Perimetric motion thresholds are elevated in glaucoma suspects and glaucoma patients

The purpose of this study was to determine if a clinically feasible perimetric motion test utilizing random-dot kinematograms could identify glaucomatous visual field defects. Using a staircase procedure, an automated perimetric motion test and a larger foveally presented target were given to normal (n = 30), glaucoma suspects (n = 31) and primary open-angle glaucoma patients (n = 19). Motion thresholds at specific locations throughout the whole visual field were significantly elevated in glaucoma patients (P < or = 0.001). Perimetric motion testing identified 84.2% of the primary open-angle glaucoma patients and 25.8% of the glaucoma suspects as abnormal. A larger foveal stimulus was unable to distinguish between the different subject groups (P < or = 0.185). Perimetric motion thresholds were significantly correlated with Humphrey standard visual field thresholds in the glaucoma and glaucoma-suspect patients (P < or = 0.0002).     

Integrated services for treatment of schizophrenic substance abusers: demographics, symptoms, and substance abuse patterns

We have previously described a model of outpatient integrated treatment for patients with comorbid psychoactive substance use disorders and schizophrenia (PSUD/S)(1). Here we review relevant literature on comorbidity and outline the rationale for integrated services. Further, we describe results from 3 related studies: First, we document the approximate incidence of PSUD among a heterogeneous group of 602 schizophrenic inpatient admissions to our hospital. Second, we describe in greater detail the psychiatric symptoms and patterns of substance abuse among a subsample of 106 inpatients with PSUD/S, contrasting them with 112 patients with PSUD and mixed psychotic disorders, but who are not schizophrenic. Third, we present a prospective research project and describe a sample of 30 patients with PSUD/S, detailing demographic characteristics, psychiatric symptoms and substance abuse history. Attention is given to current issues in the differential diagnosis of patients with PSUD/S using standardized instruments.     

Acral lentiginous melanoma

BACKGROUND: Ossification of the posterior longitudinal ligament (OPLL) may cause neuropathic bladder dysfunction due to spinal cord involvement. OPLL, unlike a traumatic spinal cord lesion, progresses insidiously and sometimes affects longer cord segments. As the manifestation of bladder dysfunction may depend on the development of OPLL, we studied the relationship between bladder function and roentgenographic changes in the spinal canals of OPLL patients. PATIENTS AND METHODS: Eighteen surgical candidates (11 males and 7 females, 34 to 85 years old) were studied urodynamically. Sixteen underwent CO2-filling cystometry, uroflowmetry and measurement of their residual urine volume. Cystometry was omitted in the remaining 2 patients. The vertical extent of OPLL and the degree of stenosis in the spinal canal was estimated by x-ray films and CT. RESULTS: The cystometric study revealed detrusor hyperreflexia in 2 patients and areflexic or underactive detrusors in 5 patients. Intermittent flows or considerable amounts of residual urine were also observed in the arefilexia/underactive group. Uroflowmetry showed a normal flow with little residual urine in both patients in whom cystometry was omitted. Bladder sensation was maintained in all patients. The occurrence of abnormal detrusor activity had no relationship to the degree of canal stenosis, while the occurrence of an areflexic or underactive detrusor correlated with the vertical extent of OPLL. CONCLUSION: Although detrusor hyperreflexia is common in an upper spinal cord lesion, attention should also be paid to the development of detrusor underactivity in patients with a wide vertical extent of OPLL.     

Molecular characterization of Borrelia burgdorferi sensu lato from Slovenia revealing significant differences between tick and human isolates

The aim of the study was to evaluate the morphological and functional status of the liver in acute, oral cholinesterase inhibitors poisoning using static scintigraphy, hepatography and measurements of chosen enzymes activity. Considering the different clinical picture of cholinesterase inhibitors poisonings in people, it was necessary to estimate the poisoning severity and its dependence on the frequency and intensification of the liver lesion. Under examination there were 37 cholinesterase inhibitors orally poisoned patients, treated at the Department of Toxicology in the years 1992-1995. The examined group comprised 7 women (19%) and 30 men (81%). Organophosphate compounds poisoning was noted in 14 patients, and carbamates poisonings in 23 patients. The reference group comprised 30 healthy men aged 24 to 59 years not exposed to hepatotoxic agents. More than 90% of patients were classified as severe poisoned. Any fatal case was not noted. A differently intensified pathological changes of the liver dependent on age and poisoning severity were found in 97.2% of patients and their frequency was significantly higher than in the control group. Hepatographic picture revealed in 96.6% of cases the liver lesion. Hepatographic picture of the liver was also dependent on poisoning severity. The higher activity of AST, ALT, AP and higher bilirubin concentration in blood were noted in poisoned men compared to the control group. Control scintigraphic examination revealed a considerable improvement in the intensification of the liver scintigraphic picture in 40% of the patients and a higher intensification in 13% of the subjects. In 46.6% of the patients the intensification of scintigraphic changes remained at the same level. Considering arbitrary criteria for the degree of the liver lesion, the improvement in the intensification of hepatographic changes was noted in 42.8% of the patients; the intensification of the liver lesion was not noted even in one case. Analyzing the percentage of the liver lesion for each individual patient, improvement was noted in 92.8% of the examined patients, and the changes with the same level of intensification in 7.2%. Deterioration was not noted at all. Conclusion: The liver scintigraphy and hepatography combined with biochemical analysis allows to assess the liver condition in acute cholinesterase inhibitors poisoning.     

Transport-mediated release of endogenous glutamate in the vertebrate retina

In the present study we measured calcium-dependent, vesicular glutamate release, and calcium-independent, transport-mediated glutamate release patterns in the vertebrate retina to better understand the sources of elevated glutamate in neural tissue under ischemic conditions. A potassium concentration of 40 mM, which mimics the extracellular potassium concentration in the central nervous system during ischemia, was applied to the bathing medium of a retinal slice prepared from zebrafish. High external potassium evoked release of endogenous glutamate that was measured using a glutamate-specific fluorometric assay applied to the bath. The slice was visualized under 668 nm light using Normarski optics and fluorescent images were captured using a cooled charge-coupled device (CCD) camera. Following the elevation of external potassium to 40 mM several bands of glutamate fluorescence, reflecting the spatial distribution of glutamate release, were observed. A calcium-dependent cloud of glutamate was observed in the inner plexiform layer, that was antagonized by bath-applied nifedipine. A relatively dense glutamate cloud (1-10 microM) was observed over the ganglion cell layer, which was blocked by dihydrokainate, a glutamate transport antagonist. In contrast, nifedipine, an inhibitor of calcium-dependent neurotransmitter release in the retina, failed to block the cloud of released glutamate in the ganglion cell layer. These data suggest that under pathological conditions in the eye where glutamate levels are elevated surrounding retinal ganglion cells, such as observed in some forms of glaucoma, a possible source of the elevated glutamate is through a glutamate transporter operating in a reversed direction. A likely candidate for mediating this reversed transport of glutamate is the retinal Muller cell.     

Antithrombins Wibble and Wobble (T85M/K): archetypal conformational diseases with in vivo latent-transition, thrombosis, and heparin activation

The inherent variability of conformational diseases is demonstrated by two families with different mutations of the same conserved aminoacid in antithrombin. Threonine 85 underlies the opening of the main beta-sheet of the molecule and its replacement, by the polar lysine, in antithrombin Wobble, resulted in a plasma deficiency of antithrombin with an uncharacteristically severe onset of thrombosis at 10 years of age, whereas the replacement of the same residue by a nonpolar methionine, antithrombin Wibble, gave near-normal levels of plasma antithrombin and more typical adult thromboembolic disease. Isolated antithrombin Wibble had a decreased thermal stability (Tm 56.2, normal 57.6 degreesC) but was fully stabilized by the heparin pentasaccharide (Tm 71.8, normal 71.0 degreesC), indicating that the prime abnormality is a laxity in the transition of the main sheet of the molecule from the 5- to 6-stranded form, as was confirmed by the ready conversion of antithrombin Wibble to the 6-stranded latent form on incubation. That this transition can occur in vivo was shown by the finding of nearly 10% of the proband's plasma antithrombin in the latent form and also, surprisingly, of small but definitive amounts of latent antithrombin in normal plasma. The latent transition will be predictably accelerated not only by gross mutations, as with antithrombin Wobble, to give severe episodic thrombosis, but also by milder mutations, as with antithrombin Wibble, to trigger thrombosis in the presence of other predisposing factors, including the conformational stress imposed by the raised body temperatures of fevers. Both antithrombin variants had an exceptional (25-fold) increase in heparin affinity and this, together with an increased inhibitory activity against factor Xa, provides evidence of the direct linkage of A-sheet opening to the conformational basis of heparin binding and activation.     

Low prevalence of coronary artery spasm in patients with normal coronary angiograms and unexplained ventricular fibrillation

AIMS: The aetiology of ventricular fibrillation in patients without identifiable structural heart disease is unknown. Recently, high prevalence of silent ischaemia due to coronary artery spasm has been reported in such patients. However, in at least one report, all patients had non-critical coronary artery lesions. Identification of coronary artery spasm as the underlying aetiology of ventricular fibrillation has important therapeutic implications. METHODS AND RESULTS: We performed ergonovine provocation tests in 18 patients (14 males, and four females; mean age, 36 years) with documented ventricular fibrillation in the absence of identifiable structural heart disease who had undergone aborted sudden death. In group I (n = 7) ergonovine provocation tests were performed at a mean interval of 31 months (range 21-42 months) after the index episode. These patients had already received an implantable cardioverter defibrillator, after failed electrophysiologically guided antiarrhythmic therapy. In group II (n = 11) the ergonovine provocation test was performed prospectively as part of the diagnostic evaluation. All patients were off antiarrhythmic drugs, calcium entry or beta-adrenoceptor blockers at the time of the ergonovine provocation test. Ergonovine was administered intravenously as a bolus injection, beginning with 0.05 mg followed every 3 min by incremental doses up to a cumulative maximum dose of 0.45 mg. Predefined end-points were (1) recording of ischaemic ST segment shifts of > or = 1 mm in at least two corresponding leads of the 12-lead electrocardiogram; (2) induction of ventricular tachycardia or ventricular fibrillation; and (3) administration of a cumulative dose of 0.45 mg. A positive response to ergonovine was seen in only one patient (5%) in group I in whom there developed ST segment elevation without angina and a short burst of rapid ventricular tachycardia. CONCLUSIONS: This study found a low prevalence of coronary artery spasm in patients with aborted sudden death resulting from documented ventricular fibrillation and non-apparent underlying heart disease. All patients had normal coronary angiograms and a negative history for spontaneous episodes of chest pain. The mechanism of arrhythmogenesis in such patients remains largely unknown.     

The influence of the bolus injection rate of propofol on its cardiovascular effects and peak blood concentrations in sheep

The influence of the bolus injection rate of propofol on its cardiovascular effects has not been extensively studied. We therefore examined the influence of the injection rate of i.v. bolus doses of propofol on its acute cardiovascular effects and peak blood concentrations in seven chronically instrumented sheep. Each received i.v. propofol (200 mg) over 2 min (slow injection) and 0.5 min (rapid injection) on separate occasions in random order. The rapid injection was associated with more profound decreases in mean arterial blood pressure than slow injection (35.7% vs 23.7% maximal reductions from baseline, respectively; P = 0.02). There were no significant differences between the injection rates for peak reductions in myocardial contractility, increases in heart rate, or degree of respiratory depression. Concurrently, the rapid injections were associated with significantly higher arterial (26.9 vs 11.9 mg/L) propofol concentrations in a manner consistent with indicator dilution principles. There were no differences in the peak coronary sinus concentrations between the injection rates. We conclude that the rapid injection of propofol in the context of the induction of anesthesia produced significantly higher peak arterial propofol concentrations and suggest that it is these higher concentrations that produced relatively greater reductions in arterial blood pressure from rapid injections. Implications: Propofol is injected into a vein to initiate anesthesia. It can cause a rapid decrease in blood pressure, which may be dangerous to the patient. We examined the effect of rapid and slow injection rates of propofol in sheep and found that rapid injection caused a greater decrease in blood pressure. This was because rapid injection caused higher concentrations of propofol in the blood immediately after the injection. We believe that if the same processes occur in humans, there may be little advantage in injecting propofol rapidly.     

Epidemiology, laboratory detection, and therapy of penicillin-resistant streptococcal infections

The excitatory effect of presynaptically released glutamate is tightly regulated and terminated by high affinity sodium-dependent glutamate transporters. The regulation of the glial glutamate transporter GLT-1 is potentially important in synaptic modulation. Using astroglial cultures prepared from the rat cerebral cortex, we found that the delta-opioid receptor agonist [D-pen2,D-pen5]-enkephalin decreases and glutamate increases the expression of the GLT-1 transporter mRNA. Corresponding changes in the uptake kinetics were found after incubation for 48 h with the respective agonists when glial glutamate uptake was measured in primary astroglial cultures. The data suggest that long-term receptor activation induces alterations in glial glutamate uptake properties.