RESUMO

The quality of meat in prepared dishes deteriorates due to excessive protein denaturation resulting from precooking, freezing, and recooking. This study aimed to link the precooked state with chicken breast's recooked quality. Cooked Value (CV), based on protein denaturation kinetics, was established to indicate the doneness of meat during pre-heating. The effects of CVs after pre-heating on recooked qualities were investigated compared to fully pre-heated samples (control). Mild pre-heating reduced water migration and loss. While full pre-heating inhibited protein oxidation during freezing, intense oxidation during pre-heating led to higher oxidation levels. Surface hydrophobicity analysis revealed that mild pre-heating suppressed aggregation during recooking. These factors contributed to a better texture and microstructure of prepared meat with mild pre-heating. Finally, a potential mechanism of how pre-heating affects final qualities was depicted. This study underlines the need for finely controlling the industrial precooking process to regulate the quality of prepared meat.

Assuntos

Galinhas , Culinária , Temperatura Alta , Carne , Oxirredução , Desnaturação Proteica , Água , Animais , Cinética , Carne/análise , Água/química , Interações Hidrofóbicas e Hidrofílicas

RESUMO

BACKGROUND: Gastric cancer, a prevalent malignancy, poses a severe threat to the health of residents in China. Timely intervention in early stages can extend patients' survival. AIM: To analyze clinical characteristics of patients with early gastric cancer and efficacy and risk of complications associated with endoscopic resection. METHODS: This study included 175 patients with early gastric cancer treated at our hospital, with no restrictions on sex or age. General data, pathological information, and endoscopic biopsy results were obtained. The clinical characteristics of early gastric cancer were analyzed, and endoscopic resection was performed. Postoperative efficacy and incidence of complications were monitored. Statistical analysis was performed using SPSS 26.0 and GraphPad Prism 8.0 software. RESULTS: A total of 175 patients with early gastric cancer were included, with 75.43% (n = 132) males and 24.57% (n = 43) females. 38.29% (n = 67) and 35.43% (n = 62) of patients had a history of smoking and alcohol consumption, respectively. Comorbidities included diabetes (8.57%, n = 15), coronary heart disease (10.29%, n = 18), and hypertension (43.43%, n = 76), which was highly prevalent. A history of abdominal surgery and family history of digestive system cancer accounted for 21.14% and 17.14%, respectively. The most common lesion location was the antral part of the stomach (52.00%, n = 91), followed by the gastric angle, body, and fundus. The pathological types were predominantly high-grade intraepithelial neoplasia (28.00%, n = 49) and well-differentiated adenocarcinoma (26.86%, n = 47), followed by moderately differentiated adenocarcinoma, high-moderately differentiated adenocarcinoma, and moderate-lowly differentiated adenocarcinoma. 89.14% of the patients had intestinal metaplasia and 85.14% had atrophy. After endoscopic resection, re-examination revealed that 13 patients had cancer cells at the tissue margin, with a positive margin rate of 7.43%. Postoperative complications included no cases of gastrointestinal obstruction, but incisional infection (2.86%, n = 5), gastric perforation (1.14%, n = 2), and gastric bleeding (4%, n = 7) were present, with an overall incidence of 8.00%. CONCLUSION: Analysis of the clinical characteristics indicated that early gastric cancer is more prevalent in males with a history of hypertension, with lesions most commonly occurring in the antral region of the stomach. The pathological types are often high-grade intraepithelial neoplasia and well-differentiated adenocarcinoma, with over 85% of patients having comorbid intestinal metaplasia and atrophy. Despite endoscopic resection, a positive margin rate persisted, indicating a probability of residual cancer at the margins. Postoperative complications, such as gastrointestinal obstruction, incisional infection, gastric perforation, and gastric bleeding can occur and require timely symptomatic treatment.

RESUMO

Background: Microangiogenesis and lymphangiogenesis are essential for tumor growth in the tumor microenvironment, contributing to tumor invasion and metastasis. Limited literature exists on these processes in esophageal squamous cell carcinoma (ESCC). Therefore, the purpose of this study is to explore the impacts of microangiogenesis and lymphangiogenesis on the occurrence, progression, and prognosis assessment of ESCC. Methods: Surgical specimens and paraffin-embedded human tissues were procured from ESCC patients, encompassing 100 ESCC tissues and 100 cancer-adjacent normal (CAN) tissues. CD34 and D2-40 were utilized as markers for microvessel endothelial cells and lymphatic vessel endothelial cells, respectively. Microvascular density (MVD) and lymphatic vessel density (LVD) were evaluated through immunohistochemical quantification. Results: We found that tumor tissues in ESCC patients had significantly higher MVD and LVD than cancer-adjacent normal (CAN) tissues. High MVD and LVD were associated with lymph node metastasis and advanced tumor clinical stages. Additionally, both high MVD and high LVD were strongly linked to poorer prognosis among cancer patients. Furthermore, a positive correlation was found between high MVD and high LVD (p < 0.05). The presence of these markers individually indicated a worse prognosis, with their combined assessment showcasing enhanced prognostic value. Conclusions: Overall, the increased MVD and LVD indicates higher invasion and metastasis of ESCC, closely correlating with unfavorablefor poor prognosis of ESCC patients.

Assuntos

Carcinoma de Células Escamosas , Neoplasias Esofágicas , Carcinoma de Células Escamosas do Esôfago , Vasos Linfáticos , Densidade Microvascular , Humanos , Neoplasias Esofágicas/patologia , Neoplasias Esofágicas/mortalidade , Neoplasias Esofágicas/irrigação sanguínea , Masculino , Feminino , Prognóstico , Pessoa de Meia-Idade , Vasos Linfáticos/patologia , Carcinoma de Células Escamosas do Esôfago/patologia , Carcinoma de Células Escamosas do Esôfago/irrigação sanguínea , Carcinoma de Células Escamosas do Esôfago/mortalidade , Carcinoma de Células Escamosas/patologia , Carcinoma de Células Escamosas/mortalidade , Carcinoma de Células Escamosas/irrigação sanguínea , Metástase Linfática/patologia , Linfangiogênese/fisiologia , Idoso , Neovascularização Patológica/patologia , Microvasos/patologia , Antígenos CD34/metabolismo , Imuno-Histoquímica

RESUMO

Apoptosis associated speck like protein containing a card (ASC), the key adaptor protein of the assembly and activation of canonical inflammasomes, has been found to play a significant role in neuroinflammation after spinal cord injury (SCI). The previous studies indicated that widely block or knockout ASC can ameliorate SCI. However, ASC is ubiquitously expressed in infiltrated macrophages and local microglia, so further exploration is needed on which type of cell playing the key role. In this study, using the LysMcre;Ascflox/flox mice with macrophage-specifc ASC conditional knockout (CKO) and contusive SCI model, we focus on evaluating the specific role of ASC in lysozyme 2 (LysM)+ myeloid cells (mainly infiltrated macrophages) in this pathology. The results revealed that macrophage-specifc Asc CKO exhibited the follow effects: (1) A significant reduction in the numbers of infiltrated macrophages in the all phases of SCI, and activated microglia in the acute and subacute phases. (2) A significant reduction in ASC, caspase-1, interleukin (IL)-1ß, and IL-18 compared to control mice. (3) In the acute and subacute phases of SCI, M1 subset differentiation was inhibited, and M2 differentiation was increased. (4) Histology and hindlimb motor recoveries were improved. In conclusion, this study elucidates that macrophage-specific ASC CKO can improve nerve function recovery after SCI by regulating M1/M2 polarization through inhibiting ASC-dependent inflammasome signaling axis. This indicates that ASC in peripheral infiltrated macrophages may play an important role in SCI pathology, at least in mice, could be a potential target for treatment.

RESUMO

Recently, Clarireedia jacksonii has emerged as a significant pathogen threatening turfgrass, and its escalating resistance to multiple drugs often undermines field interventions. This study highlighted the critical role of the fungus-specific transcription factor CjXDR1 (formerly ShXDR1) in regulating multidrug resistance (MDR) in C. jacksonii. This was demonstrated through experiments involving CjXDR1-knockout and CjXDR1-complemented strains. Our sequence analysis revealed five mutations in CjXDR1: G445D, K453E, S607F, D676H, and V690A. All five gain-of-function (GOF) mutations were confirmed to directly contribute to MDR against three different classes of fungicides (propiconazole: demethylation inhibitor, boscalid: succinate dehydrogenase inhibitor, and iprodione: dicarboximide) using the genetic transformation system and in vitro fungicide-sensitivity assay. Comparative transcriptome analysis revealed that CjXDR1 and its GOF mutations led to the overexpression of downstream genes encoding a Phase I metabolizing enzyme (CYP68) and two Phase III transporters (CjPDR1 and CjAtrD) previously reported. Knockout mutants of CYP68, CjPDR1, CjAtrD, and double-knockout mutants of CjPDR1 and CjAtrD exhibited increased sensitivity to all three fungicides tested. Among these, the CYP68-knockout mutants displayed the highest sensitivity to propiconazole, while the CjPDR1 knockout mutant exhibited significantly increased sensitivity to all three fungicides. Double-knockout mutants of CjPDR1 and CjAtrD displayed greater sensitivity than the single knockouts. In conclusion, multiple GOF mutants in CjXDR1 contribute to MDR by upregulating the expression of CjPDR1, CjAtrD, and CYP68. This study enhances our understanding of the molecular mechanisms underlying MDR in plant pathogenic fungi, providing valuable insights into GOF mutation structures and advancing the development of antifungal drugs.

RESUMO

BACKGROUND: Positive regulators of T-cell function (PTFRs), integral to T-cell proliferation and activation, have been identified as potential prognostic markers in colorectal cancer (CRC). Despite this, their role within the tumor microenvironment (TME) and their response to immunotherapy are not yet fully understood. METHODS: This study delved into PTFR-related CRC subtypes by analyzing four independent transcriptome datasets, emphasizing the most significant prognostic PTFRs. We identified differentially expressed genes (DEGs) between two subtypes and developed a PTFR risk model using LASSO and Cox regression methods. The model's associations with survival time, clinical features, TME characteristics, tumor mutation profiles, microsatellite instability (MSI), cancer stem cell (CSC) index, and responses to chemotherapy, targeted therapy, and immunotherapy were subsequently explored. RESULTS: The PTFR risk model demonstrated a strong predictive capacity for CRC. It facilitated the estimation of immune cell composition, HLA expression levels, immune checkpoint expression, mutation burden, CSC index features, and the effectiveness of immunotherapy. CONCLUSIONS: This study enhances our understanding of the role of PTFRs in CRC progression and introduces an innovative assessment framework for CRC immunotherapy. This framework improves the prediction of treatment outcomes and aids in the customization of therapeutic strategies.

Assuntos

Neoplasias Colorretais , Imunoterapia , Instabilidade de Microssatélites , Microambiente Tumoral , Neoplasias Colorretais/genética , Neoplasias Colorretais/imunologia , Neoplasias Colorretais/terapia , Neoplasias Colorretais/patologia , Humanos , Microambiente Tumoral/imunologia , Microambiente Tumoral/genética , Imunoterapia/métodos , Prognóstico , Linfócitos T/imunologia , Transcriptoma , Biomarcadores Tumorais/genética , Células-Tronco Neoplásicas/imunologia , Feminino , Mutação

RESUMO

Particle size effects significantly impact the concentration and toxicity of heavy metals (HMs) in dust. Nevertheless, the differences in concentrations, sources, and risks of HMs in dust with different particle sizes are unclear. Therefore, guided by the definition of atmospheric particulate matter, dust samples with particle sizes under 1000 µm (DT1000), 100 µm (DT100), and 63 µm (DT63) from Beijing kindergartens were collected. The concentrations of HMs (e.g., Cd, Pb, Zn, Ni, Cr, Ba, Cu, V, Mn, Co, and Ti) in dust samples with different particle sizes were measured. Besides, the differences in HM concentrations, contamination levels, sources, and source-oriented health risks in dust samples of different particle sizes were systematically explored. The results show that the concentrations of Mn, V, Zn, and Cd gradually increase with decreasing dust particle sizes, the concentrations of Ba and Pb show a decreasing trend, and the concentrations of Cr, Cu, Ni, and Co display an increasing and then decreasing trend. The degree of contamination of HMs in dust of different particle sizes varies, with Cd being the most dominant contaminant. Compared with DT1000 and DT63, DT100 is the most polluted. In addition, the sources of HMs in DT1000, DT100, and DT63 become more single with decreasing particle size, which may be mainly due to the particle-size effect inducing the redistribution of HMs in different sources. Notably, the potential health risk is higher in DT100 than in DT1000 and DT63. The highest contribution of industrial sources to the health risk is found in DT100, which is mainly caused by highly toxic chromium (Cr). This work emphasizes the importance of considering particle size in risk assessment and pollution control, which can provide a theoretical basis for precise management of HMs pollution in dust.

RESUMO

BACKGROUND: Kidney transplantation is the optimal renal replacement therapy for children with end-stage renal disease; however, delayed graft function (DGF), a common post-operative complication, may negatively impact the long-term outcomes of both the graft and the pediatric recipient. However, there is limited research on DGF in pediatric kidney transplant recipients. This study aims to develop a predictive model for the risk of DGF occurrence after pediatric kidney transplantation by integrating donor and recipient characteristics and utilizing machine learning algorithms, ultimately providing guidance for clinical decision-making. METHODS: This single-center retrospective cohort study includes all recipients under 18 years of age who underwent single-donor kidney transplantation at our hospital between 2016 and 2023, along with their corresponding donors. Demographic, clinical, and laboratory examination data were collected from both donors and recipients. Univariate logistic regression models and differential analysis were employed to identify features associated with DGF. Subsequently, a risk score for predicting DGF occurrence (DGF-RS) was constructed based on machine learning combinations. Model performance was evaluated using the receiver operating characteristic curves, decision curve analysis (DCA), and other methods. RESULTS: The study included a total of 140 pediatric kidney transplant recipients, among whom 37 (26.4%) developed DGF. Univariate analysis revealed that high-density lipoprotein cholesterol (HDLC), donor after circulatory death (DCD), warm ischemia time (WIT), cold ischemia time (CIT), gender match, and donor creatinine were significantly associated with DGF (P < 0.05). Based on these six features, the random forest model (mtry = 5, 75%p) exhibited the best predictive performance among 97 machine learning models, with the area under the curve values reaching 0.983, 1, and 0.905 for the entire cohort, training set, and validation set, respectively. This model significantly outperformed single indicators. The DCA curve confirmed the clinical utility of this model. CONCLUSIONS: In this study, we developed a machine learning-based predictive model for DGF following pediatric kidney transplantation, termed DGF-RS, which integrates both donor and recipient characteristics. The model demonstrated excellent predictive accuracy and provides essential guidance for clinical decision-making. These findings contribute to our understanding of the pathogenesis of DGF.

Assuntos

Função Retardada do Enxerto , Transplante de Rim , Aprendizado de Máquina , Doadores de Tecidos , Humanos , Transplante de Rim/efeitos adversos , Feminino , Masculino , Criança , Estudos Retrospectivos , Adolescente , Pré-Escolar , Lactente

RESUMO

Argonaute (AGO), a component of RNA-induced silencing complexes (RISCs), is a representative RNA-binding protein (RBP) known to bind with mature microRNA (miRNA) and is directly involved in post-transcriptional gene silencing. However, despite the biological significance of miRNA, the roles of other micro RNA-binding proteins (miRBPs) remain unclear in regulation of miRNA loading, dissociation from RISC, and extracellular release. In this study, we perform protein arrays to profile miRBPs and identify 118 RNA-binding proteins directly binding with miRNAs. Among those proteins, RBP quaking (QKI) inhibits extracellular release of mature microRNA let-7b by controlling the loading of let-7b into extracellular vesicles via additional miRBPs such as hnRNPD/AUF1 and hnRNPK. The enhanced extracellular release of let-7b after QKI depletion activates the Toll-like Receptor 7 (TLR7) and promotes the production of proinflammatory cytokines in recipient cells, leading to brain inflammation in mouse cortex. Thus, this study reveals contribution of QKI to the inhibition of brain inflammation via regulation of extracellular let-7b release.

RESUMO

Activating enhancer-binding protein 2 (AP-2) is a family of transcription factors (TFs) that play crucial roles in regulating embryonic and oncogenic development. In addition to splice isoforms, five major family members encoded by the TFAP2A/B/C/D/E genes have been identified in humans, i.e., AP-2α/ß/γ/δ/ε. In general, the first three TFs have been studied more thoroughly than AP-2δ or AP-2ε. Currently, there is a relatively limited body of literature focusing on the AP-2 family in the context of gastroenterological research, and a comprehensive overview of the existing knowledge and recommendations for further research directions is lacking. Herein, we have collected available gastroenterological data on AP-2 TFs, discussed the latest medical applications of each family member, and proposed potential future directions. Research on AP-2 in gastrointestinal tumors has predominantly been focused on the two best-described family members, AP-2α and AP-2γ. Surprisingly, research in the past decade has highlighted the importance of AP-2ε in the drug resistance of gastric cancer (GC) and colorectal cancer (CRC). While numerous questions about gastroenterological disorders await elucidation, the available data undoubtedly open avenues for anti-cancer targeted therapy and overcoming chemotherapy resistance. In addition to gastrointestinal cancers, AP-2 family members (primarily AP-2ß and marginally AP-2γ) have been associated with other health issues such as obesity, type 2 diabetes, liver dysfunction, and pseudo-obstruction. On the other hand, AP-2δ has been poorly investigated in gastroenterological disorders, necessitating further research to delineate its role. In conclusion, despite the limited attention given to AP-2 in gastroenterology research, pivotal functions of these transcription factors have started to emerge and warrant further exploration in the future.

Assuntos

Fator de Transcrição AP-2 , Humanos , Fator de Transcrição AP-2/metabolismo , Fator de Transcrição AP-2/genética , Gastroenteropatias/genética , Gastroenteropatias/metabolismo , Animais

RESUMO

BACKGROUND: Coronary artery thrombosis and myocardial ischemia caused by giant coronary aneurysms are the main causes of death in children with Kawasaki disease. The use of thrombolytic therapy in children with Kawasaki disease who have coronary thrombosis is a controversial topic, especially with respect to the timing of treatment. CASE PRESENTATION: In this article, we report a case of a child aged two years and nine months with Kawasaki disease whose coronary arteries had no involvement in the acute phase. However, by only one week after discharge, the patient returned because we found giant coronary aneurysms complicated by thrombosis via echocardiography. Despite aggressive thrombolytic therapy, the child developed myocardial ischemia during thrombolytic therapy. Fortunately, because of timely treatment, the child's thrombus has dissolved, and the myocardial ischemia has resolved. CONCLUSIONS: This case suggests that for patients at high risk of coronary artery aneurysms, echocardiography may need to be reviewed earlier. Low-molecular-weight heparin should be added to antagonize the early procoagulant effects of warfarin when warfarin therapy is initiated. In the case of first-detected coronary thrombosis, aggressive thrombolytic therapy may be justified, particularly during the acute and subacute phases of the disease course.

Assuntos

Aneurisma Coronário , Trombose Coronária , Síndrome de Linfonodos Mucocutâneos , Isquemia Miocárdica , Terapia Trombolítica , Humanos , Síndrome de Linfonodos Mucocutâneos/complicações , Síndrome de Linfonodos Mucocutâneos/diagnóstico , Síndrome de Linfonodos Mucocutâneos/tratamento farmacológico , Trombose Coronária/diagnóstico por imagem , Trombose Coronária/etiologia , Aneurisma Coronário/diagnóstico por imagem , Aneurisma Coronário/etiologia , Resultado do Tratamento , Pré-Escolar , Isquemia Miocárdica/etiologia , Isquemia Miocárdica/tratamento farmacológico , Isquemia Miocárdica/diagnóstico por imagem , Masculino , Anticoagulantes/uso terapêutico , Fibrinolíticos/uso terapêutico , Angiografia Coronária

RESUMO

The Nab-paclitaxel combined with gemcitabine (AG) regimen is the main chemotherapy regimen for pancreatic cancer, but drug resistance often occurs. Currently, the ability to promote sensitization in drug-resistant cases is an important clinical issue, and the strategy of repurposing conventional drugs is a promising strategy. This study aimed to identify a classic drug that targets chemotherapy resistance's core signaling pathways and combine it with the AG regimen to enhance chemosensitivity. We also aimed to find reliable predictive biomarkers of drug combination sensitivity. Using RNA sequencing, we found that abnormal PI3K/Akt pathway activation plays a central role in mediating resistance to the AG regimen. Subsequently, through internal and external verification of randomly selected AG-resistant patient-derived organoid (PDO) and PDO xenograft models, we discovered for the first time that the classic anti-inflammatory drug sulindac K-80003, an inhibitor of the PI3K/Akt pathway that we focused on, promoted sensitization in half (14/28) of AG-resistant pancreatic ductal adenocarcinoma cases. Through RNA-sequencing, multiplex immunofluorescent staining, and immunohistochemistry experiments, we identified cFAM124A as a novel biomarker through which sulindac K-80003 promotes AG sensitization. Its role as a sensitization marker is explained via the following mechanism: cFAM124A enhances both the mRNA expression of cathepsin L and the activity of the cathepsin L enzyme. This dual effect stimulates the cleavage of RXRα, leading to large amounts of truncated RXRα, which serves as a direct target of K-80003. Consequently, this process results in the pathological activation of the PI3K/Akt pathway. In summary, our study provides a new treatment strategy and novel biological target for patients with drug-resistant pancreatic cancer.

Assuntos

Albuminas , Protocolos de Quimioterapia Combinada Antineoplásica , Desoxicitidina , Resistencia a Medicamentos Antineoplásicos , Gencitabina , Paclitaxel , Neoplasias Pancreáticas , Sulindaco , Ensaios Antitumorais Modelo de Xenoenxerto , Desoxicitidina/análogos & derivados , Desoxicitidina/farmacologia , Humanos , Paclitaxel/farmacologia , Paclitaxel/uso terapêutico , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Neoplasias Pancreáticas/tratamento farmacológico , Neoplasias Pancreáticas/metabolismo , Neoplasias Pancreáticas/patologia , Animais , Camundongos , Albuminas/farmacologia , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia , Sulindaco/farmacologia , Sulindaco/análogos & derivados , Linhagem Celular Tumoral , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais/efeitos dos fármacos , Fosfatidilinositol 3-Quinases/metabolismo , Feminino , Carcinoma Ductal Pancreático/tratamento farmacológico , Carcinoma Ductal Pancreático/patologia , Carcinoma Ductal Pancreático/metabolismo , Masculino , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos

RESUMO

Malassezia, the most abundant fungal commensal on the mammalian skin, has been linked to several inflammatory skin diseases such as atopic dermatitis, seborrheic dermatitis and psoriasis. This study reveals that epicutaneous application with Malassezia globosa (M. globosa) triggers skin inflammation in mice. RNA-sequencing of the resulting mouse lesions indicates activation of Interleukin-17 (IL-17) signaling and T helper 17 (Th17) cells differentiation pathways by M. globosa. Furthermore, our findings demonstrate a significant upregulation of IL-23, IL-23R, IL-17A, and IL-22 expressions, along with an increase in the proportion of Th17 and pathogenic Th17 cells in mouse skin exposed to M. globosa. In vitro experiments illustrate that M. globosa prompts human primary keratinocytes to secrete IL-23 via TLR2/MyD88/NF-κB signaling. This IL-23 secretion by keratinocytes is shown to be adequate for inducing the differentiation of pathogenic Th17 cells in the skin. Overall, these results underscore the significant role of Malassezia in exacerbating skin inflammation by stimulating IL-23 secretion by keratinocytes and promoting the differentiation of pathogenic Th17 cells.

Assuntos

Diferenciação Celular , Interleucina-23 , Queratinócitos , Malassezia , Células Th17 , Malassezia/imunologia , Queratinócitos/microbiologia , Queratinócitos/imunologia , Queratinócitos/metabolismo , Células Th17/imunologia , Animais , Interleucina-23/metabolismo , Humanos , Camundongos , Transdução de Sinais , NF-kappa B/metabolismo , Receptor 2 Toll-Like/metabolismo , Interleucina-17/metabolismo , Pele/microbiologia , Pele/patologia , Pele/imunologia , Modelos Animais de Doenças , Fator 88 de Diferenciação Mieloide/metabolismo , Fator 88 de Diferenciação Mieloide/genética , Células Cultivadas , Camundongos Endogâmicos C57BL , Interleucina 22

RESUMO

Dollar spot, a highly destructive turfgrasses disease worldwide, is caused by multiple species within the genus Clarireedia. Previous research indicated varying sensitivity to boscalid among Clarireedia populations not historically exposed to succinate dehydrogenase inhibitors (SDHIs). This study confirms that the differential sensitivity pattern is inherent among different Clarireedia spp., utilizing a combination of phylogenetic analyses, in vitro cross-resistance assays, and genetic transformation of target genes with different mutations. Furthermore, greenhouse inoculation experiments revealed that the differential boscalid sensitivity did not lead to pathogenicity issues or fitness penalties, thereby not resulting in control failure by boscalid. This research underscores the importance of continuous monitoring of fungicide sensitivity trends and highlights the complexity of chemical control of dollar spot due to the inherent variability in fungicide sensitivity among different Clarireedia spp.

Assuntos

Compostos de Bifenilo , Fungicidas Industriais , Niacinamida , Doenças das Plantas , Fungicidas Industriais/farmacologia , Compostos de Bifenilo/farmacologia , Doenças das Plantas/microbiologia , Niacinamida/análogos & derivados , Niacinamida/farmacologia , Poaceae/microbiologia , Filogenia , Farmacorresistência Fúngica/genética , Succinato Desidrogenase/genética , Succinato Desidrogenase/antagonistas & inibidores , Basidiomycota/genética , Basidiomycota/efeitos dos fármacos

RESUMO

In microgravity conditions, the consumption of Spirulina platensis (SP) as a renewable food source shows promise in mitigating osteoporosis due to its high nutritional content photosynthetic efficiency, environmental adaptability and positive effects on bone density, though the exact bioactive components and mechanisms remain unclear. Using a hindlimb suspension (HLS) model, this study investigated SP components: proteins (SPP), polysaccharides (SPS), lipids (SPL), and residue (SPR) on bone density and metabolism. Findings revealed that SPP and SPS significantly enhanced bone density and reduced oxidative stress. Activation of the FoxO3/Wnt/ß-catenin pathway reduced FoxO3a expression and increased Wnt signaling molecules and ß-catenin protein, boosting bone formation. Moreover, these components promoted beneficial gut bacteria like Turicibacter, reduced the Firmicutes-to-Bacteroidetes ratio, and enhanced SCFAs production, crucial for bone health. This study emphasized the potential of Spirulina nutrients in addressing space-induced osteoporosis and developing functional foods for long-term space missions.

RESUMO

Drug-eluting bead transcatheter arterial chemoembolization (D-TACE) is one of the first-line treatment for intermediate hepatocellular carcinoma (HCC). However, the dual hypoxia microenvironment, due to inherent tumor hypoxia and TACE-induced hypoxia, triggers drug resistance in HCC. To address this challenge, the study develops multicavitary microspheres capable of encapsulating oxygen and harnessing magnetic hyperthermia to enhance oxygen permeability. The novel multicavitary oxygen-encapsulated magnetothermal drug-eluting microspheres (OTD-Ms) effectively reduce hypoxia-related proteins (HIF-1α, VEGF-A) and drug resistance (P-gp) both in vitro and in vivo. Moreover, these microspheres demonstrate improved TACE efficacy and enhance survival rates in a rabbit VX-2 tumor model, suggesting their potential for HCC treatment.

RESUMO

Correction for 'Polymer mechanochemistry: from single molecule to bulk material' by Qifeng Mu et al., Phys. Chem. Chem. Phys., 2024, 26, 679-694, https://doi.org/10.1039/D3CP04160C.

RESUMO

Objectives: A systematic review and meta-analysis was performed to evaluate the preventive effectiveness of Helicobacter pylori eradication against metachronous gastric cancer (MGC) or dysplasia following endoscopic resection (ER) for early gastric cancer (EGC) or dysplasia. Methods: PubMed, Cochrane Library, MEDLINE, and EMBASE were searched until 31 October 2023, and randomized controlled trials or cohort studies were peer-reviewed. The incidence of metachronous gastric lesions (MGLs) including MGC or dysplasia was compared between Helicobacter pylori persistent and negative groups, eradicated and negative groups, and eradicated and persistent groups. Results: Totally, 21 eligible studies including 82,256 observations were analyzed. Compared to those never infected, Helicobacter pylori persistent group (RR = 1.58, 95% CI = 0.98-2.53) trended to have a higher risk of MGLs and significantly in partial subgroups, while the post-ER eradicated group (RR = 0.79, 95% CI = 0.43-1.45) did not increase the risk of MGLs. Moreover, successful post-ER eradication could significantly decrease the risk of MGLs (RR = 0.54, 95% CI = 0.44-0.65) compared to those persistently infected. Sensitivity analysis obtained generally consistent results, and no significant publication bias was found. Conclusion: The persistent Helicobacter pylori infection trends to increase the post-ER incidence of MGC or dysplasia, but post-ER eradication can decrease the risk correspondingly. Post-ER screening and eradication of Helicobacter pylori have preventive effectiveness on MGC, and the protocol should be recommended to all the post-ER patients.Systematic review registration: The PROSPERO registration identification was CRD42024512101.

RESUMO

Background: Hypoxic pulmonary hypertension (HPH) is one of the important pathophysiological changes in chronic pulmonary heart disease. Hypoxia promotes the phenotypic transformation of pulmonary artery smooth muscle cells (PASMCs). Extracellular exosomes regulate vascular smooth muscle cell (VSMC) phenotypic switch. Aim: Given the importance of exosomes and alveolar epithelial cells (AECs) in HPH, the present study aimed to address the issue of whether AEC-derived exosomes promote HPH by triggering PASMC phenotypic switch. Methods: Cell Counting Kit-8 (CCK-8), TRITC-phalloidin staining, and Western blotting were used to examine the effects of AEC-derived exosomes on cell proliferation, intracellular actin backbone distribution, and expression of phenotypic marker proteins in PASMCs. Transcriptomics sequencing was used to analyze differentially expressed genes (DEGs) between groups. Results: Hypoxia-induced exosomes (H-exos) could promote the proliferation of PASMCs, cause the reduction of cellular actin microfilaments, promote the expression of synthetic marker proteins (ELN and OPN), reduce the expression of contractile phenotypic marker proteins (SM22-α and α-SMA), and induce the phenotypic transformation of PASMCs. Transcriptomics sequencing analysis showed that the Rap1 signaling pathway was involved in the phenotypic transformation of PASMCs induced by H-exos. Conclusion: The present study identified that hypoxia-induced AEC-derived exosomes promote the phenotypic transformation of PASMCs and its mechanism is related to the Rap1 signaling pathway.

Assuntos

Proliferação de Células , Exossomos , Miócitos de Músculo Liso , Fenótipo , Artéria Pulmonar , Transdução de Sinais , Exossomos/metabolismo , Artéria Pulmonar/metabolismo , Miócitos de Músculo Liso/metabolismo , Animais , Células Epiteliais Alveolares/metabolismo , Ratos , Proteínas rap1 de Ligação ao GTP/metabolismo , Proteínas rap1 de Ligação ao GTP/genética , Músculo Liso Vascular/metabolismo , Hipertensão Pulmonar/metabolismo , Ratos Sprague-Dawley , Células Cultivadas , Hipóxia/metabolismo , Hipóxia Celular/fisiologia

RESUMO

Severe pneumonia (SP) is a prevalent respiratory ailment characterized by high mortality and poor prognosis. Current scoring systems for pneumonia are not only time-consuming but also exhibit limitations in early SP prediction. To address this gap, this study aimed to develop a machine-learning model using inflammatory markers from peripheral blood for early prediction of SP. A total of 204 pneumonia patients from seven medical centers were studied, with 143 (68 SP cases) in the training cohort and 61 (32 SP cases) in the test cohort. Clinical characteristics and laboratory test results were collected at diagnosis. Various models including Logistic Regression, Random Forest, Naïve Bayes, XGBoost, Support Vector Machine, and Decision Tree were built and evaluated. Seven predictors-age, sex, WBC count, T-lymphocyte count, NLR, CRP, TNF-α, IL-4/IFN-γ ratio, IL-6/IL-10 ratio-were selected through LASSO regression and clinical insight. The XGBoost model, exhibiting best performance, achieved an AUC of 0.901 (95 % CI: 0.827 to 0.985) in the test cohort, with an accuracy of 0.803, sensitivity of 0.844, specificity of 0.759, and F1_score of 0.818. Indeed, SHAP analysis emphasized the significance of elevated WBC counts, older age, and elevated CRP as the top predictors. The use of inflammatory biomarkers in this concise predictive model shows significant potential for the rapid assessment of SP risk, thereby facilitating timely preventive interventions.