Cover Crop and Crop Rotation Effects on Tissue and Soil Population Dynamics of and Yield Under No-Till System.

The effects of crop rotation and winter cover crops on soybean yield and colony-forming (CFU) units of , the causal agent of charcoal rot (CR), are poorly understood. A field trial was conducted from 2011 to 2015 to evaluate (i) the impact of crop rotation consisting of soybean ( [L.] Merr.

Screening Tall Fescue for Resistance to and Using Digital Image Analysis.

Brown patch, caused by , is a destructive disease on tall fescue. Compared with , causes indistinguishable symptoms in the field but varies in geographic distribution. This may contribute to geographic variability observed in the resistance response of improved brown patch-resistant cultivars.

Differential expression of procollagen genes between mid- and late-gestational fetal fibroblasts.

Background: Previously, we have shown that cutaneous wounds in mid-gestational (E15) mice heal in a scarless manner with decreased procollagen 1 and increased procollagen 3 production compared with wounds in late-gestational (E18) mice, which heal with scars. The aim of the current work was to determine whether E15 and E18 fibroblasts respond to stimulation in culture with differential procollagen expression, suggesting they may preserve their phenotype in vitro. Further, we wanted to determine if fetal fibroblast gene expression patterns persisted in tissue culture.

Scarless fetal mouse wound healing may initiate apoptosis through caspase 7 and cleavage of PARP.

Introduction: Apoptotic mechanisms are thought to be important in wound healing for the removal of inflammatory cells and evolution of granulation tissue. However, little is understood about the signal, propagation, and mechanisms responsible for triggering cell death in tissue injury, particularly during fetal wound repair. Understanding these signals may lead to insights regarding scarless wound healing.

Homeobox genes Hoxd3 and Hoxd8 are differentially expressed in fetal mouse excisional wounds.

Background: Cell signaling pathways underlying wound repair are under extensive investigation; however, there is still a poor understanding of the mechanisms orchestrating these processes. Hox genes, which are a subgroup of homeobox genes, encode for a family of transcription factors that play a critical role in tissue migration and cell differentiation during embryogenesis and may also serve as master regulatory genes of postnatal wound repair. We have developed a fetal excisional wound healing model whereby mid-gestational wounds heal in a regenerative manner while late-gestational wounds display scar formation.

Differential use of Erk1/2 and transforming growth factor beta pathways by mid- and late-gestational murine fibroblasts.

Background: Previously, we demonstrated the rapid closure of mid-gestational excisional murine wounds at 32 hours. In this study, we theorized that mid-gestational wounds would be completely regenerated, whereas late-gestational wounds would heal with scar formation at 48 hours. Furthermore, we theorized that mid- and late-gestational fibroblasts differentially use the transforming growth factor beta and mitogen-activated protein kinase pathways.

Altered procollagen gene expression in mid-gestational mouse excisional wounds.

Introduction: Many pathologic conditions are characterized by excessive tissue contraction and scar formation. Previously, we developed a murine model of excisional wound healing in which mid-gestational wounds heal scarlessly compared with late-gestational wounds. We theorized that variations in procollagen gene expression may contribute to the scarless and rapid closure.

Rapid closure of midgestational excisional wounds in a fetal mouse model is associated with altered transforming growth factor-beta isoform and receptor expression.

Background: Many pediatric diseases are characterized by excessive tissue contraction. Because of a poor understanding of contraction, few therapies exist. We developed a murine fetal excisional wound model of contraction and theorize that wound closure is associated with changes in transforming growth factor-beta (TGF-beta) expression.

Association of a single nucleotide polymorphism in the matrix metalloproteinase-1 promoter with glioblastoma.

A key feature in the malignant behavior of glioblastoma is the tendency to invade host brain tissue surrounding the primary tumor site. Several members of the matrix metalloproteinase family are thought to contribute to this invasive capacity. A single nucleotide polymorphism has been described in the matrix metalloproteinase-1 (MMP-1) promoter that consists of either the presence or absence of a guanine nucleotide at position -1607.