MNCs) were cultured with intact flagellin, heat-denatured flagellin, TLR-5 antagonist, Pseudomonas aeruginosa, and TLR-4 antagonist each alone or in combinations. Supernatants were collected at 4 hours post incubation to assess the levels of IL-12 and TNF-α by Enzyme-Linked ImmunoAssay (ELISA). Furthermore, groups of BALB/c mice were injected intraperitoneally (IP) with Pseudomonas aeruginosa, LPS-RS, intact flagellin, and denatured flagellin, each alone or in different combinations. Serum levels of IL-12 and TNF-α were measured at 2, 4, and 6 hours post injections of Pseudomonas aeruginosa or intact flagellin. RESULTS: Pretreatment with denatured flagellin significantly reduced the amount of TNF-α and IL-12 produced both in vitro and in vivo by intact flagellin or Pseudomonas aeruginosa. CONCLUSION: Denatured flagellin suppressed the production of the pro-inflammatory cytokines induced by intact flagellin or Pseudomonas aeruginosa both in vitro and in vivo, probably by blocking TLR5. Denatured flagellin might be considered as an anti-septic shock agent.


Assuntos
Flagelina/metabolismo , Leucócitos Mononucleares/metabolismo , Infecções por Pseudomonas/metabolismo , Pseudomonas aeruginosa/metabolismo , Salmonella typhimurium/metabolismo , Receptor 5 Toll-Like/metabolismo , Animais , Células Cultivadas , Modelos Animais de Doenças , Feminino , Flagelina/administração & dosagem , Flagelina/química , Interações Hospedeiro-Patógeno , Interleucina-12/sangue , Leucócitos Mononucleares/microbiologia , Camundongos Endogâmicos BALB C , Ligação Proteica , Desnaturação Proteica , Infecções por Pseudomonas/sangue , Infecções por Pseudomonas/microbiologia , Pseudomonas aeruginosa/patogenicidade , Transdução de Sinais , Fator de Necrose Tumoral alfa/sangue
5.
Immunopharmacol Immunotoxicol ; 34(6): 951-5, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-22551050

RESUMO

CONTEXT: Alum is thought to induce inflammation resulting in the release of danger signals such as uric acid (UA) which in turn enhances the immune response to an antigen. Hydrogen peroxide (H(2)O(2)) is produced as a byproduct in the purine catabolic pathway that leads to the production of UA. In addition, serum nitric oxide (NO) levels are increased in inflammation. OBJECTIVE: To further explore the mechanism of action of alum, this study was designed to determine the effects of catalase and 1400W on the number of interleukin-4 (IL-4) and interferon-γ (IFN-γ) secreting spleen cells in mice given ovalbumin (OVA) with alum. MATERIALS AND METHODS: Groups of BALB/c mice were injected intraperitoneally with alum + OVA, alum, OVA, catalase, or 1400W. Other groups were treated with catalase or 1400W and given alum + OVA. The number of IL-4 and IFN-γ secreting spleen cells were determined at days 4 and 7 postinjection by enzyme-linked immunosorbent spot (ELISPOT). RESULTS: Catalase and 1400W caused a decrease in the number of IL-4 secreting spleen cells induced by alum + OVA. 1400W caused a decline in the IFN-γ secreting spleen cells induced by alum + OVA. Catalase caused an increase in IFN-γ secreting spleen cells. DISCUSSION AND CONCLUSION: It appears that H(2)O(2) and NO are needed for alum-induced production of a T-helper 2 cytokine. NO also appears to be needed, whereas H(2)O(2) appeared to inhibit an alum-induced production of a T-helper 1 cytokine. These results might explain why alum is mainly a promoter of a T-helper 2 response.


Assuntos
Adjuvantes Imunológicos/farmacologia , Compostos de Alúmen/farmacologia , Amidinas/farmacologia , Benzilaminas/farmacologia , Catalase/farmacologia , Inibidores Enzimáticos/farmacologia , Interferon gama/metabolismo , Interleucina-4/metabolismo , Ovalbumina/farmacologia , Baço/metabolismo , Animais , Bovinos , Contagem de Células , Feminino , Peróxido de Hidrogênio/imunologia , Peróxido de Hidrogênio/metabolismo , Interferon gama/imunologia , Interleucina-4/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Óxido Nítrico/imunologia , Óxido Nítrico/metabolismo , Baço/citologia , Baço/imunologia
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