Occult head injury: its incidence in spinal cord injury

This study investigated the suspicion that a significant proportion of individuals having spinal cord injury (SCI) also sustain a concomitant undiagnosed occult head injury during the trauma accident. The criteria for high risk of head injury included the following: (1) quadriplegia with high energy deceleration accident, (2) loss of consciousness at time of injury, (3) brainstem or cortical neurologic indicators, or (4) respiratory support required at time of injury. In this study, 67 patients admitted to the rehabilitation unit were given a neuropsychologic evaluation a median of 48 days after injury. Motor free scales used were the Galveston Orientation and Amnesia Test (GOAT), Quick Test, Raven Progressive matrices, serial 7s, Shipley Hartford, Stroop Color/Word Interference, and the Wechsler Memory Scale Associate Learning Tests. Forty-three of the 67 patients (64%) scored mildly to profoundly impaired on the test battery. Evidence of poor premorbid academic history was present in 19 (44%) of those with impaired performance on the neurologic evaluation and in only three (13%) of those scoring unimpaired. Consequently, 56% (24/43) of the impaired had no previous record of scholastic difficulties, presumably acquiring cognitive impairment at the time of injury. The implications of this high incidence of impaired cognitive functioning for treatment of individuals with SCI are significant.     

Neurogenic Respiratory Failure: A 5-Year Experience Using Implantable Phrenic Nerve Stimulators

During the past 5 years, 20 phrenic nerve stimulators have been implanted in 11 patients who were ventilator dependent because of neurogenic respiratory failure. Ten patients had traumatic spinal cord lesions; the remaining patient suffered from a progressive demyelinating disease. There was no operative mortality. Complications included 1 stimulator malfunction and 1 pneumothorax. In spite of adjacent tracheostomies, there were no infections or wound complications. Of the 20 stimulators implanted, 13 initially produced good diaphragmatic function, 2 had fair function, and 5 had little or no function. Three patients became completely independent of their ventilators; 6 became partially independent, thus simplifying nursing care. There were no late complications. As of December, 1979, 7 patients had benefited or were continuing to benefit from phrenic nerve stimulation.     

Competitive quenching: a possible novel approach in protecting RPE cells from damage during PDT

PURPOSE: The purpose of this study is to demonstrate feasibility of using our novel concept, termed competitive quenching, for protecting the choroidal extravascular compartment and retinal pigment epithelium (RPE) from verteporfin (VP)-induced phototoxicity using hypericin. Furthermore, we aim to achieve partitioning of the quencher, hypericin, in the extravascular space and VP within the microvascular compartment of the chorio-retinal complex in vivo. METHODS: We protect RPE cells from damage inflicted by photoactivated VP by introducing hypericin into these cells prior to photosensitization to quench the photosensitizing activity of VP. Cell protection levels were measured by MTT and Hemacolor viability assays. Wavelength range used for VP photoexcitation (700 +/- 40 nm) excludes the absorption range of hypericin, preventing the latter from photoactivation. Pharmacokinetic conditions, in which hypericin spreads throughout the choroidal and retinal extravascular space while VP is confined to the vasculature, are delineated using double-fluorescence imaging. RESULTS: Cell viability increased 3- to 5-fold when 10-20 microM hypericin were present in RPE cells during photosensitization with 0.1-0.5 microM VP. VP fluorescence intensity was unchanged by the presence of hypericin in the cells. Hypericin administered intravenously to rats was confined to the choroidal vasculature after 15 min to 2 hr. Subsequently, hypericin partitioned to the choroidal and retinal extravascular space. VP administered at this time was confined to the microvasculature. CONCLUSIONS: RPE and choroid may potentially be protected by compartmentalizing hypericin to the extravascular compartment while VP administered shortly before photosensitization is confined to the microvasculature. Adverse photodynamic therapy (PDT) damage to choroidal tissues adjacent to neovasculature targeted for photoablation have the potential of being prevented by competitive quenching with hypericin.     

A loss-of-function nonsynonymous polymorphism in the osmoregulatory TRPV4 gene is associated with human hyponatremia

Disorders of water balance are among the most common and morbid of the electrolyte disturbances, and are reflected clinically as abnormalities in the serum sodium concentration. The transient receptor potential vanilloid 4 (TRPV4) channel is postulated to comprise an element of the central tonicity-sensing mechanism in the mammalian hypothalamus, and is activated by hypotonic stress in vitro. A nonsynonymous polymorphism in the TRPV4 gene gives rise to a Pro-to-Ser substitution at residue 19. We show that this polymorphism is significantly associated with serum sodium concentration and with hyponatremia (serum sodium concentration ≤135 mEq/L) in 2 non-Hispanic Caucasian male populations; in addition, mean serum sodium concentration is lower among subjects with the TRPV4^P19S allele relative to the wild-type allele. Subjects with the minor allele were 2.4−6.4 times as likely to exhibit hyponatremia as subjects without the minor allele (after inclusion of key covariates). Consistent with these observations, a human TRPV4 channel mutated to incorporate the TRPV4^P19S polymorphism showed diminished response to hypotonic stress (relative to the wild-type channel) and to the osmotransducing lipid epoxyeicosatrienoic acid in heterologous expression studies. These data suggest that this polymorphism affects TRPV4 function in vivo and likely influences systemic water balance on a population-wide basis.     

Effective prevention of microbial biofilm formation on medical devices by low-energy surface acoustic waves

Low-energy surface acoustic waves generated from electrically activated piezo elements are shown to effectively prevent microbial biofilm formation on indwelling medical devices. The development of biofilms by four different bacteria and Candida species is prevented when such elastic waves with amplitudes in the nanometer range are applied. Acoustic-wave-activated Foley catheters have all their surfaces vibrating with longitudinal and transversal dispersion vectors homogeneously surrounding the catheter surfaces. The acoustic waves at the surface are repulsive to bacteria and interfere with the docking and attachment of planktonic microorganisms to solid surfaces that constitute the initial phases of microbial biofilm development. FimH-mediated adhesion of uropathogenic Escherichia coli to guinea pig erythrocytes was prevented at power densities below thresholds that activate bacterial force sensor mechanisms. Elevated power densities dramatically enhanced red blood cell aggregation. We inserted Foley urinary catheters attached with elastic-wave-generating actuators into the urinary tracts of male rabbits. The treatment with the elastic acoustic waves maintained urine sterility for up to 9 days compared to 2 days in control catheterized animals. Scanning electron microscopy and bioburden analyses revealed diminished biofilm development on these catheters. The ability to prevent biofilm formation on indwelling devices and catheters can benefit the implanted medical device industry.