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Biomedical subjects
Publications and source records attributed to P Hickey.
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This case-control study assessed whether office workers who report more severe levels of musculoskeletal symptoms of the upper extremities demonstrate higher levels of keyforce in comparison to controls with less severe symptoms. Office workers reporting working on computer keyboards for four hours per day were classified as cases or controls based upon a median split on a Composite Symptom Severity score (cases = 23, controls = 25). Keyboard force and keying rate were measured during a 15-minute keyboarding task. Measures of task-related discomfort, muscular fatigue, pain, upper extremity symptoms, psychological distress and force were collected at baseline, post-keyboard task, and recovery. Ratings of perceived effort and task credibility were also obtained. Measures of work demands, perceived job stress, and upper extremity strength and flexibility were also collected. The results indicated group equivalence on reported work demands and upper extremity strength. Cases were more likely to receive a medical diagnosis of upper extremity cumulative trauma disorder, awaken from sleep due to symptoms, report higher levels of pain during work, experience greater impact of pain on function, and report higher workload pressure and lower support. Cases generated significantly higher keyboarding forces than controls, although both groups produced forces well above that required to operate the keyboard (4-5 times activation force). Cases reported higher levels of upper extremity symptoms and discomfort than controls, and these measures were highest after the keyboarding task for both groups. No significant correlation between keyforce and key rate was observed in either group. Results suggest that generation of excessive force while working on a computer keyboard may contribute to the severity of upper extremity symptoms. Clinically, the findings suggest that evaluating how an individual worker performs keyboarding tasks, or his or her workstyle, may be helpful in the management of these symptoms and disorders.
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The survival of infants with congenital heart disease has improved dramatically. However, the incidence of neurological injury in infants surviving cardiac surgery remains considerable. These neurological sequelae are attributable at least in part to hypoxia-ischemia/reperfusion, which inevitably accompanies infant heart surgery with deep hypothermia, cardiopulmonary bypass, and circulatory arrest. To begin to identify mechanisms of brain injury during infant cardiac surgery, we used near-infrared spectroscopy to study the relationship between cerebral intravascular (hemoglobin) and mitochondrial (cytochrome aa3) oxygenation in 63 infants (aged 1 day to 9 months) undergoing deep hypothermic repair of congenital heart defects, throughout the intraoperative period. Moreover, we assessed the effect of postnatal age on these changes. The cerebral concentration of oxidized cytochrome aa3 decreased from the onset of deep hypothermic cardiopulmonary bypass, despite apparent abundant intravascular oxygenation manifested by a simultaneous increase in the cerebral concentration of oxyhemoglobin. During this interval infants older than 2 weeks had a greater decrease in oxidized cytochrome aa3 than did infants 2 weeks old or younger. During deep hypothermic circulatory arrest, cerebral levels of oxidized cytochrome aa3 remained depressed while those of oxyhemoglobin declined. With reperfusion following circulatory arrest, the recovery of oxidized cytochrome aa3 was delayed, despite a rapid recovery of intravascular oxygenation (HbO2). After rewarming and 60 minutes of reperfusion, only 46% of infants recovered to the baseline level of cerebral oxidized cytochrome aa3. These findings demonstrate a paradoxical dissociation of changes in intravascular and mitochondrial oxygenation during hypothermic cardiopulmonary bypass; a pronounced decrease of mitochondrial oxygenation is established during induction of hypothermia and a delay in recovery of mitochondrial oxygenation occurs following circulatory arrest. These effects were more pronounced in infants older than 2 weeks than in younger infants. The data suggest potentially deleterious impairments of intrinsic mitochondrial function or of delivery of intravascular oxygen to the mitochondrion or both, effects previously undetected and apparently influenced by cerebral maturation.
Certain sigma receptor ligands have been shown to block locomotor stimulation produced by cocaine at doses that do not have significant behavioral activity when given alone. Using a potent and selective ligand of sigma binding sites, 6-[6-(4-hydroxypiperidinyl)hexyloxy]-3-methylflavone (NPC 16377), we further investigated the influence of sigma ligands on additional behavioral and toxic effects of cocaine in mice. A behaviorally inactive dose of NPC 16377 shifted the dose-effect function for the locomotor stimulant effects of cocaine to the right by a factor of 2.5. A higher dose of NPC 16377 produced an insurmountable blockade of this stimulant effect of cocaine. Prior exposure to cocaine enhances the locomotor stimulant effects of cocaine (sensitization). NPC 16377 prevented the development of cocaine sensitization without producing behavioral effects of its own. However, NPC 16377 was unable to block the expression of sensitization in mice previously exposed to cocaine. NPC 16377 also did not consistently alter the discriminative stimulus effects of cocaine or methamphetamine in rats discriminating either 3 or 10 mg/kg of cocaine, or 1 mg/kg of methamphetamine from saline. The potential phencyclidine-like behavioral effects of NPC 16377 were also evaluated. Unlike the NMDA channel ligand, dizocilpine, NPC 16377 did not increase responding under a fixed-interval schedule of food presentation in rats nor did it substitute for the discriminative stimulus effects of either 1.5 mg/kg of phencyclidine or 0.2 mg/kg of dizocilpine in rats discriminating these drugs from saline. NPC 16377 displayed limited but significant anticonvulsant activity against diazepam-sensitive cocaine convulsions. The lethal effects of higher doses of cocaine were neither significantly blocked nor enhanced in rats or mice with NPC 16377. These findings extend earlier observations on the cocaine-blocking effects of sigma ligands to a novel structure with exceptional selectivity for sigma sites. These data indicate that some sigma ligands may be capable of altering certain behavioral and toxic actions of cocaine without notable behavioral side effects as evidenced in preclinical tests. As such, these compounds may ultimately be useful in the treatment of cocaine abuse.
The prevalence of work-related upper extremity disorders has significantly increased in the past decade. Persistent pain, loss of function, and associated work disability in patients with work-related upper extremity disorders appears to be affected by multiple factors including physical capabilities in relation to work demands, ergonomic risk factors on the job, and psychological factors related to worker traits, psychological readiness to return to work, and ability to manage symptoms. The complex nature of these disorders suggests the utility of a multidisciplinary program targeted at these factors. The present study is an investigation of the long-term vocational outcome of a multicomponent rehabilitation program that includes physical conditioning, work conditioning, work-related pain and stress management, ergonomic consultation, and vocational counseling/placement. Two groups equivalent on measures of duration of work disability, pain severity, fear of reinjury, psychological distress, perceived work environment, age, and education level were exposed to either the comprehensive work rehabilitation intervention (n = 19) or usual care (n = 15). Return-to-work status was determined at an average of 17 months posttreatment (range, 3 to 35 months) for the treatment group and an average of 18 months postevaluation (range, 5 to 30 months) for the usual care group. Findings indicated that 74% of the treatment group returned to work or were involved in state-supported vocational training in contrast to 40% of the control group (P < .05). For those who returned to work, 91% of the treatment group were working full-time in contrast to 50% of the control group (P < .05). Although the treatment group demonstrated a higher return-to-work rate than controls, the work reentry rate was not as high as similar approaches with work-related low back pain (80% to 88% return-to-work rate). These findings suggest the need to modify treatment components to facilitate an increased return-to-work rate. Areas that may prove useful include a greater emphasis ergonomic modifications at the workplace to reduce the risks of repetitiveness, force, awkward posture, and insufficient work/rest cycles, as well as efforts to modify work style directly in order to reduce the impact of ergonomic stressors on the ability to perform essential job tasks. In combination with traditional work hardening efforts directed at improving strength and flexibility of the upper extremities and work-related pain and stress management training, these ergonomic and work-style modification efforts may contribute to increases in the percentage of work disabled cases who successfully return to competitive work.
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After Norwood's initial report of successful first-stage palliation of hypoplastic left heart syndrome in neonates, an improved understanding of both the pathologic anatomy and physiology of this common condition has led to improving surgical results. Twenty-five neonates have been treated by modifications of the Norwood procedure, and the early mortality between January, 1984, and July, 1985, has been 24% (six deaths). Two premature neonates weighing less than 2 kg died, as did two neonates who could not be resuscitated with prostaglandin E1 and had cardiac arrests immediately preoperatively. There have been four late deaths. The frequent occurrence (80%) of a juxtaductal coarctation or coarctation shelf necessitates alteration of surgical technique. Failure to do so will be reflected in an early persistent postoperative metabolic acidosis with an arterial oxygen tension greater than 35 to 40 mm Hg in the operating room or greater than 40 to 45 mm Hg in the intensive care unit. A similar acid-base derangement will be seen if the systemic-to-pulmonary shunt is excessively large. Careful ventilatory and pharmacologic management of the ratio of pulmonary to systemic vascular resistance is an essential part of the perioperative management of these neonates with two parallel competing circulations. Late postoperative catheterization findings have emphasized the importance of a wide atrial septectomy, because restrictive atrial septal defects have developed in a number of children, despite partial surgical atrial septectomy. Central pulmonary artery reconstruction must be carefully performed to avoid distorted hypoplastic pulmonary arteries that would be unsuitable for a second-stage modified Fontan procedure.
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