To analyze the disease burden of acute lymphoid leukemia(ALL) and its changing trends in China and globally from 1990 to 2021, aiming to provide a theoretical basis for disease prevention, treatment, and policy formulation.

ObjectiveTo explore the potential mechanism of Shenqi Jianxin Formula （参芪健心方） in the treatment of chronic heart failure （CHF） from the perspective of regulating mitochondrial autophagy via the PTEN-induced kinase 1 （PINK1）/E3 ubiquitin ligase （Parkin） pathway. MethodsMale SD rats were subjected to abdominal aortic constriction to establish the CHF model. Twenty-four successfully modeled rats were randomly divided into the model group， sacubitril/valsartan group， and low- and high-dose Shenqi Jianxin Formula groups， with 6 rats in each group. Six other rats were set as the sham surgery group， which were only separated the abdominal aorta and then closed the abdomen. Rats in the low-dose and high-dose Shenqi Jianxin Formula groups were given intragastric administration of Shenqi Jianxin Formula suspension at doses of 4.41 g/（kg·d） and 17.64 g/（kg·d）， respectively； the sacubitril/valsartan group received intragastric administration of sacubitril/valsartan sodium tablet suspension at 10 mg/（kg·d）； the sham surgery group and the model group were given normal saline at 10 ml/（kg·d） via intragastric gavage. The intervention lasted for 4 consecutive weeks. Cardiac function indices including left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） were detected， and serum brain natriuretic peptide （BNP） content was measured. HE staining and Masson staining were used to observe myocardial histopathological changes. Transmission electron microscopy was employed to examine the ultrastructure of cardiac tissues. Quantitative real-time polymerase chain reaction （Rt-qPCR） was performed to determine the mRNA expressions of PINK1/Parkin pathway-related factors and autophagy-associated proteins including Beclin-1， p62， and microtubule-associated protein 1 light chain 3 （LC3） in myocardial tissues. ResultsCompared with the sham surgery group， the model group showed significant decreases in LVEF and LVFS levels， an increase in serum BNP content， down-regulated mRNA and protein expressions of PINK1， Parkin and Beclin-1 in cardiac tissues， up-regulated mRNA and protein expressions of p62， as well as significant reductions in LC3B mRNA expression， phosphorylated PTEN-induced kinase 1 （p-PINK1） and phosphorylated E3 ubiquitin ligase （p-Parkin） protein levels， and the ratio of microtubule-associated protein 1 light chain 3-Ⅱ to microtubule-associated protein 1 light chain 3-Ⅰ （LC3Ⅱ/LC3Ⅰ） （P＜0.05）. Pathological results revealed obvious myocardial cell edema， necrosis and degeneration， increased disorder of myocardial fiber arrangement， extensive inflammatory cell infiltration， moderate to severe mitochondrial swelling， a few mitochondrial vacuolar changes， and no obvious autophagy in the field of vision in the model group. Compared with the model group， all the above indicators were significantly improved in the high-dose Shenqi Jianxin Formula group and the sacubitril/valsartan group （P＜0.05）. Moreover， the improvement of each index in the high-dose Shenqi Jianxin Formula group was superior to that in the low-dose group （P＜0.05）. In the high-dose Shenqi Jianxin Formula group， myocardial myofibrils were arranged regularly with orderly orientation， the striated structure was clear， and necrotic cells significantly reduced. ConclusionShenqi Jianxin Formula can activate the PINK1/Parkin signaling pathway in myocardial tissues， enhance mitochondrial autophagy， and clear dysfunctional mitochondria， thereby improving cardiac function and delaying the progression of CHF.

Liver transplantation is a radical treatment for progressive and irreversible end-stage liver disease. However, its clinical application has always been restricted by the core bottleneck of donor liver shortage. Living donor liver transplantation can alleviate the shortage of donor livers to a certain extent, but it requires simultaneous assurance of sufficient residual liver volume in donors to avoid liver insufficiency, as well as an adequate graft-to-recipient weight ratio to prevent small-for-size syndrome, which limits its clinical application. Dual-donor liver transplantation utilizes partial liver tissues from two donors as grafts. While ensuring donor safety, avoiding small-for-size syndrome in recipients, and expanding the donor pool, this technique significantly improves the utilization rate of donor livers and effectively eases the clinical contradiction of donor liver shortage. Based on recent domestic and international clinical practices and the latest diagnosis and treatment guidelines, this article systematically reviews the developmental background, donor and recipient evaluation and selection, surgical procedures and postoperative complications of dual-donor liver transplantation, aiming to provide references for the standardized promotion and clinical optimization of this technique.

OBJECTIVE To investigate the relationship between 23-site chip genetic screening failures and the results of newborns hearing screening,and to provide clinical reference for the diagnosis and treatment of genetic screening failures.METHODS There were 1 916 newborns born in the Beijing area from November 2022 to May 2024,who did not pass the 23-site chip genetic screening tests and underwent newborn hearing screening with definite initial screening results.Chi-square test was used to analyze the relationship between different mutation types and genotypes and the initial hearing screening results.RESULTS The overall neonatal hearing screening failure rate was 5.27%(101/1 916),with a higher failure rate of 61.54%(56/91)for homozygous and compound heterozygous mutations than the failure rate of 2.54%(45/1 772)for heterozygous mutations,0%(0/34)for digenic gene heterozygous mutations,and 0(0/19)for mtDNA 12S rRNA mutations,with a statistically significant difference(P<0.001).Among the homozygous and compound heterozygous mutations,the failure rates of homozygous and compound heterozygous for GJB2 gene and SLC26A4 gene were 59.76%(49/82)and 77.78%(7/9),respectively,with no statistically significant difference between the two groups(P=0.488).The homozygous and compound heterozygous for GJB2 gene were divided into three groups based on genotype:c.109G>A homozygous mutations,c.109G>A compound heterozygous mutations,and other homozygous and compound heterozygous mutations.The hearing screening failure rates of the three groups,from highest to lowest,were as follow:other homozygous and compound heterozygous mutations(88.89%,8/9),c.109G>A homozygous mutations(65.12%,28/43),and c.109G>A compound heterozygous mutations(43.33%,13/30),with a statistically significant difference(P=0.029).The failure rates of heterozygous for GJB2 gene,SLC26A4 gene and GJB3 gene were 2.86%(40/1 398),1.25%(4/321)and 1.89%(1/53),respectively,with no statistically significant difference among the three groups(P=0.241).The failure rate of hearing screening for individuals with GJB2 heterozygotes of different genotypes and individuals with SLC26A4 heterozygotes of different genotypes did not show statistically significant differences.CONCLUSION The failure rate of newborn hearing screening for homozygous and compound heterozygous mutation of 23-site chip genetic screening is higher than that of other mutation types,verifying the effectiveness of the newborn hearing screening program.Some newborns of homozygous and compound heterozygous mutation can pass the hearing screening,especially those with the c.109G>A homozygous and compound heterozygous mutation,who need clinical follow-up.

Objective:To investigate the role of heme oxygenase-1(HO-1)regulating autophagy and its impact on the intracel-lular growth of Mycobacterium abscessus(M.abs).Methods:The standard strain of M.abs ATCC19977 was used to stimulate mouse RAW264.7 macrophages with a specified multiple of infection(MOI)for a specified time.Western blot analysis was performed to detect the expression levels of HO-1 protein and autophagy related proteins Atg5,LC3Ⅱ and p62.Macrophages were pretreated with HO-1 specific inducer CoPP and enzyme activity inhibitor SnPP for 12 h,and incubated with M.abs for 2 h.Amikacin removed extra-cellular bacteria and continued to culture until the specified time,and cell activity was detected by CCK-8 method.Western blot and LysoTracker Red were used to detect the regulatory relationship between HO-1 protein and autophagy related proteins.Bacterial survival and TNF-α secretion levels were detected by colony count and ELISA.Results:Compared with the control group,M.abs could induce increased expression of HO-1,Atg5,LC3Ⅱ and p62 proteins.Over-expression and inhibition of HO-1 were found to effectively regu-late the expressions of Atg5,LC3Ⅱ and p62 induced by M.abs.LysoTracker Red,colony count,and ELISA results demonstrated that SnPP promoted the increasement of intracellular lysosomes,significantly inhibited M.abs intracellular proliferation,and reduced TNF-α secretion.Conclusion:Inhibition of HO-1 can enhance the autophagy flow induced by M.abs and reduce the intracellular growth of M.abs,which provides scientific basis for the development of targeted drugs targeting HO-1.

Iron is involved in several activities in the brain, including energy metabolism, neurotransmitter transmission, and myelination. Disorder of peripheral iron metabolism and excessive iron accumulation in the brain can reduce cognitive and behavioral ability through pathological mechanisms such as inflammatory response and abnormal protein expression, leading to cognitive disorders. Quantitative susceptibility mapping (QSM), as a new non-invasive magnetic resonance technique, can quantitatively measure brain iron deposition, clarify the relationship between cognitive disorders and iron homeostasis imbalance, and provide a basis for clinical diagnosis and treatment of the diseases. This article reviews the latest research progress of QSM in brain iron deposition associated with cognitive disorders.

Objective To investigate the sequencing results of the SLC26A4 gene in 34 nuclear families and the genetic diagnosis on the offspring in the nuclear families who have been screened for SLC26A4 gene single-allele mutation in the deafness genetic screening,to provide a basis for genetic consulting.Methods A retrospective anal-ysis was performed on the results of SLC26A4 gene testing in 34 nuclear families,in which the offspring with SLC26A4 gene single-allele mutation in deafness genetic screening of each nuclear family.The offspring of 34 nucle-ar families with the second mutation site detected by sequencing,their audiological results were included in the anal-ysis;and if they suffered from hearing loss,the results of temporal bone CT or inner ear MRI were also included in the analysis.Results The sequencing results of 34 nuclear families showed that there were 23 offsprings(67.65％,23/34)with SLC26A4 gene single-allele mutation,and one parent was SLC26A4 gene single-allele mutation.There were 11 offsprings(32.35％,11/34)with second site,among which 7 offsprings(63.64％,7/11)with SLC26A4 gene complex heterozygous mutations,and their parents were SLC26A4 gene single-allele mutations.Among the 7 offsprings with SLC26A4 gene complex heterozygous mutation,3 cases were with hearing loss,all of which were diagnosed as large vestibular aqueduct syndrome,and the other 4 cases were normal.While 4 offsprings(36.36％,4/11)with SLC26A4 gene double heterozygous mutation(cis mutation),and one parent was SLC26A4 gene double heterozygous mutation.The hearing 4 offsprings with SLC26A4 gene double heterozygous mutations were normal.Among the 34 nuclear families,3 pairs of parents were SLC26A4 gene single-allele mutation,and both mutation sites were pathogenic,risk of reproducing children with hereditary hearing loss was 25％.Conclusion The detec-tion sites of deafness gene chip are limited.Using gene sequencing technology to sequence the nuclear family can fur-ther clarify the gene mutation type in offspring and provide guidance for parents to reproduce.

Objective:To investigate the role of heme oxygenase-1(HO-1)regulating autophagy and its impact on the intracel-lular growth of Mycobacterium abscessus(M.abs).Methods:The standard strain of M.abs ATCC19977 was used to stimulate mouse RAW264.7 macrophages with a specified multiple of infection(MOI)for a specified time.Western blot analysis was performed to detect the expression levels of HO-1 protein and autophagy related proteins Atg5,LC3Ⅱ and p62.Macrophages were pretreated with HO-1 specific inducer CoPP and enzyme activity inhibitor SnPP for 12 h,and incubated with M.abs for 2 h.Amikacin removed extra-cellular bacteria and continued to culture until the specified time,and cell activity was detected by CCK-8 method.Western blot and LysoTracker Red were used to detect the regulatory relationship between HO-1 protein and autophagy related proteins.Bacterial survival and TNF-α secretion levels were detected by colony count and ELISA.Results:Compared with the control group,M.abs could induce increased expression of HO-1,Atg5,LC3Ⅱ and p62 proteins.Over-expression and inhibition of HO-1 were found to effectively regu-late the expressions of Atg5,LC3Ⅱ and p62 induced by M.abs.LysoTracker Red,colony count,and ELISA results demonstrated that SnPP promoted the increasement of intracellular lysosomes,significantly inhibited M.abs intracellular proliferation,and reduced TNF-α secretion.Conclusion:Inhibition of HO-1 can enhance the autophagy flow induced by M.abs and reduce the intracellular growth of M.abs,which provides scientific basis for the development of targeted drugs targeting HO-1.

F-FDG PET/CT is an ideal auxiliary tool for early and accurate diagnosis of malignant tumors in children.This guideline aimed to standardize 18F-FDG PET/CT examination process for malignant tumors in children,hence providing references for nuclear medicine professionals.

Objective:To understand the incidence of adverse pregnancy outcome in HIV-infected pregnant women and influencing factors in China and provide reference for the improvement of the health status of HIV-infected pregnant women and their newborns.Methods:Based on a mother-child cohort of HIV-infected pregnant women and children (PMTCT-MC-2005) established in Guangxi Zhuang Autonomous Region, Yunnan Province and Xinjiang Uygur Autonomous Region, this study enrolled pregnant women with or without HIV infection as study subjects from January 2017 to June 2023, a total of 1 646 pregnant women (558 HIV-infected and 1 088 HIV-uninfected) were included, and 34 cases with missing data were excluded. The χ2 test was used to analyze the difference in the incidence adverse pregnancy outcome between two groups, and used logistic regression model to identify the influencing factors of adverse pregnancy outcome in HIV-infected pregnant women. Results:A total of 1 612 pregnant women were included in the study, in whom 541 were infected with HIV and 1 071 were not infected with HIV. The incidence of adverse pregnancy outcome was 18.8% (303/1 612), the incidence of adverse pregnancy outcome was 33.1% (179/541) in the HIV-infected pregnant women and 11.6% (124/1 071) in the pregnant women without HIV infection. The results of multivariable logistic regression analysis showed that the influencing factors of adverse pregnancy outcome were age <35 years at delivery (a OR=0.64, 95% CI: 0.43-0.95) compared with the age ≥35 years and the duration of antiviral treatment over 10 years (a OR=0.43, 95% CI: 0.23-0.79) compared with less than one year. Conclusions:The incidence of adverse pregnancy outcome in HIV-infected pregnant women was high in some regions of China during 2017-2023. It is necessary for HIV-infected women to get pregnancy at appropriate time based on antiretroviral treatment effect and strengthen self-care to reduce the incidence of adverse pregnancy outcome.