Rapid and selective uptake, metabolism, and cellular distribution of docosahexaenoic acid among rod and cone photoreceptor cells in the frog retina

The uptake, metabolism, and cellular distribution of 3H-docosahexaenoic acid (3H-22:6) in the frog retina during in vitro incubation were studied. An initial diffuse labeling throughout the retina was detected by autoradiography and was followed by an active steady increase in labeled photoreceptor cells. After 6 hr of incubation, 92% of the label was concentrated in photoreceptor cells. Among these cells, 435-rods (green rods) labeled heavily and showed two to three times higher uptake than the 502-rods (red rods). Cone uptake labeling was the lowest, showing negligible labeling throughout the cytoplasm. However, oil droplets of the 575-cones actively concentrated 22:6. The high uptake of 3H-22:6 by photoreceptor cells was followed by its rapid esterification into phospholipids. After 6 hr of labeling, only 5% of the radioactivity in the retina was free 22:6, whereas 88% was esterified into phospholipids. The remaining 22:6 was distributed equally in triacylglycerols (TAGs) and diacylglycerols. When 3H-22:6 (0.11 microM) of high specific activity was used, early incubation times showed phosphatidylinositol (PI) labeling to be of the same order of magnitude or greater than that of phosphatidylcholine (PC) or phosphatidylethanolamine (PE). Although the amount of endogenous 22:6 esterified into PI accounted for less than 2% of the 22:6 in retinal phospholipids, 27% of 3H-22:6 labeling was recovered in this phospholipid. When 14C-22:6 at a final concentration of 70 microM was used, a different profile of lipid labeling was observed. Forty percent of the labeling remained in the free fatty acid pool, followed by TAG (24%), PC (14%), and PE (12%). PI showed the smallest increase in picomoles of 14C-22:6 incorporated, when compared with 3H-22:6. In conclusion, a selective and differential uptake of 3H-22:6 by photoreceptor cells is coupled to its active utilization for phospholipid biosynthesis, mainly that of PC, PE, and PI. The differential uptake of 3H-22:6 among photoreceptor cells may reflect involvement of this fatty acid in cell-specific functions.     

Blunt thoracic trauma. Analysis of 515 patients.

A retrospective analysis of 515 cases of blunt chest trauma is presented. The overall thoracic morbidity rate was 36% and mortality rate was 15.5%. Atelectasis was the most common complication. Severe chest trauma can be present in the absence of rib or other thoracic bony fractures. Emergency thoracotomies for resuscitation of the patient with blunt chest trauma with absent vital signs proved unsuccessful in 39 of 39 patients. A high index of suspicion for blunt chest injury occurring in blunt trauma, coupled with an aggressive diagnostic and therapeutic approach, remains the cornerstone of treatment to minimize the morbidity and mortality of such injuries.     

Regulation of neurotransmitter enzyme by quisqualate subtype glutamate receptors in cultured cerebellar and hippocampal neurons

The possible involvement of ionotropic and metabotropic quisqualate (QA) receptors in neuronal plasticity was studied in cultured glutamtergic cerebellar or hippocampal cells in terms of the specific activity of phosphate-activated glutaminase, an enzyme important in the synthesis of the putative neurotransmitter pool of glutamate. When cerebellar of hippocampal neurons were treated with QA, it elevated the specific activity of glutaminase in a dose-dependent manner. The half-maximal effect was obtained at about 0.1 μM, the maximum increase was at about 1 μM, but levels higher than 10 μM QA produced progressive reduction in glutaminase activity. In contrast, QA had little effects on the activities of lactate dehydrogenase and aspartate aminotransferase and the amount of protein, indicating that the increase in glutaminase was relatively specific. The QA-mediated increase in glutaminase was mimicked by the ionotropic QA receptor agonist -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA; EC₅₀, about 0.5 μM), but not by the metabotropic QA receptor agonist trans-(±)-1-aino-cyclopentyl-1,3,dicarboxyalte (t-ACPD; up to 0.5 mM). The specific ionotropic QA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) inhibited QA- and AMPA-mediated increases in glutaminase activity in a dose-dependent manner, whereas other glutamate receptor antagonists, -2-amino-5-phosphonovalerate, γ- -glutamyl aminomethyl sulphonic acid and γ- -glutamyl diethyl ester were ineffective. The elevation of neurotransmitter enzyme was Ca²⁺-dependent. The increase in Ca²⁺ influx essentially through the activation of L-type voltage-operated Ca²⁺ channels, and not the mobilization of internal Ca²⁺ stores, was responsible for these QA receptor-mediated long-term plastic changes in hippocampal and cerebellar neurons.     

Cerebral Effects in Superior Vena Caval Cannula Obstruction: The Role of Brain Monitoring

A pediatric cardiac case of transient obstruction of the superior vena cava by the venous cannula before cardiopulmonary bypass is presented. With venous obstruction and increase in central venous pressure, reduced cerebral blood flow velocities and absence of diastolic Doppler flow were detected. This was followed by regional cerebral venous oxygen desaturation and global electroencephalographic slowing. Reposition of the venous cannula led to the recovery of these physiologic indicators and a noncomplicated clinical outcome.     

An evaluation of the mechanical failure modalities of a rotating hinge knee prosthesis

The clinical and metallurgical performance of 12 retrieved Noiles total knee prostheses was investigated. Clinical histories and serial roentgenograms were used in conjunction with the American Society for Testing and Materials (ASTM) standard implant retrieval and analysis techniques to assess device performance. All of the devices were removed because of implant loosening with pain, while two devices also had a late infection. The average time in situ for all devices was four years. Roentgenographically, all of the devices showed signs of progressive radiolucencies. Ten (83%) of the devices migrated proximally within the femur. A marked varus drift was observed in eight (67%) of the retrieved prostheses. Hypertrophy of the femoral cortex was observed in eight (67%) of the cases. Seventy-three percent of the polyethylene tibial stems exhibited extensive wear on the anterior and medial aspects of the articulating surface. Extensive wear was also seen on the anterior and extreme posterior aspects in 92% of the polyethylene tibial plateau bearings. This wear was a consequence of the migration of the femoral component leading to buttressing of the plastic components against bone or bone cement. This study indicates serious design flaws in the Noiles knee prosthesis that unless corrected would question the use of the device in either primary or revision knee surgery.     

Impairments in vasopressin-stimulated inositol lipid metabolism in hepatocytes of septic rats

Vasopressin (VP)-stimulated 32P-inositol lipid metabolism was studied in hepatocytes obtained from rats rendered septic by cecal ligation and puncture. Basal 32P-phosphatidylinositol (PI) labeling, as well as its hormone-stimulated turnover, were greatly reduced in septic rats compared with sham-operated rats. The earliest VP-induced degradation of 32P-polyphosphoinositides (poly-PI) was greatly attenuated in septic rats. Moreover, while 32P-poly-PI labeling reached its lowest value by 60 sec of VP stimulation in cells from sham-operated rats, maximal changes in 32P-phosphatidylinositol 4,5-bisphosphate (32PIP2) occurred within 30 sec in septic rats. In contrast, the recovery of 32PIP2 labeling was more active in cells from septic rats, overcoming the impairment in its resynthesis triggered by surgical trauma in cells from sham-operated rats. The lower uptake of 32P into phosphatidic acid (PA) at the different time points analyzed was a sensitive indicator of the lower production of diacylglycerols from the VP-induced degradation of inositol phospholipids in septic rats. These observations support the idea that sepsis is associated with perturbations in the earliest events of the hepatocyte signal transmission pathway, namely, at the level of a receptor coupled to inositol lipid metabolism. Such perturbations are likely to be involved in the previously reported defective cell physiologic response to external hormone stimulation.     

Procedural learning in schizophrenia can reflect the pharmacologic properties of the antipsychotic treatments.

BACKGROUND: Conventional and atypical antipsychotics have different affinities for D2 receptors, and these receptors are principally located in the striatum. Given that this cerebral structure was previously found to play a major role in procedural learning, the antipsychotic treatment in schizophrenia may be determinant for the procedural learning profile of these patients. OBJECTIVE: The current study was aimed at verifying whether procedural learning differs in patients with schizophrenia treated with conventional antipsychotics and patients treated with atypical antipsychotics. METHOD: Forty-five patients with schizophrenia were divided into 3 different groups according to their pharmacologic treatment: (1) haloperidol, a classical neuroleptic with high D2 receptor affinity; (2) clozapine, an atypical neuroleptic with practically no D2 receptor affinity; and (3) risperidone, an atypical neuroleptic that nevertheless shows high D2 receptor affinity. Patients were compared to 35 control subjects on a visuomotor procedural learning task (mirror drawing). RESULTS: All patients were able to learn the task. However, those treated with haloperidol showed some degree of learning impairment, while those treated with clozapine or risperidone did not show this impairment. In addition, performance per se, regardless of the learning, was found to be affected in the haloperidol and risperidone, but not in the clozapine groups. CONCLUSION: Procedural learning in schizophrenia may be differentially affected, depending on the pharmacologic profiles of the antipsychotics used for the treatment of this illness.     

Management of acute visual loss in children.]

Acute or rapidly progressive visual loss in children needs urgent attention and treatment. It may be unilateral orbilateral. Etiology depends upon the involved areas: eye ball, optic nerve, retro-chiasmatic pathways. Psychogenic origin is quite common in school-age children, however, it has to be considered last. Unilateral visual loss may be overlooked. Acute total transitory visual loss may be due to epilepsy or to migraine. Rapidly progressive visual loss may be due to retinal disease, optic neuritis or cortical blindness. Management of visual loss depends on clinical features, associated symptoms, and aspect of the optic disc. It needs collaboration between ophthalmologist,pediatrician and neuropediatrician. Retinal hemorrhages first call to mind a traumatic origin. Swelling of the optic disc may be due to increased intracranial pressure or due to optic neuritis. When the optic disc is normal it is necessary to rule out organic diseases before establishing the diagnosis of a psychogenic vision disturbance. In emergency, brain neuroimaging is the best way to diagnose intracranial mass and visualize optic pathways.     

Paramedic and emergency department care of stroke: baseline data from a citywide performance improvement study.

BACKGROUND: Rapid diagnosis and transport by paramedics and efficient, effective emergency management are essential to improving care of acute stroke patients. OBJECTIVES: To measure the performance of paramedics and emergency departments providing care for patients with suspected acute stroke. METHODS: Two stroke centers and 4 other hospitals where most patients with acute stroke in Houston, Tex, are admitted participated. Hospital and paramedic performance data were collected prospectively on 446 patients with suspected acute stroke transported by paramedics between September 1999 and February 2000. RESULTS: Paramedics had a sensitivity of 66%, specificity of 98%, and overall accuracy of 72% in diagnosing stroke. For patients with suspected stroke, 58.5% arrived in the emergency department within 120 minutes of symptom onset; in confirmed cases, that percentage was 67%. Mean total transport time was 42.2 minutes and was significantly longer (P < .001) to inner-city hospitals (44 minutes) than to suburban, community-based centers (39 minutes). Door to computed tomography times were significantly (P < .001) shorter for the 2 stroke centers than the other hospitals. Overall thrombolysis treatment rate among patients with confirmed ischemic stroke was 7.4% (range, 0-19.4%); treatment rates at the 2 stroke centers were 5.9% and 19.4%. CONCLUSIONS: More than half of patients with suspected stroke arrive at hospitals while thrombolytic treatment is still feasible. Although the current rate for thrombolytic treatment in Houston exceeds the national rate, performance of paramedics and hospitals in treating acute stroke can be improved by increasing efficiency and standardizing medical practices.