Application of Crus of Helix Incision Through the Posterior Parotid Gland Approach in the Mid-Level or High-Level Mandibular Condylar Fractures.

OBJECTIVE: This study is to explore the clinical effect of crus of helix incision through the posterior parotid gland approach in the treatment of Mid-or High-Level mandibular condylar fractures. METHODS: From September 2020 to June 2023, we performed incision reduction internal fixation of 23 patients with mid-level or high-level fractures of the mandibular condylar through the approach of the posterior parotid gland, and observed the effect of the operation. RESULTS: After a follow-up period of 6 to 12 months, all patients showed no signs of postoperative facial paralysis or salivary gland fistula. In addition, satisfactory scars were observed in the operation area, and the occlusion function had recovered well. CONCLUSION: The approach of using a crus of helix incision through the posterior parotid gland proved to be an effective method for treating mid-level or high-level fractures of the condylar fractures. This technique offers several advantages, including adequate exposure, minimal facial nerve injury, ease of incision and reduction, inconspicuous scarring, and a more concealed incision.

Effect of GVHD on the gut and intestinal microflora.

Graft-versus-host disease (GVHD) is one of the most important cause of death in patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT). The gastrointestinal tract is one of the most common sites affected by GVHD. However, there is no gold standard clinical practice for diagnosing gastrointestinal GVHD (GI-GVHD), and it is mainly diagnosed by the patient's clinical symptoms and related histological changes. Additionally, GI-GVHD causes intestinal immune system disorders, damages intestinal epithelial tissue such as intestinal epithelial cells((IEC), goblet, Paneth, and intestinal stem cells, and disrupts the intestinal epithelium's physical and chemical mucosal barriers. The use of antibiotics and diet alterations significantly reduces intestinal microbial diversity, further reducing bacterial metabolites such as short-chain fatty acids and indole, aggravating infection, and GI-GVHD. gut microbe diversity can be restored by fecal microbiota transplantation (FMT) to treat refractory GI-GVHD. This review article focuses on the clinical diagnosis of GI-GVHD and the effect of GVHD on intestinal flora and its metabolites.

LGALS3BP/Gal-3 promotes osteogenic differentiation of human periodontal ligament stem cells.

OBJECTIVE: To identify the role of LGALS3BP/Gal-3 in the process of human periodontal ligament stem cells (hPDLSCs) differentiating into osteoblasts. METHODS: IP-WB experiments were carried out to examine the binding of LGALS3BP and Gal-3. Western blot was performed to detect the expressions of LGALS3BP and Gal-3 in hPDLSCs with or without osteogenic differentiation inducement. The expressions of differentiation-related Oct4, Sox2 and Runx2 were also detected by western blot. Alkaline Phosphatase (ALP) Assay Kit was used to measure ALP activity in hPDLSCs. The mineralization ability of hPDLSCs was observed by staining with Alizarin Red S solution. RESULTS: LGALS3BP bound with Gal-3 in hPDLSCs, and the expression of LGALS3BP and Gal-3 was improved after osteogenic differentiation of hPDLSCs. Recombinant GAL-3 promoted the expression of differentiation-related proteins Oct4 and Sox2 and Runx2 in osteogenic differentiation-induced hPDLSCs. Recombinant GAL-3 also promoted the differentiation of osteogenesis-induced hPDLSCs. Furthermore, LGALS3BP had a facilitating effect on differentiation-related protein expression, while it could be reversed by shGal-3. LGALS3BP also promoted osteogenic capacity of hPDLSCs, and shGal-3 could reverse this effect. CONCLUSION: LGALS3BP binds to Gal-3, producing a promoting effect on the osteogenic differentiation of human periodontal ligament stem cells.

Ionized calcium: whole blood, plasma or serum?

OBJECTIVES: To determine an optimal specimen type to be used for measurements of ionized calcium (iCa) so that it applies properly to the reference interval. Also to determine the validity of the pH correction that is applied to iCa measurements. METHODS: A reference interval study of normal volunteers was performed using four sample types namely balanced heparin (BH) whole blood, lithium heparin (LH) whole blood, plasma and serum. The sample was treated in an anaerobic fashion and analyzed at 0 and 40 minutes after venipuncture. The effect of pH correction as well as analysis time after collection was also studied. RESULTS: The mean iCa was the highest in BH-treated whole blood when measured immediately. However, it was slightly lower at 40 min after collection (p < 0.001). In contrast, there did not appear to be a significant difference in results when LH-treated whole blood was analyzed at 0 or 40 min. The reference interval for serum was similar to that of whole blood. The reference interval for plasma was dramatically lower than whole blood and plasma. The reference intervals for pH adjusted ionized calcium (iCa-adj) were dramatically lower than those from all specimens without adjustment. The reason for this was that the reference interval for pH in this study had a strong alkaline bias on one instrument and a strong acidic bias on the other. CONCLUSIONS: The sample of choice for ionized calcium analysis appears to be whole blood with either BH or LH. For the LH specimen, there is no significant change over 40 min whereas there is significant change for the BH specimens (-0.030 mmol/L, p < 0.0001). iCa-adj should not be used unless (i) very strict attention is paid to standardization of both the calcium and the pH and (ii) there is a very good reason to believe that the patients' pH is normal at 7.4.

Adriamycin-induced oxidative stress, activation of MAP kinases and apoptosis in isolated cardiomyocytes.

BACKGROUND: Adriamycin (ADR) induced heart failure is associated with an increase in oxidative stress and apoptosis. Changes due to ADR in mitogen-activated protein kinases (ERK1/2 and p38 MAPKs), pro- and anti-apoptotic proteins (Bax and Bcl-xl) and apoptosis were examined in isolated adult rat cardiomyocytes. METHODS: Isolated adult rat cardiomyocytes were exposed to different concentrations of ADR (0.1, 1 and 10mumol/L) and analyzed at different post-treatment durations. Antioxidant, trolox (20mumol/L) was used to determine involvement of oxidative stress on these changes. RESULTS: Total ERK1/2 and p38 did not show any significant change. However, phosphorylated ERK1/2 showed a rapid increase (497%) after 5min of ADR treatment, peaking (610%) at 10min followed by a decline to submaximal levels at 30min (280%) and 60min (247%). Phosphorylated p38 showed no changes until after 30min, peaking (284%) at 1h, followed by a small decline at 2h. These changes were found to be dose-dependent (0.1, 1 and 10mumol/L of ADR). Adriamycin induced apoptosis was confirmed by Hoechst staining. The ratio of Bax/Bcl-xl increased in a dose-dependent manner. At 10mumol/L, this ratio increased to a maximum at 1h, remained steady at the level for up to 12h, followed by a decline below the base line at 24h. Antioxidant, trolox modulated the ADR-induced increase in phosphorylation of ERK1/2 and p38 MAPKs as well as in the ratio of Bax/Bcl-xl. CONCLUSION: It is suggested that ADR activates MAP kinases, followed by an activation of pro-apoptotic protein Bax which results in cardiomyocyte apoptosis and these effects appear to be mediated by ADR-induced oxidative stress.

Oxidative stress and apoptosis in heart dysfunction.

BACKGROUND: Heart disease is a major cause of morbidity and mortality due to its complex pathogenesis. Myocyte cell loss through apoptosis has been reported in a variety of cardiovascular disease conditions including myocardial infarction (MI), ischemia-reperfusion injury, end-stage heart failure and adriamycin cardiomyopathy. POTENTIAL APOPTOTIC FACTORS AND THERAPEUTIC TARGET: The cell biology of the apoptotic regulatory processes and the precise role of apoptosis in the development of cardiac dysfunction need to be established. The upregulation of proapoptic proteins, like Bax (a member of the Bcl-2 family proteins), caspases and cytochrome c, with or without the downregulation of antiapoptic proteins, including Bcl-2 (another member of the Bcl family), Akt and inhibitory apoptotic proteins (IAPs), has been documented in different cardiac disease conditions. However, mitogen-activated protein kinases (MAPKs) have been shown to be involved in both apoptosis and cell survival. Apoptosis can be blocked by inhibiting apoptotic regulatory pathways with caspase inhibitors and overexpression of Bcl-2 and Akt. More recently, increased oxidative stress has been shown to promote apoptosis, and antioxidants have been shown to inhibit this process. CONCLUSION: The ability of antioxidants to inhibit these apoptotic pathways has raised the possibility of newer therapeutic treatment for various heart diseases.

Maintenance of myocardial levels of vitamin A in heart failure due to adriamycin.

The therapeutic use of adriamycin (doxorubicin), a potent antitumor antibiotic, is limited by the development of dose-dependent cardiomyopathy. Increased oxidative stress due to adriamycin is considered to play a role in the pathogenesis of this toxic effect. In this study, we examined the levels and redistribution of vitamin A (a potent non-enzymatic antioxidant) in adriamycin-induced cardiomyopathy in rats. Three weeks after the adriamycin (ADR) treatment, animals were hemodynamically assessed and different tissues were analyzed for total retinol (vitamin A), (3)H-radio-labeled retinol, retinol palmitate and vitamin E. At 3 weeks, animals in the ADR group were hemodynamically and clinically confirmed to be in heart failure. In the ADR group, total retinol levels in heart and plasma were unchanged. However, levels of the (3)H radio-labeled fraction of retinol were significantly increased in both organs suggesting increased turnover. In the liver, the levels of total retinol and retinol palmitate were significantly decreased, while the radio-labeled fraction of retinol was significantly increased suggesting mobilization of retinol from this organ. Alpha tocopherol (vitamin E) levels were found unchanged in hearts of the ADR animals, while its levels in the plasma and liver were significantly increased. Increased radio-labeled fraction, without any change in the total retinol in the heart, suggested that vitamin A is utilized more by the heart under increased oxidative stress due to adriamycin. Its levels in the plasma and the heart may have been maintained at the expense of the loss from the liver.