The removal of antibiotic resistant bacteria and antibiotic resistance genes by sulfidated nanoscale zero-valent iron activating periodate: Efficacy and mechanism.

Antibiotic resistant bacteria (ARB) and antibiotic resistance genes (ARGs) have drawn much more attention due to their high risk on human health and ecosystem. In this study, the performance of sulfidated nanoscale zero-valent iron (S-nZVI)/periodate (PI) system toward ARB inactivation and ARGs removal was systematically investigated. The S-nZVI/PI system could realize the complete inactivation of 1 × 108 CFU/mL kanamycin, ampicillin, and tetracycline-resistant E. coli HB101 within 40 min, meanwhile, possessed the ability to remove the intracellular ARGs (iARGs) (including aphA, tetA, and tnpA) carried by E. coli HB101. Specifically, the removal of aphA, tetA, and tnpA by S-nZVI/PI system after 40 min reaction was 0.31, 0.47, and 0.39 log10copies/mL, respectively. The reactive species attributed to the E. coli HB101 inactivation were HO• and O2•-, which could cause the destruction of E. coli HB101 morphology and enzyme system (such as superoxide dismutase and catalase), the loss of intracellular substances, and the damage of iARGs. Moreover, the influence of the dosage of PI and S-nZVI, the initial concentration of E. coli HB101, as well as the co-existing substance (such as HCO3-, NO3-, and humic acid (HA)) on the inactivation of E. coli HB101 and its corresponding iARGs removal was also conducted. It was found that the high dosage of PI and S-nZVI and the low concentration of E. coli HB101 could enhance the disinfection performance of S-nZVI/PI system. The presence of HCO3-, NO3-, and HA in S-nZVI/PI system showed inhibiting role on the inactivation of E. coli HB101 and its corresponding iARGs removal. Overall, this study demonstrates the superiority of S-nZVI/PI system toward ARB inactivation and ARGs removal.

Effect of total knee arthroplasty for valgus knee correction on clinical outcome and patellar position.

PURPOSE: The purpose was to investigate the effect of different degrees of valgus deformity correction on patellar position and clinical outcome in patients with valgus knees after total knee arthroplasty (TKA). METHODS: We retrospectively analyzed and followed 118 patients with valgus knees. Based on the post-operative hip-knee-ankle (HKA), patients were divided into three groups: neutral (±3°), mild (3-6°), and severe (> 6°). Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), range of motion (ROM), and Knee Society Score (KSS) were used to evaluate post-operative clinical efficacy. Also, the patellar tilt angle (ε-angle), congruence angle (θ-angle), and Insall-Salvati index (ISI) were used to represent the patellar position. Post-operative observation indicators included HKA, angle of the femur (α-angle), tibial angle (ß-angle), femoral component flexion angle (γ-angle), and tibial component posterior slope angle (δ-angle). RESULTS: All patients showed significant improvements in HKA, ROM, WOMAC, and KSS after operation (P < 0.001). Regarding patellar position, the ISI values decreased to varying degrees (P < 0.05). The patellar tilt angle was significantly increased in the severe valgus group compared to that in the mild valgus and neutral groups (P < 0.001). Univariate analysis showed that the degree of post-operative residual valgus was significantly affected by WOMAC, KSS, α-, ε-, and θ-angles. CONCLUSION: Minor valgus undercorrection did not affect the short-term outcome after TKA; however, when the residual valgus angle was > 6°, the post-operative scores were significantly reduced. Inadequate valgus correction does not result in significant changes in patellar height but may increase the risk of poor patellar tracking.

Exosomes derived from human umbilical cord mesenchymal stem cells (HUCMSC-EXO) regulate autophagy through AMPK-ULK1 signaling pathway to ameliorate diabetic cardiomyopathy.

One of the main causes of severe diabetic heart failure and mortality is diabetic cardiomyopathy (DCM), a cardiovascular condition attributable to diabetes with a high incidence, a complicated and unexplained pathophysiology, and poor treatment results. Current findings have demonstrated that the onset of diabetic cardiomyopathy involves autophagy, inflammation, and mitochondrial damage. Myocardial autophagy behaves differently in different states,and one of the targets for the detection and treatment of cardiovascular illnesses like diabetic cardiomyopathy may be the control of autophagy. The role of human umbilical cord Mesenchymal stem cells-derived exosomes (HUCMSC-EXO) as a non-cellular system in the repair of cardiomyocytes, the evolution of diabetic cardiomyopathy and their cardioprotective effects are gradually being recognized. This study's objectives were to assess the therapeutic benefits of HUCMSC-EXO for diabetic cardiomyopathy and to look into their potential mechanisms of action. High-speed centrifugation was used to extract HUCMSC-EXO, and the shape of the exosomes was examined using transmission electron microscopy. Immunoblotting was used to determine the expression of CD9, CD63, and TSG101 molecules on the surface of the exosomes. A high-fat, high-sugar diet mixed with streptozotocin was used to build a rat model of type 2 diabetic cardiomyopathy. Cardiac function, ventricular wall thickness and cardiac histological changes were examined by cardiac ultrasound, serum BNP and histology. In cardiac myocytes, HUCMSC-EXO reduced the levels of autophagy-related protein expression. Additionally, immunoblotting supported our suspicion that this mechanism is strongly tied to the activation of the AMPK-ULK1 signaling pathway. So, we propose that it would be a good strategy to follow for treating diabetic cardiomyopathy. These findings offer both fresh concepts for building a model of diabetic cardiomyopathy and a creative theoretical framework for using HUCMSC-EXO to treat diabetic cardiomyopathy in a clinical setting.

Descending thoracic aortic dissection after covered stent for adult aortic coarctation: Technical or physiopathologic?

Covered stent graft implantation is currently the most commonly used modality for the management of adult aortic coarctation. Although the risk of descending thoracic aortic dissection after covered stent graft implantation is low, sometimes it may cause serious medical consequences or even death. We report one adult aortic coarctation patient with early postoperative descending thoracic aortic dissection after covered stent graft implantation. The patient underwent second operation of thoracic endovascular aortic reconstruction and was discharged 6 days after the operation. This case is not rare, but we hope that the complete diagnosis and treatment process of this case and discussion pertaining to surgical treatment method and its complications could serve as a reference for clinicians in dealing with such situations.

Astragaloside IV Inhibits NLRP3 Inflammasome-Mediated Pyroptosis via Activation of Nrf-2/HO-1 Signaling Pathway and Protects against Doxorubicin-Induced Cardiac Dysfunction.

BACKGROUND: Doxorubicin (DOX) is an effective broad-spectrum antitumor drug, but its clinical application is limited due to the side effects of cardiac damage. Astragaloside IV (AS-IV) is a significant active component of Astragalus membranaceus that exerts cardioprotective effects through various pathways. However, whether AS-IV exerts protective effects against DOX-induced myocardial injury by regulating the pyroptosis is still unknown and is investigated in this study. METHODS: The myocardial injury model was constructed by intraperitoneal injection of DOX, and AS-IV was administered via oral gavage to explore its specific protective mechanism. Cardiac function and cardiac injury indicators, including lactate dehydrogenase (LDH), cardiac troponin I (cTnI), creatine kinase isoenzyme (CK-MB), and brain natriuretic peptide (BNP), and histopathology of the cardiomyocytes were assessed 4 weeks post DOX challenge. Serum levels of IL-1ß, IL-18, superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) and the expression of pyroptosis and signaling proteins were also determined. RESULTS: Cardiac dysfunction was observed after the DOX challenge, as evidenced by reduced ejection fraction, increased myocardial fibrosis, and increased BNP, LDH, cTnI, and CK-MB levels (p < 0.05, N = 3-10). AS-IV attenuated DOX-induced myocardial injury. The mitochondrial morphology and structure were also significantly damaged after DOX treatment, and these changes were restored after AS-IV treatment. DOX induced an increase in the serum levels of IL-1ß, IL-18, SOD, MDA and GSH as well as an increase in the expression of pyroptosis-related proteins (p < 0.05, N = 3-6). Besides, AS-IV depressed myocardial inflammatory-related pyroptosis via activation of the expressions of nuclear factor E2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1) (p < 0.05, N = 3). CONCLUSIONS: Our results showed that AS-IV had a significant protective effect against DOX-induced myocardial injury, which may be associated with the activation of Nrf-2/HO-1 to inhibit pyroptosis.