Acquired hepatocerebral degeneration: MR similarity with Wilson disease

Acquired hepatocerebral degeneration (AHD) is a neurologic syndrome occurring in the presence of chronic hepatic disease, which results in permanent neurologic aberrations. The syndrome shares many of the clinical manifestations of Wilson disease, however, distinction can be made with slit lamp examination and biochemical studies. Cranial magnetic resonance (MR) imaging of a patient with AHD revealed increased signal intensity in the dentate nuclei bilaterally on T2-weighted images indistinguishable from Wilson disease. The MR findings of Wilson disease as described in the literature are not specific and further investigation with slit lamp examination and biochemical studies is warranted to distinguish between the two entities.     

Fibrinolysis inhibitors.

The fibrinolytic system involves a series of enzymatic reactions that results in the conversion of the proenzyme, plasminogen, into the trypsin-like lytic enzyme, plasmin. The major physiologic target of plasmin is fibrin. Free plasmin in plasma is a nonspecific lytic enzyme that will degrade other proteins such as fibrinogen and coagulation factors V and VIII. Plasmin and activators of plasminogen also play a role in ovulation, embryo implantation, tissue remodeling, and inflammation.     

Why all finger fractures should be referred to a hand surgery service: a prospective study of primary management

The quality of the treatment of finger fractures by Accident and Emergency Department staff has been prospectively assessed during a six-month period. 678 finger fractures were seen in the A. & E. Department. The primary treatment of 624 of these was performed by the A. & E. staff, but in 169 of these (27%), the treatment was inappropriate. Most management errors were elementary; they included failure to prescribe antibiotics for compound fractures, failure to reduce displaced fractures accurately and unsatisfactory splintage. It is recommended that all finger fractures should be assessed and treated by surgeons with training in the management of hand injuries.     

Chronic haloperidol and chlorpromazine treatment alters in vitro beta-endorphin metabolism in rat brain

To determine if chronic haloperidol (3.0 mg/kg per day) or chlorpromazine (4.2 mg/kg per day) treatment alters central beta-endorphin metabolism, haloperidol and chlorpromazine were perfused via Alzet minipumps into male Sprague-Dawley rats for 8 days. Crude twice-washed membranes, purified synaptic plasma membranes and Golgi-enriched membranes, respectively, were isolated from rat brains and time course incubated with beta-endorphin. All samples were analyzed by high resolution, reversed-phase high performance liquid chromatography. The half-lives of beta-endorphin for animals treated with haloperidol or chlorpromazine were not statistically different from control animals at the crude washed membranes. At the purified synaptic plasma membranes, however, the half-lives of beta-endorphin from haloperidol (t 1/2 = 45.1 min)- and chlorpromazine (t1/2 = 47.0 min)-treated animals were significantly decreased as compared to the control animals (t1/2 = 78.0 min). The half-life of beta-endorphin at the Golgi-enriched membranes was increased for haloperidol (t1/2 = 112.3 min) and chlorpromazine (t1/2 = 103.0 min)-treated animals when compared to control animals (t1/2 = 80.2 min). The findings indicate a differential effect of the dopamine receptor antagonists haloperidol and chlorpromazine on the extracellular fate at the synaptic plasma membranes of beta-endorphin and the intracellular processing at the Golgi-enriched membranes in vitro.     

Sensitivity and specificity of clinical case definitions for pertussis

We evaluated the diagnostic performance of 15 clinical case definitions for pertussis in 233 patients who developed acute respiratory illness during community outbreaks in Wisconsin and Delaware. Using results from culture (Regan-Lowe media) and serology (Ig-class-specific ELISA) as diagnostic standards, cough for greater than or equal to 14 days was both sensitive (84 per cent-92 per cent) and specific (63 percent-90 per cent) in identifying patients with pertussis. This definition may be useful in monitoring pertussis outbreaks and for investigating contacts of culture-positive cases.     

Brain Death Further Promotes Ischemic Reperfusion Injury of the Rabbit Myocardium

Background. Little is known about preload-dependent cardiac function after brain death (BD) and subsequent graft preservation.

Methods. A validated model of BD in rabbits was developed and myocardial performance was studied after BD induction and 1 hour of subsequent global hypothermic ischemia using a validated rabbit model and an isolated work-performing heart preparation.

Results. Significant decreases in stroke work, left ventricular contractility, and left ventricular relaxation were observed 2 hours after BD. After global hypothermic ischemia, significant decreases in stroke work, left ventricular contractility, and left ventricular relaxation were observed in the BD group compared with controls. Cardiac output and coronary flow were also significantly decreased in BD hearts compared with controls. Creatine kinase release was increased by 32.5% in BD hearts compared with controls.

Conclusions. In a rabbit model, BD combined with global hypothermic ischemia causes a significant decrease in left ventricular function compared with global hypothermic ischemia. This dysfunction may be attributed to a significant decrease in coronary flows in BD hearts.     

SDZ 208-911, an amino-ergoline with partial dopamine agonist properties,dose dependently increases cocaine self-administration in the rat

Brain dopamine neurotransmission appears to be an important component of the neural pathways involved in the maintenance of intravenous (IV) cocaine self-administration in rats. The effects of a novel partial dopamine agonist, SDZ 208–911, on intravenous cocaine self-administration in rats was studied. SDZ 208–911 at a dose range of 0.025–1.6 mg/kg SC dose-dependently increased the number of lever presses and drug intake in rats exposed to limited (3-h) daily access to cocaine on a continuous reinforcement schedule (0.75 mg/kg per injection). This behavioral profile is similar to that observed following administration of dopamine antagonist drugs and has been hypothesized to reflect a compensatory increase in drug intake due to a reduction of the reinforcing efficacy of the drug, probably because of functional antagonism at the receptor site. These results suggest that dopamine partial agonists may act as functional dopamine antagonists in the face of pharmacologically induced activation of brain dopamine function.     

Na+ currents near and away from endplates on human fast and slow twitch muscle fibers

Fast and slow twitch muscle fibers have distinct contractile properties. Here we determined that membrane excitability also varies with fiber type. Na⁺ currents (I_NA) were studied with the loose-patch voltage clamp technique on 29 histochemically classified human intercostal skeletal muscle fibers at the endplate border and <200 μm from the endplate (extrajunctional). Fast and slow twitch fibers showed slow inactivation of endplate border and extrajunctional I_NA and had increased I_NA at the endplate border compared to extrajunctional membrane. The voltage dependencies of I_NA were similar on the endplate border and extrajunctional membrane, which suggests thatboth regions have physiclogically similar channels. Fast twitch fibers had larger I_NA on the endplate border and extrajunctional membrane and manifest fast and slow inactivation of I_NA at more negative potentials than slow twitch fibers. For normal muscle, the differences between I_NA on fast and slow twitch fibers might: (1) enable fast twitch fibers to operate at high firing frequencies for brief periods; and (2) enable slow twitch fibers to operate at low firing frequencies for prolonged times. Disorders of skeletal membrane excitability, such as the periodic paralyses and myotonias, may impact fast and slow twitch fibers differently due to the distinctive Na⁺ channel properties of each fiber type. © 1993 John Wiley & Sons, Inc.