Myopia has evolved into a global public health concern, highlighting the critical importance of myopia prevention and control. This paper elaborates on the pathogenetic mechanisms of myopia and relevant therapeutic interventions, with a focused discussion on the action mechanisms and research advances of low-dose atropine combined with other interventional measures for myopia control. By comparing the advantages and limitations of such combined regimens, this review aims to provide scientific and safe strategies for myopia prevention and management.

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder worldwide, causing dementia and affecting millions of individuals. One prominent characteristic in the brains of AD patients is glucose hypometabolism. In the context of galactose metabolism, intracellular glucose levels are heightened. Galactose mutarotase (GALM) plays a crucial role in maintaining normal galactose metabolism by catalyzing the conversion of β-D-galactose into α-D-galactose (α-D-G). The latter is then converted into glucose-6-phosphate, improving glucose metabolism levels. However, the involvement of GALM in AD progression is still unclear. In the present study, we found that the expression of GALM was significantly increased in AD patients and model mice. Genetic knockdown of GALM using adeno-associated virus did not change the expression of amyloid precursor protein (APP) and APP-cleaving enzymes including a disintegrin and metalloprotease 10 (ADAM10), β-site APP-cleaving enzyme 1 (BACE1), and presenilin-1 (PS1). Interestingly, genetic overexpression of GALM reduced APP and Aβ deposition by increasing the maturation of ADAM10, although it did not alter the expression of BACE1 and PS1. Further electrophysiological and behavioral experiments showed that GALM overexpression significantly ameliorated the deficits in hippocampal CA1 long-term potentiation (LTP) and spatial learning and memory in AD model mice. Importantly, direct α-D-G (20 mg/kg, i.p.) also inhibited Aβ deposition by increasing the maturation of ADAM10, thereby improving hippocampal CA1 LTP and spatial learning and memory in AD model mice. Taken together, our results indicate that GALM shifts APP processing towards α-cleavage, preventing Aβ generation by increasing the level of mature ADAM10. These findings indicate that GALM may be a potential therapeutic target for AD, and α-D-G has the potential to be used as a dietary supplement for the prevention and treatment of AD.
Animals ; ADAM10 Protein/metabolism* ; Alzheimer Disease/pathology* ; Amyloid Precursor Protein Secretases/metabolism* ; Disease Models, Animal ; Humans ; Mice ; Amyloid beta-Peptides/metabolism* ; Male ; Mice, Transgenic ; Membrane Proteins/metabolism* ; Cognitive Dysfunction/pathology* ; Mice, Inbred C57BL ; Amyloid beta-Protein Precursor/metabolism* ; Female ; Hippocampus/metabolism* ; Long-Term Potentiation/physiology*

Objective To improve the awareness of fetal cardiac rhabdomyomas (CRs) and investigate a better model for prenatal diagnosis and treatment through analyzing imaging findings and prognosis.Methods A retrospective study was conducted on 23 cases of CRs which were diagnosed by ultrasound in Obstetrics and Gynecology Hospital of Fudan University from January 2008 to November 2015.General conditions,imaging features,prognosis and follow-up data of the 23 cases were described.Results The average gestational age of the 23 fetuses at diagnosis was (29.8±4.1) (22.4-35.7) weeks.Seventeen out of the 23 gravidas received prenatal multidisciplinary consultation.Among all 23 gravidas,three (13％) were lost to follow-up,12 (52％) decided to terminate the pregnancy,and the other eight (35％) continued to term pregnancy and their babies were followed up for three years.Of these eight cases,two cases received prenatal brain MRI and no tuberous sclerosis complex (TSC) was detected,no CRs was identified during the follow-up,and their physical and mental developments were both normal.One case was diagnosed with suspected subependymal nodules by prenatal brain MRI in our hospital,but the MRI images was normal when scanned in the other hospital,and follow-up data revealed neither CRs nor abnormal physical and mental developments.Four cases did not received prenatal brain MRI,but the MRI images of neonatal brains indicated TSC,besides,follow-up data showed that seizures were observed,physical developments were all normal,but three of the four cases had mental retardation;CRs disappeared in only two of the four cases.One case had neither prenatal nor neonatal MRI,but follow-up data showed that CRs had disappeared and physical and mental developments were both normal.Conclusions Prenatal diagnosis of fetal tuberous sclerosis is crucial to the prognosis of CRs.Prenatal ultrasonography in combination with cranial MRI improves the accuracy of prenatal diagnosis of CRs complicated with TSC and assists in clinical decision-making and prognosis analysis.