21 research outputs found
Heparin therapy reduces 28-day mortality in adult severe sepsis patients: a systematic review and meta-analysis
Mechanical ventilation modes for respiratory distress syndrome in infants: a systematic review and network meta-analysis
Endogenous FGF1 Deficiency Aggravates Doxorubicin-Induced Hepatotoxicity
Doxorubicin (DOX) is a broad-spectrum antineoplastic agent that widely used in clinic. However, its application is largely limited by its toxicity in multiple organs. Fibroblast growth factor 1 (FGF1) showed protective potential in various liver diseases, but the role of endogenous FGF1 in DOX-induced liver damage is currently unknown. Both wild-type (WT) and FGF1 knockout (FGF1-KO) mice were treated with DOX. DOX induced loss of body weight and liver weight and elevation of ALT and AST in WT mice, which were aggravated by FGF1 deletion. FGF1 deletion exacerbated hepatic oxidative stress mirrored by further elevated 3-nitrosative modification of multiple proteins and malondialdehyde content. These were accompanied by blunted compensatively antioxidative responses indicated by impaired upregulation of nuclear factor erythroid 2-related factor 2 and its downstream antioxidant gene expression. The aggravated oxidative stress was coincided with exacerbated cell apoptosis in DOX-treated FGF1-KO mice reflected by further increased TUNEL positive cell staining and BCL-2-associated X expression and caspase 3 cleavage. These detrimental changes in DOX-treated FGF1-KO mice were associated with worsened intestinal fibrosis and increased upregulation fibrotic marker connective tissue growth factor and α-smooth muscle actin expression. However, DOX-induced hepatic inflammatory responses were not further affected by FGF1 deletion. These results demonstrate that endogenous FGF1 deficiency aggravates DOX-induced liver damage and FGF1 is a potential therapeutic target for treatment of DOX-associated hepatoxicity
Significant Factors Influencing Rural Residents’ Well-Being with Regard to Electricity Consumption: An Empirical Analysis in China
pDeep: Predicting MS/MS Spectra of Peptides with Deep Learning
In
tandem mass spectrometry (MS/MS)-based proteomics, search engines
rely on comparison between an experimental MS/MS spectrum and the
theoretical spectra of the candidate peptides. Hence, accurate prediction
of the theoretical spectra of peptides appears to be particularly
important. Here, we present pDeep, a deep neural network-based model
for the spectrum prediction of peptides. Using the bidirectional long
short-term memory (BiLSTM), pDeep can predict higher-energy collisional
dissociation, electron-transfer dissociation, and electron-transfer
and higher-energy collision dissociation MS/MS spectra of peptides
with >0.9 median Pearson correlation coefficients. Further, we
showed
that intermediate layer of the neural network could reveal physicochemical
properties of amino acids, for example the similarities of fragmentation
behaviors between amino acids. We also showed the potential of pDeep
to distinguish extremely similar peptides (peptides that contain isobaric
amino acids, for example, GG = N, AG = Q, or even I = L), which were
very difficult to distinguish using traditional search engines
Influence of different surfactants on crystal growth behavior and sinterability of La2Ce2O7 solid solution
Liraglutide Improves the Angiogenic Capability of EPC and Promotes Ischemic Angiogenesis in Mice under Diabetic Conditions through an Nrf2-Dependent Mechanism
The impairment in endothelial progenitor cell (EPC) functions results in dysregulation of vascular homeostasis and dysfunction of the endothelium under diabetic conditions. Improving EPC function has been considered as a promising strategy for ameliorating diabetic vascular complications. Liraglutide has been widely used as a therapeutic agent for diabetes. However, the effects and mechanisms of liraglutide on EPC dysfunction remain unclear. The capability of liraglutide in promoting blood perfusion and angiogenesis under diabetic conditions was evaluated in the hind limb ischemia model of diabetic mice. The effect of liraglutide on the angiogenic function of EPC was evaluated by cell scratch recovery assay, tube formation assay, and nitric oxide production. RNA sequencing was performed to assess the underlying mechanisms. Liraglutide enhanced blood perfusion and angiogenesis in the ischemic hindlimb of db/db mice and streptozotocin-induced type 1 diabetic mice. Additionally, liraglutide improved tube formation, cell migration, and nitric oxide production of high glucose (HG)-treated EPC. Assessment of liraglutide target pathways revealed a network of genes involved in antioxidant activity. Further mechanism study showed that liraglutide decreased the production of reactive oxygen species and increased the activity of nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 deficiency attenuated the beneficial effects of liraglutide on improving EPC function and promoting ischemic angiogenesis under diabetic conditions. Moreover, liraglutide activates Nrf2 through an AKT/GSK3β/Fyn pathway, and inhibiting this pathway abolished liraglutide-induced Nrf2 activation and EPC function improvement. Overall, these results suggest that Liraglutide represents therapeutic potential in promoting EPC function and ameliorating ischemic angiogenesis under diabetic conditions, and these beneficial effects relied on Nrf2 activation
Genome-Wide Characterization, Evolution, and Expression Profiling of VQ Gene Family in Response to Phytohormone Treatments and Abiotic Stress in Eucalyptus grandis
Salvia ranzaniana Makino
原著和名: ハルノタムラサウ科名: シソ科 = Labiatae採集地: 奈良県 玉置山 (大和 玉置山)採集日: 1982/5/16採集者: 萩庭丈壽整理番号: JH031613国立科学博物館整理番号: TNS-VS-98161