Mitocytosis, a migrasome-mediated mitochondrial quality-control process.

Damaged mitochondria need to be cleared to maintain the quality of the mitochondrial pool. Here, we report mitocytosis, a migrasome-mediated mitochondrial quality-control process. We found that, upon exposure to mild mitochondrial stresses, damaged mitochondria are transported into migrasomes and subsequently disposed of from migrating cells. Mechanistically, mitocytosis requires positioning of damaged mitochondria at the cell periphery, which occurs because damaged mitochondria avoid binding to inward motor proteins. Functionally, mitocytosis plays an important role in maintaining mitochondrial quality. Enhanced mitocytosis protects cells from mitochondrial stressor-induced loss of mitochondrial membrane potential (MMP) and mitochondrial respiration; conversely, blocking mitocytosis causes loss of MMP and mitochondrial respiration under normal conditions. Physiologically, we demonstrate that mitocytosis is required for maintaining MMP and viability in neutrophils in vivo. We propose that mitocytosis is an important mitochondrial quality-control process in migrating cells, which couples mitochondrial homeostasis with cell migration.

PDCdb: the biological activity and pharmaceutical information of peptide-drug conjugate (PDC).

Peptide-drug conjugates (PDCs) have emerged as a promising class of targeted therapeutics with substantial pharmaceutical advantages and market potentials, which is a combination of a peptide (selective to the disease-relevant target), a linker (stable in circulation but cleavable at target site) and a cytotoxic/radioactive drug (efficacious/traceable for disease). Among existing PDCs, those based on radiopharmaceuticals (a.k.a. radioactive drugs) are valued due to their accurate imaging and targeted destruction of disease sites. It's demanded to accumulate the biological activity and pharmaceutical information of PDCs. Herein, a database PDCdb was thus constructed to systematically describe these valuable data. Particularly, biological activities for 2036 PDCs were retrieved from literatures, which resulted in 1684, 613 and 2753 activity data generated based on clinical trial, animal model and cell line, respectively. Furthermore, the pharmaceutical information for all 2036 PDCs was collected, which gave the diverse data of (a) ADME property, plasma half-life and administration approach of a PDC and (b) chemical modification, primary target, mode of action, conjugating feature of the constituent peptide/linker/drug. In sum, PDCdb systematically provided the biological activities and pharmaceutical information for the most comprehensive list of PDCs among the available databases, which was expected to attract broad interest from related communities and could be freely accessible at: https://idrblab.org/PDCdb/.

Ablation of CD44 attenuates adipogenesis in white adipocytes via the TPH2/5-HT axis to protect mice from high-fat diet induced obesity.

CD44 is a transmembrane protein that plays an essential role in transducing extracellular stimuli into intracellular signaling cascades especially in cancer cells. Recent studies have shown that CD44 contributes to metabolic regulation. However, the effect of CD44 on adipogenesis in white adipose tissue (WAT) remains unclear. Here, the results showed that the expression of CD44 was largely increased in the inguinal and epididymal WAT of obese mice. Ablation or neutralization of CD44 inhibits adipogenesis in cultured adipocytes. CD44 deficient mice are resistant to high-fat diet (HFD) induced obesity and metabolic dysfunction. RNA-seq, together with functional studies, revealed that reduced expression of tryptophan 5-hydroxylase 2 (Tph2) in WAT is responsible for the repressed adipogenesis in the absence of CD44. The application of 5-hydroxytryptamine (5-HT), a product of TPH2, rescues the repressed adipogenesis induced by CD44 neutralization. Moreover, the inhibition of TPH2 by p-chlorophenylalanine (pCPA) recapitulates the beneficial phenotypes observed in CD44 deficient mice. Taken together, these data indicate that CD44 plays a pivotal role in adipogenesis in WAT. In this regard, CD44 and its downstream target TPH2 may hold great therapeutic potential for treating excessive adiposity-related metabolic disorders such as obesity, insulin resistance, and type 2 diabetes.

Recapitulating familial hypercholesterolemia in a mouse model by knock-in patient-specific LDLR mutation.

Familial hypercholesterolemia (FH) is one of the most prevalent monogenetic disorders leading to cardiovascular disease (CVD) worldwide. Mutations in Ldlr, encoding a membrane-spanning protein, account for the majority of FH cases. No effective and safe clinical treatments are available for FH. Adenine base editor (ABE)-mediated molecular therapy is a promising therapeutic strategy to treat genetic diseases caused by point mutations, with evidence of successful treatment in mouse disease models. However, due to the differences in the genomes between mice and humans, ABE with specific sgRNA, a key gene correction component, cannot be directly used to treat FH patients. Thus, we generated a knock-in mouse model harboring the partial patient-specific fragment and including the Ldlr W490X mutation. LdlrW490X/W490X mice recapitulated cholesterol metabolic disorder and clinical manifestations of atherosclerosis associated with FH patients, including high plasma low-density lipoprotein cholesterol levels and lipid deposition in aortic vessels. Additionally, we showed that the mutant Ldlr gene could be repaired using ABE with the cellular model. Taken together, these results pave the way for ABE-mediated molecular therapy for FH.

Cold-inducible lncRNA266 promotes browning and the thermogenic program in white adipose tissue.

Cold-induced nonshivering thermogenesis has contributed to the improvement of several metabolic syndromes caused by obesity. Several long noncoding RNAs (lncRNAs) have been shown to play a role in brown fat biogenesis and thermogenesis. Here we show that the lncRNA lnc266 is induced by cold exposure in inguinal white adipose tissue (iWAT). In vitro functional studies reveal that lnc266 promotes brown adipocyte differentiation and thermogenic gene expression. At room temperature, lnc266 has no effects on white fat browning and systemic energy consumption. However, in a cold environment, lnc266 promotes white fat browning and thermogenic gene expression in obese mice. Moreover, lnc266 increases core body temperature and reduces body weight gain. Mechanistically, lnc266 does not directly regulate Ucp1 expression. Instead, lnc266 sponges miR-16-1-3p and thus abolishes the repression of miR-16-1-3p on Ucp1 expression. As a result, lnc266 promotes preadipocyte differentiation toward brown-like adipocytes and stimulates thermogenic gene expression. Overall, lnc266 is a cold-inducible lncRNA in iWAT, with a key role in white fat browning and the thermogenic program.

Overexpression of DUSP26 gene suppressed the proliferation, migration, and invasion of human prostate cancer cells.

Prostate cancer (PCa) is threatening the health of millions of people, the pathological mechanism of prostate cancer has not been fully elaborated, and needs to be further explored. Here, we found that the expression of DUSP26 is dramatically suppressed, and a positive connection of its expression with PCa prognosis was also observed. In vitro, overexpression of DUSP26 significantly inhibited the proliferative, migrative, and invasive capacities of PC3 cells, DUSP26 silencing presented opposite results. Tumor formation experiments in subcutaneous nude mice demonstrated that DUSP26 overexpression could significantly suppress PC3 growth in vivo. Moreover, the mechanism of DUSP26 gene and PCa was discovered by RNA-Seq analysis. We found that DUSP26 significantly inhibited MAPK signaling pathway activation, and further experiments displayed that DUSP26 could impair TAK1, p38, and JNK phosphorylation. Interestingly, treatment with the TAK1 inhibitor (iTAK1) attenuated the effect of DUSP26 on PC3 cells. Together, these results suggested that DUSP26 may serve as a novel therapeutic target for PC3 cell type PCa, the underlying mechanism may be through TAK1-JNK/p38 signaling.

Oncogenic ß-catenin stimulation of AKT2-CAD-mediated pyrimidine synthesis is targetable vulnerability in liver cancer.

CTNNB1, encoding ß-catenin protein, is the most frequently altered proto-oncogene in hepatic neoplasms. In this study, we studied the significance and pathological mechanism of CTNNB1 gain-of-function mutations in hepatocarcinogenesis. Activated ß-catenin not only triggered hepatic tumorigenesis but also exacerbated Tp53 deletion or hepatitis B virus infection-mediated liver cancer development in mouse models. Using untargeted metabolomic profiling, we identified boosted de novo pyrimidine synthesis as the major metabolic aberration in ß-catenin mutant cell lines and livers. Oncogenic ß-catenin transcriptionally stimulated AKT2, which then phosphorylated the rate-limiting de novo pyrimidine synthesis enzyme CAD (carbamoyl-phosphate synthetase 2, aspartate transcarbamoylase, dihydroorotase) on S1406 and S1859 to potentiate nucleotide synthesis. Moreover, inhibition of ß-catenin/AKT2-stimulated pyrimidine synthesis axis preferentially repressed ß-catenin mutant cell proliferation and tumor formation. Therefore, ß-catenin active mutations are oncogenic in various preclinical liver cancer models. Stimulation of ß-catenin/AKT2/CAD signaling cascade on pyrimidine synthesis is an essential and druggable vulnerability for ß-catenin mutant liver cancer.

Targeting dysregulated lipid metabolism for the treatment of Alzheimer's disease and Parkinson's disease: Current advancements and future prospects.

Alzheimer's and Parkinson's diseases are two of the most frequent neurological diseases. The clinical features of AD are memory decline and cognitive dysfunction, while PD mainly manifests as motor dysfunction such as limb tremors, muscle rigidity abnormalities, and slow gait. Abnormalities in cholesterol, sphingolipid, and glycerophospholipid metabolism have been demonstrated to directly exacerbate the progression of AD by stimulating Aß deposition and tau protein tangles. Indirectly, abnormal lipids can increase the burden on brain vasculature, induce insulin resistance, and affect the structure of neuronal cell membranes. Abnormal lipid metabolism leads to PD through inducing accumulation of α-syn, dysfunction of mitochondria and endoplasmic reticulum, and ferroptosis. Great progress has been made in targeting lipid metabolism abnormalities for the treatment of AD and PD in recent years, like metformin, insulin, peroxisome proliferator-activated receptors (PPARs) agonists, and monoclonal antibodies targeting apolipoprotein E (ApoE). This review comprehensively summarizes the involvement of dysregulated lipid metabolism in the pathogenesis of AD and PD, the application of Lipid Monitoring, and emerging lipid regulatory drug targets. A better understanding of the lipidological bases of AD and PD may pave the way for developing effective prevention and treatment methods for neurodegenerative disorders.

A bibliometric analysis of m6A methylation in viral infection from 2000 to 2022.

BACKGROUND: N6-methyladenosine (m6A) methylation has become an active research area in viral infection, while little bibliometric analysis has been performed. In this study, we aim to visualize hotspots and trends using bibliometric analysis to provide a comprehensive and objective overview of the current research dynamics in this field. METHODS: The data related to m6A methylation in viral infection were obtained through the Web of Science Core Collection form 2000 to 2022. To reduce bias, the literature search was conducted on December 1, 2022. Bibliometric and visual analyzes were performed using CiteSpace and Bibliometrix package. After screening, 319 qualified records were retrieved. RESULTS: These publications mainly came from 28 countries led by China and the United States (the US), with the US ranking highest in terms of total link strength.The most common keywords were m6A, COVID-19, epitranscriptomics, METTL3, hepatitis B virus, innate immunity and human immunodeficiency virus 1. The thematic map showed that METTL3, plant viruses, cancer progression and type I interferon (IFN-I) reflected a good development trend and might become a research hotspot in the future, while post-transcriptional modification, as an emerging or declining theme, might not develop well. CONCLUSIONS: In conclusion, m6A methylation in viral infection is an increasingly important topic in articles. METTL3, plant viruses, cancer progression and IFN-I may still be research hotspots and trends in the future.

The Amino Acid Homoarginine Inhibits Atherogenesis by Modulating T-Cell Function.

BACKGROUND: Amino acid metabolism is crucial for inflammatory processes during atherogenesis. The endogenous amino acid homoarginine is a robust biomarker for cardiovascular outcome and mortality with high levels being protective. However, the underlying mechanisms remain elusive. We investigated the effect of homoarginine supplementation on atherosclerotic plaque development with a particular focus on inflammation. METHODS: Female ApoE-deficient mice were supplemented with homoarginine (14 mg/L) in drinking water starting 2 weeks before and continuing throughout a 6-week period of Western-type diet feeding. Control mice received normal drinking water. Immunohistochemistry and flow cytometry were used for plaque- and immunological phenotyping. T cells were characterized using mass spectrometry-based proteomics, by functional in vitro approaches, for example, proliferation and migration/chemotaxis assays as well as by super-resolution microscopy. RESULTS: Homoarginine supplementation led to a 2-fold increase in circulating homoarginine concentrations. Homoarginine-treated mice exhibited reduced atherosclerosis in the aortic root and brachiocephalic trunk. A substantial decrease in CD3+ T cells in the atherosclerotic lesions suggested a T-cell-related effect of homoarginine supplementation, which was mainly attributed to CD4+ T cells. Macrophages, dendritic cells, and B cells were not affected. CD4+ T-cell proteomics and subsequent pathway analysis together with in vitro studies demonstrated that homoarginine profoundly modulated the spatial organization of the T-cell actin cytoskeleton and increased filopodia formation via inhibition of Myh9 (myosin heavy chain 9). Further mechanistic studies revealed an inhibition of T-cell proliferation as well as a striking impairment of the migratory capacities of T cells in response to relevant chemokines by homoarginine, all of which likely contribute to its atheroprotective effects. CONCLUSIONS: Our study unravels a novel mechanism by which the amino acid homoarginine reduces atherosclerosis, establishing that homoarginine modulates the T-cell cytoskeleton and thereby mitigates T-cell functions important during atherogenesis. These findings provide a molecular explanation for the beneficial effects of homoarginine in atherosclerotic cardiovascular disease.

Synthesis of 3,4,5-Trisubstituted 1,2,4-Triazoles via I2-Catalyzed Cycloaddition of Amidines with Hydrazones.

A general and practical method for the construction of various 3,4,5-trisubstituted 1,2,4-triazoles via I2-catalyzed cycloaddition of N-functionalized amidines with hydrazones is reported. This strategy features cheap and readily available catalyst and starting materials, broader substrate scope, and moderate-to-good yields. The mechanism study shows that the existence of hydrogen on the nitrogen of hydrazones is crucial for this transformation.

Community Assembly Processes of Deadwood Mycobiome in a Tropical Forest Revealed by Long-Read Third-Generation Sequencing.

Despite the importance of wood-inhabiting fungi on nutrient cycling and ecosystem functions, their ecology, especially related to their community assembly, is still highly unexplored. In this study, we analyzed the wood-inhabiting fungal richness, community composition, and phylogenetics using PacBio sequencing. Opposite to what has been expected that deterministic processes especially environmental filtering through wood-physicochemical properties controls the community assembly of wood-inhabiting fungal communities, here we showed that both deterministic and stochastic processes can highly contribute to the community assembly processes of wood-inhabiting fungi in this tropical forest. We demonstrated that the dynamics of stochastic and deterministic processes varied with wood decomposition stages. The initial stage was mainly governed by a deterministic process (homogenous selection), whereas the early and later decomposition stages were governed by the stochastic processes (ecological drift). Deterministic processes were highly contributed by wood physicochemical properties (especially macronutrients and hemicellulose) rather than soil physicochemical factors. We elucidated that fine-scale fungal-fungal interactions, especially the network topology, modularity, and keystone taxa of wood-inhabiting fungal communities, strongly differed in an initial and decomposing deadwood. This current study contributes to a better understanding of the ecological processes of wood-inhabiting fungi in tropical regions where the knowledge of wood-inhabiting fungi is highly limited.

MicroRNA miR-210 Modulates the Water Flea Daphnia magna Response to Cyanobacterial Toxicity.

As a key form of post-transcriptional regulation, microRNAs (miRNAs) regulate gene expression by binding to target mRNAs, leading to mRNA decay or translational repression. Recently, the role of miRNAs in the response of aquatic organisms to environmental stressors has emerged. Daphnia, widely distributed cladocerans, play a crucial role in aquatic ecosystems. Cyanobacterial blooms often cause Daphnia populations to decrease, thereby disrupting ecosystem functionality and water quality. However, the post-transcriptional mechanisms behind Daphnia's response to toxic cyanobacteria are insufficiently understood. This study investigated the role of miR-210, a multifunctional miRNA involved in stress response and toxicity pathways, and its target genes (MLH3, CDHR5, and HYOU1) in two Daphnia magna clones exposed to toxic Microcystis aeruginosa. Results showed that M. aeruginosa inhibited somatic growth rates, led to microcystin accumulation, caused abnormal ultrastructural alterations in the digestive tract, and induced DNA damage in both clones. Notably, exposure significantly increased miR-210 expression and decreased the expression of its target genes compared with the controls. We identified miR-210s regulation on clonal-tolerance variations in D. magna to M. aeruginosa, emphasizing miRNAs' contribution to adaptive responses. Our work uncovered a novel post-transcriptional mechanism of cyanobacterial impact on zooplankton and provided essential insights for assessing cyanobacterial toxicity risks.

Effective Detection of Cu(II) Ions Based on Carbon Dots@Exfoliated Layered Double Hydroxides Composites Fluorescence Probe.

A series of carbon dots@exfoliated layered double hydroxides (CDs@LDH) composites were hydrothermally fabricated by Mg/Al LDH and formamide. The results of FTIR, UV-vis, and XPS spectra in company with HRTEM images showed that crystalline nano CDs formed on the single layer of LDH by Mg-C bond. With the increase of solvothermal reaction time from 2 to 6 h, the band gap and the binding energy of aminic and graphitic N species of CDs@LDH composites decreased, whereas the crystallinity increased. The fluorescence peaks of CDs@LDH composites could be deconvoluted into short-wavelength (416 nm) and large-wavelength (443 nm) components by Gaussian function, and the fluorescence intensities of both components enhanced with the extension of the solvothermal reaction time. The simultaneous enhancements of fluorescence lifetime and quantum yield resulted from the relatively high electron density in graphitic nitrogen of CDs@LDH, whereas the reduction of nonradiative rate was due to the high crystallinity in the carbon core of CDs@LDH. A strong exciton-lattice interaction also has been validated based on the excitation and emission spectra of CDs@LDH, so the fluorescence emission of CDs@LDH composite was heavily related to its crystalline carbon core and nitrogen-containing groups. CDs@LDH with high nitrogen-containing exhibited a superior detection property for Cu2+ ion sensing with the linear range of 26.90 ~ 192.20 µM and a limit of detection of 0.1957 µM. The photo-induced electron transfer (PET) process dominated the fluorescence quenching of CDs@LDH by Cu2+ ion since the fluorescence lifetime decreased with the increase of Cu2+ ion concentration.

Genetically modified indigenous Pseudomonas aeruginosa drove bacterial community to change positively toward microbial enhanced oil recovery applications.

AIMS: Microbial enhanced oil recovery (MEOR) is cost-effective and eco-friendly for oil exploitation. Genetically modified biosurfactants-producing high-yield strains are promising for ex-situ MEOR. However, can they survive and produce biosurfactants in petroleum reservoirs for in-situ MEOR? What is their effect on the native bacterial community? METHODS AND RESULTS: A genetically modified indigenous biosurfactants-producing strain Pseudomonas aeruginosa PrhlAB was bioaugmented in simulated reservoir environments. Pseudomonas aeruginosa PrhlAB could stably colonize in simulated reservoirs. Biosurfactants (200 mg l-1) were produced in simulated reservoirs after bio-augmenting strain PrhlAB. The surface tension of fluid was reduced to 32.1 mN m-1. Crude oil was emulsified with an emulsification index of 60.1%. Bio-augmenting strain PrhlAB stimulated the MEOR-related microbial activities. Hydrocarbon-degrading bacteria and biosurfactants-producing bacteria were activated, while the hydrogen sulfide-producing bacteria were inhibited. Bio-augmenting P. aeruginosa PrhlAB reduced the diversity of bacterial community, and gradually simplified the species composition. Bacteria with oil displacement potential became dominant genera, such as Shewanella, Pseudomonas, and Arcobacter. CONCLUSIONS: Culture-based and sequence-based analyses reveal that genetically modified biosurfactants-producing strain P. aeruginosa PrhlAB are promising for in-situ MEOR as well.

Analytical strategies to identify multicomponent quality markers for commercial Hua-ju-hong using multidimensional chemical analysis.

Hua-ju-hong (HJH) is a Chinese medicinal material obtained from Citrus grandis 'Tomentosa' (CGT) and Citrus grandis (L.) Osbeck (CG) with various commercial specifications. It is known for relieving cough and dispelling phlegm. To reveal the quality marker for distinguishing the various HJH, 215 batches of commercial HJH were studied systematically using multidimensional chemical analysis. Ten major components were identified by high-performance liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry and quantified via high-performance liquid chromatography coupled with diode array detection. In this study, a rapid, efficient, and low-cost chromatographic method was established. Total coumarin-hemiterpene and total coumarin-monoterpene were first classified and analyzed in HJH. The result indicated that the main component, naringin, was not the quality marker for differentiating CGT from CG. For reflecting the unique medicinal and food value of HJH, coumarins should be the more potential quality markers. Flavonoids were the possible quality markers for distinguishing two growth stages of fruit-exocarp and young fruit. For the first time, two chemotypes of HJH were identified in CG. This study provides a convenient yet reliant chromatographic method and novel yet systematic strategies for overall quality control of commercial HJH.

The role of NLRP3 inflammasome in aging and age-related diseases.

The gradual aging of the global population has led to a surge in age-related diseases, which seriously threaten human health. Researchers are dedicated to understanding and coping with the complexities of aging, constantly uncovering the substances and mechanism related to aging like chronic low-grade inflammation. The NOD-like receptor protein 3 (NLRP3), a key regulator of the innate immune response, recognizes molecular patterns associated with pathogens and injury, initiating an intrinsic inflammatory immune response. Dysfunctional NLRP3 is linked to the onset of related diseases, particularly in the context of aging. Therefore, a profound comprehension of the regulatory mechanisms of the NLRP3 inflammasome in aging-related diseases holds the potential to enhance treatment strategies for these conditions. In this article, we review the significance of the NLRP3 inflammasome in the initiation and progression of diverse aging-related diseases. Furthermore, we explore preventive and therapeutic strategies for aging and related diseases by manipulating the NLRP3 inflammasome, along with its upstream and downstream mechanisms.

Reprogramming of lipid metabolism in the tumor microenvironment: a strategy for tumor immunotherapy.

Lipid metabolism in cancer cells has garnered increasing attention in recent decades. Cancer cells thrive in hypoxic conditions, nutrient deficiency, and oxidative stress and cannot be separated from alterations in lipid metabolism. Therefore, cancer cells exhibit increased lipid metabolism, lipid uptake, lipogenesis and storage to adapt to a progressively challenging environment, which contribute to their rapid growth. Lipids aid cancer cell activation. Cancer cells absorb lipids with the help of transporter and translocase proteins to obtain energy. Abnormal levels of a series of lipid synthases contribute to the over-accumulation of lipids in the tumor microenvironment (TME). Lipid reprogramming plays an essential role in the TME. Lipids are closely linked to several immune cells and their phenotypic transformation. The reprogramming of tumor lipid metabolism further promotes immunosuppression, which leads to immune escape. This event significantly affects the progression, treatment, recurrence, and metastasis of cancer. Therefore, the present review describes alterations in the lipid metabolism of immune cells in the TME and examines the connection between lipid metabolism and immunotherapy.

Application of 'CDC- Public Security Bureau-NGO' Joint Prevention and Control Mechanism Allied AIDS prevention and control in Guigang, Guangxi.

BACKGROUND: HIV/AIDS has emerged as a nationwide epidemic and has taken the forefront position as the primary infectious killer of adults in China. The control and prevention of the disease have been hampered by a weak link in the form of heterosexual transmission. However, conventional intervention measures have demonstrated suboptimal efficacy in reducing the incidence of new HIV infections. In light of the current epidemiological characteristics, we have developed and executed an innovative intervention model known as the Joint Prevention and Control Mechanism of the 'CDC-Public Security Bureau-NGO'. The purpose of this research is to assess the impact of this model on the AIDS awareness, HIV infection rates, sexual behavior, and associated factors among female sex workers and elderly clients. Through the provision of robust evidence of the efficacy of this innovative model, we seek to advocate for its implementation in future interventions. METHODS: The research design of this study incorporates both a serial cross-sectional study and time-series analysis from 2014 to 2021, including a 4-year traditional intervention (2014-2017) and the 4-year 'CDC-Public Security Bureau-NGO' innovative intervention (2018-2021), was conducted to evaluate the effects of the new intervention. The GM(1, 1) model was performed to predict the proportion of HIV infection without implementing the innovative intervention in 2018-2021; P and C values were used to evaluate the performance of the model. Mann-Kendall test and descriptive methods were used to analyzed the trend of traditional and innovative interventions models on HIV positive detection rate in FSWs and elderly clients. RESULTS: The condom usage rates during the last commercial sexual encounter for FSWs and elderly clients improved from 74.9% and 9.1%, respectively, to 96.9% and 28.1%. (P < 0.05), newly reported cases of HIV have decreased by 15.56% yearly and the HIV positive detection rate among middle-aged and elderly people has dropped by 14.47%. The innovative intervention model has significantly reduced the HIV infection rates. CONCLUSIONS: The 'CDC-Public Security Bureau-NGO' innovative intervention has achieved beneficial effects on HIV/AIDS prevention and control and provides a good reference for Guangxi, China.

Nutritional improvement status of primary and secondary school students in the pilot nutrition improvement areas of Hainan, China from 2014 to 2021.

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 ï¿¥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.