Biomedical subjects

A L McMurtry

Publications and source records attributed to A L McMurtry.

3 recordsLinked to original sources

PubMed2000

Differential regulation of c-jun expression in liver and lung of mice after thermal injury.

In addition to skin injury, burns may also damage distant organs. Understanding the mechanisms of distant organ injury will substantially improve the survival of burn patients. Transcription factors are the major regulators of gene expression in response to most types of injury. C-Jun, which is a part of the activator protein-1 transcription factor complex, is one of the major immediate-early response genes, which is rapidly induced after injury. The expression of c-Jun in mouse liver and lung at different time points (3 h to 29 days) after thermal injury was examined by using Reverse Transcription-Polymerase Chain Reaction (RT-PCR), Western blot, and immunohistochemistry. Rapid induction of c-Jun mRNA and protein was observed in the liver 3 h after an 18% TBSA burn. C-Jun expression returned to basal levels within 3 days after injury. In contrast to the up-regulation observed in liver, lungs from the same mice expressed c-Jun constitutively throughout the same time points. The finding that thermal injury leads to up-regulation of c-Jun in liver but not lungs suggests that either the liver has a lower threshold for early response to injury or that different cellular events exist when each organ is stressed.

Animals↗

PubMed1999

Expression of HSP70 in healing wounds of diabetic and nondiabetic mice.

BACKGROUND: Heat shock proteins (HSPs) stabilize intracellular processes of cells under stress. Little is known about the role of HSPs in wound healing, or whether their expression is altered by systemic disease. The focus of this study was to examine the local heat shock response to wounding in diabetic mice. METHODS: Congenitally diabetic and phenotypically normal mice underwent standardized full-thickness cutaneous wounding. Mice were sacrificed at sequential time points and the wound beds excised. Tissues underwent immunohistochemical (IHC) and RT-PCR analyses for inducible HSP70. RESULTS: HSP70 protein expression in the wound bed by IHC peaked at 24 h in the nondiabetic mice. Expression of HSP70 was delayed in the diabetic mice until Day 3, which correlates with the clinical delay in healing seen in this model. The protein was especially prominent in the epithelium and in inflammatory cells migrating into the granulation tissue matrix. RT-PCR demonstrated upregulation of HSP70 mRNA within 12 h after wounding, lasting until Day 3, and decreasing thereafter in both the nondiabetic and the diabetic animals. CONCLUSION: Cutaneous wounding produces a HSP response in inflammatory cells, and expression of inducible HSP70 is delayed in diabetic mice. This delay may be related to the impaired inflammatory response of diabetics, and may contribute to impaired wound healing. The wound may be a continuing source of the heat shock response in inflammatory cells after injury.

Animals↗

PubMed1999

Increased use of prophylactic vena cava filters in trauma patients failed to decrease overall incidence of pulmonary embolism.

BACKGROUND: Recent studies have reported that placement of vena cava filters (VCFs) early after injury may decrease the incidence of pulmonary embolism (PE) in high-risk trauma patients. STUDY DESIGN: This was a retrospective review of all trauma patients with placement of VCFs admitted to a single level-1 trauma center between 1989 and 1997. Two cohorts corresponding to years of high or low prophylactic VCF use (PVCF) were compared. RESULTS: Records were reviewed for 299 trauma patients identified as having had placement of a VCE Two hundred forty-eight filters were placed before the diagnosis of PE. During years of low PVCF use, the overall PE incidence was 0.31%; during years of high PVCF use, the incidence of PE was higher at 0.48% (p = 0.045, chi-square). CONCLUSIONS: Increased use of PVCFs failed to decrease the overall rate of PE in our trauma patient population.

Adult↗