Biomedical subjects
Publications and source records attributed to T O'Brien.
A survey of 426 children with unilateral distal forearm fractures was performed to examine the role of hand dominance. Results showed a significant preponderance of fractures occurring in the non-dominant arm (p < .01). This finding has implications for possible preventive strategies in these common injuries.
L-arginine (L-Arg) may be limiting for inducible nitric oxide synthase (NOS) activity and under certain circumstances, such as increased concentrations of a NOS inhibitor, may also be limiting for endothelial NOS activity. It is unknown if L-Arg is limiting for recombinant eNOS activity in the vascular wall after adenoviral mediated gene transfer. Our aim was to examine, if L-Arg is limiting for recombinant eNOS activity in the normal or atherosclerotic vessel wall. Rings of rabbit aorta from chow or cholesterol fed animals were transduced with adenovirus vector encoding eNOS (AdeNOS) or beta-galactosidase (AdbetaGal). After 24 h, transgene expression was confirmed and vasomotor studies were performed in the absence or presence of L-Arg. During maximal contractions to phenylephrine (10(-5) M), L-Arg (3 mM) was added to the organ chamber for 30 min. Subsequently, relaxations to acetylcholine during half-maximal contractions were obtained. In the chow- and cholesterol-fed animals, relaxations were significantly enhanced in the NOS and NOS + L-Arg groups compared to the betaGal and betaGal + L-Arg groups. There was no difference between NOS and NOS + L-Arg or betaGal and betaGal + L-Arg rings from chow- or cholesterol-fed animals. While gene transfer of eNOS enhances endothelium-dependent vasorelaxation in the normal and atherosclerotic vessel wall, L-arginine is not limiting for recombinant eNOS activity.
Endothelial dysfunction is frequently involved in the pathogenesis of vascular disease. While nitric oxide (NO) inhibits smooth muscle cell proliferation, its effect on endothelial cell proliferation is unclear. The aim of this study was to determine if adenoviral-mediated gene transfer of endothelial NO synthase (eNOS) to human umbilical vein endothelial cells (HUVECs) would result in increased generation of NO and affect endothelial cell proliferation. HUVECs were transduced with adenoviral vectors encoding eNOS (AdeNOS) or beta-galactosidase (Ad beta gal) or exposed to diluent (control). AdeNOS-transduced cells showed increased eNOS expression as detected by Western blot analysis, and increased concentrations of cGMP (control 0.7 +/- 0.1; Ad beta gal 0.9 +/- 0.2; AdeNOS 3.1 +/- 0.5 pmol/mg protein; p < 0.001) and nitrite (control 11.8 +/- 1.2; Ad beta gal 13.3 +/- 1.7; AdeNOS 21.1 +/- 2.2 nmol/mg protein/hour; p < 0.01). DNA synthesis as assessed by [(3)H]thymidine incorporation and cell counts were significantly reduced (by approximately 30%) in AdeNOS-transduced HUVECs. Expression of mitogen-activated protein kinase was also decreased in AdeNOS-transduced cells. This study shows that adenoviral-mediated gene transfer of eNOS to HUVECs inhibits endothelial cell proliferation.
No universally accepted management protocol is available for dealing with the protective equipment worn by a neck-injured football player. The purpose of this cadaveric study was to determine the effects of the helmet and shoulder pads on the alignment of 1) the intact lower cervical spine and 2) the partially destabilized C5-6 motion segment. In Group I cadavers (N = 15), the lower cervical spine was tested in an intact condition. In Group II (N = 8), the C5-6 motion segment was tested in both an intact and a partially destabilized condition. Each cadaver was placed supine on a backboard and four lateral cervical radiographs were obtained as follows: no protective equipment, helmet only, helmet and shoulder pads, and shoulder pads only. Results for Group I showed that wearing both helmet and shoulder pads did not result in a significant change in cervical lordosis when compared with the neutral position (i.e., the no-equipment test). Cervical lordosis was significantly decreased in the helmet-only category (mean, 9.6 degrees) and significantly increased in the shoulder pads-only category (mean, 13.6 degrees). In Group II, destabilized specimens under the helmet test situation showed a significant mean increase in C5-6 forward angulation (16.5 degrees), posterior disk space height (3.8 mm), and dorsal element distraction (8.3 mm). Immobilizing the neck-injured football player with only the helmet or only the shoulder pads in place violates the principle of splinting the cervical spine in neutral alignment, according to our findings. We support the concept that removal of the helmet and shoulder pads should be an all-or-none proposition.
We describe a case of an adolescent with sickle-beta+ thalassemia who developed fatal fat embolism syndrome. After presenting with bone pain, the patient developed mental status changes, hypoxemia, and died following cardiorespiratory arrest.
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OBJECTIVE: To explore the current status and future potential of gene therapy for the inherited dyslipidemias. METHODS: A brief overview of the inherited dyslipidemias, a review of the currently available means of transferring genetic material in vivo, and a discussion of two examples of conditions in which gene therapy may be useful--familial hypercholesterolemia and reduced high-density lipoprotein cholesterol syndromes--are presented. RESULTS: Although substantial progress has been made in the management of inherited dyslipidemia, optimal treatment regimens are not available in all cases. Gene therapy has recently emerged as a potential solution to some of these problems. For gene therapy to be successful, several factors are necessary: an efficient means of gene transfer, long-term transgene expression, and lack of toxicity. Although the feasibility of this approach has been demonstrated, currently available vectors have a number of technical and safety limitations. CONCLUSION: Gene therapy for inherited dyslipidemias has many technical hurdles that must be overcome before it will have widespread clinical application.
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OBJECTIVE: To discuss nutritional support in a patient with hypertriglyceridemia and liver dysfunction. METHODS: We describe the hospital course of a critically ill patient with hepatic dysfunction and hypertriglyceridemia who required nutritional support, and we provide an overview of lipid metabolism. RESULTS: A 27-year-old man with hepatic dysfunction and hypertriglyceridemia, who had undergone kidney transplantation 4 months previously, was admitted to the intensive-care unit with upper gastrointestinal bleeding. He was unable to tolerate enteral feeding, and central parenteral nutrition was initiated. Calories from dextrose and fat were limited because of the presence of increased liver enzyme levels and hypertriglyceridemia. A modified regimen of parenteral nutrition was developed for the patient. The short-term reduction of total calories to 75% of the predicted need is safe. CONCLUSION: Nutritional support in patients with liver dysfunction and hypertriglyceridemia is complicated and may require temporary underfeeding because of the need to limit fat and dextrose intake.
We assessed the pattern of gait in children with spastic hemiplegia and a leg-length discrepancy, particularly in relation to the uninvolved limb. The kinematics of the uninvolved limbs were compared with the pattern in normal children. The uninvolved limbs in children with hemiplegia and a significant leg-length discrepancy were compared with the uninvolved limb in those children who did not have a leg-length discrepancy. We found that the involved and uninvolved legs in patients with hemiplegia had characteristic patterns that were significantly different from normal. The kinematics of the involved leg were not affected by the presence of a leg-length discrepancy. The abnormal pattern in the uninvolved limb was more exaggerated in children with a leg-length discrepancy. The abnormal sagittal plane kinematics in the uninvolved lower limb in hemiplegic children appears to be related to the presence of an actual or functional leg-length discrepancy and have not previously been described. Our findings suggest that attention be paid to the functional and actual leg-length discrepancy that exists in these children, and early consideration be given to epiphysiodesis of the uninvolved limb.
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Twenty-six patients with progressive neuromuscular scoliosis underwent anterior/posterior (AP) spinal fusion. Thirteen of the patients underwent a one-stage fusion, and 13 underwent a two-stage fusion. Although one-stage AP spinal fusion provides adequate correction of severe curves and allows a more expeditious recovery without increasing patient morbidity or mortality, current third-party payor reimbursement policies provide little incentive for 1-day operations. In addition, the procedure is mentally and physically demanding and the apparent benefits must be weighed against the potential harm that can result from surgeon fatigue or lack of appropriate planning.
The authors attempt to redefine the anatomic origin of the tibialis posterior muscle, and correlate it with the location of medial tibial stress syndrome that occurs in the lower third of the tibia. Contrary to what is commonly described, the authors show on all ten dissected specimens, that the origin of the tibialis posterior does include a portion of the lower third of the tibia. The mean distance from tibialis posterior's origin to the medial malleolus was only 7.77 cm. In addition, to further explain lower leg pain, the authors investigated the crossing point of tibialis posterior and flexor digitorum longus; a mean distance for this to occur in the same ten specimens was 8.16 cm. proximal to the medial malleolus. These findings provide insight to anatomic reasons behind biomechanical factors responsible for medial tibial stress syndrome. This is also important to consider when performing surgery for a deep compartment syndrome.
Eleven hips in nine children were identified with acetabular dysplasia, which presented as developmental dislocation of the hip. The clinical signs of dislocation--tight abductors and a limp, associated with a plain radiograph showing the femoral head protruding from the pelvis--were not evident among this group. Arthrography showed acetabular dysplasia but no dislocation. Accurate grading of hip dysplasia can help to avoid such misdiagnoses, which have presented a recurring problem in the management tof this condition.
Several rhythmic components were previously mapped for salivary and/or urinary CA125 and CA130. On the background of such reference standards, OVX1 and M-CSF were assayed on 242 urine samples and 160 saliva samples provided by a 71-year-old patient with a Müllerian/ovarian adenocarcinoma. Serum OVX1 correlates with serum CA125 (P = 0.002); when circulating CA125 concentrations decreased (from 122 to 14 U/ml), the urinary excretion rate of OVX1 decreased (P = 0.005), whereas the urinary excretion rate of CA125 increased (P < 0.001). Salivary OVX1 and urinary M-CSF show ultradian variations (with a frequency of one cycle in 14-17 hours), which could be utilized to guide treatment timing targeted first to optimize treatment efficacy and as a second consideration to minimize treatment toxicity.
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