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Pulmonary atresia with ventricular septal defect is a complex congenital heart defect whose management varies depending on the anatomy of pulmonary circulation and surgeon’s preferences. The surgical outcomes of complete repair in small infants and neonates in Vietnam have been seldomly reported. We reported our medium-term results of complete repair of this complex lesion using valved conduit in infants and neonates at our institution. The study included 25 patients with the body weight of less than 5kg who underwent definitive repair using valved conduit between January 2016 and December 2021. The median age at surgery was 66 days (IQR 45 – 116 days), and the mean body weight was 4 kg (3 – 5). Most (96%) attended all follow-up visits, and the average follow-up time was 37.4 months (8.4 – 69.3). There was 1 in-hospital death and 2 late mortalities. The 30-days and 5 years survival rate were 96% and 83%, respectively. One patient required conduit replacement at 3 years post operative because of conduit failure. The proportion of patients with freedom from conduit replacement at 5 years was 95%. Three cases required balloon dilatation of the left pulmonary artery due to stenosis. Freedom from all reinterventions and reoperations at 5 years was 52%. Definitive repair of this type of complex heart defect in small infants can be performed safely and resulted in good surgical outcomes.

Objectives Aortopulmonary window (APW) associated with interrupted aortic arch (IAA) is a rare cardiac malformation with significant mortality and morbidity. This study aimed to report the intermediate outcomes of single-stage stage repair concentrating on the surgical techniques and postoperative reintervention for this rare cardiac lesion. Methods Eleven patients were diagnosed with IAA-associated APW and underwent single-stage surgical repair at Vietnam National Children’s Hospital. Results The APW anatomy types were the types I, II, and III in 1, 4, and 6 patients, respectively. The IAA morphology was type A in nine patients and type B in two patients. The median age was 27 (interquartile range [IQR] 6–79) days, and median weight was 3.5 (IQR 2.8–4.5) kg. The aortic arch was repaired using direct end-to-side tissue anastomosis in seven patients, and patch aortoplasty was performed in four patients. Six patients underwent APW closure with an intra-aortic baffle, and five patients required right pulmonary artery detachment and reimplantation. One early death occurred. Four patients required reinterventions: one patient required reoperation due to aortic stenosis and three required balloon angioplasty for either recurrent aortic arch stenosis (n = 1) or right pulmonary stenosis (n = 2) with a mean follow-up time of 3.1 (IQR 0.5–4.3 years). Conclusions Single-stage repair of IAA-associated APW can be achieved with good survival outcomes in children. However, the need for repeat reintervention or reoperation remains high, and the growth of both the aorta and pulmonary arteries should follow carefully with patient’s growth. Clinical registration number VNCH-RICH-18-96

The cytidine deaminases APOBEC3A and APOBEC3B (A3B) are prominent mutators of human cancer genomes. However, tumor-specific genetic modulators of APOBEC-induced mutagenesis are poorly defined. Here, we utilized a screen to identify 61 gene deletions that increase A3B-induced mutations in yeast. Also, we determined whether each deletion was epistatic with UNG1 loss, which indicated whether the encoded factors participate in the error-free bypass of A3B/Ung1-dependent abasic sites or suppress A3B-catalyzed deamination by protecting against aberrant formation of single stranded DNA (ssDNA). Additionally, we determined that the mutation spectra of A3B-induced mutations revealed genotype-specific patterns of strand-specific ssDNA formation and nucleotide incorporation across APOBEC-induced lesions. Combining these three metrics we were able to establish a multifactorial signature of APOBEC-induced mutations specific to (1) failure to remove H3K56 acetylation, which results in extremely high A3B-induced mutagenesis, (2) defective CTF18-RFC complex function, which results in high levels of A3B induced mutations specifically on the leading strand template that synergistically increase with loss of UNG1, and (3) defective HR-mediated bypass of APOBEC-induced lesions, which were epistatic with Ung1 loss and result from increased Rev1-mediated C-to-G substitutions. We extended these results by analyzing mutation data for human tumors and found BRCA1/2-deficient breast cancer tumors display 3- to 4-fold more APOBEC-induced mutations. Mirroring our results in yeast, for BRCA1/2 deficient tumors Rev1-mediated C-to-G substitutions are solely responsible for increased APOBEC-signature mutations and these mutations occur on the lagging strand during DNA replication. Together these results identify important factors that influence the dynamics of DNA replication and likely the abundance of APOBEC-induced mutation during tumor progression as well as a novel mechanistic role for BRCA1/2 during HR-dependent lesion bypass of APOBEC-induced lesions during cancer cell replication.

The development of the Fifth Generation (5G) New Radio (NR) provides several significant advantages when compared to the fourth generation (4G) Long Term Evolution (LTE) in mobile communications. Due to the outstanding characteristics of Low-Density Parity-Check (LDPC) codes such as high decoding performance, high throughput, low complexity, they have been accepted as the standard codes for the 5G NR. In this paper, we propose two LDPC decoding algorithms: Hybrid Offset Min-Sum (HOMS) and Variable Offset Min-Sum (VOMS), which are aimed at improving the error correction performance. The main idea of the HOMS/VOMS algorithm is to apply modified factors to both variable-nodes and check-nodes updated processing in order to compensate the extrinsic messages overestimation of the MS-based algorithms and increase the protection ability for degree-1 variable-nodes. The simulation results show that at the Bit-Error-Rate (BER) of 10-5, the proposed HOMS/VOMS algorithm achieves the decoding gain up to 0.2 dB compared to the Offset Min-Sum (OMS) algorithm, with a slight increase in decoding complexity.

Mục tiêu: Nhận xét kết quả điều trị đóng xương ức thì hai ở bệnh nhi sau phẫu thuật tim mở tại Bệnh viện Nhi Trung ương. Đối tượng và phương pháp: Hồi cứu mô tả trên 61 bệnh nhi phẫu thuật tim mở và được đóng xương ức thì hai sau phẫu thuật từ tháng 5/2020 đến tháng 4/2021. Kết quả: Trong 61 bệnh nhân được nghiên cứu, tuổi trung vị là 2 (1 - 11,5) tháng, cân nặng trung vị là 4,5 (3,4 - 7,8) kg, thời gian đóng xương ức thì 2 trung bình là 46 giờ. Chỉ định để hở xương ức sau phẫu thuật chủ yếu do hội chứng cung lượng tim thấp (55,7%). Tỷ lệ thành công đóng xương ức là 60/61 bệnh nhân (98,4%). Tỉ lệ tử vong trong nhóm nghiên cứu là 13,1%. Các yếu tố nguy cơ ảnh hưởng tới tử vong có ý nghĩa thống kê bao gồm: Chỉ số lactat khi ra Khoa Hồi sức ngoại tim mạch, thời gian thở máy kéo dài, thời gian nằm hồi sức kéo dài, nhiễm trùng xương ức, nhiễm khuẩn huyết sau mổ, ECMO sau mổ. Kết luận: Đóng xương ức thì 2 là một phương pháp hỗ trợ hiệu quả đối với bệnh nhân có tình trạng huyết động không ổn định sau khi phẫu thuật tim mở phức tạp ở trẻ em trong giai đoạn hậu phẫu sớm.