METHODS: The English DC/TMD was translated into the Malay language using the forward-backward translation procedures specified in the INfORM guideline. The initial Malay instrument was pre-tested, and any discrepancies were identified and reconciled before producing the final Malay DC/TMD. Psychometric properties of the M-GCPS and M-JFLS were evaluated using a convenience sample of 252 subjects and were assessed using internal consistency and test-retest reliability, as well as face, content, concurrent, and construct validity testing. Internal consistency was assessed using Cronbach's alpha, while test-retest reliability was examined using intraclass correlation coefficient (ICC). Concurrent and construct validity of both domains were performed using Spearman ρ correlation test. In addition, construct and discriminant validity were appraised using Kruskal-Wallis and Mann-Whitney U tests, respectively.
RESULTS: Cronbach's alpha values for the M-GCPS and M-JFLS were 0.95 and 0.97, respectively. The ICC was 0.98 for the M-GCPS and 0.99 for M-JFLS. The majority of the tested associations for both domains were found to be statistically significant, with good positive correlations.
CONCLUSION: The M-GCPS and M-JFLS were found to be reproducible and valid. The Malay DC/TMD shows potential for use among Malay-speaking adults.
MATERIALS AND METHODS: The lentivirus transfection method was used to establish ARC-overexpressing BMSCs. The CCK-8 method was used to detect cell proliferation. The BD Pharmingen™ APC Annexin V Apoptosis Detection kit was used to detect cell apoptosis. The osteogenic capacity was investigated by OCN immunofluorescence staining, ALP analysis, ARS assays, and RT-PCR analysis. Cells were seeded into calcium phosphate cement (CPC) scaffolds and then inserted subcutaneously into nude mice and the defect area of the rat calvarium. Histological analysis was conducted to evaluate the in vivo cell apoptosis and new bone formation of the ARC-overexpressing BMSCs. RNA-seq was used to detect the possible mechanism of the effect of ARC on BMSCs.
RESULTS: ARC promoted BMSC proliferation and inhibited cell apoptosis. ARC enhanced BMSC osteogenic differentiation in vitro. An in vivo study revealed that ARC can inhibit BMSC apoptosis and increase new bone formation. ARC regulates BMSCs mainly by activating the Fgf-2/PI3K/Akt pathway.
CONCLUSIONS: The present study suggests that ARC is a powerful agent for promoting bone regeneration of BMSCs and provides a promising method for bone tissue engineering.
METHODS: Twenty-four male, 8-week old Sprague Dawley rats with an initial weight of 160 to 200 g were randomised into three groups (n = 6 for each group): groups A (standard rat chow), B (high-fat, high-sucrose diet), and C (high-fat, high-sucrose diet + 100 mg/kg/d of glycyrrhizic acid via oral administration). The rats were treated accordingly for 4 wk. Glycaemic parameters, lipid profile, stress hormones, and adiponectin levels were measured after the treatment. Relative gene expressions of peroxisome proliferator-activated receptor α and γ, lipoprotein lipase as well as gluconeogenic enzymatic activities in different tissues were also determined.
RESULTS: Consumption of high-fat, high-sucrose diet triggered hyperglycaemia, insulin resistance, and dyslipidemia, which were effectively attenuated by supplementation with glycyrrhizic acid. Glycyrrhizic acid supplementation also effectively reduced circulating adrenaline, alleviated gluconeogenic enzymes overactivity, and promoted the upregulation of lipoprotein lipase expression in the cardiomyocytes and skeletal muscles. A high calorie diet also triggered hypoadiponectinaemia and suppression of peroxisome proliferator-activated receptor γ expression, which did not improve with glycyrrhizic acid treatment.
CONCLUSION: Supplementation with glycyrrhizic acid could alleviate high calorie diet-induced glucose and lipid metabolic dysregulations by reducing circulatory stress hormones, normalizing gluconeogenic enzyme activities, and elevating muscular lipid uptake. The beneficial effects of these bioactivities outweighed the adverse effects caused by diet-induced repression of peroxisome proliferator-activated receptor γ expression, resulting in the maintenance of lipid and glucose homeostasis.
METHODS: The FAI-M was created according to international guidelines. Internal consistency/test-retest reliability were assessed with Cronbach's alpha/intra-class correlation (ICC) coefficients. Construct and convergent validity were appraised by relating the FAI-M to the Global Oral Health (GOH) questionnaire and Short-form Oral Health Impact Profile (S-OHIP) using Kruskal-Wallis and Spearman's rho correlation (α = 0.05).
RESULTS: Of the 243 participants enrolled, 54.7% (n = 133) had no TMDs, while TMDs were present in 45.3% (n = 110). The FAI-M presented very good internal consistency (α = 0.90) and test-retest reliability (ICC = 0.99). Theoretically predicted FAI-M score patterns matched the GOH categories, and strong correlations were discerned between FAI-M and S-OHIP (rs = 0.71).
CONCLUSION: The FAI-M exhibited good psychometric properties and can be applied in Malay-speaking populations.
MATERIALS AND METHODS: An advance search from PubMed and Hindawi was performed with keywords; oral leukoplakia/oral squamous cell carcinoma, salivary biomarker and diagnosis/prognosis. An additional search of articles was done through a manual search from the Google Scholar database.
RESULTS: Twenty studies involving salivary biomarkers as diagnostic tools for oral squamous cell carcinoma and/or oral leukoplakia were identified. A narrative review was carried out.
CONCLUSION: Single or multiple salivary biomarkers reported by most studies have shown great potential as diagnostic tools for oral squamous cell carcinoma and oral leukoplakia. However, the validation of sensitivity and specificity should be carried out to ensure the accuracy of the biomarkers. Furthermore, a standardised method for saliva collection should be established to prevent variability in the expression of biomarkers.
METHODS: A cross-sectional study was conducted among 784 participants (mean age: 20.9 years; 66.1% female). Validated instruments included the Short-Form Fonseca Anamnestic Index, Patient Health Questionnaire (PHQ)-4, Big Five Inventory-10, PHQ-15 and Oral Behaviours Checklist. Statistical analyses comprised Mann-Whitney U, Chi-square, Spearman's correlation and Hayes' PROCESS macro (Models 1 and 4) to examine moderation and mediation in terms of indirect associations (α = 0.05).
RESULTS: Symptoms consistent with TMDs were identified in 19.0% of participants. Moderate-to-severe psychological distress and somatization were significantly associated with greater TMD symptom severity, higher oral behaviour frequency and specific personality traits. Moderate correlations were observed among psychological distress, somatization, oral behaviours and TMD symptom severity (rs = 0.40-0.53). No significant moderation pathways were detected. Partial mediation pathways indicated indirect associations for psychological distress via agreeableness (β = 0.05), somatization (β = 0.46) and oral behaviours (β = 0.63), and for somatization via psychological distress (β = 0.12) and oral behaviours (β = 0.42).
CONCLUSION: Psychological distress and TMD symptom severity showed indirect associations involving personality, somatization and oral behaviours. These findings highlight the value of biopsychosocial screening and culturally sensitive approaches for TMDs in young adults.
METHODS: MetS was induced in Sprague Dawley rats on an HFD, followed by a daily oral gavage of geraniin (25 mg/kg) for 4 wk. The outcomes of geraniin-treated rats were compared with those of untreated rats on either a control diet or an HFD and with rats with MetS treated with metformin on a daily basis (200 mg/kg).
RESULTS: The supplementation of geraniin ameliorated multiple metabolic abnormalities caused by HFD, including hypertension, impaired glucose and lipid metabolism, ectopic fat deposition in the visceral fat and liver, and disturbed antioxidant mechanism and inflammatory response. The benefits conferred by geraniin were comparable to metformin. Transcriptomic analysis revealed a profound influence of geraniin on the hepatic expression profiles. The lipid and steroid metabolic processes that were aberrantly activated by HFD were suppressed by geraniin. Based on the differential transcriptomes, geraniin also exerted a significant modulatory effect on the expression of mitochondrial genes, potentially influencing the mitochondrial activity and leading to the observed beneficial effects.
CONCLUSION: Geraniin supplementation mitigated metabolic anomalies of MetS in rats, making it an attractive drug candidate for further investigation.