No abstract

MMP inhibition leads to myocardial stiffness with negative functional consequences for the RV and LV in NE-treated rat hearts.

This paper gives recommendations for treatment of thoracolumbar and lumbar spine injuries. The recommendations are based on the experience of the involved spine surgeons, who are part of a study group of the "Deutsche Gesellschaft für Unfallchirurgie" and a review of the current literature. Basics of diagnostic, conservative, and operative therapy are demonstrated. Fractures are evaluated by using morphologic criteria like destruction of the vertebral body, fragment dislocation, narrowing of the spinal canal, and deviation from the individual physiologic profile. Deviations from the individual sagittal profile are described by using the monosegmental or bisegmental end plate angle. The recommendations are developed for acute traumatic fractures in patients without severe osteoporotic disease.

Serum depletion led to cell death of isolated cardiac fibroblasts. Survival was associated with the increase in the expression of various ECM proteins. The transcription factor CREB was activated after serum removal. Inhibition of PKA improved the serum depletion induced decrease in the survival rate. The increase in collagen I, collagen III, MMP-2, TIMP-2, and colligin evoked by serum depletion was also diminished by PKA inhibition.

The pro-inflammatory cytokines interleukin (IL)-1beta and IL-6 have been shown to be upregulated in the myocardium after injury and after adrenergic receptor stimulation. Together with other cytokines, such as the transforming growth factor (TGF)-beta, the pro-inflammatory cytokines have been implicated in the initiation of tissue repair and wound healing after myocardial infarction (MI). In the present study, the effect of beta-adrenergic receptor blockade with propranolol (2 mg/kg x h s.c. by miniosmotic pumps) on cardiac cytokine expression and on wound healing was analyzed in rats from 6-72 h after MI. IL-1beta and IL-6 gene expression strongly increased in the infarcted myocardium 6 h after MI and peaked after 12 h, while TGF-beta, progressively increased from 12 h onwards. Also, TGF-beta2 increased after 12 h, peaked after 24 h and declined thereafter, while TGF-beta, was only elevated after 72 h. Treatment with propranolol had a negative chronotropic effect throughout the observation period of 72 h. It attenuated the initial elevation in LVEDP and increased cardiac output ultimately. Furthermore, propranolol attenuated IL-1beta mRNA expression, but had not effect on the other cytokines. Moreover, MMP-9 gelatinolytic activity was markedly attenuated by propranolol indicating a delayed resorption of the necrotic tissue and, possibly, collagen turnover. Replacement by scar tissue, however, was not affected as indicated by normal collagen expression.