Trunk Testing Using a Prototype Cybex II lsokinetic Dynamometer Stabilization System

This pilot study represents Cybex II isokinetic dynamometer trunk testing on 160 subjects (98 males, 62 females). A prototype apparatus which provides stabilization in the standing (functional) position was used in the testing. The testing protocols were performed first for trunk flexion and then trunk extension. The protocols consisted of two isometric tests for 5 seconds at 0 degrees trunk angle and 45 degrees trunk angle followed by three repetitions each at the isokinetic speeds of 30, 60, 90, and 120 degrees per second. Peak torque values were measured for the isometric tests. lsokinetic data interpretation consisted of: peak torque, time rate of tension development, range of motion where peak torque occurred, and total work performed. The ratios of trunk flexors to extensors at each test were also calculated. The conclusion from this pilot study is that the use of an isokinetic testing of trunk musculature and establishing normative data provide clinically useful guidelines for sports screening, industrial medicine screening, and objective parameters for discharging patients with trunk dysfunction. J Orthop Sports Phys Ther 1982;3(4):164-170.     

Regulatory effects of reboxetine treatment alone, or following paroxetine treatment, on brain noradrenergic and serotonergic systems.

When patients do not respond to an initial antidepressant, one clinical approach is to switch to an agent in a different pharmacological class. However, few studies have examined the neurochemical consequences of this practice. To study this, we examined changes in binding sites in rat brain for norepinephrine (NET) and serotonin transporters (SERT), alpha1, alpha2, and beta1 adrenergic receptors after chronic administration of paroxetine (PRX), reboxetine (RBX), or PRX followed by RBX. We also examined the effects of these treatments on mRNA expression for tyrosine hydroxylase (TH). RBX treatment for 3 weeks reduced NET binding significantly, by approximately 40% in terminal field areas, and 6 weeks of RBX reduced it even more, by approximately 60%. RBX treatment for 3 and 6 weeks reduced beta1 adrenergic receptor-binding sites equally, by 50-60%. At no time did RBX treatment reduce SERT-binding sites. PRX treatment had no effect on beta1 adrenergic or NET-binding sites, but reduced SERT-binding sites by 75-80%. Neither treatment altered mRNA for TH, alpha1, or alpha2 adrenergic receptor-binding sites. When 3 weeks of RBX treatment followed 3 weeks of PRX treatment, NET-binding sites were reduced to the same extent as measured after 6 weeks of RBX treatment alone, indicating that PRX pretreatment may have 'primed' the subsequent regulatory effect of RBX on the NET. Thus, pretreatment of rats with PRX actually enhanced at least one regulatory effect of RBX treatment on the noradrenergic system, and did not interfere with any other pharmacological effect caused by RBX treatment.     

Strontium-90 in newborns and childhood disease

Radioactive strontium-90 concentrations in baby teeth obtained from Suffolk County, New York, rose steadily during the 1980s. Recent levels of strontium-90 are similar to those reported for babies born in the late 1950s-at the height of atmospheric nuclear weapons testing in Nevada. Strontium-90 concentrations increased concomitantly with increases in cancer incidence among Suffolk children under the age of 5 y, a result that mimicked parallel trends observed in the 1950s and early 1960s. Given that effects of strontium-90 on developing cells are most pronounced during the fetal and infant periods, escalating levels should be viewed as a factor in the recent decline in various child health status measures.     

Antioxidant-rich diets improve cerebellar physiology and motor learning in aged rats

The free radical theory of aging predicts that reactive oxygen species are involved in the decline in function associated with aging. The present paper reports that diets supplemented with either spinach, strawberries or blueberries, nutritional sources of antioxidants, reverse age-induced declines in beta-adrenergic receptor function in cerebellar Purkinje neurons measured using electrophysiological techniques. In addition the spinach diet improved learning on a runway motor task, previously shown to be modulated by cerebellar norepinephrine. Motor learning is important for adaptation to changes in the environment and is thus critical for rehabilitation following stroke, spinal cord injury, and the onset of some neurodegenerative diseases. These data are the first to indicate that age-related deficits in motor learning and memory can be reversed with nutritional interventions.     

Five cases of brain injury following amniocentesis in mid-term pregnancy

This paper describes the neuroimaging and neuropathological findings in five cases of severe brain damage after traumatic mid-trimester amniocentesis, all performed between 1986 and 1994. Although fetal injury after amniocentesis has been reported, reports of brain injury are infrequent. Continuous ultrasound monitoring may reduce the risk of fetal injury but follow-up ultrasound scans can be falsely reassuring. Withdrawal of blood-stained fluid, particularly if it contains tissue fragments, should alert the operator to the possibility of fetal damage. Histological examination of such tissue fragments may confirm the nature of the fetal damage. The consequences of fetal brain injury are severe, all five of our cases showed evidence of disruption of brain development compatible with mid-term injury. Obstetricians and their patients should be aware of the small but significant risk of brain damage after mid-term amniocentesis.     

A possible role for nerve growth factor in the augmentation of sodium channels in models of chronic pain

Inflammation induces an upregulation of sodium channels in sensory neurons. This most likely occurs as a result of the retrograde transport of cytochemical mediators released during the inflammatory response. The purpose of this study was to determine the effect of the subcutaneous administration of one such mediator, nerve growth factor (NGF), on the production of sodium channels in neurons of the rat dorsal root ganglion. For this, hindpaw withdrawal from either a thermal or mechanical stimulus was measured in rats at selected intervals for up to 2 weeks following injections of NGF. Sodium channel augmentation was then examined in dorsal root ganglia using site-specific, anti-sodium channel antibodies. Both thermal and mechanical allodynia was observed between 3 and 12 h post-injection. The hyperalgesic response returned to baseline by approximately 24 h post-injection. Sodium channel labeling was found to increase dramatically in the small neurons of the associated dorsal root ganglia beginning at 23 h, reached maximum intensity by 1 week, and persisted for up to 3 months post-injection. Pre-blocking NGF with anti-NGF prevented the NGF-induced decrease in paw withdrawal latencies and significantly reduced the intensity of sodium channel labeling. The results indicate that NGF is an important mediator both in the development of acute hyperalgesia and in the stimulation of sodium channel production in dorsal root ganglia during inflammation.     

Cd36 and molecular mechanisms of insulin resistance in the stroke-prone spontaneously hypertensive rat

Insulin resistance is of pathogenic importance in several common human disorders including type 2 diabetes, hypertension, obesity and hyperlipidemia, but the underlying mechanisms are unknown. The spontaneously hypertensive rat (SHR) is a model of these human insulin resistance syndromes. Quantitative trait loci (QTLs) for SHR defects in glucose and fatty acid metabolism, hypertriglyceridemia, and hypertension map to a single region on rat chromosome 4. Genetic analysis of an SHR derived from a National Institutes of Health colony led to the identification of a causative mutation in the SHR Cd36. We have investigated glucose and fatty acid metabolism in the stroke-prone SHR (SHRSP). We demonstrate defects in insulin action on 2-deoxy-D-glucose transport (SHRSP 3.3 +/- 1.5 vs. 21.0 +/- 7.4 pmol x min(-1) x [20 microl packed cells](-1), SHRSP vs. WKY, respectively, P = 0.01) and inhibition of catecholamine-stimulated lipolysis (P < 0.05 at all concentrations of insulin) in adipocytes isolated from SHRSP. In contrast, basal levels of catecholamine-stimulated nonesterified free fatty acid (NEFA) release and plasma levels of NEFA are similar in SHRSP and WKY. These results are in agreement with the data on the SHR.4 congenic strain, which suggested that the QTL containing Cd36 mutations accounted for the entire defect in basal catecholamine action but only for approximately 40% of the SHR defect in insulin action. In the SHR, both abnormalities appear consequent of defective Cd36 expression. Because Cd36 sequence and expression are apparently normal in SHRSP, it is likely that the molecular mechanism for defective insulin action in this strain is caused by a gene(s) different than Cd36.     

Chloramphenicol resistance in vancomycin-resistant enterococcal bacteremia: impact of prior fluoroquinolone use?

OBJECTIVE: The prevalence of vancomycin-resistant enterococci (VRE) has increased markedly during the past decade. Few data exist regarding the epidemiology of resistance of VRE to chloramphenicol, one of the few therapeutic options. DESIGN: Survey and case-control study. SETTING: A 725-bed, tertiary-care academic medical center and a 344-bed urban community hospital. PATIENTS: Hospitalized patients with blood cultures demonstrating VRE. METHODS: We examined the trends in the prevalence of chloramphenicol resistance in VRE blood isolates at our institution from 1991 through 2002 and conducted a case-control study to identify risk factors for chloramphenicol resistance among these isolates. RESULTS: From 1991 through 2002, the annual prevalence of chloramphenicol-resistant VRE increased from 0% to 12% (P < .001, chi-square test for trend). Twenty-two case-patients with chloramphenicol-resistant VRE bloodstream isolates were compared with 79 randomly selected control-patients with chloramphenicol-susceptible VRE. Independent risk factors for chloramphenicol-resistant VRE were prior chloramphenicol use (odds ratio [OR], 10.9; 95% confidence interval [CI95], 1.72-68.91; P = .01) and prior fluoroquinolone use (OR, 4.74; CI95, 1.15-19.42; P = .03). Chloramphenicol-resistant VRE isolates were more likely to be susceptible to beta-lactams and resistant to tetracycline than were chloramphenicol-susceptible VRE isolates. CONCLUSIONS: Significant increases in the prevalence of chloramphenicol-resistant VRE may limit the future utility of chloramphenicol in the treatment of VRE infections, and close monitoring of susceptibility trends should continue. The association between fluoroquinolone use and chloramphenicol-resistant VRE, reflecting possible co-selection of resistance, suggests that recent dramatic increases in fluoroquinolone use may have broader implications than previously recognized.