NEC Mice & Touchpads Driver

29-03-2021 admin

NEC is likely a NETs dependent process and markers of NETosis are predictive of NEC in mice and humans

Nec Mice & Touchpads Driver Downloads
Nec Mice & Touchpads Driver Download

Abstract

2020-21 Men's Ice Hockey Roster. The incidence of severe NEC was higher in pups with low birth weight. Conclusions: we have simplified and characterized a neonatal mouse NEC model that shares several risk factors with human NEC. Now that transgenic mice are available, this model will be useful to study the role played by specific proteins in vivo in NEC development.

Necrotizing enterocolitis (NEC) is one of the most devastating diseases affecting premature and mature infants. It is hypothesized that NEC is the result of neutrophils' active role in hyperinflammation after bacterial gut colonization, through their nuclear DNA release and formation of neutrophil extracellular traps (NETs) to combat pathogens. The aim of this study was to evaluate the importance of NETs in NEC pathogenesis, as well as to identify and validate markers of NETosis to predict NEC. NEC was induced in mice by gavage feeding of Neocate and lipopolysaccharide, followed by ten minutes of hypoxia (5% O2) q12h for five days, starting on day four postpartum (p.p.). The interrelation of NEC and neutrophils, including NETs, was assessed macroscopically (i.e. NEC score, SYTOX Orange), microscopically (i.e. Chiu score, citrullinated histone H3, neutrophil elastase), and in blood samples (i.e. cell-free DNA (cfDNA), DNase). In order to determine the exact role of NETs in NEC pathogenesis, a protein arginine deiminase (PAD) inhibition model was established (preventing NETs formation in mice) by injecting BB-Cl-amidine once daily, starting on day one p.p. Additionally, human intestinal samples of diagnostically verified NEC were analyzed. In total, 76 mice were analyzed in the experiment. Serum cfDNA correlated positively with NEC manifestation, as measured by macroscopic NEC score (r = 0.53, p = 0.001), and microscopic evaluation with Chiu score (r = 0.56, p < 0.001). Markers of neutrophil activation and NETosis were significantly increased in animals with NEC and in human samples as compared to controls. Further, prevention of NETosis by protein arginine deiminase (PAD) inhibition in mice significantly reduced mortality, tissue damage, and inflammation in mice induced with NEC. Our results suggest that the hyperinflammation observed in NEC is a NETs-dependent process, as NEC severity was significantly reduced in mice incapable of forming NETs (PAD inhibition) and markers for NEC and NETs correlated positively during the time course of NEC induction. Further, serum surrogate markers of NETosis (such as cfDNA and DNase) appear to predict NEC in neonatal mice. As findings of the mouse NEC model correlate positively with human NEC samples immunohistochemically, the hyperinflammation reaction observed in mice could potentially be applied to human NEC pathogenesis.

Administration of Nec-1 or Nec-1s in mice with brain ischemic injury 12 or existing AAA 16 proved in principle that blocking necroptosis may slow and even reverse disease progression.
Forty mice were divided into four groups (n = 10 per group): (1) sham group: sham-operated mice administered 15 μL vehicle (5% DMSO, 45% PEG300, and ddH 2 O), (2) the sham + Nec-1 group: sham-operated mice treated with 15 μL Nec-1 (0.0468 mg/Kg), (3) the DMM group: DMM surgery mice administered 15 μL vehicle, and (4) the DMM + Nec-1 group.