MATERIALS AND METHODS: Thirty-Two Sprague Dawley (SD) male rats were divided into four groups. The group 1 was administrated with distilled water intragastrically and injected sterile saline subcutaneously. The group 2 was administrated with EA orally and injected with sterile saline subcutaneously. The groups 3 & 4 were subcutaneously exposed to Ni for 4 weeks twice daily before tooth extraction procedure, and maintained Ni injection until the animals were sacrificed. After one month Ni exposure, the group 4 was fed with EA while continuing Ni injection. All the groups were anesthetized, and the upper left incisor was extracted. Four rats from each group were sacrificed on 14(th) and 28(th) days. Tumour necrosis factor alpha (TNFα), Interleukin-1 beta (IL-1β) and Interleukin-6 (IL-6) were applied to assess in serum rat at 14th and 28(th) days. Superoxide dismutase (SOD) and Thiobarbituric acid reactive substances (TBRAS) levels were assessed to evaluate the antioxidant status and lipid peroxidation accordingly after tooth extraction in homogenized gingival maxilla tissue of rat at 14(th) and 28(th) days. The socket hard tissue was stained by eosin and hematoxylin (H&E); immunohistochemical technique was used to assess the healing process by Osteocalcin (OCN) and Alkaline Phosphatase (ALP) biomarkers.
RESULTS: Ni-induced rats administered with EA compound (Group 4) dropped the elevated concentration of pro-inflammatory cytokines significantly when compared to Ni-induced rats (Group 3) (p<0.05). Ni-induced rats administrated with EA compound (Group 4) showed significant production of SOD and recession in TBRAS level when compared to Ni-induced rats (Group 3) (p<0.05). The immunohistochemistry analysis has revealed that OCN and ALP have presented stronger expression in Ni-induced rats treated with EA (Group 4), as against Ni-induced rats (Group 3).
CONCLUSION: We have concluded that, Ni-induced rats, treated with EA have exerted positive effect on the trabecular bone formation after tooth extraction in nicotinic rats could be due to the antioxidant activity of EA which lead to upregulate of OCN and ALP proteins which are responsible for osteogenesis.
MATERIALS AND METHODS: Sixteen New Zealand white rabbits were randomly divided into four groups. Modified Hyrax expanders were placed across the midsagittal sutures and secured with miniscrew implants with the following activations: group 1 (control), 0.5 mm expansion/day for 12 days; group 2, 1 mm instant expansion followed by 0.5 mm expansion/day for 10 days; group 3, 2.5 mm instant expansion followed by 0.5 mm expansion/day for 7 days; and group 4, 4 mm instant expansion followed by 0.5 mm expansion/day for 4 days. After 6 weeks, sutural expansion and new bone formation were evaluated histomorphometrically. Statistical analysis was performed using Kruskal-Wallis/Mann-Whitney U tests and Spearman's rho correlation (p
METHODS: This was a retrospective cohort study involving two hepatobiliary centres from January 1, 2012, to June 30, 2018. Medical records were analysed for sociodemographic, clinical characteristics, laboratory testing, and HCC treatment information. Survival outcomes were examined using the Kaplan-Meier and log-rank test. Prognostic factors were determined using multivariate Cox regression.
RESULTS: A total of 212 patients were included in the study. The median survival time was 22 months. The 1-, 3-, and 5-year survival rates were 64.2%, 34.2%, and 18.0%, respectively. Palliative treatment (adjusted hazard ratio [AHR] = 2.82, 95% confidence interval [CI] 1.75-4.52), tumour size ≥ 5 cm (AHR = 2.02, 95%CI: 1.45-2.82), traditional medication (AHR = 1.94, 95%CI: 1.27-2.98), raised alkaline phosphatase (AHR = 1.74, 95%CI: 1.25-2.42), and metformin (AHR = 1.44, 95%CI: 1.03-2.00) were significantly associated with poor prognosis for HCC survival. Antiviral hepatitis treatment (AHR = 0.54, 95% CI: 0.34-0.87), nonalcoholic fatty liver disease (NAFLD) (AHR = 0.50, 95% CI: 0.30-0.84), and family history of malignancies (AHR = 0.50, 95%CI: 0.26-0.96) were identified as good prognostic factors for HCC survival.
DISCUSSION: Traditional medication, metformin treatment, advanced stage and raised alkaline phosphatase were the poor prognostic factors, while antiviral hepatitis treatment, NAFLD, and family history of malignancies were the good prognostic factors for our HCC cases comorbid with T2D.