RESUMEN
Preterm birth is the leading cause of death in children under five years old, and is associated with a wide sequence of complications in both short and long term. In view of rapid neurodevelopment during the neonatal period, preterm neonates may exhibit considerable functional alterations compared to term ones. However, the identified functional alterations in previous studies merely achieve moderate classification performance, while more accurate functional characteristics with satisfying discrimination ability for better diagnosis and therapeutic treatment is underexplored. To address this problem, we propose a novel brain structural connectivity (SC) guided Vision Transformer (SCG-ViT) to identify functional connectivity (FC) differences among three neonatal groups: preterm, preterm with early postnatal experience, and term. Particularly, inspired by the neuroscience-derived information, a novel patch token of SC/FC matrix is defined, and the SC matrix is then adopted as an effective mask into the ViT model to screen out input FC patch embeddings with weaker SC, and to focus on stronger ones for better classification and identification of FC differences among the three groups. The experimental results on multi-modal MRI data of 437 neonatal brains from publicly released Developing Human Connectome Project (dHCP) demonstrate that SCG-ViT achieves superior classification ability compared to baseline models, and successfully identifies holistically different FC patterns among the three groups. Moreover, these different FCs are significantly correlated with the differential gene expressions of the three groups. In summary, SCG-ViT provides a powerfully brain-guided pipeline of adopting large-scale and data-intensive deep learning models for medical imaging-based diagnosis.
Asunto(s)
Conectoma , Nacimiento Prematuro , Femenino , Niño , Humanos , Recién Nacido , Preescolar , Encéfalo/diagnóstico por imagen , Imagen por Resonancia Magnética/métodos , Conectoma/métodos , Suministros de Energía EléctricaRESUMEN
Tea polyphenols have received much attention from the pharmaceutical and food industries owing to their extraordinary antioxidant and antibacterial characteristics. However, tea polyphenols are very unstable in processing and storage, since they are sensitive to the environmental factors like temperature, light and pH. Therefore, the effective application of tea polyphenols requires a protective mechanism to maintain its activity. The utilization of compounded tea polyphenols, instead of raw materials, can potentially help to improve their stability. This review focuses on the summarization of the compounding technologies for tea polyphenols, including physical technologies, chemical-interfacial technologies and nano-scale compounding technologies. Of which, the emerging nano cellulose bio-carrier, as a promising technology, is particularly proposed.
Asunto(s)
Antibacterianos/farmacología , Antineoplásicos/farmacología , Antioxidantes/farmacología , Neoplasias/tratamiento farmacológico , Polifenoles/farmacología , Té/química , Antibacterianos/química , Antineoplásicos/química , Antioxidantes/química , Bacterias/efectos de los fármacos , Enfermedades Cardiovasculares/tratamiento farmacológico , Estabilidad de Medicamentos , Enfermedades Neurodegenerativas/tratamiento farmacológico , Polifenoles/químicaRESUMEN
Triptolide, a traditional Chinese medicine, has anti-inflammatory, antiproliferative, and proapoptotic properties. As interstitial inflammation and tubular apoptosis are features of cisplatin-induced acute kidney injury (AKI), we determined the effect of the water-soluble triptolide derivative 14-succinyl triptolide sodium salt (PG490-88) in a mouse model of cisplatin-induced AKI. PG490-88 resulted in a significant decrease in blood urea nitrogen (BUN), serum creatinine, and acute tubular necrosis (ATN) score, and a nonsignificant increase in tubular apoptosis score in AKI. The mitogen-activated protein kinase (MAPK) pathway is activated in AKI. On immunoblot analysis, phosphoextracellular signal-regulated kinase (p-ERK) was increased 3.6-fold in AKI and 2.0-fold inhibited by PG490-88. Phospho-c-Jun N-terminal kinase (p-JNK) was increased in AKI. PG490-88 resulted in a nonsignificant decrease in p-JNK. Phospho-p38 was not affected by cisplatin or PG490-88. MAPK phosphatase-1 (MKP-1) that negatively regulates MAPK signaling has not previously been studied in AKI. MKP-1 activity was not affected by cisplatin or PG490-88. Changes in p-ERK, p-JNK, and MKP-1 were confirmed on reverse protein phase analysis. The ERK inhibitor U0126 resulted in lower BUN and serum creatinine, suggesting a mechanistic role of ERK in AKI. The increase in interleukin-1α (IL-1α), IL-1ß, IL-6, CXCL1, and IL-33 in the kidney in AKI was unaffected by PG490-88. In summary, PG490-88 protects against AKI and ATN despite no decrease in tubular apoptosis. The protection of PG490-88 against AKI was associated with a decrease in p-ERK and was independent of MKP-1 and proinflammatory cytokines. In conclusion, PG490-88 protects against cisplatin-induced AKI possibly by decreasing p-ERK.
Asunto(s)
Lesión Renal Aguda/prevención & control , Antineoplásicos/toxicidad , Cisplatino/toxicidad , Diterpenos/química , Diterpenos/uso terapéutico , Fenantrenos/química , Lesión Renal Aguda/inducido químicamente , Lesión Renal Aguda/enzimología , Lesión Renal Aguda/patología , Animales , Apoptosis/efectos de los fármacos , Citocinas/inmunología , Diterpenos/administración & dosificación , Diterpenos/farmacología , Compuestos Epoxi/química , Pruebas de Función Renal , MAP Quinasa Quinasa 4/antagonistas & inhibidores , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Masculino , Ratones , Ratones Endogámicos C57BL , Proteínas Quinasas p38 Activadas por Mitógenos/antagonistas & inhibidoresRESUMEN
In this study, the potential of using bleached wheat straw pulp (BWSP) was explored to improve the tensile strength of the high-yield pulp (HYP) while preserving its high bulk property. The results showed that with the addition of 5-10% refined BWSP, the HYP tensile strength can be increased by about 10-20% without sacrificing the bulk. Similar results were obtained by adding refined BWSP into a mixed furnish of bleached kraft pulps (BKPs) and HYP. The explanation was that micro fines from refined BWSP can act as binders to improve the HYP interfiber bonding, as a result, the HYP tensile strength can be improved by using a small amount of BWSP, while the HYP bulk is not significantly affected.