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1.
BMC Genomics ; 25(1): 494, 2024 May 20.
Artículo en Inglés | MEDLINE | ID: mdl-38764031

RESUMEN

BACKGROUND: Mammary gland development is a critical process in mammals, crucial for their reproductive success and offspring nourishment. However, the functional roles of key candidate genes associated with teat number, including ABCD4, VRTN, PROX2, and DLST, in this developmental process remain elusive. To address this gap in knowledge, we conducted an in-depth investigation into the dynamic expression patterns, functional implications, and regulatory networks of these candidate genes during mouse mammary gland development. RESULTS: In this study, the spatial and temporal patterns of key genes were characterized in mammary gland development. Using time-series single-cell data, we uncovered differences in the expression of A bcd4, Vrtn, Prox2, and Dlst in cell population of the mammary gland during embryonic and adult stages, while Vrtn was not detected in any cells. We found that only overexpression and knockdown of Abcd4 could inhibit proliferation and promote apoptosis of HC11 mammary epithelial cells, whereas Prox2 and Dlst had no significant effect on these cells. Using RNA-seq and qPCR, further analysis revealed that Abcd4 can induce widespread changes in the expression levels of genes involved in mammary gland development, such as Igfbp3, Ccl5, Tlr2, and Prlr, which were primarily associated with the MAPK, JAK-STAT, and PI3K-AKT pathways by functional enrichment. CONCLUSIONS: These findings revealed ABCD4 as a candidate gene pivotal for regulating mammary gland development and lactation during pregnancy by influencing PRLR expression.


Asunto(s)
Glándulas Mamarias Animales , Animales , Glándulas Mamarias Animales/crecimiento & desarrollo , Glándulas Mamarias Animales/metabolismo , Femenino , Ratones , Apoptosis/genética , Proliferación Celular , Regulación del Desarrollo de la Expresión Génica , Redes Reguladoras de Genes , Células Epiteliales/metabolismo , Transducción de Señal
2.
Neuropathology ; 2024 May 22.
Artículo en Inglés | MEDLINE | ID: mdl-38775061

RESUMEN

Multiple sclerosis (MS), the leading cause of disability in young adults, is an inflammatory disease of the central nervous system characterized by localized areas of demyelination. Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase that has been shown to be implicated in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Interestingly, ASK1 signaling regulates glial cell interactions and drives neuroinflammation in EAE mice. To further investigate its clinical significance, in the present study, we examined the activation of ASK1 in the post-mortem brain of MS patients. ASK1 activation was found in active lesions of the corpus callosum in both microglia/macrophages and astrocytes. Moreover, ASK1 activation in astrocytes was higher than that in microglia/macrophages, which was in line with our findings in EAE mice. Our results suggest an important role of ASK1 in glial cells, indicating that ASK1 might be a good therapeutic target for MS.

3.
Aging (Albany NY) ; 16(8): 6852-6867, 2024 Apr 17.
Artículo en Inglés | MEDLINE | ID: mdl-38637126

RESUMEN

BACKGROUND: Globally, ischemic stroke (IS) is ranked as the second most prevailing cause of mortality and is considered lethal to human health. This study aimed to identify genes and pathways involved in the onset and progression of IS. METHODS: GSE16561 and GSE22255 were downloaded from the Gene Expression Omnibus (GEO) database, merged, and subjected to batch effect removal using the ComBat method. The limma package was employed to identify the differentially expressed genes (DEGs), followed by enrichment analysis and protein-protein interaction (PPI) network construction. Afterward, the cytoHubba plugin was utilized to screen the hub genes. Finally, a ROC curve was generated to investigate the diagnostic value of hub genes. Validation analysis through a series of experiments including qPCR, Western blotting, TUNEL, and flow cytometry was performed. RESULTS: The analysis incorporated 59 IS samples and 44 control samples, revealing 226 DEGs, of which 152 were up-regulated and 74 were down-regulated. These DEGs were revealed to be linked with the inflammatory and immune responses through enrichment analyses. Overall, the ROC analysis revealed the remarkable diagnostic potential of ITGAM and MMP9 for IS. Quantitative assessment of these genes showed significant overexpression in IS patients. ITGAM modulation influenced the secretion of critical inflammatory cytokines, such as IL-1ß, IL-6, and TNF-α, and had a distinct impact on neuronal apoptosis. CONCLUSIONS: The inflammation and immune response were identified as potential pathological mechanisms of IS by bioinformatics and experiments. In addition, ITGAM may be considered a potential therapeutic target for IS.


Asunto(s)
Accidente Cerebrovascular Isquémico , Mapas de Interacción de Proteínas , Humanos , Accidente Cerebrovascular Isquémico/genética , Mapas de Interacción de Proteínas/genética , Perfilación de la Expresión Génica , Metaloproteinasa 9 de la Matriz/genética , Metaloproteinasa 9 de la Matriz/metabolismo , Redes Reguladoras de Genes , Bases de Datos Genéticas , Apoptosis/genética
4.
Hum Brain Mapp ; 45(5): e26672, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-38549429

RESUMEN

Mother-child interaction is highly dynamic and reciprocal. Switching roles in these back-and-forth interactions serves as a crucial feature of reciprocal behaviors while the underlying neural entrainment is still not well-studied. Here, we designed a role-controlled cooperative task with dual EEG recording to explore how differently two brains interact when mothers and children hold different roles. When children were actors and mothers were observers, mother-child interbrain synchrony emerged primarily within the theta oscillations and the frontal lobe, which highly correlated with children's attachment to their mothers (self-reported by mothers). When their roles were reversed, this synchrony was shifted to the alpha oscillations and the central area and associated with mothers' perception of their relationship with their children. The results suggested an observer-actor neural alignment within the actor's oscillations, which was related to the actor-toward-observer emotional bonding. Our findings contribute to the understanding of how interbrain synchrony is established and dynamically changed during mother-child reciprocal interaction.


Asunto(s)
Encéfalo , Madres , Femenino , Humanos , Madres/psicología , Encéfalo/diagnóstico por imagen , Lóbulo Frontal , Relaciones Madre-Hijo/psicología , Diencéfalo
5.
Hum Cell ; 37(3): 689-703, 2024 May.
Artículo en Inglés | MEDLINE | ID: mdl-38551774

RESUMEN

Polycystic ovary syndrome (PCOS) is a complex gynaecological endocrine disease that occurs in women of childbearing age. The pathogenesis of PCOS is still unclear and further exploration is needed. Here, proteomic analysis indicated that the expression of farnesyl diphosphate synthase (FDPS) protein in ovarian tissue of PCOS mice was significantly decreased. The purpose of this study is to investigate the relationship between potential biomarkers of PCOS and granulosa cells (GCs) function. The mechanisms by which FDPS affected the proliferation of granulosa cells were also explored both in vitro and in vivo. We found that knockdown of FDPS inhibited the proliferation of KGN (human ovarian granulosa cell line), while overexpression of FDPS had the opposite effect. FDPS activated Rac1 (Rac Family Small GTPase 1) activity and regulated MAPK/ERK signalling pathway, which affecting the proliferation of KGN cells significantly. In addition, treatment with the adeno-associated virus (AAV)-FDPS reverses the dehydroepiandrosterone (DHEA)-induced PCOS-phenotype in mice. Our data indicated that FDPS could regulate the proliferation of ovarian GCs by modulating MAPK/ERK (mitogen-activated protein kinase/extracellular regulated protein kinases) pathway via activating Rac1 activity. These findings suggest that FDPS could be of great value for the regulation of ovarian granulosa cell function and the treatment of PCOS.


Asunto(s)
MicroARNs , Síndrome del Ovario Poliquístico , Humanos , Femenino , Ratones , Animales , Síndrome del Ovario Poliquístico/genética , Geraniltranstransferasa/metabolismo , Proteómica , Células de la Granulosa/metabolismo , Proliferación Celular , MicroARNs/metabolismo , Apoptosis , Proteína de Unión al GTP rac1/genética , Proteína de Unión al GTP rac1/metabolismo
6.
J Pharmacol Sci ; 154(4): 326-333, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-38485351

RESUMEN

PURPOSE: To determine whether combination of topical ripasudil and brimonidine has more effective neuroprotection on retinal ganglion cells (RGCs) following injury to axons composing the optic nerve. METHODS: Topical ripasudil, brimonidine, or mixture of both drugs were administered to adult mice after optic nerve injury (ONI). The influence of drug conditions on RGC health were evaluated by the quantifications of surviving RGCs, phosphorylated p38 mitogen-activated protein kinase (phospho-p38), and expressions of trophic factors and proinflammatory mediators in the retina. RESULTS: Topical ripasudil and brimonidine suppressed ONI-induced RGC death respectively, and mixture of both drugs further stimulated RGC survival. Topical ripasudil and brimonidine suppressed ONI-induced phospho-p38 in the whole retina. In addition, topical ripasudil suppressed expression levels of TNFα, IL-1ß and monocyte chemotactic protein-1 (MCP-1), whereas topical brimonidine increased the expression level of basic fibroblast growth factor (bFGF). CONCLUSIONS: Combination of topical ripasudil and brimonidine may enhance RGC protection by modulating multiple signaling pathways in the retina.


Asunto(s)
Isoquinolinas , Traumatismos del Nervio Óptico , Sulfonamidas , Ratones , Animales , Tartrato de Brimonidina , Traumatismos del Nervio Óptico/tratamiento farmacológico , Traumatismos del Nervio Óptico/metabolismo , Neuroprotección , Combinación de Medicamentos
7.
Plant Cell ; 36(4): 963-986, 2024 Mar 29.
Artículo en Inglés | MEDLINE | ID: mdl-38301274

RESUMEN

Soybean cyst nematode (SCN; Heterodera glycines Ichinohe), one of the most devastating soybean (Glycine max) pathogens, causes significant yield loss in soybean production. Nematode infection triggers plant defense responses; however, the components involved in the upstream signaling cascade remain largely unknown. In this study, we established that a mitogen-activated protein kinase (MAPK) signaling module, activated by nematode infection or wounding, is crucial for soybeans to establish SCN resistance. GmMPK3 and GmMPK6 directly interact with CDG1-LIKE1 (GmCDL1), a member of the receptor-like cytoplasmic kinase (RLCK) subfamily VII. These kinases phosphorylate GmCDL1 at Thr-372 to prevent its proteasome-mediated degradation. Functional analysis demonstrated that GmCDL1 positively regulates immune responses and promotes SCN resistance in soybeans. GmMPK3-mediated and GmMPK6-mediated phosphorylation of GmCDL1 enhances GmMPK3 and GmMPK6 activation and soybean disease resistance, representing a positive feedback mechanism. Additionally, 2 L-type lectin receptor kinases, GmLecRK02g and GmLecRK08g, associate with GmCDL1 to initiate downstream immune signaling. Notably, our study also unveils the potential involvement of GmLecRKs and GmCDL1 in countering other soybean pathogens beyond nematodes. Taken together, our findings reveal the pivotal role of the GmLecRKs-GmCDL1-MAPK regulatory module in triggering soybean basal immune responses.


Asunto(s)
Infecciones por Nematodos , Tylenchoidea , Animales , Proteínas Quinasas Activadas por Mitógenos/genética , Proteínas Quinasas Activadas por Mitógenos/metabolismo , Glycine max/genética , Sistema de Señalización de MAP Quinasas , Transducción de Señal/genética , Enfermedades de las Plantas/genética , Quinasas de Proteína Quinasa Activadas por Mitógenos/metabolismo
8.
New Phytol ; 242(1): 262-277, 2024 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-38332248

RESUMEN

Plants are simultaneously attacked by different pests that rely on sugars uptake from plants. An understanding of the role of plant sugar allocation in these multipartite interactions is limited. Here, we characterized the expression patterns of sucrose transporter genes and evaluated the impact of targeted transporter gene mutants and brown planthopper (BPH) phloem-feeding and oviposition on root sugar allocation and BPH-reduced rice susceptibility to Meloidogyne graminicola. We found that the sugar transporter genes OsSUT1 and OsSUT2 are induced at BPH oviposition sites. OsSUT2 mutants showed a higher resistance to gravid BPH than to nymph BPH, and this was correlated with callose deposition, as reflected in a different effect on M. graminicola infection. BPH phloem-feeding caused inhibition of callose deposition that was counteracted by BPH oviposition. Meanwhile, this pivotal role of sugar allocation in BPH-reduced rice susceptibility to M. graminicola was validated on rice cultivar RHT harbouring BPH resistance genes Bph3 and Bph17. In conclusion, we demonstrated that rice susceptibility to M. graminicola is regulated by BPH phloem-feeding and oviposition on rice through differences in plant sugar allocation.


Asunto(s)
Hemípteros , Oryza , Tylenchoidea , Animales , Femenino , Hemípteros/fisiología , Azúcares/metabolismo , Oryza/metabolismo
9.
J Sep Sci ; 47(3): e2300900, 2024 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-38356233

RESUMEN

Reasonable design and construction of functionalized materials are of great importance for the enrichment of global phosphopeptides. In this work, Ti4+ functionalized hydrophilic covalent organic frameworks by introducing glutathione (GSH) and 2,3,4-trihydroxy benzaldehyde (THBA) via click chemistry and Schiff base reaction (COF-V@GSH-THBA-Ti4+ ) was constructed and applied for selective enrichment of phosphopeptides in serum. Benefit from the high surface area, excellent hydrophilicity as well as regular mesoporous structure, COF-V@GSH-THBA-Ti4+ displayed high selectivity (molar ratio of 2000:1), low limit of detection (0.5 fmol), high load capacity (100.0 mg/g) and excellent size-exclusion effect (1:10000) for enrichment of phosphopeptides. For actual bio-sample analysis, 15 phosphopeptides assigned to 10 phosphoproteins with 16 phosphorylated sites and 33 phosphopeptides assigned to 25 phosphoproteins with 34 phosphorylated sites were detected from the serum of patients with chronic obstructive pulmonary disease (COPD), and normal controls. Biological processes and molecular functions analysis further disclosed the difference of serums with phosphoproteomics between COPD and normal controls.


Asunto(s)
Estructuras Metalorgánicas , Enfermedad Pulmonar Obstructiva Crónica , Humanos , Fosfopéptidos/química , Estructuras Metalorgánicas/química , Química Clic , Bases de Schiff , Fosfoproteínas , Cromatografía de Afinidad/métodos , Titanio/química
10.
Sci Rep ; 14(1): 4129, 2024 Feb 19.
Artículo en Inglés | MEDLINE | ID: mdl-38374150

RESUMEN

This paper investigates Regional Integrated Energy Systems (RIES), emphasizing the connection of diverse energy supply subsystems to address varied user needs and enhance operational efficiency. A novel low-carbon economic dispatch method, utilizing the multi-objective chaotic artificial hummingbird algorithm, is introduced. The method not only optimizes economic and environmental benefits but also aligns with "carbon peak and carbon neutrality" objectives. The study begins by presenting a comprehensive low-carbon economic dispatch model, followed by the proposal of the multi-objective chaotic artificial hummingbird algorithm, crucial for deriving the Pareto frontier of the low-carbon economic dispatch model. Additionally, we introduce a TOPSIS approach based on combined subjective and objective weights, this approach harnesses the objective data from the Pareto solution set deftly, curbs the subjective biases of dispatchers effectively and facilitates the selection of an optimal system operation plan from the Pareto frontier. Finally, the simulation results highlight the outstanding performance of our method in terms of optimization outcomes, convergence efficiency, and solution diversity. Noteworthy among these results is an 8.8% decrease in system operational economic costs and a 14.2% reduction in carbon emissions.

11.
BMC Med ; 22(1): 73, 2024 Feb 19.
Artículo en Inglés | MEDLINE | ID: mdl-38369461

RESUMEN

BACKGROUND: Annual screening through low-dose computed tomography (LDCT) is recommended for heavy smokers. However, it is questionable whether all individuals require annual screening given the potential harms of LDCT screening. This study examines the benefit-harm and cost-effectiveness of risk-based screening in heavy smokers and determines the optimal risk threshold for screening and risk-stratified screening intervals. METHODS: We conducted a comparative cost-effectiveness analysis in China, using a cohort-based Markov model which simulated a lung cancer screening cohort of 19,146 heavy smokers aged 50 ~ 74 years old, who had a smoking history of at least 30 pack-years and were either current smokers or had quit for < 15 years. A total of 34 risk-based screening strategies, varying by different risk groups for screening eligibility and screening intervals (1-year, 2-year, 3-year, one-off, non-screening), were evaluated and were compared with annual screening for all heavy smokers (the status quo strategy). The analysis was undertaken from the health service perspective with a 30-year time horizon. The willingness-to-pay (WTP) threshold was adopted as three times the gross domestic product (GDP) of China in 2021 (CNY 242,928) per quality-adjusted life year (QALY) gained. RESULTS: Compared with the status quo strategy, nine risk-based screening strategies were found to be cost-effective, with two of them even resulting in cost-saving. The most cost-effective strategy was the risk-based approach of annual screening for individuals with a 5-year risk threshold of ≥ 1.70%, biennial screening for individuals with a 5-year risk threshold of 1.03 ~ 1.69%, and triennial screening for individuals with a 5-year risk threshold of < 1.03%. This strategy had the highest incremental net monetary benefit (iNMB) of CNY 1032. All risk-based screening strategies were more efficient than the status quo strategy, requiring 129 ~ 656 fewer screenings per lung cancer death avoided, and 0.5 ~ 28 fewer screenings per life-year gained. The cost-effectiveness of risk-based screening was further improved when individual adherence to screening improved and individuals quit smoking after being screened. CONCLUSIONS: Risk-based screening strategies are more efficient in reducing lung cancer deaths and gaining life years compared to the status quo strategy. Risk-stratified screening intervals can potentially balance long-term benefit-harm trade-offs and improve the cost-effectiveness of lung cancer screenings.


Asunto(s)
Neoplasias Pulmonares , Fumadores , Humanos , Anciano , Análisis Costo-Beneficio , Análisis de Costo-Efectividad , Detección Precoz del Cáncer/métodos , Neoplasias Pulmonares/diagnóstico por imagen , Neoplasias Pulmonares/epidemiología , Tamizaje Masivo , Años de Vida Ajustados por Calidad de Vida
12.
Toxicology ; 503: 153758, 2024 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-38367942

RESUMEN

Benzene exposure leads to hematotoxicity, and epigenetic modification is considered to be a potential mechanism of benzene pathogenesis. As a newly discovered post-transcriptional modification, the roles of N6-methyladenosine (m6A) in benzene hematotoxicity are still unclear. m6A can only exert its gene regulatory function after being recognized by m6A reading proteins. In this study, we found that the expression of m6A reader IGF2BP1 decreased in benzene poisoning workers and in 20 µM benzene metabolite 1,4-BQ-treated AHH-1 cells. Further overexpression of IGF2BP1 in mice alleviated 50 ppm benzene-induced hematopoietic damage, suggesting that IGF2BP1 plays a critical role in benzene hematotoxicity. Next, we examined transcriptome-wide m6A methylation in vitro to search for target genes of IGF2BP1. We found that benzene metabolite 1,4-BQ treatment altered the m6A methylation levels of various genes. The comprehensive analysis of mRNA expression and m6A methylation uncovered that the hypomethylated Ribosomal Protein L36 (RPL36) and its consequent reduced expression impaired cell proliferation. Mechanically, m6A modification reduced RNA stability to down-regulate RPL36 expression. Moreover, overexpression of IGF2BP1 relieved RPL36 reduction and cell proliferation inhibition caused by benzene in vitro and in vivo by directly binding with RPL36 mRNA. In conclusion, the m6A reader IGF2BP1 attenuates the stability of RPL36 and cell proliferation to mediate benzene hematotoxicity by recognizing m6A modification. IGF2BP1 and RPL36 may be key molecules and potential therapeutic targets for benzene hematotoxicity.


Asunto(s)
Adenina/análogos & derivados , Benceno , Ratones , Animales , Benceno/toxicidad , Metilación , ARN Mensajero/metabolismo , Biomarcadores/metabolismo , Proliferación Celular
13.
Org Biomol Chem ; 22(12): 2370-2374, 2024 Mar 20.
Artículo en Inglés | MEDLINE | ID: mdl-38416487

RESUMEN

An efficient method was developed for the one-pot construction of pyrrolo[1,2-a]quinoxalines via a Cu(II)-catalyzed domino reaction between 2-(1H-pyrrol-1-yl)anilines and alkylsilyl peroxides. This reaction proceeds through C-C bond cleavage and new C-C and C-N bond formation. A mechanistic study suggests that alkyl radical species participate in the cascade reaction.

14.
Front Biosci (Landmark Ed) ; 29(2): 66, 2024 Feb 06.
Artículo en Inglés | MEDLINE | ID: mdl-38420815

RESUMEN

BACKGROUND: Gynecological malignancies, such as endometrial cancer (EC) and uterine cancer are prevalent. Increased Acyl-CoA synthetase long-chain family member 1 (ACSL1) activity may contribute to aberrant lipid metabolism, which is a potential factor that contributes to the pathogenesis of endometrial cancer. This study aimed to elucidate the potential molecular mechanisms by which ACSL1 is involved in lipid metabolism in endometrial cancer, providing valuable insights for targeted therapeutic strategies. METHODS: Xenograft mouse models were used to assess the effect of ACSL1 on the regulation of endometrial cancer progression. ACSL1 protein levels were assessed via immunohistochemistry and immunoblotting analysis. To assess the migratory potential of Ishikawa cells, wound-healing and Transwell invasion assays were performed. Changes in lipids in serum samples from mice with endometrial cancer xenotransplants were examined in an untargeted lipidomic study that combined multivariate statistical methods with liquid chromatography‒mass spectrometry (LC/MS). RESULTS: Patient sample and tissue microarray data suggested that higher ACSL1 expression is strongly associated with the malignant progression of EC. Overexpression of ACSL1 enhances fatty acid ß-oxidation and 5'-adenylate triphosphate (ATP) generation in EC cells, promoting cell proliferation and migration. Lipidomic analysis revealed that significant changes were induced by ACSL1, including changes to 28 subclasses of lipids and a total of 24,332 distinct lipids that were detected in both positive and negative ion modes. Moreover, pathway analysis revealed the predominant association of these lipid modifications with the AMPK/CPT1C/ATP pathway and fatty acid ß-oxidation. CONCLUSIONS: This study indicates that ACSL1 regulates the AMPK/CPT1C/ATP pathway, which induces fatty acid ß-oxidation, promotes proliferation and migration, and then leads to the malignant progression of EC.


Asunto(s)
Neoplasias Endometriales , Ácidos Grasos , Humanos , Ratones , Animales , Femenino , Ácidos Grasos/metabolismo , Proteínas Quinasas Activadas por AMP/metabolismo , Metabolismo de los Lípidos , Neoplasias Endometriales/genética , Adenosina Trifosfato/metabolismo , Coenzima A Ligasas/genética , Coenzima A Ligasas/metabolismo
15.
Food Chem ; 442: 138433, 2024 Jun 01.
Artículo en Inglés | MEDLINE | ID: mdl-38237292

RESUMEN

In this work, a switchable deep eutectic solvent (SDES) based on fatty acid and polyetheramine ion pair was prepared for liquid-phase microextraction (LPME) of phenoxyacetic acid herbicides in drinking water, beverage and honey matrices. The as-synthesized SDES equipped with an interesting characteristic of fast and reversible polarity switching, achieving homogeneous extraction and rapid bi-phase separation simultaneously. Several key parameters affecting the extraction performance were investigated comprehensively by Box-Behnken design. Under the optimal conditions, the method exhibited excellent linearity (15-4000 µg L-1), low detection limits (3-5 µg L-1), desirable precision (RSD < 8.1 %), and satisfactory recovery (72.6-98.7 %). More importantly, the introduction of SDES can simplify the pre-treatment procedure, shorten extraction time (4 min), and avoid the usage of traditional organic solvent during the whole extraction process. In addition, the switching mechanism of SDES was characterized by FT-IR and 1H NMR, and the forming mechanism of SDES was investigated using density-functional theory. The green of the method was estimated using the analytical ecological scale, the analytical green calculator, and the green analytical procedure index. The cytotoxicity of SDES was investigated and the result displayed that toxicity of the SDES was very low with the EC50 > 500 mg/L. Therefore, the proposed method was green and efficient and revealed considerable application prospects for the extraction of trace analytes from complex materials.


Asunto(s)
Acetatos , Agua Potable , Herbicidas , Microextracción en Fase Líquida , Solventes/química , Disolventes Eutécticos Profundos , Espectroscopía Infrarroja por Transformada de Fourier , Microextracción en Fase Líquida/métodos , Límite de Detección
16.
Insect Sci ; 2024 Jan 12.
Artículo en Inglés | MEDLINE | ID: mdl-38214204

RESUMEN

The gregarious lifestyle of lepidopteran larvae is diverse and shaped by a complex interplay of ecological and evolutionary factors. Our review showed that the larval-aggregation behavior has been reported in 23 lepidopteran families, indicating multiple evolution of this behavior. Some larvae live in sibling groups throughout all larval instars and even pupation stages, which may result from the kin-selection. In contrast, group fusion may occur among different sibling or foraging groups of larvae and form larger aggregates, and the gregariousness of these species might be driven by the group-selection. While group size and foraging patterns vary greatly across species, it is generally associated with improved larval survivorship and accelerated development. However, the advantages of group living, such as facilitating feeding activities, adjusting the temperature, and defending natural enemies, may diminish along with development, with strong intraspecific competition occurring at later instars, even when food is abundant. Therefore, the group sizes and fission-fusion dynamics of certain gregarious lepidopteran larvae may be a consequence of their cost-benefit balance depending on various biotic and abiotic factors. Trail and aggregation pheromones, silk trails, or body contact contribute to collective movement and group cohesion of gregarious lepidopteran larvae. However, frequent contact among group members may cause the horizontal transmission of pathogens and pesticides, which may bring an integrated pest management strategy controlling gregarious lepidopteran pests.

17.
Reprod Sci ; 2024 Jan 31.
Artículo en Inglés | MEDLINE | ID: mdl-38294667

RESUMEN

In this study, we examined the changes in the mitochondrial structure and function in cumulus granulosa cells of patients with diminished ovarian reserve (DOR) to explore the causes and mechanisms of decreased mitochondrial quality. The mitochondrial ultrastructure was observed by transmission electron microscope, and the function was determined by detecting the ATP content, reactive oxygen species (ROS) levels, the number of mitochondria, and the mitochondrial membrane potential. The expression of ATP synthases in relation to mitochondrial function was analyzed. Additionally, protein immunoblotting was used to compare the expression levels of mitochondrial kinetic protein, the related channel protein in the two groups. Patients with DOR had abnormal granulosa cell morphology, increased mitochondrial abnormalities, decreased mitochondrial function, and disturbed mitochondrial dynamics. Additionally, the silent information regulator 1 (SIRT1)/phospho-AMP-activated protein kinase (P-AMPK)-peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) pathway expression was decreased, which was speculated to be associated with the decreased mitochondrial mass in the DOR group. The mitochondrial mass was decreased in granulosa cells of patients in the DOR group. The mitochondrial dysfunction observed in granulosa cells of patients in the DOR group may be associated with dysregulation of the SIRT1/P-AMPK-PGC-1α-mitochondrial transcription factor A (TFAM) pathway.

18.
Sensors (Basel) ; 24(2)2024 Jan 05.
Artículo en Inglés | MEDLINE | ID: mdl-38257406

RESUMEN

To improve the classification of pig vocalization using vocal signals and improve recognition accuracy, a pig vocalization classification method based on multi-feature fusion is proposed in this study. With the typical vocalization of pigs in large-scale breeding houses as the research object, short-time energy, frequency centroid, formant frequency and first-order difference, and Mel frequency cepstral coefficient and first-order difference were extracted as the fusion features. These fusion features were improved using principal component analysis. A pig vocalization classification model with a BP neural network optimized based on the genetic algorithm was constructed. The results showed that using the improved features to recognize pig grunting, squealing, and coughing, the average recognition accuracy was 93.2%; the recognition precisions were 87.9%, 98.1%, and 92.7%, respectively, with an average of 92.9%; and the recognition recalls were 92.0%, 99.1%, and 87.4%, respectively, with an average of 92.8%, which indicated that the proposed pig vocalization classification method had good recognition precision and recall, and could provide a reference for pig vocalization information feedback and automatic recognition.


Asunto(s)
Tos , Reconocimiento en Psicología , Porcinos , Animales , Redes Neurales de la Computación , Análisis de Componente Principal
19.
Neurotherapeutics ; 21(2): e00320, 2024 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-38262102

RESUMEN

Mirror therapy (MT) has been proposed to promote motor recovery post-stroke through activation of mirror neuron system, recruitment of ipsilateral motor pathways, or/and increasing attention toward the affected limb. However, neuroimaging evidence for these mechanisms is still lacking. To uncover the underlying mechanisms, we designed a randomized controlled study and used a voxel-based whole-brain analysis of resting-state fMRI to explore the brain reorganizations induced by MT. Thirty-five stroke patients were randomized to an MT group (n â€‹= â€‹16) and a conventional therapy (CT) group (n â€‹= â€‹19) for a 4-week intervention. Before and after the intervention, the Fugl-Meyer Assessment Upper Limb subscale (FMA-UL) and resting-state fMRI were collected. A healthy cohort (n â€‹= â€‹16) was established for fMRI comparison. The changes in fractional amplitude of low-frequency fluctuation (fALFF) and seed-based functional connectivity were analyzed to investigate the impact of intervention. Results showed that greater FMA-UL improvement in the MT group was associated with the compensatory increase of fALFF in the contralesional precentral gyrus (M1) region and the re-establishment of functional connectivity between the bilateral M1 regions, which facilitate motor signals transmission via the ipsilateral motor pathways from the ipsilesional M1, contralesional M1, to the affected limb. A step-wise linear regression model revealed these two brain reorganization patterns collaboratively contributed to FMA-UL improvement. In conclusion, MT achieved motor rehabilitation primarily by recruitment of the ipsilateral motor pathways. Trial Registration Information: http://www.chictr.org.cn. Unique Identifier. ChiCTR-INR-17013644, submitted on December 2, 2017.


Asunto(s)
Rehabilitación de Accidente Cerebrovascular , Accidente Cerebrovascular , Humanos , Imagen por Resonancia Magnética/métodos , Terapia del Movimiento Espejo , Accidente Cerebrovascular/diagnóstico por imagen , Accidente Cerebrovascular/terapia , Encéfalo/diagnóstico por imagen , Vías Eferentes , Recuperación de la Función/fisiología
20.
IEEE Trans Biomed Eng ; 71(2): 400-409, 2024 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-37535480

RESUMEN

OBJECTIVE: Electroencephalography (EEG) with high time-resolution allows for recording dynamic cortical activity during walking and provides new insight into the underlying pathophysiology of gait impairments in PD. However, traditional gait-phase-specific EEG analysis only measures the brain activities in the isolated gait phase, but neglects the between-gait-phase interactions as well as the whole-gait-cycle characteristics, and therefore is unable to effectively reflect the abnormal cortical gait control. METHODS: In this study, we introduced three whole-gait-cycle measures of intra-stride EEG activity (i.e., mean desynchronization, amplitude of fluctuations, and coupling to the gait phase), and investigated their abnormalities in PD and relationships with gait impairments, which were further compared with the traditional gait-phase-specific measures. RESULTS: Compared with healthy controls, PD patients showed overwhelming stronger desynchronizations (ERD) across the whole gait cycle in θ, α and low-ß bands, implying a cortical compensatory strategy in response to the low efficiency of the motor network. Patients also exhibited weaker intra-stride ERD fluctuations in the central area in α and low-ß bands, with reduced amplitude and less coupling to the gait phase, which were correlated with gait impairments in walking speed, gait rhythm and walking stability. However, gait-phase-specific EEG measures did not show any significant correlation with gait impairments in PD. CONCLUSION: Our results demonstrated the efficiency of whole-gait-cycle EEG measures in characterizing the abnormal cortical gait control, and for the first time, associated gait impairments with weak intra-stride electrocortical fluctuations. SIGNIFICANCE: The findings may shed light on the development of cortical-targeted interventions for PD.


Asunto(s)
Enfermedad de Parkinson , Humanos , Marcha/fisiología , Caminata/fisiología , Electroencefalografía , Velocidad al Caminar
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