Analysis and experimental validation of genes and their transcription factor prediction in contused rat spinal cord at the intermediate phase.

The intermediate phase of spinal cord injury (SCI) serves as an important target site for therapeutic mediation of SCI. However, there is a lack of insight into the mechanism of the intermediate phase of SCI. The present study aimed to investigate the molecular mechanism and the feasible treatment targets in the intermediate phase of SCI. We downloaded GSE2599 from GEO and identified 416 significant differentially expressed genes (DEGs), including 206 downregulated and 210 upregulated DEGs. Further enrichment analysis of DEGs revealed that many important biological processes and signal pathways were triggered in the injured spinal cord. Furthermore, a protein-protein interaction (PPI) network was constructed and the top 10 high-degree hub nodes were identified. Furthermore, 27 predicted transcription factors (TFs) and 136 predicted motifs were identified. We then selected insulin-like growth factor 1 (IGF1) and its predicted transcription factor, transcription factor A, mitochondrial (TFAM) for further investigation. We speculated and preliminarily confirmed that TFAM may regulate gene transcription of IGF1 and effected alterations in the function recovery of rats after SCI. These findings together provide novel information that may improve our understanding of the pathophysiological processes during the intermediate phase of SCI.

Identification of complexes of Nd(III) with dithiophosphinic acids verifying the difference in complexation between Ln(III) and An(III).

Five complex species of Nd(III) with HA have been spectroscopically and compositionally identified as NdA3, NdA3(HA), NdA3(HA)H2O, NdA3(H2O)3, and Nd(H2O)23·3A (HA, bis(2,4,4-trimethylpentyl)dithiophosphinic acid) with the help of X-ray diffraction analysis on single crystals of Nd(H2O)9·H2O·3B (HB = bis(iso-butyl)dithiophosphinic acid.

Spatial statistics and random forest approaches for traffic crash hot spot identification and prediction.

Crash hot spot identification and prediction using spatial statistics and random forest methods on the interstate of Michigan are evaluated. The Getis-Ord statistics are adopted to identify hot spots using location, frequency, and equivalent property damage only weights computed from the cost and severity of crashes. In the random forest approach, data patterns between 2010 and 2017 are determined to predict hot spots of crashes in 2018. Accordingly, the results indicate that: (i) interstate routes have witnessed 13,089 crashes on significant hot spots, 7,413 on cold spots, and the rest in other locations; (ii) random forest shows 76.7% and 74% accuracy for validation and prediction, respectively. The performance of the model is further affirmed with precision, recall, and F-scores of 75%, 74%, and 70%, respectively; and (iii) clustering of the crashes exhibits spatial dependence of high and low equivalent property damage only crashes. The practical significance of the approach is highlighted in the identification and prediction of hot spots.

Effects of Granulocyte Colony-Stimulating Factor on Opsonin Receptor Expression and Neutrophil Antibacterial Activity in a Mouse Model of Severe Acute Pancreatitis.

The antimicrobial function of neutrophils, which is dependent on opsonin receptors, deteriorates in severe acute pancreatitis (SAP). Granulocyte colony-stimulating factor (G-CSF) putatively enhanced levels of the opsonin receptors CD11b and CD32/16 in healthy human subjects, and provided protection against infection in animal models of SAP. A statistically convincing study of the effect of G-CSF on CD32/16 expression in an SAP model is lacking. We used a mouse model of SAP to investigate the association between G-CSF administration and CD32/16 levels on neutrophils and bacterial translocation. G-CSF or saline was subcutaneously injected into SAP-induced mice. The pancreases were histologically examined, and leukocytes were stained to count neutrophils. The expression of CD11b and CD32/16 on neutrophils was measured by flow cytometry, and bacterial translocation was observed by bacterial culture. The numbers of CD11b and CD32/16-positive neutrophils were significantly elevated in the SAP mice treated with G-CSF, and the mean fluorescence intensities of these receptors on neutrophils were significantly elevated. Bacterial translocations to cavity organs were suppressed from 17% to 6% by G-CSF treatment. Our results indicated that the number of neutrophils significantly increased with increasing expression of CD11b and CD32/16 and their mean fluorescence intensities (MFIs). This inhibited bacterial translocation to other organs. These results are in accord with other studies in SAP dogs and SAP mice. Our findings suggest that G-CSF was effective in protecting against bacterial infection in SAP mice.