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Global climate change and the collection of environmental protection taxes are accelerating the green transformation of thermal power enterprises. This study selected Chinese thermal power listed companies as samples and used a dynamic three-stage (operational, green transformation, and market performance) network DEA model to evaluate their transformation efficiency and corporate performance. This paper incorporates targeted indicators such as ESG (environment, society, governance) and stock prices into the model and conducts a comparative study on the basis of macro policies and the geographical location of the enterprise. A comparative analysis was conducted on the efficiency of enterprises before and after the adjustment of the environmental tax burden, using the environmental tax burden as an exogenous variable. Thus, the following conclusions can be drawn: there is a certain positive correlation between the collaborative efficiency of the two links of thermal power enterprises and the economic development of their respective regions. Moreover, the green transformation efficiency of most thermal power enterprises is superior to the market performance efficiency. The environmental tax burden mainly improves the overall efficiency of thermal power enterprises by improving their operational efficiency and efficiency in the green transformation stage without affecting market performance. To further improve efficiency, thermal power enterprises should actively communicate with stakeholders to strive for more financial relief.
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Background: Leukaemia is a devastating disease with an incidence that progressively increases with advancing age. The World Health Organization has designated 2021-30 as the decade of healthy ageing, highlighting the need to address age-related diseases. We estimated the disease burden of leukaemia and forecasted it by 2030. Methods: Based on the Global Burden of Disease 2019 database, we systematically analysed the geographical distribution of leukaemia and its subtypes. We used Joinpoint regression and Bayesian age-period-cohort models to evaluate incidence and mortality trends from 1990 to 2019 and projections through 2030. We analysed five leukaemia subtypes and the impact of age, gender, and social development. Decomposition analysis revealed the effects of disease burden on ageing and population growth. We used frontier analysis to illustrate the potential of each country to reduce its burden based on its development levels. Results: Globally, the absolute numbers of leukaemia incidence and mortality have increased, while the age-standardised rates (ASRs) have shown a decreasing trend. The disease burden was more pronounced in men, the elderly, and regions with a high socio-demographic index (SDI), where ageing and population growth played varying roles across subtypes. From 2000 to 2006, disease burdens were most effectively controlled. Global ASRs of incidence might stabilise, while ASRs of death are expected to decrease until 2030. Frontier analysis showed that middle and high-middle SDI countries have the most improvement potential. Smoking and high body mass index were the main risk factors for leukaemia-related mortality and disability-adjusted life years. Conclusions: The absolute number of leukaemia cases has increased worldwide, but there has been a sharp decline in ASRs over the past decade, primarily driven by population growth and ageing. Countries with middle and high-middle SDI urgently need to take action to address this challenge.
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Carga Global da Doença , Leucemia , Humanos , Leucemia/epidemiologia , Leucemia/mortalidade , Carga Global da Doença/tendências , Masculino , Feminino , Fatores de Risco , Pessoa de Meia-Idade , Idoso , Adulto , Incidência , Adolescente , Adulto Jovem , Pré-Escolar , Saúde Global/estatística & dados numéricos , Criança , Previsões , Lactente , Idoso de 80 Anos ou mais , Recém-NascidoRESUMO
Korla pear has a unique taste and aroma and is a breeding parent of numerous pear varieties. It is susceptible to Valsa mali var. pyri, which invades bark wounded by freezing injury. Its genetic relationships have not been fully defined and could offer insight into the mechanism for freezing tolerance and disease resistance. We generated a high-quality, chromosome-level genome assembly for Korla pear via the Illumina and PacBio circular consensus sequencing (CCS) platforms and high-throughput chromosome conformation capture (Hi-C). The Korla pear genome is ~ 496.63 Mb, and 99.18% of it is assembled to 17 chromosomes. Collinearity and phylogenetic analyses indicated that Korla might be derived from Pyrus pyrifolia and that it diverged ~ 3.9-4.6 Mya. During domestication, seven late embryogenesis abundant (LEA), two dehydrin (DHN), and 54 disease resistance genes were lost from Korla pear compared with P. betulifolia. Moreover, 21 LEA and 31 disease resistance genes were common to the Korla pear and P. betulifolia genomes but were upregulated under overwintering only in P. betulifolia because key cis elements were missing in Korla pear. Gene deletion and downregulation during domestication reduced freezing tolerance and disease resistance in Korla pear. These results could facilitate the breeding of novel pear varieties with high biotic and abiotic stress resistance.
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Cromossomos de Plantas , Genoma de Planta , Pyrus , Pyrus/genética , Pyrus/fisiologia , Cromossomos de Plantas/genética , Filogenia , Estações do Ano , Resistência à Doença/genética , CongelamentoRESUMO
Live imaging of primary neural cells is crucial for monitoring neuronal activity, especially multiscale and multifunctional imaging that offers excellent biocompatibility. Multiscale imaging can provide insights into cellular structure and function from the nanoscale to the millimeter scale. Multifunctional imaging can monitor different activities in the brain. However, this remains a challenge because of the lack of dyes with a high signal-to-background ratio, water solubility, and multiscale and multifunctional imaging capabilities. In this study, we present a neural dye with near-infrared (NIR) emissions (>700 nm) that enables ultrafast staining (in less than 1 min) for the imaging of primary neurons. This dye not only enables multiscale neural live-cell imaging from vesicles in neurites, neural membranes, and single neurons to the whole brain but also facilitates multifunctional imaging, such as the monitoring and quantifying of synaptic vesicles and the changes in membrane potential. We also explore the potential of this NIR neural dye for staining brain slices and live brains. The NIR neural dye exhibits superior binding with neural membranes compared to commercial dyes, thereby achieving multiscale and multifunctional brain neuroimaging. In conclusion, our findings introduce a significant breakthrough in neuroimaging dyes by developing a category of small molecular dyes.
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Encéfalo , Corantes Fluorescentes , Neurônios , Animais , Encéfalo/diagnóstico por imagem , Corantes Fluorescentes/química , Neurônios/metabolismo , Camundongos , Neuroimagem/métodos , Espectroscopia de Luz Próxima ao Infravermelho/métodos , Ratos , Raios Infravermelhos , Imagem ÓpticaRESUMO
Fe single atoms (Fe SAs) based catalysts have received much attention in electrocatalytic oxygen reduction reaction (ORR) due to its low-cost and high activity. Yet, the facile synthesis of efficient and stable Fe SAs catalysts are still challenging. Here, we reported a Fe SAs anchored on N-doped mesoporous carbon microspheres (NC) catalyst via spraying drying and pyrolysis processes. The highly active Fe SAs are uniformly distributed on the NC matrix, which prevented the aggregation benefiting from the enhanced Fe-N bonds. Also, the mesoporous carbon structure is favorable for fast electron and mass transfer. The optimized Fe@NC-2-900 catalyst shows positive half wave potential (E1/2 = 0.86 V vs reversible hydrogen electrodes (RHE)) and starting potential (Eonset = 0.98 V vs RHE) in ORR, which is comparable to the commercial Pt/C catalyst (E1/2= 0.87 V, Eonset = 1.08 V). Outstanding stability with a current retention rate of 92.5% for 9 hours and good methanol tolerance are achieved. The assembled zinc-air batteries showed good stability up to 500 hours at a current density of 5 mA cm-2. This work shows potentials of Fe SAs based catalysts for the practical application in ORR and pave a new avenue for promoting their catalytic performances.
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BACKGROUND: Hemorrhagic stroke is a devastating cerebrovascular event with a high rate of early mortality and long-term disability. The therapeutic potential of mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) for neurological conditions, such as intracerebral hemorrhage (ICH), has garnered considerable interest, has garnered considerable interest, though their mechanisms of action remain poorly understood. METHODS: EVs were isolated from human umbilical cord MSCs, and SPECT/CT was used to track the 99mTc-labeled EVs in a mouse model of ICH. A series of comprehensive evaluations, including magnetic resonance imaging (MRI), histological study, RNA sequencing (RNA-Seq), or miRNA microarray, were performed to investigate the therapeutic action and mechanisms of MSC-EVs in both cellular and animal models of ICH. RESULTS: Our findings show that intravenous injection of MSC-EVs exhibits a marked affinity for the ICH-affected brain regions and cortical neurons. EV infusion alleviates the pathological changes observed in MRI due to ICH and reduces damage to ipsilateral cortical neurons. RNA-Seq analysis reveals that EV treatment modulates key pathways involved in the neuronal system and metal ion transport in mice subjected to ICH. These data were supported by the attenuation of neuronal ferroptosis in neurons treated with Hemin and in ICH mice following EV therapy. Additionally, miRNA microarray analysis depicted the EV-miRNAs targeting genes associated with ferroptosis, and miR-214-3p was identified as a regulator of neuronal ferroptosis in the ICH cellular model. CONCLUSIONS: MSC-EVs offer neuroprotective effects against ICH-induced neuronal damage by modulating ferroptosis highlighting their therapeutic potential for combating neuronal ferroptosis in brain disorders.
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Hemorragia Cerebral , Vesículas Extracelulares , Ferroptose , Células-Tronco Mesenquimais , Neurônios , Vesículas Extracelulares/metabolismo , Animais , Hemorragia Cerebral/terapia , Hemorragia Cerebral/metabolismo , Hemorragia Cerebral/patologia , Células-Tronco Mesenquimais/metabolismo , Camundongos , Humanos , Neurônios/metabolismo , Modelos Animais de Doenças , Masculino , MicroRNAs/metabolismo , MicroRNAs/genética , Camundongos Endogâmicos C57BLRESUMO
Various copper-related defects in the absorption layer have been a key factor impeding the enhancement of the efficiency of Cu2ZnSn(S,Se)4 (CZTSSe) solar cells. Alkali metal doping is considered to be a good strategy to ameliorate this problem. In this article, Rb-doped CZTSSe (RCZTSSe) thin films were synthesized using the sol-gel technique. The results show that the Rb atom could successfully enter into the CZTSSe lattice and replace the Cu atom. According to SEM results, a moderate amount of Rb doping aided in enhancing the growth of grains in CZTSSe thin films. It was proven that the RCZTSSe thin film had the densest surface morphology and the fewest holes when the doping content of Rb was 2%. In addition, Rb doping successfully inhibited the formation of CuZn defects and correlative defect clusters and promoted the electrical properties of RCZTSSe thin films. Finally, a remarkable power conversion efficiency of 7.32% was attained by the champion RCZTSSe device with a Rb content of 2%. Compared with that of un-doped CZTSSe, the efficiency improved by over 30%. This study offers new insights into the influence of alkali metal doping on suppressing copper-related defects and also presents a viable approach for improving the efficiency of CZTSSe devices.
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Background: Small cell lung cancer (SCLC) presents considerable challenges regarding the availability of second-line treatment options, which remain limited. The paucity of effective therapeutic choices at this setting emphasizes the urgent requirement for rigorous research and investigation into novel treatment strategies. To address this clinical gap, the current study aimed to compare the efficacy and safety of anlotinib with the standard second-line treatment, topotecan, in patients with relapsed SCLC. Methods: This retrospective collected data from SCLC patients who received either anlotinib or topotecan as second-line treatment. The primary endpoints were progression-free survival (PFS), while the secondary endpoints included the overall survival (OS), objective response rate (ORR), disease control rate (DCR), and safety assessment. Results: The study included 46 SCLC patients, with 20 receiving anlotinib and 26 receiving topotecan as second-line treatment. The anlotinib group showed a significantly longer median PFS compared to the topotecan group [5.6 vs. 2.2 months; hazard ratio (HR) =0.50; 95% confidence interval (CI): 0.27-0.92; P=0.02]. However, there was no statistically significant difference in OS between the two groups (9.1 vs. 7.7 months; HR =0.88; 95% CI: 0.46-1.70; P=0.71). The ORRs were 20.0% and 7.7% (P=0.48), and the DCRs were 70.0% and 23.1% (P=0.007) for the anlotinib and topotecan groups, respectively. Treatment-related adverse events (TRAEs) occurred in 13 patients (65.0%) in the anlotinib group and 20 (76.9%) in the topotecan group (P=0.49). Conclusions: Anlotinib shows the potential to extend PFS and manageable adverse events (AEs) compared to topotecan in the second-line setting for relapsed SCLC.
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BACKGROUND: Type 2 diabetes mellitus (T2D) is associated with an increased risk of cognitive dysfunction. Angiopoietin-like protein 8 (ANGPTL8) is an important regulator in T2D, but the role of ANGPTL8 in diabetes-associated cognitive dysfunction remains unknown. Here, we explored the role of ANGPTL8 in diabetes-associated cognitive dysfunction through its interaction with paired immunoglobulin-like receptor B (PirB) in the central nervous system. METHODS: The levels of ANGPTL8 in type 2 diabetic patients with cognitive dysfunction and control individuals were measured. Mouse models of diabetes-associated cognitive dysfunction were constructed to investigate the role of ANGPTL8 in cognitive function. The cognitive function of the mice was assessed by the Barnes Maze test and the novel object recognition test, and levels of ANGPTL8, synaptic and axonal markers, and pro-inflammatory cytokines were measured. Primary neurons and microglia were treated with recombinant ANGPTL8 protein (rA8), and subsequent changes were examined. In addition, the changes induced by ANGPTL8 were validated after blocking PirB and its downstream pathways. Finally, mice with central nervous system-specific knockout of Angptl8 and PirB-/- mice were generated, and relevant in vivo experiments were performed. RESULTS: Here, we demonstrated that in the diabetic brain, ANGPTL8 was secreted by neurons into the hippocampus, resulting in neuroinflammation and impairment of synaptic plasticity. Moreover, neuron-specific Angptl8 knockout prevented diabetes-associated cognitive dysfunction and neuroinflammation. Mechanistically, ANGPTL8 acted in parallel to neurons and microglia via its receptor PirB, manifesting as downregulation of synaptic and axonal markers in neurons and upregulation of proinflammatory cytokine expression in microglia. In vivo, PirB-/- mice exhibited resistance to ANGPTL8-induced neuroinflammation and synaptic damage. CONCLUSION: Taken together, our findings reveal the role of ANGPTL8 in the pathogenesis of diabetes-associated cognitive dysfunction and identify the ANGPTL8-PirB signaling pathway as a potential target for the management of this condition.
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Proteína 8 Semelhante a Angiopoietina , Proteínas Semelhantes a Angiopoietina , Disfunção Cognitiva , Diabetes Mellitus Tipo 2 , Camundongos Knockout , Receptores Imunológicos , Transdução de Sinais , Animais , Camundongos , Disfunção Cognitiva/metabolismo , Disfunção Cognitiva/prevenção & controle , Disfunção Cognitiva/etiologia , Transdução de Sinais/fisiologia , Transdução de Sinais/efeitos dos fármacos , Proteínas Semelhantes a Angiopoietina/metabolismo , Proteínas Semelhantes a Angiopoietina/genética , Humanos , Masculino , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/metabolismo , Receptores Imunológicos/metabolismo , Receptores Imunológicos/genética , Camundongos Endogâmicos C57BL , Sinapses/metabolismo , Sinapses/patologia , Sinapses/efeitos dos fármacos , Hormônios Peptídicos/metabolismo , Pessoa de Meia-Idade , FemininoRESUMO
Parkinson's disease (PD) is one of the most common neurodegenerative diseases and involves various pathogenic mechanisms, including oxidative stress and neuroinflammation. Niacin, an important cofactor in mitochondrial energy metabolism, may play a key role in the pathogenesis of PD. An in-depth exploration of the relationship between niacin and mitochondrial energy metabolism may provide new targets for the treatment of PD. The present study was designed to examine the association between dietary niacin intake and the risk of PD in US adults. Data from adults aged 40 years and older collected during cycles of the United States (US) National Health and Nutrition Examination Survey (NHANES) from 2005 to 2018 were used. A multiple logistic regression model was used to analyze the relationship between dietary niacin intake and the risk of PD. Further linear tests using restricted cubic splines (RCS) were performed to explore the shape of the dose-response relationship. Subgroup stratification and interaction analyses were conducted according to years of education, marital status, smoking, and hypertension to evaluate the stability of the association between different subgroups. A total of 20,211 participants were included in this study, of which 192 were diagnosed with PD. In the fully adjusted multiple logistic regression model, dietary niacin intake was negatively associated with the risk of PD (OR: 0.77, 95%CI: 0.6-0.99; p = 0.042). In the RCS linear test, the occurrence of PD was negatively correlated with dietary niacin intake (nonlinearity: p = 0.232). In stratified analyses, dietary niacin intake was more strongly associated with PD and acted as an important protective factor in patients with fewer years of education (OR: 0.35, 95%CI: 0.13-0.93), married or cohabitating (OR: 0.71, 95%CI: 0.5-0.99), taking dietary supplements (OR: 0.6, 95%CI: 0.37 0.97), non-smokers (OR: 0.57, 95%CI: 0.39-0.85), those with hypertension (OR: 0.63, 95%CI: 0.63-0.95), coronary artery disease (OR: 0.77, 95%CI: 0.6-1), and stroke (OR: 0.75, 95%CI: 0.88-0.98), but the interaction was not statistically significant in all subgroups. Dietary niacin intake was inversely associated with PD risk in US adults, with a 23% reduction in risk for each 10 mg increase in niacin intake.
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As vastly modified on secreted proteins, N-glycosylation is found on milk proteins and undergo dynamic changes during lactation, characterizing milk protein glycosylation would benefit the elucidation of glycosylation pattern differences between samples. However, their low abundance required specific enrichment. Herein, through rational design and controllable synthesis, we developed a novel multi-functional polymer for the isolation of protein glycosylation. It efficiently separated glycopeptides from complex background inferences with mutual efforts of hydrophilic interaction chromatography (HILIC), metal ion affinity and ion exchange. By fine-tuning Ca2+ as regulators of aldehyde hyaluronic acid (HA) conformation, the grafting density of HA was remarkably improved. Moreover, grafting Ti4+ further enhanced the enrichment performance. Application of this material to characterize bovine milk and colostrum proteins yields 479 and 611 intact glycopeptides, respectively. Comparative analysis unraveled the distinct glycosylation pattern as well the different distribution of glycoprotein abundances between the two samples, offering insights for functional food development.
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Breast cancer (BC) is the most common tumor in women worldwide. TRIM28 (RNF96) plays pleiotropic biological functions, such as silencing target genes, facilitating DNA repair, stimulating cellular proliferation and differentiation, and contributing to cancer progression. TRIM28 plays an increasingly crucial role in cancer, but its impact on BC, including breast invasive carcinoma, remains poorly understood. In the current study, analyses of online databases, quantitative real-time quantitative PCR, immunohistochemistry, and western blotting were performed on patients with breast invasive carcinoma (BRCA). Cordycepin (CD) was used to monitor BC progression and TRIM28 expression in vivo. As a result, we observed that TRIM28 is highly expressed in breast invasive carcinoma tissues compared with the corresponding normal tissues and is correlated with metastatic / invasive progression. High expression of TRIM28 might serve as a prognostic marker for long-term survival in triple-negative BC, advanced BC, or breast invasive carcinoma. Although TRIM28 methylation in tumor tissues of breast invasive carcinoma is not significantly changed compared to the matched normal tissues, the expressions and methylation of TRIM28 are significantly reversely correlated. TRIM28 expression was inhibited by CD in the mouse model, indicating its role in preventing BC progression. Thus, TRIM28 might be a potentially valuable molecular target for forecasting the progression / prognosis of patients with breast invasive carcinoma. CD, which represses BC growth/metastasis, may be involved partially through suppressing TRIM28 expression.
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Excessive phosphorus (P) levels can disrupt nutrient balance in plants, adversely affecting growth. The molecular responses of Pennisetum species to high phosphorus stress remain poorly understood. This study examined two Pennisetum species, Pennisetum americanum × Pennisetum purpureum and Pennisetum americanum, under varying P concentrations (200, 600 and 1000 µmol·L- 1 KH2PO4) to elucidate transcriptomic alterations under high-P conditions. Our findings revealed that P. americanum exhibited stronger adaption to high-P stress compared to P. americanum× P. purpureum. Both species showed an increase in plant height and leaf P content under elevated P levels, with P. americanum demonstrating greater height and higher P content than P. americanum× P. purpureum. Transcriptomic analysis identified significant up- and down-regulation of key genes (e.g. SAUR, GH3, AHP, PIF4, PYL, GST, GPX, GSR, CAT, SOD1, CHS, ANR, P5CS and PsbO) involved in plant hormone signal transduction, glutathione metabolism, peroxisomes, flavonoid biosynthesis, amino acid biosynthesis and photosynthesis pathways. Compared with P. americanum× P. purpureum, P. americanum has more key genes in the KEGG pathway, and some genes have higher expression levels. These results contribute valuable insights into the molecular mechanisms governing high-P stress in Pennisetum species and offer implications for broader plant stress research.
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Perfilação da Expressão Gênica , Pennisetum , Fósforo , Folhas de Planta , Estresse Fisiológico , Pennisetum/genética , Pennisetum/metabolismo , Folhas de Planta/genética , Folhas de Planta/metabolismo , Fósforo/metabolismo , Estresse Fisiológico/genética , Regulação da Expressão Gênica de Plantas , Transcriptoma , Genes de PlantasRESUMO
Melanoma is a primary malignant tumor with high lethality, which occurs in the skin and eye tissues, while the molecular mechanisms of melanomagenesis remain largely unknown. Here, we show that death-associated protein-like 1 (DAPL1) expression is lower in melanoma tissues than in paracancerous tissues or nevus tissues, and Uveal melanoma patients with lower DAPL1 expression have a poorer survival rate than those with higher expression of DAPL1. Overexpression of DAPL1 inhibits proliferation of cultured melanoma cells, whereas knockdown of DAPL1 increases cell proliferation. Tumor transplantation experiment results also demonstrate that DAPL1 inhibits tumorigenesis of melanoma cells both in subretinal and subcutaneous tissues of nude mice in vivo. Finally, DAPL1 inhibits proliferation of melanoma cells by increasing the protein level of P21 via decreasing the ubiquitin mediated degradation of P21 and promoting its stability. Conversely, knockdown of P21 neutralizes the effects of inhibition of DAPL1 on melanoma cell proliferation and enhances the severity of melanoma tumorigenesis. These results suggest that DAPL1 is a novel melanoma tumor suppressor gene and thus a potential therapeutic target for melanoma.
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Background: It is difficult to obtain 18-fluorodeoxyglucose positron emission tomography (18FDG-PET) data from normal children, and changes in brain metabolism in children due to growth and development are poorly understood. For the first time, we established a normal control model of brain 18FDG-PET in children and evaluated its feasibility. The association of PET with age in children aged 0-14 years was analyzed. This study aimed to establish a normal control model of brain 18FDG-PET in children for the first time and to verify its feasibility, and to analyze the trend of PET with age in children aged 0-14 years. Methods: In this retrospective cohort study, the 18FDG-PET imaging data of patients with no epileptiform discharge involvement contralateral to the epileptogenic zone were consecutively collected from January 2015 to June 2022 according to strictly defined screening criteria. For the normal control data, the hemisphere contralateral to the epileptogenic zone was mirrored and spliced to form an intact brain. The cohort of children aged 0-14 years was divided into 14 groups according age by year. Subsequently, patients who underwent lesionectomy with clear hypometabolism that roughly coincided with the extent of surgical resection were examined. The PET scan was compared with the control model, and the ratio of overlapping parts (hypometabolic areas â© surgical resection area) to hypometabolic parts (ROH) was calculated. Multiple regression analysis was performed on the normal control model for every 3- to 4-year age interval. Results: A total of 159 normal control models were established. Five patients were randomly selected to verify the reliability of each yearly model. The average ROH was 0.968. Metabolism increasing with age in the different brain regions was observed at ages 0-2~, 3-5~, and 6-10 years. No age-related metabolic increase or decrease was found in the 10- to 14-year-old group. The metabolism in the 7- to 8-year-old group was higher than that in the 13- to 14-year-old group. Conclusions: With strict screening criteria, the method of mirroring the contralateral hemisphere of the epileptic zone and splicing it into a complete brain as a means of creating a normal control group is feasible. The method offers convenience to the studies that lack healthy pediatric controls. Children under 10 years of age (especially 0-6 years old) experience considerable metabolic changes year on year. After the age of 10 years, the changes in metabolism gradually decrease, and metabolism also slowly decreases. Our findings provide guidance the clinical interpretation of areas with hypometabolism and emphasize the importance of establishing a normal control model of the child's brain, which should not be replaced by an adult model.
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The intricate process of shell biomineralization in marine molluscs is governed by a complex interplay of regulatory elements, encompassing secretomes, transporters, and noncoding RNA. This review delves into recent advancements in understanding these regulatory mechanisms, emphasizing their significance in elucidating the functions and evolutionary dynamics of the molluscan shell biomineralization process. Central to this intricate orchestration are secretomes with diverse functional domains, selectively exported to the extrapallial space, which directly regulate crystal growth and morphology. Transporters are crucial for substrate transportation in the calcification and maintenance of cellular homeostasis. Beyond proteins and transporters, noncoding RNA molecules are integral components influencing shell biomineralization. This review underscores the nonnegligible roles played by these genetic elements at the molecular level. To comprehend the complexity of biomineralization in mollusc, we explore the origin and evolutionary history of regulatory elements, primarily secretomes. While some elements have recently evolved, others are ancient genes that have been co-opted into the biomineralization toolkit. These elements undergo structural and functional evolution through rapidly evolving repetitive low-complexity domains and domain gain/loss/rearrangements, ultimately shaping a distinctive set of secretomes characterized by both conserved features and evolutionary innovations. This comprehensive review enhances our understanding of molluscan biomineralization at the molecular and genetic levels.
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Pregnancy is normally contraindicated in pulmonary arterial hypertension (PAH). Thanks to medical advances, the prognosis for pregnancy in patients with PAH has improved. The aim of our study was to investigate pregnancy conditions and outcomes in patients with mild, moderate and severe PAH. We searched PubMed, Embase, CNKI, Wanfang and Weipu databases for studies published before May 2024. Data from 29 included studies from 1898 references were pooled and analyzed. We calculated the rates for each group as well as the risk ratio (RR) and 95% confidence interval (CI) between pairwise. There was no statistical difference in maternal and neonatal survival between the mild and moderate groups. Maternal survival in the mild, moderate and severe groups was 100.0%, 99.7% and 88.8%, respectively, and neonatal survival was 100.0%, 99.7% and 96.0%, respectively. The incidence of NYHA class III-IV, pregnancy loss, intensive care unit (ICU) admission, fetal growth restriction, and neonatal asphyxia was lowest in patients with mild PAH and highest in patients with severe PAH (P < 0.001). The incidence of vaginal deliveries and term pregnancies was highest in the mild group and lowest in the severe group (P < 0.001). In conclusion, pregnant women with mild PAH can safely deliver a newborn. Given similar survival rates but greater economic and medical burdens, caution is advised in the moderate group. Pregnancy in the severe group is considered contraindicated.
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Concerted conservation efforts have brought the giant panda (Ailuropoda melanoleuca) back from the brink of extinction, but pandas continue to face anthropogenic threats in the wild and breeding success in captivity remains low. Because stress can have detrimental impacts on reproduction, monitoring stress- and sex-steroid levels would help assess the effectiveness of conservation mitigation measures in panda populations as well as monitor the welfare and reproductive health of captive animals. In this proof-of-concept study, we used faecal sex steroid and cortisol concentrations (n = 867 samples collected from five males and five females at Beijing Zoo every 4 days over the course of 12 months) as a reference to investigate if testosterone, estradiol, progesterone and cortisol can be meaningfully measured in panda hair (n = 10) using radio-immuno-assays. Additionally, we calculated the ratio of testosterone to cortisol (T:C ratio) for each male, which can provide a biomarker of stress and physical performance. Our findings revealed distinct monthly variations in faecal sex-steroid and cortisol concentrations, reflecting reproductive seasonality and visitor-related stress among individual pandas. Notably, the oldest male had a significantly lower T:C ratio than other males. Our results confirm that the level of sex steroids and cortisol can be assayed by panda hair, and the hair cortisol concentrations correlate significantly with that in faeces with one month lag behind (r = 0.68, P = 0.03). However, the concentrations of hormones detected in saliva are lower than those in faeces by two orders of magnitude, making it difficult to ensure accuracy. By assessing the applicability of hair, faecal and salivary sampling, we can infer their utility in monitoring the reproductive status and acute and chronic stress levels of giant pandas, thereby providing a means to gauge the success of ongoing habitat restoration efforts and to discuss the feasibility of sample collection from wild populations.
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Exosomes represent a type of extracellular vesicles derived from the endosomal pathway that transport diverse molecular cargoes such as proteins, lipids, and nucleic acids. These cargoes have emerged as crucial elements impacting disease diagnosis, treatment, and prognosis, and are integral to the process of exosome formation. This review delves into the essential molecular cargoes implicated in the phases of exosome production and release. Emphasis is placed on their significance as cancer biomarkers and potential therapeutic targets, accompanied by an exploration of the obstacles and feasible applications linked to these developments.
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Exossomos , Neoplasias , Exossomos/metabolismo , Humanos , Neoplasias/diagnóstico , Neoplasias/metabolismo , Animais , Biomarcadores Tumorais/metabolismoRESUMO
BACKGROUND: Despite improved treatments for acute myocardial infarction (AMI), myocardial fibrosis remains a key driver of adverse left ventricular (LV) remodeling and increased mortality. Fibroblast activation and proliferation significantly contribute to this process by enhancing cardiac fibrosis, which can lead to detrimental changes in LV structure. This study evaluates the effectiveness of 99mTc-labeled fibroblast activation protein inhibitor (99mTc-HFAPi) SPECT imaging in predicting LV remodeling over 12 months in post-AMI patients. METHODS: A cohort of 58 AMI patients (46 males, median age 61 [53, 67] years) underwent baseline 99mTc-HFAPi imaging (5 ± 2 days post-MI), perfusion imaging (6 ± 2 days post-MI), and echocardiography (2 ± 2 days post-MI). Additionally, 15 patients had follow-up 99mTc-HFAPi and perfusion imaging, while 30 patients had follow-up echocardiography. Myocardial 99mTc-HFAPi activity was assessed at the patient level. LV remodeling was defined as a ≥10% increase in LV end-diastolic diameter (LVEDD) or LV end-systolic diameter (LVESD) from baseline to follow-up echocardiography. RESULTS: AMI patients displayed localized but non-uniform 99mTc-HFAPi uptake, exceeding perfusion defects. Baseline 99mTc-HFAPi activity exhibited significant correlations with BNPmax, LDHmax, cTNImax, and WBCmax, inversely correlating with LVEF. After 12 months, 11 patients (36.66%) experienced LV remodeling. Univariate regression analysis demonstrated an association between baseline 99mTc-HFAPi uptake extent and LV remodeling (OR = 2.14, 95%CI, 1.04, 4.39, P = 0.038). CONCLUSIONS: 99mTc-HFAPi SPECT imaging holds promise in predicting LV remodeling post-MI, providing valuable insights for patient management and prognosis.