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Objective: By meticulously tracking the evolving growth, development, and nutritional status of primary and secondary school students in Qiongzhong County from 2014 to 2021 post-implementation of the "Nutrition Improvement Program for Rural Compulsory Education Students"(NIPRCES, This project provides a supplementary food allowance of at least ￥4 per person per day for primary and secondary school students. The project area undergoes annual routine monitoring.), this study aims to offer a scientific basis for enhancing and promoting the project. Through thorough monitoring of students' nutritional status changes influenced by this program, we strive to establish a comprehensive and evidence-based framework for its future advancement. Methods: From 2014 to 2021, this study employed a multi-stage sampling method utilizing cluster sampling to select six primary and six secondary schools in Qiongzhong County, Hainan Province. Data on the growth and development of respondents were collected. This cohort was a dynamic cohort with a total of 18,762 final data recovered. The prevalence of malnutrition was evaluated using the Cochran Armitage Trend Test (CATT) to assess year-to-year changes. Furthermore, height/weight and the prevalence of malnutrition between groups were compared using the t-test, χ2 test, and Bonferroni's corrected analysis. Results: The average height of both boys and girls has increased. In 2021, boys and girls of all ages showed an average height increase of 2.31 cm and 1.98 cm, respectively, compared to 2014. Nevertheless, the growth and development levels, and rate of improvement of these students remain comparatively lower than their rural counterparts across China, who are of the same age. From 2014 to 2021, the prevalence of undernutrition (mainly wasting) showed a significant downward trend (P < 0.05) from 29.30% to 22.19%, and the prevalence of overnutrition showed an upward trend (both P < 0.05). The prevalence of undernutrition was higher among boys, students in grades 1–3 and those of Li nationality. Meanwhile, the prevalence of overnutrition was higher among boys, students in grades 1–3 and those of Han nationality. Conclusions: Over the 8-year period of NIPRCES, there has been progress in the growth and development of students, yet levels still lag behind the national average for rural students of the same age. While malnutrition prevalence have decreased, they remain high, with a concerning rise in overnutrition prevalence. Undernutrition and overweight/obesity are more prevalent among boys and younger students. Li students show higher prevalence of undernutrition, while overnutrition is a growing issue among Han students. Simultaneously, local education and health care departments must acknowledge the disparities in growth and nutritional status among primary and secondary school students residing in rural areas within the tropics and those in rural areas across the entire nation. Nutritional improvement measures should be tailored to local conditions. [ABSTRACT FROM AUTHOR]

Sjogren's syndrome (SS) is a complex systemic autoimmune disease. This study aims to elucidate a humanized NOD-PrkdcscidIl2rgem1/Smoc (NSG) murine model to better clarify the pathogenesis of SS. NSG female mice were adoptively transferred with 10 million peripheral blood mononuclear cells (PBMCs) through the tail vein from healthy controls (HCs), primary Sjogren's syndrome (pSS), and systemic lupus erythematosus (SLE) patients on D0. The mice were subcutaneously injected with C57/B6j submandibular gland (SG) protein or phosphate-buffered saline on D3, D17 and D31, respectively. NSG mice were successfully transplanted with human PBMCs. Compared with NSG-HC group, NSG-pSS and NSG-SLE mice exhibited a large number of lymphocytes infiltration in the SG, decreased salivary flow rate, lung involvement, decreased expression of genes related to salivary secretion, and the production of autoantibodies. Type I interferon-related genes were increased in the SG of NSG-pSS and NSG-SLE mice. The ratio of BAX/BCL2, BAX, cleaved caspase3, and TUNEL staining were increased in the SG of NSG-pSS and NSG-SLE mice. The expressions of p-MLKL and p-RIPK3 were increased in the SG of NSG-pSS and NSG-SLE mice. Increased expression of type I interferon-related genes, PANoptosis (apoptosis and necroptosis) were identified in the SG of this typical humanized NSG murine model of SS. [ABSTRACT FROM AUTHOR]

Aims: HNF1B syndrome is caused by defects in the hepatocyte nuclear factor 1B (HNF1B) gene, which leads to maturity‐onset diabetes of the young type 5 and congenital organ malformations. This study aimed to identify a gene defect in a patient presenting with diabetes and severe diarrhea, while also analyzing the prevalence of hypomagnesemia and its correlation with the HNF1B genotype. Materials and Methods: Whole exome sequencing was used to identify responsible point mutations and small indels in the proband and their family members. Multiplex ligation‐dependent probe amplification was carried out to identify HNF1B deletions. Furthermore, an analysis of published data on 539 cumulative HNF1B cases, from 29 literature sources, was carried out to determine the correlation between the HNF1B genotype and the phenotype of serum magnesium status. Results: Using multiplex ligation‐dependent probe amplification, we identified a de novo heterozygous HNF1B deletion in the patient, who showed dorsal pancreas agenesis and multiple kidney cysts, as detected by magnetic resonance imaging. Magnesium supplementation effectively alleviated the symptoms of diarrhea. Hypomagnesemia was highly prevalent in 192 out of 354 (54.2%) patients with HNF1B syndrome. Compared with patients with intragenic mutations, those with HNF1B deletions were more likely to suffer from hypomagnesemia, with an odds ratio of 3.1 (95% confidence interval 1.8–5.4). Conclusions: Hypomagnesemia is highly prevalent in individuals with HNF1B syndrome, and those with HNF1B deletion are more susceptible to developing hypomagnesemia compared with those with intragenic mutations. The genotype–phenotype associations in HNF1B syndrome have significant implications for endocrinologists in terms of genotype detection, treatment decisions and prognosis assessment. [ABSTRACT FROM AUTHOR]