Radiographic comparison of atelocollagen versus deproteinized bovine bone minerals covered with a collagen membrane in alveolar ridge preservation: a retrospective study.

BACKGROUND: Atelocollagen (AC) is a low-immunogenic collagen derivative with longer degradation time, which can be a suitable material for alveolar ridge preservation (ARP). However, there are few human studies on AC using for ARP. This research aims to radiographically evaluate the efficacy of AC in comparison to deproteinized bovine bone minerals covered with a collagen membrane (DBBM/CM) in ARP. METHODS: Medical records in the Implantology Department of the Hospital of Stomatology of Wuhan University were screened for patients who received flapless ARP using either AC or DBBM/CM. A total of 58 patients were included in this retrospective study. 28 patients were treated with AC, while 30 patients were used DBBM/CM. Cone-beam computed tomography (CBCT) scans were taken before extraction and after 6 months of healing. To assess the dimensional change of the extraction sockets, the scanning data were output and transferred to the digital software to measure horizontal bone width change, vertical bone height change and bone volume change in region of interest. To evaluate the bone quality of healed sockets, the bone density of virtual implants was evaluated. RESULTS: The horizontal bone width changes at all five different levels showed no significant difference between the two groups. The largest horizontal bone width decrement in both groups occurred at the crest of ridge, which decreased 3.71 ± 1.67 mm in AC group and 3.53 ± 1.51 mm in DBBM/CM group (p = 0.68). At the central buccal aspect, the ridge height reduced 0.10 ± 1.30 mm in AC group, while increased 0.77 ± 2.43 mm in DBBM/CM group (p = 0.10). The vertical bone height differences between two groups showed no statistical significance. The percentages of volume absorption in AC group and DBBM/CM group were 12.37%±6.09% and 14.54%±11.21%, respectively. No significant difference in volume absorption was found (p = 0.36). The average bone density around virtual implants in AC group (649.41 ± 184.71 HU) was significantly lower than that in DBBM/CM group (985.23 ± 207.85 HU) (p < 0.001). CONCLUSIONS: ARP with AC had a similar effect on limiting the dimensional alteration of alveolar ridge, when radiographically compared with DBBM/CM.

Uric acid as a prognostic factor and critical marker of COVID-19.

The purpose of this study is to explore whether uric acid (UA) can independently act as a prognostic factor and critical marker of the 2019 novel corona virus disease (COVID-19). A multicenter, retrospective, and observational study including 540 patients with confirmed COVID-19 was carried out at four designated hospitals in Wuhan. Demographic, clinical, laboratory data were collected and analyzed. The primary end point was in-hospital death of patients with COVID-19. The concentration of admission UA (adUA) and the lowest concentration of uric acid during hospitalization (lowUA) in the dead patients were significantly lower than those in the survivors. Multivariate logistic regression analysis showed the concentration of lowUA (OR 0.986, 95% CI 0.980-0.992, p < 0.001) was able to independently predict the risk of in-hospital death. The mean survival time in the low-level group of lowUA was significantly lower than other groups. When lowUA was ≤ 166 µmol/L, the sensitivity and specificity in predicting hospital short-term mortality were 76.9%, (95% CI 68.5-85.1%) and 74.9% (95% CI 70.3-78.9%). This retrospective study determined that the lowest concentration of UA during hospitalization can be used as a prognostic indicator and a marker of disease severity in severe patients with COVID-19.

Nutritional risk and therapy for severe and critical COVID-19 patients: A multicenter retrospective observational study.

OBJECTIVE: To evaluate the nutritional risk and therapy in severe and critical patients with COVID-19. METHODS: A total of 523 patients enrolled from four hospitals in Wuhan, China. The inclusion time was from January 2, 2020 to February 15. Clinical characteristics and laboratory values were obtained from electronic medical records, nursing records, and related examinations. RESULTS: Of these patients, 211 (40.3%) were admitted to the ICU and 115 deaths (22.0%). Patients admitted to the ICU had lower BMI and plasma protein levels. The median Nutrition risk in critically ill (NUTRIC) score of 211 patients in the ICU was 5 (4, 6) and Nutritional Risk Screening (NRS) score was 5 (3, 6). The ratio of parenteral nutrition (PN) therapy in non-survivors was greater than that in survivors, and the time to start nutrition therapy was later than that in survivors. The NUTRIC score can independently predict the risk of death in the hospital (OR = 1.197, 95%CI: 1.091-1.445, p = 0.006) and high NRS score patients have a higher risk of poor outcome in the ICU (OR = 1.880, 95%CI: 1.151-3.070, p = 0.012). After adjusted age and sex, for each standard deviation increase in BMI, the risk of in-hospital death was reduced by 13% (HR = 0.871, 95%CI: 0.795-0.955, p = 0.003), and the risk of ICU transfer was reduced by 7% (HR = 0.932, 95%CI:0.885-0.981, p = 0.007). The in-hospital survival time of patients with albumin level ≤35 g/L was significantly decreased (15.9 d, 95% CI: 13.7-16.3, vs 24.2 d, 95% CI: 22.3-29.7, p < 0.001). CONCLUSION: Severe and critical patients with COVID-19 have a high risk of malnutrition. Low BMI and protein levels were significantly associated with adverse events. Early nutritional risk screening and therapy for patients with COVID-19 are necessary.

[Visfatin upregulates MMP-2 and MMP-9 expressions in human monocytes through activating NF-kappaB].

OBJECTIVE: To investigate the effects of visfatin on the MMP-2 and MMP-9 expressions in human monocytes and related mechanisms. METHODS: Human monocytes were isolated from blood, the expressions of MMP-2 and MMP-9 at mRNA and protein levels were detected in visfatin stimulated monocytes (0, 100, 200, 400 ng/ml) in the absence and presence of NF-kappaB inhibitor specific Bay11-7082 by Realtime PCR or Western blot, the MMP-2 and MMP-9 enzyme activity in the culture media was also detected by Gelatin Zymography. The NF-kappaB protein level and NF-kappaBp65 expression in visfatin stimulated cells were measured by Western blot and ELISA, respectively. RESULTS: Visfatin upregulated MMP-2 and MMP-9 expressions in human monocytes in a dose dependent manner. After treatment with visfatin 400 ng/ml for 24 h, comparing with the free visfatin treatment, the protein expressions of MMP-2 and MMP-9 were up-regulated to 1.644 +/- 0.052 and 3.578 +/- 0.081 (all P < 0.001); the enzyme activities of MMP-2 and MMP-9 were enhanced by 1.661 +/- 0.036 (P < 0.001) and 1.662 +/- 0.100 (P < 0.001). NF-kappaB was also activated in these cells by visfatin and these effects could be significantly attenuated by Bay11-7082. Visfatin induced a dose-dependent (100 - 400 ng) increase of NF-kappaBp65 nuclear translocation from 0.763 +/- 0.056 to 1.290 +/- 0.065 at 100 and 400 ng/ml, comparing with free visfatin treatment 0.467 +/- 0.046 (all P < 0.05). Bay11-7082 decreased the protein expression of MMP-2 and MMP-9 to 1.183 +/- 0.030 and 2.024 +/- 0.056 (all P < 0.001 comparing with 400 ng/ml visfatin treatment). CONCLUSION: Visfatin enhanced the expression and activity of MMP-2 and MMP-9 in human monocytes via activating NF-kappaB signaling pathway.

Leptin-induced vascular smooth muscle cell proliferation via regulating cell cycle, activating ERK1/2 and NF-kappaB.

Leptin is a peptide hormone primarily involved in the regulation of food intake and energy expenditure. Recent studies have suggested that leptin is one of the risk factors for cardiovascular diseases including atherosclerosis and hypertension. Vascular smooth muscle cells (VSMCs) play a vital role in arterial intimal thickening and vascular remodeling. In this study, we investigated the effect of leptin on VSMC cell-cycle regulation and the possible pathway. We found that leptin stimulated VSMC proliferation and increased cell progression to S and G2/M phases. The expression of cyclinD1, phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), and nuclear factor (NF)-kappaBp65 was increased. Treatment of the cells with leptin antagonist triple mutant attenuated the leptininduced ERK1/2 and NF-kappaB activation. These results suggested that leptin stimulated VSMC proliferation by promoting transition from G1 to S phase and ERK1/2 and NF-kappaB pathway might contribute to this procession.