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"Cheng, Dongmei"
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LAX1 as a core biomarker in Alzheimer’s disease and periodontitis via the STAT signaling pathway
Background
The relationship between Alzheimer’s disease (AD) and chronic periodontitis (PD) rarely share the medical spotlight, yet epidemiological mirroring hints at a common inflammatory root.
Methods
Mining four GEO (Gene Expression Omnibus) cohorts (211 AD + 27 controls; 24 PD + 23 controls), batch-corrected and validated by principal component analysis (PCA)/t-distributed stochastic neighbour embedding (t-SNE)/uniform manifold approximation and projection (UMAP), we identified 61 shared differentially expressed genes (DEGs) with lymphocyte transmembrane adaptor 1 (LAX1) ranked first in weighted gene co-expression network analysis (WGCNA), maximum clique centrality (MCC), Degree, edge percolated component (EPC) and Stress algorithms, tightly co-expressed with colony-stimulating factor 3 receptor (CSF3R) and signal transducer and activator of transcription 1/3 (STAT1/3). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene set enrichment analysis (GSEA) uniquely highlighted the “LAX1/CSF3R/STAT” triad in apoptosis and JAK-STAT cascades. CIBERSORT de-convolution showed LAX1 covaried with plasma-cell, mast-cell and M0-macrophage infiltration.
Results
Plasma from 42 AD and 38 stage-III/IV PD patients showed elevated soluble LAX1 (sLAX1) correlating with Mini-Mental State Examination (MMSE) decline (
r
=—0.67) and clinical attachment loss (
r
= 0.71), outperforming Aβ42 and receptor activator of nuclear factor-κB ligand (RANKL) in receiver operating characteristic (ROC) analyses (area under the curve [AUC] = 0.91). We hypothesised that LAX1 orchestrates the dialogue via the STAT axis. In human periodontal-ligament fibroblasts and 5 × FAD glia exposed to Porphyromonas gingivalis LPS or amyloid-β42 (Aβ42), LAX1 overexpression (pCMV6-LAX1) amplified STAT1/3 phosphorylation, elevated interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) by 2.3—3.1-fold and escalated p53, cleaved caspase-3 and FAS, whereas LAX1 small interfering RNA (siRNA) abolished these effects. In other words, targeting of the LAX1 validated that the inflammatory/apoptotic signature scales with LAX1 abundance.
Conclusion
LAX1 gates STAT-dependent neuroinflammation and periodontal destruction, offering a druggable checkpoint and blood-based biomarker for these convergent chronic diseases.
Journal Article
Isolation, identification, biological characteristics, and pathogenicity of an entomogenous fungus against the Egyptian mealybug, Icerya aegyptiaca (J.) (Hemiptera: Monophlebidae)
Background
In this study, an entomogenous, fungus was isolated from the Egyptian mealybug,
Icerya aegyptiaca
(J.) (Hemiptera: Monophlebidae) on the parasol leaf tree,
Macaranga tanarius
, in China where evaluated as a biocontrol fungus to reduce the population of the target insect. The strain was identified as
Aspergillus parasiticus
by morphological and phylogenetic analysisand named ZHKUAP1. The biological characteristics, pathogenicity, and field control effect of the strain were determined.
Results
The most suitable medium for the mycelial growth of strain ZHKUAP1 was PPDA medium, with an optimum temperature of 30 °C and pH 7, in addition to glucose and peptone as carbon and nitrogen sources. The optimum sporulation conditions were the PPDA medium at 30 °C and pH 6, using the soluble starch and beef extract as carbon and nitrogen sources. The mycelial growth and spore production of strain ZHKUAP1 were stopped at 70 °C and above, indicating that it was not resistant to high temperatures. High concentrations of spore suspension, against young insect age, resulted high corrected mortality, as well as decreased the median lethal time. When the spore concentration was 1 × 10
8
cfu/ml, the corrected mortality of the second nymph was 88.33%, and the LT
50
was 0.66 day. After 10 days of inoculation, the LC
50
of the second instar nymph was the smallest, reaching 4.07 × 10
4
cfu/ml. On the 10th day of the field experiment, the corrected mortality was 76.45%, indicating that the
A. parasiticus
strain ZHKUAP1 had strong pathogenicity on
I. aegyptiaca
population.
Conclusions
The indoor toxicity of the strain to
I. aegyptiaca
was determined, and the field control effect of the pathogen was explored on this basis. The results have important application prospects in the biological control of
I. aegyptiaca.
Journal Article
U1 small nuclear ribonucleoprotein complex and RNA splicing alterations in Alzheimer’s disease
Deposition of insoluble protein aggregates is a hallmark of neurodegenerative diseases. The universal presence of β-amyloid and tau in Alzheimer’s disease (AD) has facilitated advancement of the amyloid cascade and tau hypotheses that have dominated AD pathogenesis research and therapeutic development. However, the underlying etiology of the disease remains to be fully elucidated. Here we report a comprehensive study of the human brain-insoluble proteome in AD by mass spectrometry. We identify 4,216 proteins, among which 36 proteins accumulate in the disease, including U1-70K and other U1 small nuclear ribonucleoprotein (U1 snRNP) spliceosome components. Similar accumulations in mild cognitive impairment cases indicate that spliceosome changes occur in early stages of AD. Multiple U1 snRNP subunits form cytoplasmic tangle-like structures in AD but not in other examined neurodegenerative disorders, including Parkinson disease and frontotemporal lobar degeneration. Comparison of RNA from AD and control brains reveals dysregulated RNA processing with accumulation of unspliced RNA species in AD, including myc box-dependent-interacting protein 1, clusterin, and presenilin-1 . U1-70K knockdown or antisense oligonucleotide inhibition of U1 snRNP increases the protein level of amyloid precursor protein. Thus, our results demonstrate unique U1 snRNP pathology and implicate abnormal RNA splicing in AD pathogenesis.
Journal Article
Psychometric properties of screening tools for mild cognitive impairment in older adults based on COSMIN guidelines: a systematic review
Background
The prevalence of mild cognitive impairment in older adults is understood to be as high as 40%, and early screening for MCI may slow the progression of Alzheimer's disease. However, no systematic review has summarized the psychometric properties of instruments.
Objective
This systematic review aimed to assess the psychometric properties of existing scales for screening older adults for mild cognitive impairment and to provide an evidence-based basis for selecting the most appropriate assessment tool for older adults.
Design
This study systematically reviewed the measurement properties using the consensus-based Criteria for the Selection of Instruments for Measuring Health (COSMIN) method.
Methods
Eight electronic databases (PubMed, Embase, Web of Science, Scopus, Cochrane, CNKI, Wanfang, and Proquest) were systematically searched from inception up to October 26, 2024. Methodological quality was assessed using the COSMIN risk of bias checklist, and psychometric properties were summarized and evaluated using the COSMIN criteria.
Results
Thirty-one studies reported 30 different versions of screening instruments, with 15 studies examining more than 5 psychometric properties. Limited information on construct validity and reliability was found. No data were found on cross-cultural validity/measurement invariance, measurement error, or responsiveness. The final three instruments, AV-MoCA, HKBC, and Qmci-G, received class A recommendations and were recommended for use. The TICS-M study had insufficient psychometric properties and received a class C recommendation; thus, it was not recommended for use. The other 26 instruments were class B recommendations, indicating potential for use, although further research is needed to assess their psychometric properties.
Conclusion
The AV-MoCA, HKBC, and Qmci-G can be used to screen older adults for MCI. Future research is needed to further validate the cross-cultural applicability of these instruments and to fully assess their psychometric properties.
Journal Article
WNT3A promotes the cementogenic differentiation of dental pulp stem cells through the FOXO1 signaling pathway
Background
Dental pulp stem cells (DPSCs) possess capability of multidirectional differentiation, and their cementogenic differentiation potential enables them to participate in cementum repair and regeneration. The molecular mechanisms underlying cementogenic differentiation of DPSCs remain unclear.
Methods
DPSC data set GSE138179 was retrieved from gene expression omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was employed to identify significant modules. Pathway enrichment exploration was conducted utilizing gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA), and Metascape tools. CIBERSORT was utilized to analyze immune cell infiltration analysis. The comparative toxicogenomics database (CTD) was utilized for the validation of core targets. Subsequently, cell experiments were conducted to validate the core targets. Changes in protein expression related to the FOXO1 signaling pathway, cell cycle, and apoptosis were evaluated using western blotting (WB).
Results
Differentially expressed genes (DEGs) associated with DPSC cementogenic differentiation were predominantly enriched in crucial pathways such as the signaling pathway, cell apoptosis, and Wnt signaling pathway. Bioinformatics analysis confirmed WNT3A as a pivotal biomarker for DPSC cementogenic differentiation, and WNT3A was highly expressed in the cementogenic differentiation group. Western blotting results demonstrated that compared to the DPSC group, molecules such as Caspase-3, Caspase-9, FAS, P53, and BAX were downregulated in the CDDPSC group, suggesting reduced apoptosis. Furthermore, upregulation of WNT3A expression in CDDPSC–OE further suppressed the expression of these apoptotic molecules, suggesting a mitigated apoptotic response. Downregulation of WNT3A expression in CDDPSC–KO resulted in increased expression of apoptosis-related molecules, thereby enhancing apoptosis.
Conclusions
WNT3A is highly expressed in the cementogenic differentiation of DPSC, and WNT3A mediates FOXO1 pathway to promote differentiation of dental pulp stem cells into cementogenic differentiation, thus realizing the formation and maintenance of cementum tissue.
Journal Article
Using Azadirachtin to Transform Spodoptera frugiperda from Pest to Natural Enemy
Spodoptera frugiperda and Rhopalosiphum maidis, as main pests, seriously harm the safety of maize. At present, chemical pesticides are mainly used to control these pests. However, due to residue and resistance problems, more green, environmentally benign, simple preventive control technology is needed. In this study, we reported the reason for the antifeedant activity of azadirachtin on S. frugiperda and proposed that S. frugiperda treated with azadirachtin would turn from pest into natural enemy. S. frugiperda showed an obvious antifeeding phenomenon to maize leaf treated with various azadirachtin concentrations (0.5~20 mg/L). It was found that maize leaf treated with 1 mg/L of azadirachtin has a stimulating effect on the antenna and sensillum basiconicum of S. frugiperda, and azadirachtin can affect the feeding behavior of S. frugiperda. Additionally, after treating maize leaves or maize leaves + R. maidis with 1 mg/L of azadirachtin, the predatory behavior of S. frugiperda changed from a preference for eating maize leaves to R. maidis. Moreover, the molting of R. maidis can promote the change of this predatory behavior. Our results, for the first time, propose that the combined control technology of azadirachtin insecticide and biological control could turn S. frugiperda from pest into natural enemy, which can effectively eliminate R. maidis and protect maize. This combined control technology provides a new way for pest management and has good ecological, environmental, and economic benefits.
Journal Article
Senescent cells promote breast cancer cells motility by secreting GM-CSF and bFGF that activate the JNK signaling pathway
Background
Cellular senescence can be induced in mammalian tissues by multiple stimuli, including aging, oncogene activation and loss of tumor suppressor genes, and various types of stresses. While senescence is a tumor suppressing mechanism when induced within premalignant or malignant tumor cells, senescent cells can promote cancer development through increased secretion of growth factors, cytokines, chemokines, extracellular matrix, and degradative enzymes, collectively known as senescence-associated secretory phenotype (SASP). Previous studies indicated that senescent cells, through SASP factors, stimulate tumor cell invasion that is a critical step in cancer cell metastasis.
Methods
In the current study, we investigated the effect of senescent cells on the motility of breast cancer cells, which is another key step in cancer cell metastasis. We analyzed the motility of breast cancer cells co-cultured with senescent cells in vitro and metastasis of the breast cancer cells co-injected with senescent cells in orthotopic xenograft models. We also delineated the signaling pathway mediating the effect of senescent cells on cancer cell motility.
Results
Our results indicate that senescent cells stimulated the migration of breast cancer cells through secretion of GM-CSF and bFGF, which in turn induced activation of the JNK pathway in cancer cells. More importantly, senescent cells promoted breast cancer metastasis, with a minimum effect on the primary tumor growth, in orthotopic xenograft mouse models.
Conclusions
These results have revealed an additional mechanism by which senescent cells promote tumor cell metastasis and tumor progression, and will potentially lead to identification of novel targets for cancer therapies that suppress metastasis, the major cause of cancer mortality.
Journal Article
Patterns of gestational weight gain among women with obesity and its correlation with hypertensive disorders of pregnancy in Chinese women
Gestational weight management in obese women is critical in clinical work. Adverse pregnancy outcomes are associated with improper gestational weight gain (GWG). However, the pattern of GWG (PGWG) and its correlation with hypertensive disorders of pregnancy (HDP) in obesity are still unclear in China. This retrospective cohort study evaluates clinical data from 799 women through multivariate analyses and trajectory analyses. All the participants are stratified per first trimester weight gain category into three groups (Inadequate‐1st, <0.5 kg; Adequate‐1st, 0.5–2.0 kg; Excessive‐1st, >2.0 kg) and PGWG refers to the weekly weight gain during each gestational period. GWG is positively associated with first trimester weight gain. 78.4% of the Excessive‐1st participants have excessive total GWG, in contrast to Inadequate‐1st (32.7%) and Adequate‐1st (48.2%). After 20 weeks, the weekly weight gain rapidly accelerates, and 77.3% have a weekly weight gain exceeding the Institute of Medicine recommendations. Trajectory analysis of weekly weight gain based on HDP shows two separate weight gain curves after 20 weeks in women with and without a high risk of HDP. Especially in Excessive‐1st participants, weekly weight gain after 20 weeks over 0.32 kg/w is positively related to the risk of HDP (<0.32 kg/w vs. 0.32–0.61 kg/w, adjusted odds ratios [aOR]: 2.999, 95% confidence interval [CI]: 1.054–8.537; <0.32 kg/w vs. >0.61 kg/w, aOR: 5.362, 95% CI: 1.719–16.729). In summary, the first trimester is critical for gestational weight management in obesity. Excessive weight gain during the first trimester and after 20 weeks predicts a high risk of HDP, which should be noted in clinical practice. Although the pattern of gestational weight gain is complex, the first trimester is critical for gestational weight management in women with obesity. Excessive gestational weight gain during the first trimester and after 20 weeks predicts a high risk of hypertension disorder in pregnancy, which should be noted in clinical practice. Highlights The pattern of gestational weight gain in women with obesity is intricate. The first trimester is the critical period for gestational weight management. Improper gestational weight gain reminds a potentially high risk of hypertensive disorders of pregnancy.
Journal Article
Toxicity and Sublethal Effects of Autumn Crocus (Colchicum autumnale) Bulb Powder on Red Imported Fire Ants (Solenopsis invicta)
Autumn crocus (Colchicum autumnale L.) is a medicinal plant as it contains high concentrations of colchicine. In this study, we reported that the ground powder of autumn crocus bulb is highly toxic to invasive Solenopsis invicta Buren, commonly referred to as red imported fire ants (RIFAs). Ants fed with sugar water containing 5000 mg/L of bulb powder showed 54.67% mortality in three days compared to 45.33% mortality when fed with sugar water containing 50 mg/L of colchicine. Additionally, the effects of short-term feeding with sugar water containing 1 mg/L of colchicine and 100 mg/L of autumn crocus bulb powder were evaluated for RIFAs’ colony weight, food consumption, and aggressiveness, i.e., aggregation, grasping ability, and walking speed. After 15 days of feeding, the cumulative colony weight loss reached 44.63% and 58.73% due to the sublethal concentrations of colchicine and autumn crocus bulb powder, respectively. The consumption of sugar water and mealworm (Tenebrio molitor L.) was substantially reduced. The aggregation rates decreased 48.67% and 34.67%, grasping rates were reduced to 38.67% and 16.67%, and walking speed decreased 1.13 cm/s and 0.67 cm/s as a result of the feeding of the two sublethal concentrations of colchicine and autumn crocus bulb powder, respectively. Our results for the first time show that powder derived from autumn crocus bulbs could potentially be a botanical pesticide for controlling RIFAs, and application of such a product could be ecologically benign due to its rapid biodegradation in the environment.
Journal Article