Modern Western pediatric translated works encompassed extensive neonatal knowledge, serving as critical vehicles for the early dissemination and development of neonatology in China. The translation and circulation of foreign pediatric monographs, such as Essentials of Pediatrics, Pediatrics Synopsis, Newly Compiled Pediatrics, and The Diseases of Infancy and Childhood, played pivotal roles in this process. Key aspects of Western neonatal knowledge included scientific understanding of neonatal physiology and diseases, systematic development of neonatal care practices, and modernization of infant feeding models. The introduction of this knowledge laid the foundation for the emergence of modern neonatology in China. By examining the evolutionary trajectory of neonatal knowledge in these translated works, we gain deeper insights into the sociocultural context and developmental milestones of neonatology in China.

Modern Western pediatric translated works encompassed extensive neonatal knowledge, serving as critical vehicles for the early dissemination and development of neonatology in China. The translation and circulation of foreign pediatric monographs, such as Essentials of Pediatrics, Pediatrics Synopsis, Newly Compiled Pediatrics, and The Diseases of Infancy and Childhood, played pivotal roles in this process. Key aspects of Western neonatal knowledge included scientific understanding of neonatal physiology and diseases, systematic development of neonatal care practices, and modernization of infant feeding models. The introduction of this knowledge laid the foundation for the emergence of modern neonatology in China. By examining the evolutionary trajectory of neonatal knowledge in these translated works, we gain deeper insights into the sociocultural context and developmental milestones of neonatology in China.

Objective To investigate the expression of inflammatory factors and brain-derived neurotro-phic factor(BDNF)in the brain hippocampus of Alzheimer's disease(AD)-like mice caused by amyloid β-protein 25-35(Aβ25-35).Methods A total of 40 six-week-old male Kunming mice were taken to construct an AD-like mouse model using bilateral ventricular injection of Aβ25-35,and were divided into the 0 d,7 d,14 d,and 28 d groups for observation,with 10 mice in each group.The Y-maze and new object recognition assay were used to test the learning and memory functions of the mice.The hematoxylin-eosin(HE)staining was used to observe the neuronal damage in the hippocampal region.Immunohistochemical staining was used to detect the expression levels of phosphorylated-tau(p-tau),CD11b and BDNF in hippocampus.ELISA was used to detect the expression levels of inflammatory factors in hippocampus,including interleukin-1β(IL-1β)and tumor necrosis factor-α(TNF)-α,and real-time quantitative reverse transcription PCR(RT-qPCR)and Western blot were used to detect the mRNA and protein expression levels of BDNF.Results Aβ25-35 could impair memory and cognitive function in the mice.Compared with the 0 d group,the neuron number in the hippocampal tissue of mice in the 14 d and 28 d groups was significantly reduced(P<0.05),and the optical density values of p-Tau and CD11b,and expression levels of IL-1β and TNF-α in the hippocampal region of mice in the 14 d and 28 d groups were significantly increased(P<0.05).In addition,compared with the 0 d group,the relative expression levels of BDNF mRNA and protein in the hippocampal tissue of mice were sig-nificantly increased in the 7 d group(P<0.05),while the relative expression levels of BDNF mRNA and pro-tein were significantly decreased in the 14 d and 28 d groups(P<0.05).Conclusion Aβ25-35 may increase the expression of TNF-α,IL-1β and p-tau in hippocampal tissue by activating microglia,which in turn impaired the memory and cognitive functions of mice,and the expression level of BDNF in hippocampal tissue showed a first increase and then a decrease in the injury period.