Cobalt chloride (CoCl2) is a well-known hypoxia mimetic mediator that induces hypoxia-like responses. CoCl2, a mediator confirmed to alleviate hypoxia-inducible factor-1 (HIF-1), has been associated with a variety of hypoxic responses. HIF-1 is the foremost transcriptionfactor that is particularly activated during hypoxia and regulates various genes. Therefore, this study aimed to investigate the cellular and molecular responses of the co-cultured cells under the influence of the CoCl2-induced hypoxic condition. Mono- and co-cultured C2C12 and 3T3-L1 cells were exposed to CoCl2, and a significant induction in HIF-1, reactive oxygen species and lipid peroxidase and a reduction in glutathione and catalase were observed. The expressions of proapoptotic genes like Bax, p53, caspase-9, and caspase-3 were notably increased, whereas the antiapoptotic gene, i.e., Bcl2, was downregulated during hypoxia in mono- as well as co-cultured C2C12 cells. However, the co-cultured C2C12 cells show significantly lower induction in oxidative stress and expression of apoptotic genes in comparison to monocultured C2C12 cells. Whereas, the co-cultured 3T3-L1 cells show comparatively higher oxidative stress and apoptotic event in comparison to monocultured 3T3-L1 cells. The reason may be the communication between the cells and some soluble factors that help in cell survival/death from hypoxia. Moreover, it may also be due to the fact that fat and muscle cells interact and communicate via proximity and mutual ability when growing together. Therefore, the co-culture system provides a unique approach to intercellular communication between the two different cell types.
26 September 2019 in ACS Sustainable Chemistry & Engineering
Background: Total ankle arthroplasty (TAA) has higher complication and failure rates compared to other surgical joint replacement procedures despite technological advances. This study aimed to find the long-term survivability of the TAA procedure and identify the patient risk factors for failure with one of the largest cohorts of patients in the literature. Methods: This retrospective cohort study involving cases between 2007 and 2018 analyzed patients who received an index primary TAA procedure in Korea. A total of 5619 cases were included in the final analysis. The TAA failure was defined as either a case with revision arthroplasty or a case with TAA implant removal and arthrodesis performed after primary TAA. Results: During the study period, the 5-year survival rate was 95.4% (95% CI, 94.7–96.1%), and the 10-year survival rate was 91.1% (95% CI, 89.1–93.1%). A younger age (<55 years, adjusted hazard ratio [AHR], 1.725; 55–64 years, AHR, 1.812; p < 0.001 for both), chronic pulmonary disease (AHR, 1.476; p = 0.013), diabetes (AHR, 1.443; p = 0.014), and alcohol abuse (AHR, 1.524; p = 0.032) showed a significantly high odds ratio for primary TAA failure in Cox regression analysis. Conclusion: The 10-year TAA survivorship rate was 91.1%. A younger age, chronic pulmonary disease, diabetes, and heavy alcohol consumption are risk factors for TAA.
Surgical site infection (SSI) is a major complication after the surgical treatment of ankle fractures that can result in catastrophic consequences. This study aimed to determine the incidence of SSI in several cohorts from national insurance databases over the past 12 years and identify its predictors. The claimed data for patients (n = 1,449,692) with ankle fractures between 2007 and 2019 were investigated, and a total of 41,071 patients were included in the final analysis. The covariates included were age, sex, season, fracture type (closed vs. open), type of surgical fixation procedure, and comorbidities of each patient. All subjects were divided into two groups according to the SSI after the surgical fixation of the ankle fracture (no infection group vs. infection group). The number of SSIs after the surgical treatment of ankle fractures was 874 (2.13%). Open fractures [odds ratio, (OR) = 4.220] showed the highest risk for SSI, followed by the male sex (OR = 1.841), an increasing number of comorbidities (3–5, OR = 1.484; ≥6, OR = 1.730), a history of dementia (OR = 1.720) or of myocardial infarction (OR = 1.628), and increasing age (OR = 1.010). The summer season (OR = 1.349) showed the highest risk among the four seasons for SSI after ankle fracture surgery.
Tendon injuries account for 45% of musculoskeletal injuries. However, research on the occurrence and pathogenesis of tendinopathy is insufficient, and there is still much debate regarding treatment methods. It is important to understand the molecular mechanisms of oxidative stress and inflammatory responses because oxidative stress in tendon tissue is induced by various factors, including inflammatory cytokines, drug exposure, and metabolic abnormalities. In this study, 28 rats were divided into four groups (7 rats assigned to each group): control group (CON), collagenase injection group (CL), collagenase injection and hyaluronic acid injection group (CL + HA), and collagenase injection and EGCG-loaded hyaluronic acid injection group (CL + HA + EGCG). Seven weeks after the start of the study, all rats underwent histochemical analysis, immunofluorescence staining, and Western blot. The results showed increased inflammatory cells, disarray of collagen matrix, and degradation of the collagen matrix in the CL group. However, in the EGCG-treated group, there was a significant increase in type I collagen expression and a significant decrease in type III collagen expression, compared to the CL group. Additionally, there was an increase in the expression of antioxidant markers SOD (Superoxide Dismutase) and CAT (Catalase), tenogenic markers COLL-1 (collagen type I), and SCX (Scleraxis), and a downregulated expression of apoptosis markers cas-3 and cas-7. Our findings suggest that EGCG-loaded hyaluronic acid hydrogel exhibits potential in preventing tendon damage and promoting the regeneration process in a rat model of Achilles tendinopathy. The insights gained from our histological and molecular investigations highlight the future potential for testing novel tendinopathy treatments in human subjects.