METHODS: Murine pre-osteoblastic cells, MC3T3-E1, were cultured with the density of 1 × 104 cells/mL and treated with 4 concentrations of AnTT (0.001-1 µg/mL). Expression of HMG-CoA reductase (HMGR) gene was carried out using qPCR after treatment with AnTT for 21 days. RhoA activation and bone morphogenetic protein-2 (BMP-2) were measured using immunoassay after 9 and 15 days of AnTT treatment. Lovastatin was used as the positive control. Mineralized nodules were detected using Von Kossa staining after 21 days of AnTT treatment.
RESULTS: The results showed that HMGR was up-regulated in the lovastatin group on day 9 and 21 compared to the control. Lovastatin also inhibited RhoA activation (day 9 and 15) and increased BMP-2 protein (day 15). On the other hand, AnTT at 0.001 μg/mL (day 3) and 0.1 μg/mL (day 21) significantly down-regulated HMGR gene expression compared to the control. On day 21, HMGR gene expression was significantly reduced in all groups compared to day 15. AnTT at 0.1 μg/mL significantly decreased RhoA activation on day 9 compared to the control. AnTT at 1 μg/mL significantly increased BMP-2 protein on day 15 compared to the control (P<0.05). Mineralized calcium nodules were more abundant in AnTT treated groups compared to the control on day 21.
CONCLUSION: AnTT suppresses the mevalonate pathway by downregulating HMGR gene expression and inhibiting RhoA activation, leading to increased BMP-2 protein in MC3T3-E1 cells. This explains the stimulating effects of AnTT on osteoblast mineralization.
MATERIALS AND METHODS: We conducted extensive searches across five databases (PubMed, Scopus, Web of Science, Science Direct, and Google Scholar) following the Preferred Reporting Items for Systematic Reviews and Meta-analyses Protocols guidelines. Random-effect meta-analyses were performed using R software version 4.3.0 to estimate pooled prevalence rates. Subgroup meta-analyses were conducted based on continents, diagnostic methods, sample types, and wildcat genera.
RESULTS: A total of 71 articles on leptospirosis in domestic cats and 23 articles on leptospirosis in wild cats met the eligibility criteria. Our findings indicated a significantly higher pooled seroprevalence of leptospirosis in domestic cats compared with infection prevalence (9.95% [95% confidence interval (CI), 7.60%-12.54%] vs. 4.62% [95% CI, 2.10%-7.83%], p = 0.01). In contrast, no significant difference was observed in pooled seroprevalence and infection prevalence among wild cats (13.38% [95% CI, 6.25%-21.93%] vs. 2.9% [95% CI, 0.00%-18.91%], p = 0.21). A subgroup meta-analysis of domestic cats revealed significant differences in seroprevalence across continents, sample types, and diagnostic methods. On the contrary, wild cats had no significant differences in any of the subgroups.
CONCLUSION: Leptospira spp. have evidently been exposed to both domestic and wild cats, highlighting their potential roles as reservoir hosts for leptospirosis. These findings highlight the importance of considering felids as a possible public health threat.
METHODS: This systematic review was accorded to the guideline of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses. Three electronic databases, namely PubMed, Embase, and the Cochrane library, were used to conduct a systematic search for eligible studies from their inception until July 18, 2023. PROSPERO registration number was No. CRD42023445968.
RESULTS: We initially identified 4,774 articles. After eliminating duplicates and irrelevant articles, 11 studies met the inclusion criteria. The studies revealed important aspects of the relationship between S. mutans and Veillonella spp. in dental caries. One significant finding is that Veillonella spp. can affect the acid production capacity of S. mutans. Some studies indicate that Veillonella spp. can inhibit the acid production by S. mutans, potentially reducing the cariogenic process. Another aspect is the competition for substrates. Veillonella spp. utilize lactic acid, which is a by product of S. mutans metabolism, as a source of carbon. This metabolic interaction may decrease the availability of lactic acid for S. mutans, potentially influencing its cariogenic potential.
CONCLUSIONS: This systematic review highlights the emerging evidence on the interaction between S. mutans and Veillonella spp. in dental caries. The findings suggest that Veillonella spp. can modulate the acid production, and substrate competition of S. mutans, potentially influencing the cariogenic process.
METHODS: Genes and proteins of phase II detoxifying antioxidant enzymes were analyzed by QuantiGenePlex 2.0 Assay and Western blot analysis.
RESULTS: PB significantly induced genes and proteins of phase II and antioxidant enzymes, NAD(P)H quinone oxidoreductase 1, and catalase in aging mice (p < 0.05). The expression of these enzymes were stimulated via translocation of Nrf2 into the nucleus, indicating the involvement of ARE, a cis-acting motif located in the promoter region of nearly all phase II genes.
CONCLUSIONS: PB was testified for the first time to induce cytoprotective genes through the Nrf2/ARE signaling pathway, thus unraveling the antioxidant mechanism of PB during the aging process.
METHODS: A randomized controlled trial was carried out in a university hospital in Malaysia. Women with lifestyle-controlled gestational diabetes scheduled to receive clinically indicated antenatal corticosteroids (dexamethasone) were randomized to 12-mg 12 hourly for one day (2 × 12-mg) or 6-mg 12-hourly for two days (4 × 6-mg). 6-point (pre and 2-h postprandial) daily self-monitoring of capillary blood sugar profile for up to 3 consecutive days was started after the first dexamethasone injection. Hyperglycemia is defined as blood glucose pre-meal ≥ 5.3 or 2 h postprandial ≥ 6.7 mmol/L. The primary outcome was a number of hyperglycemic episodes in Day-1 (first 6 BSP points). A sample size of 30 per group (N = 60) was planned.
RESULTS: Median [interquartile range] hyperglycemic episodes 4 [2.5-5] vs. 4 [3-5] p = 0.3 in the first day, 3 [2-4] vs. 1 [0-3] p = 0.01 on the second day, 0 [0-1] vs. 0 [0-1] p = 0.6 on the third day and over the entire 3 trial days 7 [6-9] vs. 6 [4-8] p = 0.17 for 6-mg vs. 12-mg arms, respectively. 2/30 (7%) in each arm received an anti-glycemic agent during the 3-day trial period (capillary glucose exceeded 11 mmol/L). Mean birth weight (2.89 vs. 2.49 kg p