Objective:To study the feasibility of laparoscopic anatomical hepatectomy of segment VII for hepatocellular carcinoma (HCC) with dorsal-ventral combined approach.Methods:Clinical data of 23 patients with HCC undergoing laparoscopic anatomical hepatectomy of segment VII with dorsal-ventral combined approach in Jiangnan University Affiliated Hospital from December 2020 to April 2023 were retrospectively collected, including 11 males and 12 females, aged (58.5±7.9) years old. The patient's perio-perative data, postoperative complications, and follow-ups were analyzed.Results:All patients underwent the surgery successfully without conversion to laparotomy. The operation time was (286.7±63.4) min, the amount of intraoperative blood loss [ M( Q1, Q3)] was 200(150, 400) ml without blood transfusion. There were no major complications such as abdominal bleeding, bile leakage, liver failure or abdominal infection. Two cases had right pleural effusion and were managed with thoracic drainage. The patients could ambulate on postoperative day 2, and the postoperative hospital stay was (9.36±1.72) d. The diameter of the lesion was (4.38±1.42) cm. The serum level of alpha fetoprotein (AFP) three months after surgery was (3.26±0.93) ng/ml, lower than the preoperative baseline (46.75±9.43) ng/ml ( t=38.24, P=0.008). All patients showed normal serum levels of AFP and there were no tumor recurrence or metastasis during postoperative follow-ups. Conclusion:Laparoscopic anatomical hepatectomy of segment VII for HCC with dorsal-ventral combined approach is feasible and worth spreading.

Objective: To analyze the clinical features and summarize the experience on the diagnosis and treatment of aortic stenosis caused by Takayasu arteritis in pediatric patients. Methods: This study was a retrospective study. Five pediatric patients diagnosed as aortic stenosis caused by Takayasu arteritis in Fuwai Hospital of Chinese Academy of Medical Sciences from January 2016 to August 2018 were included. The clinical features, methods of examination, treatment and outcome were analyzed. Results: There were 2 male and 3 female patients in this cohort. The age of onset ranged from 10 to 13 years. The main clinical symptoms were as follows: intermittent claudication and hypertension (5 patients), heart failure (3 patients). Three patients with heart failure were misdiagnosed with dilated cardiomyopathy in other hospitals. Except 1 patient died due to disease aggravation before operation, the other 4 patients received interventional therapy for severe heart failure or refractory hypertension on the basis of hormone anti-inflammatory treatment, including 2 patients treated with aortic balloon dilatation and 2 patients treated with aortic balloon dilatation and stent implantation. In post-operational follow-up, clinical symptoms and laboratory examination values of the 4 patients treated with interventional therapy were significantly improved. Conclusions The clinical symptoms of pediatric patients with aortic stenosis caused by Takayasu arteritis mainly present with intermittent claudication, hypertension and heart failure. Aortic intervention strategy should be applied for pediatric patients with severe heart failure or refractory hypertension as early as possible.

Rett syndrome (RTT) is a progressive neurodevelopmental disorder, mainly caused by mutations in MeCP2 and currently with no cure. We report here that neurons from R106W MeCP2 RTT human iPSCs as well as human embryonic stem cells after MeCP2 knockdown exhibit consistent and long-lasting impairment in maturation as indicated by impaired action potentials and passive membrane properties as well as reduced soma size and spine density. Moreover, RTT-inherent defects in neuronal maturation could be pan-neuronal and occurred in neurons with both dorsal and ventral forebrain features. Knockdown of MeCP2 led to more severe neuronal deficits as compared to RTT iPSC-derived neurons, which appeared to retain partial function. Strikingly, consistent deficits in nuclear size, dendritic complexity and circuitry-dependent spontaneous postsynaptic currents could only be observed in MeCP2 knockdown neurons but not RTT iPSC-derived neurons. Both neuron-intrinsic and circuitry-dependent deficits of MeCP2-deficient neurons could be fully or partially rescued by re-expression of wild type or T158M MeCP2, strengthening the dosage dependency of MeCP2 on disease phenotypes and also the partial function of the mutant. Our findings thus reveal stable neuronal maturation deficits and unexpectedly, graded sensitivities of neuron-inherent and neural transmission phenotypes towards the extent of MeCP2 deficiency, which is informative for future therapeutic development.

New threats posed by the emerging circulating variants of SARS-CoV-2 highlight the need to find conserved neutralizing epitopes for therapeutic antibodies and efficient vaccine design. Here, we identified a receptor-binding domain (RBD)-binding antibody, XG014, which potently neutralizes β-coronavirus lineage B (β-CoV-B), including SARS-CoV-2, its circulating variants, SARS-CoV and bat SARSr-CoV WIV1. Interestingly, antibody family members competing with XG014 binding show reduced levels of cross-reactivity and induce antibody-dependent SARS-CoV-2 spike (S) protein-mediated cell-cell fusion, suggesting a unique mode of recognition by XG014. Structural analyses reveal that XG014 recognizes a conserved epitope outside the ACE2 binding site and completely locks RBD in the non-functional "down" conformation, while its family member XG005 directly competes with ACE2 binding and position the RBD "up". Single administration of XG014 is effective in protection against and therapy of SARS-CoV-2 infection in vivo. Our findings suggest the potential to develop XG014 as pan-β-CoV-B therapeutics and the importance of the XG014 conserved antigenic epitope for designing broadly protective vaccines against β-CoV-B and newly emerging SARS-CoV-2 variants of concern.
Angiotensin-Converting Enzyme 2 ; Antibodies, Neutralizing ; Antibodies, Viral ; COVID-19 ; Epitopes ; Humans ; SARS-CoV-2/genetics* ; Spike Glycoprotein, Coronavirus/genetics*