Additional file 1 of Bacterial DNA metabolism analysis by metagenomic next-generation sequencing (mNGS) after treatment of bloodstream infection

Table S2. The Pearson correlation between the E. coli DNA concentration and plasma inflammatory cytokine concentratio

Novel β-lactam/β-lactamase inhibitors versus alternative antibiotics for the treatment of complicated intra-abdominal infection and complicated urinary tract infection: a meta-analysis of randomized controlled trials

<p><b>Introduction</b>: The aim of this study is to compare the efficacy and safety of novelBL/BLIs with alternative antibiotics for the treatment of cIAI and cUTI.</p> <p><b>Area covered</b>: We performed a systematic review and meta-analysis of all randomized controlled trials comparing novel BL/BLIs with other antibiotics for the treatment of cIAI and cUTI. The primary outcome included clinical and microbiological treatment success.</p> <p><b>Expert commentary</b>: We found that novel BL/BLIs obtained a similar clinical outcome with other antibiotics in CE population (OR = 1.07, 95%CI = (0.80, 1.44), P = 0.64). However, novel BL/BLIs had better clinical treatment success in the cUTI subgroup (OR = 2.14, 95%CI = (1.06, 4.31), P = 0.03). Furthermore, novel BL/BLIs achieved significant microbiological treatment success in patie nts with cUTI (OR = 1.70, 95%CI = (1.29, 2.25), P  =  0.0002) and had higher eradication rates for Gram-negative pathogens (OR = 1.82, 95%CI = (1.26, 2.64), P = 0.001) including <i>E.coli</i> and <i>K.pneumoniae</i>. No difference was observed concerning the incidence of mortality and adverse events between the two groups. Therefore, we concluded that novel BL/BLIs are not inferior to other available antibiotics for the treatment of cIAI, and they have advantages in patients with cUTI. Simultaneously, they are sensitive to Gram-negative pathogens, especially for <i>E.coli</i> and <i>K.pneumoniae</i>.</p

Additional file 2 of Bacterial DNA metabolism analysis by metagenomic next-generation sequencing (mNGS) after treatment of bloodstream infection

Table S1. Clearance half-life of circulating E. coli DN

Confocal images of cultured control astrocytes showing the expression of GFAP (A, G, green), TNF-α (B red), IL-1β (H red) and co-localized expression of GFAP and TNF-α (C), GFAP and IL-1β (I).

<p>D–F show the expression of GFAP (D, green), TNF-α (E, red) and colocalized expression of GFAP and TNF-α (F) after treatment with 3% oxygen for 3 h. Note the elevated expression of TNF-α following treatment with 3% oxygen for 3 h (E) as compared with the control cells (B). J–L show the expression of GFAP (J, green), IL-1β (K, red) and colocalized expression of GFAP and IL-1β (L) after treatment with 3% oxygen for 3 h. The expression of IL-1β is greatly increased in the astrocytes after hypoxic exposure for 3 h. Scale bars: A–L, 50 µm.</p

Confocal images showing APC immunolabeled oligodendrocytes (arrows)(A, D, red) and caspase-3 positive apoptotic cells (B, E; green) (arrows) as detected by double immunofluorescence in the PWM of a control and a hypoxic rat at 7d after the hypoxic exposure.

<p>The colocalized expression of APC and caspase-3 labeling can be seen in C and F. Note the increase in frequency of apoptotic nuclei in the PWM after the hypoxic exposure. Bar graphs in G and H show the significant increase in percentage of caspase-3 positive apoptotic cells (H) and decrease in the number of APC positive oligodendrocytes/view (G) in the PWM after the hypoxic exposure (* <i>P</i><0.01). Scale bars: A-F, 50 µm.</p

Confocal images showing the distribution of APC (A, D, G, J, green), tumor necrosis factor receptor 1 (TNF-R₁) (B, E, red) and interleukin-1 receptor 1 (IL-1R₁) (H, K, red) in oligodendrocytes (arrows) in the PWM at 7 days after the hypoxic exposure and the corresponding control.

<p>The co-localized expression of APC with TNF-R₁ and IL-1R₁ is depicted in C and F, I and L, respectively. Note the expression of TNF-R₁ and IL-1R₁ is upregulated after the hypoxic exposure. Scale bars: A–L, 50 µm.</p

Upregulation of TNF-R₁ and IL-1R₁ expression in primary cultured oligodendrocytes following hypoxia.

<p>Confocal images showing TNF-R₁ and IL-1R₁ expression (B, E, H, K, red) in primary cultured oligodendrocytes labeled with APC (A, D, G, J, green) in both control and hypoxia for 3 h. Note TNF-R₁ and IL-1R₁ immunofluroscence intensity is markedly enhanced after hypoxic exposure (E, K) in comparison with the control (B, H). Scale bars: A–L, 50 µm.</p

Confocal images showing the distribution of GFAP-labeled (A, D, G, J green), and TNF-α (B, E red), IL-1β (H, K red) immunoreactive astrocytes (arrows) in the PWM at 7 days after the hypoxic exposure and the corresponding control rats.

<p>The co-localized expression of GFAP and TNF-α, IL-1β in astrocytes can be seen in panels C, F, I and L. Note TNF-α and IL-1β expression in astrocytes (arrows) is markedly enhanced at 7 days after the hypoxic exposure. Scale bars: A-L, 20 µm. GFAP = glial fibrillary acidic protein; PWM = periventricular white matter.</p

Hypoxia induces hypomyelination in the PWM in the hypoxic P28d rats.

<p>A–D show PLP protein expression in the PWM at 28 days after the hypoxic exposure and the corresponding control rats. Confocal images showing the expression of PLP in the PWM at 28 days of the hypoxic exposure (B) and the corresponding control rats (A). Note the PLP protein expression is saliently reduced following the hypoxic exposure (B) as compared with the control (A). C shows PLP (30 KDa) and β-actin (42 KDa) immunoreactive bands, respectively. Bar graph in D shows significant decrease in the optical density of PLP following hypoxic exposure when compared with the corresponding controls (*<i>P</i><0.01). E-I Electron micrographs show hypomyelination and aberrant ensheathment of axons in the PWM at 28d after the hypoxic exposure. Electron microscopic images of PWM in cross sections are shown at 2 different magnifications. The number of myelinated axons is markedly decreased in the PWM at 28d after the hypoxic exposure (F) when compared with corresponding control (E). Higher magnification EM images showing thinner myelin in the PWM of hypoxic rats (G, H). I is bar graph showing increased g-ratio of myelinated axons in the PWM at 28d after the hypoxic exposure. Scale bars: A–B, 100 µm. Scale bars: E–H, 500 nm.</p

Additional file 1: Figure S1. of Microglia-derived IL-1β contributes to axon development disorders and synaptic deficit through p38-MAPK signal pathway in septic neonatal rats

The CCK-8 assay (cell counting kit 8) was performed to determine the IL-1β concentration. The viability of neuronal cells was significantly reduced when neurons were treated with IL-1β at a dose exceeding 40 ng/mL. (TIF 820 kb