Troponin-I elevation in patients with increased left ventricular mass.
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Biomedical subjects
Steven A Goldstein
Publications and source records attributed to Steven A Goldstein.
Focal adhesion kinase expression during mandibular distraction osteogenesis: evidence for mechanotransduction.
Distraction osteogenesis is an established treatment strategy in the reconstruction of the craniofacial skeleton. The underlying mechanisms that drive bone formation during this process are largely unknown, but a regulatory role for mechanical force is believed to be critical. The integrin-mediated signal transduction cascade is a primary pathway by which signal transduction of mechanical stimuli (i.e., mechanotransduction) occurs. Focal adhesion kinase (FAK) is a significant regulator in this pathway. The authors hypothesize that mechanical forces created during distraction osteogenesis are responsible for the osteogenic response that takes place, and that these changes arise through integrin-dependent mechanotransduction. Using a rat model of distraction osteogenesis, the authors examined the expression of FAK in critical size defects (n = 15), subcritical size defects (n = 15), and mandibles undergoing distraction osteogenesis (n = 15). Their findings demonstrated FAK immunolocalization in mandibles undergoing distraction osteogenesis, but not in the critical size defects or in subcritical size defects, despite varying degrees of bone formation in the latter two groups. Furthermore, bone sialoprotein mRNA in situ hybridization patterns were found to mirror FAK immunolocalization patterns in mandibles undergoing distraction osteogenesis, demonstrating an association of FAK expression with the osteogenic process specific to distraction osteogenesis. These findings suggest that the bone formation in distraction osteogenesis is regulated by mechanical force by means of integrin-dependent mechanotransduction pathways.
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Brevibacterium endocarditis: a first report.
There are few case reports of infections caused by Brevibacterium species, and there have been no previously reported cases of endocarditis caused by any of the 6 known species of Brevibacterium. We report the first case of Brevibacterium endocarditis (caused by Brevibacterium otitidis) in a patient with prosthetic heart valves. The patient responded to 6 weeks of treatment with vancomycin and 2 weeks with gentamicin, and she has been receiving long-term maintenance therapy with oral azithromycin.
Actinomycetales Infections↗
Unique rodent model of distraction osteogenesis of the mandible.
Despite the increasing use of distraction osteogenesis (DO) of the mandible, the molecular mechanisms regulating new bone formation during DO remain poorly understood. The purposes of this study were (1) to establish a unique rodent model of DO capable of outlining parameters for new bone formation at the distraction site and (2) to determine a critical-size defect to differentiate osteogenesis resulting from distraction from conventional fracture healing at the osteotomy site. Adult Sprague-Dawley rats were fitted successfully with this newly developed distraction device. Analyses demonstrated that the device could distract the rat mandible reliably to 5.1 mm with complete union. Acute intersegmental gaps of 2 mm resulted in complete bony union in a manner consistent with fracture healing, whereas 3-mm acute gaps resulted in varying degrees of bony union. Acute intersegmental gaps of 5.1 mm invariably resulted in fibrous nonunion. In summary, the authors have developed a rodent model of DO of the mandible. Their distraction protocols resulted successfully in advancement to 5.1 mm with bony consolidation. Notable fracture healing occurred at immediate intersegmental spaces as large as 3 mm. A gap of 5.1 mm was sufficient to act as a critical-size defect, resulting consistently in fibrous nonunion. These findings validate the effectiveness of this distraction device and establish the critical-size defect of a rat mandible at more than 3 mm. This novel model of DO provides an effective method of examining fundamental mechanisms responsible for new bone formation in the craniofacial skeleton.
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Tissue engineering: functional assessment and clinical outcome.
The issues that should be considered as part of the design and evaluation of tissue engineering constructs with respect to their targeted clinical application are reviewed. This paper provides a general framework for the process of bringing tissue-engineering constructs from the laboratory bench to the patient's bedside, rather than presenting a detailed review of the engineering or biologic principles or mechanisms that are necessary for successful tissue engineering. Many of the principles are animated by using examples from current studies being developed in my laboratory or those of my collaborators. In all likelihood, multiple solutions or approaches will be found that lead to successful tissue-engineering constructs. The focus here is on the identification of critical parameters to be considered rather than specific design solutions. The review is therefore organized to reflect feasible sequences of activities formulated to take tissue engineering from concept to clinical reality.
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