OBJECTIVE To investigate the mechanism by which aloin （ALO） ameliorates atherosclerosis （AS）. METHODS Eight C57BL/6J mice were assigned to the control group （CON group） and fed a standard diet； thirty-two apolipoprotein E-knockout （APOE－/－） mice were randomly divided into model group （MOD group）， ALO low-dose and high-dose groups [ALO-L group， ALO-H group， 20， 40 mg/（kg·d）]， and atorvastatin positive control group [ATO group， 4 mg/（kg·d）]， with 8 mice in each group， establishing the AS model through feeding with a high-fat diet. The mice were administered the drug via gavage or given an equal volume of deionized water for 8 consecutive weeks. The lipid levels in the serum of mice were measured， and the pathological structural changes in their aortas were observed. The expressions of macrophage polarization markers （CD86+ ， CD206+） in the aorta were determined， along with the mRNA expressions of inducible nitric oxide synthase （iNOS）， tumor necrosis factor-α （TNF-α）， arginase-1 （Arg-1）， and interleukin-10 （IL-10）， as well as the protein expressions of iNOS and Arg- 1， and the phosphorylation levels of nuclear factor κB p65 （NF-κB p65） and signal transduction and activator of transcription 3 （STAT3） proteins. Additionally， a macrophage polarization model was established using lipopolysaccharide （LPS）-induced RAW264.7 cells， and the effect of ALO （400 μmol/L） on the cellular polarization phenotype was investigated. RESULTS Compared with the MOD group， administration groups all showed significant improvement in dyslipidemia （except for high-density lipoprotein cholesterol in the serum of ALO-L group） （P＜0.05）； aortic intimal structure improved significantly， plaque area was reduced significantly （P＜0.01）； the CD86+ relative fluorescence intensity in the aorta decreased significantly， the CD206+relative fluorescence intensity increased significantly （P＜0.01）， while the expressions of iNOS and TNF-α mRNA were down-regulated significantly （P＜0.05）； mRNA expressions of Arg-1 and IL-10， and protein expression of Arg-1 were increased significantly in ALO-H group and ATO group （P＜0.05）； the protein expressions of iNOS， and the phosphorylation levels of NF-κB p65 and STAT3 protein were decreased significantly （P＜0.05）. In vitro experiments further confirmed that ALO significantly reduced the proportion of LPS-induced M1-type macrophages but increased the proportion of M2-type macrophages （P＜0.01）. CONCLUSIONS ALO inhibits M1-type macrophage polarization and promotes M2-type polarization， ameliorates dyslipidemia and reduces arterial plaque formation in AS model mice， improve the structure of the aortic intima potentially through suppression of the NF-κB/STAT3 signaling pathway.

Objective:To investigate the clinical, phenotypic and genotypic features of hereditary hyperhomocysteinemia mainly involving the nervous system.Methods:The clinical data, physical examination, imaging results, blood-urine tandem mass spectrometry analysis and genetic results of 8 patients with hyperhomocysteinemia from the Department of Neurology of the Shanghai Sixth People′s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine from September 2020 to December 2023 were collected, and the clinical, genetic features and pathogenic mechanisms of these patients were summarized and analyzed.Results:Among all the 8 patients (male∶female=5∶3), the age of onset was 7 to 74 (40.4±7.4) years. Seven had adult-onset and 1 had juvenile-onset, with various types of onset symptoms, including progressive stiffness in lower limbs and walking difficulty, limb numbness, tremor, mental and behavioral abnormalities, cerebrovascular events, etc. Moderate to severe hyperhomocysteine (38.4-190.6 μmol/L) was present in all patients at first diagnosis. Among the 5 patients with cranial imaging examinations, all had white matter lesions. The genetic testing showed 7 patients with MTHFR gene pathogenic mutations (1 case with c.416C>T, and 6 cases with c.665C>T), and 1 patient with MMACHC gene pathogenic mutation (c.482G>A). Conclusions:Hereditary hyperhomocysteinemia is a metabolic disease, with complicated manifestations, varying degrees of severity, and diverse pathogenic genes. The cases with neurological involvement are not rare, such as spastic paraplegia-like manifestations, tremor, peripheral neuropathy, mental and behavioral abnormalities, cerebrovascular events.

Objective: To investigate the iodine nutrition status of children aged 8-10 in Guangming, Longhua and Yantian District of Shenzhen in 2023, and to explore the influencing factors of thyroid volume. To evaluate prevention strategies and to provide a scientific basis for the elimination of iodine deficiency disorders. Methods: Urine and household salt samples were randomly collected from 580 non-boarding students aged 8-10 years foriodine content detection. Thyroid volume was measured using a fully digital ultrasound imaging system, and goiter prevalence was calculated. Results: A total of 580 samples was tested. The median salt iodine concentration was 23.86 mg/kg, with 93.62% qualified iodized salt and 94.48% coverage rate. The median of urinary iodine was 265.00 μg/L, mainly distributed between 200 - < 300 μg/L and ≥300 μg/L. The proportion of children with ap⁃ propriate iodine was 20. 86% , and the proportion of children with insufficient or excessive urinary iodine levels was 10. 86% and 68. 28% of the total surveyed population , respectively. The median thyroid volume was 3. 27 mL , and the goiter rate was 1. 72% . Multiple linear regression analysis showed that age was the risk factor for thyroid volume (8=0 328, P<0.05). while urinary iodine was the protective factor for thyroid volume(B=-4.134x10-4,P<0.05). Conclusion The qualified iodized salt rate, median of urinary iodine,and goiter prevalence of 580 children aged 8 - 10 meet the elimination criteria for iodine deficiency disorders. Age and urinary iodine are closely related to thyroid volume change. The urinary iodine level of children is generally high and requires serious attention.

Objective:To investigate the clinical, phenotypic and genotypic features of hereditary hyperhomocysteinemia mainly involving the nervous system.Methods:The clinical data, physical examination, imaging results, blood-urine tandem mass spectrometry analysis and genetic results of 8 patients with hyperhomocysteinemia from the Department of Neurology of the Shanghai Sixth People′s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine from September 2020 to December 2023 were collected, and the clinical, genetic features and pathogenic mechanisms of these patients were summarized and analyzed.Results:Among all the 8 patients (male∶female=5∶3), the age of onset was 7 to 74 (40.4±7.4) years. Seven had adult-onset and 1 had juvenile-onset, with various types of onset symptoms, including progressive stiffness in lower limbs and walking difficulty, limb numbness, tremor, mental and behavioral abnormalities, cerebrovascular events, etc. Moderate to severe hyperhomocysteine (38.4-190.6 μmol/L) was present in all patients at first diagnosis. Among the 5 patients with cranial imaging examinations, all had white matter lesions. The genetic testing showed 7 patients with MTHFR gene pathogenic mutations (1 case with c.416C>T, and 6 cases with c.665C>T), and 1 patient with MMACHC gene pathogenic mutation (c.482G>A). Conclusions:Hereditary hyperhomocysteinemia is a metabolic disease, with complicated manifestations, varying degrees of severity, and diverse pathogenic genes. The cases with neurological involvement are not rare, such as spastic paraplegia-like manifestations, tremor, peripheral neuropathy, mental and behavioral abnormalities, cerebrovascular events.