Optimization of lung ultrasound in ultrafast-track anesthesia for non-cyanotic congenital heart disease surgery.

Objective: We aimed to explore the feasibility of lung ultrasound for perioperative assessment and the optimal effect of lung ultrasound in reducing lung complications during non-cyanotic congenital heart disease (CHD) surgery using ultrafast-track anesthesia. Methods: Sixty patients were treated at Shenzhen Children's Hospital between 2019 and 2020. Of these, 30 patients in group N had an indication for extubation and ultrafast-track anesthesia after congenital heart surgery; the tracheal catheter was removed, and the patients were sent to the cardiac intensive care unit (CICU) for further monitoring and treatment. Another 30 patients were in group L and also had an indication for extubation and ultrafast-track anesthesia; in addition we compared lung ultrasound score (LUS) before and after surgery, when we found the cases that LUS ≥ 15, for whom targeted optimization treatment would be carried out. The tracheal catheter was removed after LUS <15 days before the patients were sent to the CICU. In all cases, the LUS and PaO2/FiO2 ratios (P/F) of both groups were recorded at the time of anesthesia induction (T0), before extubation (T1), and 5 min (T2), 1 h (T3), and 24 h (T4) after extubation. The incidence of pulmonary complications, LUS, and P/F were compared between the two groups. Results: There was great consistency between LUS and radiographic findings. Comparing the data of the two groups at T2, T3 and T4, the P/F was higher and the LUS was lower in group L than in group N. The incidence of lung complications in group L (18 cases, 60 %) was lower than that in group N (26 cases, 86.7 %, χ2 = 5.46, P = 0.02); comparing LUS between T0 and T3, LUS decreased in a greater number of cases in group L (15, 50 %) than in group N (7 cases, 23.3 %, χ2 = 4.59, P = 0.032). Conclusion: Lung ultrasonography can effectively help assess lung conditions. Optimization guided by lung ultrasound in ultrafast track anesthesia can significantly reduce postoperative lung complications.

Endomyocardial fibrosis and apical calcification: A case report with unusual presentations of apical hypertrophic cardiomyopathy.

RATIONALE: Apical hypertrophic cardiomyopathy (ApHCM) is a phenotypic variant of hypertrophic cardiomyopathy. Endomyocardial fibrosis and endocardial calcification are especially rare in ApHCM. PATIENT CONCERNS: The main symptoms was chest tightness, palpitation, shortness of breath, and fatigue. Echocardiography and imaging examinations found apical hypertrophy along with endocardial calcification and endomyocardial fibrosis. Abnormal structural changes led to thrombosis and made the left ventricle a flat shape resembling an "apple." DIAGNOSES: The typical presentations, hypertrophic apex on echocardiography and an elevated N-terminal pro-brain natriuretic peptide level indicated the diagnosis of ApHCM and heart failure with preserved ejection fraction. INTERVENTIONS: Optimal medical therapy including the administration of ApHCM, heart failure and atrial fibrillation to improve symptoms and life quality. OUTCOMES: Since discharge, the patient could perform normal daily activities and had no discomfort based on the optimal medical therapy. LESSONS: We report a ApHCM patients with unusual presentations of endomyocardial fibrosis and apical calcification. This case highlights the importance of understanding the specific pathological changes of ApHCM for treatment and prognosis.

Cardiac contractility modulation ameliorates myocardial metabolic remodeling in a rabbit model of chronic heart failure through activation of AMPK and PPAR-α pathway.

Metabolic remodeling contributes to the pathological process of heart failure (HF). We explored the effects of cardiac contractility modulation (CCM) on myocardial metabolic remodeling in the rabbit model with HF. The HF in rabbit model was established by pressure uploading and then CCM was applied. We evaluated the cardiac structure and function by echocardiography, serum BNP level, and hematoxylin and eosin and Masson's trichrome staining. We detected the accumulation of glycogen and lipid droplets in myocardial tissues by periodic acid-Schiff and Oil Red O staining. Then, we measured the contents of glucose, free fatty acid (FFA), lactic acid, pyruvate, and adenosine triphosphate (ATP) levels in myocardial tissues by corresponding kits and the expression levels of key factors related to myocardial substrate uptake and utilization by western blotting were analyzed. CCM significantly restored the cardiac structure and function in the rabbit model with HF. CCM therapy further decreased the accumulation of glycogen and lipid droplets. Furthermore, CCM reduced the contents of FFA, glucose, and lactic acid, and increased pyruvate and ATP levels in HF tissues. The protein expression levels related to myocardial substrate uptake and utilization were markedly improved with CCM treatment by further activating adenosine monophosphate-activated protein kinase and peroxisome proliferator-activated receptor-α signaling pathways.

Total Glucosides of Paeony Alleviate Cell Apoptosis and Inflammation by Targeting the Long Noncoding RNA XIST/MicroRNA-124-3p/ITGB1 Axis in Renal Ischemia/Reperfusion Injury.

OBJECTIVE: Renal ischemia/reperfusion injury (RI/RI) is the main cause of acute kidney injury. Total glucosides of paeony (TGP) are a traditional Chinese medicine. This study was aimed at exploring the role of TGP in RI/RI and its underlying mechanism of action. METHODS: Rat RI/RI models were constructed by surgical operation. Serum creatinine (Scr) and blood urea nitrogen (BUN) were used to evaluate renal function. The levels of proinflammatory cytokines were detected by ELISA. RI/RI was simulated by hypoxia/reoxygenation (H/R) treatment in renal cells in vitro. The lncRNA XIST (XIST) expression was analyzed by qRT-PCR. Then, the viability and apoptosis of renal cells were detected by MTT and flow cytometry assay. Additionally, dual-luciferase reporter assay was used to determine the interactions among XIST, microRNA-124-3p (miR-124-3p), and ITGB1. RESULTS: TGP improved renal function and inhibited inflammatory responses after RI/RI. XIST expression was highly expressed in rat RI/RI models and H/R-treated renal cells, whereas treatment with TGP downregulated the XIST expression. Additionally, TGP increased viability and attenuated apoptosis and inflammation of H/R-treated renal cells via inhibiting XIST. Moreover, XIST was competitively bound to miR-124-3p, and ITGB1 was a target of miR-124-3p. miR-124-3p overexpression or ITGB1 inhibition rescued the reduction effect on viability and mitigated the promoting effects on cell apoptosis and inflammation caused by XIST overexpression in H/R-treated renal cells. CONCLUSIONS: In vivo, TGP attenuated renal dysfunction and inflammation in RI/RI rats. In vitro, TGP inhibited XIST expression to modulate the miR-124-3p/ITGB1 axis, alleviating the apoptosis and inflammation of H/R-treated renal cells.

CAR T-cell therapy for triple-negative breast cancer: Where we are.

Triple-negative breast cancer (TNBC) is the most complex and challenging breast cancer subtype to treat, and chemotherapy remains the standard of care. Clinically, TNBC has a relatively high rate of recurrence and poor prognosis, which leads to a significant effort to discover novel strategies to treat patients with these tumors. Currently, chimeric antigen receptor (CAR) T cell-based immunotherapy redirects the patient's immune system directly to recognize and eradicate tumor-associated antigens (TAAs) expressing tumor cells being explored as a treatment for TNBC. A steadily increasing research in CAR T-cell therapy targeting different TAAs in TNBC has reported. In this review, we introduce the CAR technology and summarize the potential TAAs, available CARs, the antitumor activity, and the related toxicity of CARs currently under investigation for TNBC. We also highlight the potential strategies to prevent/reduce potential "on target, off tumor" toxicity induced by CAR T-cell therapy. This review will help to explore proper targets to expand further the CAR T-cell therapy for TNBCs in the clinic.