[Plasma exchange in acute hepatic failure: effectiveness and evaluation].
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Biomedical subjects
Publications and source records attributed to H Oka.
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A 58-year-old female was admitted to our hospital because of weakness of the right lower extremity and dysesthesia of the right upper extremity. From her clinical symptoms the patient was tentatively diagnosed as having a sort of cerebral infarction and treated with administration of urokinase and antiplatelet agents. However, angiographical examination revealed a unruptured aneurysm of the A1 portion of the left anterior cerebral artery. Preoperative angiogram showed that the dome of the aneurysm compressed one of the neighboring perforating artery which arose from adjacent to the neck of the aneurysm. The patient underwent neck clipping of aneurysm successfully. During the operation, the perforator was hardly adhered to the dome of the aneurysm. So, careful dissection was made only around the neck and the perforator was spared. Her symptoms were disappeared immediately after surgery. The perforator was demonstrated with better filling in the postoperative angiogram than that in the preoperative angiogram. The pathomechanisms of cerebral ischemia caused by unruptured aneurysm were reviewed on the literature. Most of the cases were caused by release of fragmental thrombi from a large aneurysm. There was a very exceptional case whose symptoms had seemed to be related to the direct compression of the neighboring perforator by the aneurysm. The compressed perforator in this case was seemed to be corresponded with the medial proximal striate artery stated by Yaşargil.
Intracellular recording from the CM-PF neurons was performed by stimulation of the EN, the caudate nucleus (Cd), the cerebellar nuclei (CN) and the motor cortex in the cat under Nembutal anesthesia. Twenty-seven neurons in the CM-PF nuclear complex and two neurons near the habenular nucleus received monosynaptic inhibitory postsynaptic potentials (IPSPs; latency of 1.0-4.0 ms, mean 2.3 ms) by EN stimulation. Cd stimulation evoked excitatory postsynaptic potentials (EPSPs) followed by long hyperpolarizations in most of the CM-PF neurons and produced antidromic activation in 7 neurons. Six neurons received EPSPs (latencies of 4-7 ms) by cortical stimulation. CN stimulation affected only two neurons in the present study. Intracellular HRP staining revealed that some CM-PF neurons have polygonal or spindle-shaped somata with fine, long and sparsely spinous dendrites.
In human platelets, a monoclonal anti-human platelet antibody (TP82) induced platelet aggregation and release of granules (i.e., serotonin, platelet factor 4, N-acetyl-beta-D-glucosaminidase). The release reaction occurred even in the absence of aggregation and was preceded by not only the protein phosphorylation, but the transient formation of endogenous diacylglycerol (DG). These results suggest that polyphosphoinositide breakdown plays an essential role in antibody-induced release of platelet granules.
A classification of the parietal corticofugal neurons was performed in cats under Nembutal anesthesia. Eighty-eight neurons were identified with antidromic activation by the pontine stimulation. Thirteen neurons were furthermore identified with intracellular HRP staining. In these neurons, we found the close correlation between morphological features and conduction velocities. The faster conducting group of the neurons had relatively large somata, sparsely spinous apical dendrites, tap root basal dendrites and wide apical dendritic fields. The slower group had small somata and numerous dendritic spines.
We examined effects of arachidonic acid (AA) on eicosapentaenoic acid (EPA) metabolism in washed human platelets. Although human platelets had been considered to metabolize scarcely EPA, a simultaneous addition of EPA and AA to washed platelet suspensions stimulated markedly EPA metabolism. In addition, the stimulatory effect was more potent over the formation of thromboxane (TX) B3 than that of 12-hydroxy-5,8,10,14,17-eicosapentaenoic acid (HEPE). The stimulation by AA can be due to AA itself and/or AA metabolites. Indomethacin decreased the stimulatory effect of AA on the HEPE formation, suggesting that cyclooxygenase product(s) of AA stimulated the HEPE formation. Among the metabolites of AA investigated, prostaglandin (PG)G2 and 12-hydroperoxy-5,8,10,14-eicosatetraenoic acid had the stimulatory effect on both TXB2 and HEPE formations, whereas PGH2, PGD2, TXB2 and 12-hydroxy-5, 8,10,14-eicosatetraenoic acid were ineffective.
We examined platelet aggregation and serotonin release, induced by less than 60 micro M arachidonic acid, using washed platelet suspensions in the absence of albumin. The concentration of arachidonic acid used did not cause platelet lysis. Platelet responses induced by less than 20 micro M arachidonic acid were inhibited by aspirin, whereas those induced by above 30 micro M arachidonic acid were not inhibited, even by both aspirin and 5,8,11,14-eicosatetraynoic acid. Although phosphatidic acid and 1,2-diacylglycerol increased after the addition of arachidonic acid in aspirin-treated platelets, the amounts were not parallel to platelet aggregation. Oleic, linoleic and linolenic acids also induced platelet responses, while palmitic, stearic and arachidic acids did not. EDTA, dibutyryl cyclic AMP, apyrase and creatine phosphate/creatine phosphokinase brought about almost the same effects in platelet responses induced by the unsaturated fatty acids, other than arachidonic acid, as those induced by 40 micro M arachidonic acid. These results suggest that the mechanism of the actions of more than 30 micro M arachidonic acid on platelets is the same as that of the other unsaturated fatty acids and is independent of prostaglandin endoperoxides, thromboxane A2 and, perhaps, phosphatidic acid and 1,2-diacylglycerol.
A 78-year-old Japanese man with chronic liver disease developed hypervascular liver tumors accompanied by marked elevation of alphafetoprotein value (the highest level; 26200 ng/ml) and pathologic fracture of the femur. After an operation for the fracture followed by gastrointestinal bleeding and repeated transfusions of blood, the tumors disappeared with normalization of the alpha-fetoprotein level, and the radiolucent area around the fracture site of the femur became consolidated. The necrotic tissue responsible for the fracture histologically showed an appearance of hepatocellular carcinoma. The patient survives 62 months after the initial increase in alpha-fetoprotein level. This is a case of spontaneous regression of both hypervascular liver tumors which are highly suggestive of hepatocellular carcinoma and their metastasis.
We examined effects of small dose (1 microM or less) of exogenous 12-hydroperoxy-5,8,10,14-eicosatetraenoic acid (12-HPETE) on the formation of cyclooxygenase products from exogenous arachidonic acid (AA) in washed human platelets. With a simultaneous addition of AA, 12-HPETE did not affect the formation of thromboxane (TX)B2 and 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT). However, by being preincubated with platelets before an addition of AA, 0.1 microM or greater of 12-HPETE inhibited the formation of TXB2 and HHT dose-dependently. In addition, the inhibitory effect of 12-HPETE increased as the preincubation time was prolonged. These results suggest that 12-HPETE is a strong inhibitor for the cyclooxygenase pathway.
The lipoprotein profile of patients with primary biliary cirrhosis (PBC) has been assessed by high performance liquid chromatography (HPLC). Without exception, all subjects with PBC had an abnormal high density lipoprotein (HDL), which was larger than normal HDL. The elution time from an HPLC column of the abnormal HDL separated it clearly from normal HDL. The HDL of subjects with asymptomatic and symptomatic PBC could also be distinguished. The HDL of asymptomatic subjects was eluted between that of normal and symptomatic subjects. The lipid and protein composition of abnormal HDL was characterized by an increase in phospholipid and a decrease in protein, resulting in an increase in the ratio of phospholipid/protein. This ratio was higher in symptomatic than in asymptomatic PBC. Incubation of dimyristoyl phosphatidylcholine liposomes with normal serum resulted in the formation of an altered high density lipoprotein. These findings suggest that an overload of phospholipid may play a role in the formation of the abnormal HDL in primary biliary cirrhosis.
Electrical stimulation of the medial septal nucleus produced field potentials in the hippocampal CA1 region of the rat. The laminar field-potential analysis suggested that the electromotive force of the septum-induced responses might be attributable mainly to excitatory postsynaptic potential currents generated in the stratum oriens (layer of distribution of basal dendrites of hippocampal pyramidal cells). Neural cell bodies in the medial septum-diagonal band complex were retrogradely labeled with horseradish peroxidase (HRP) injected into the stratum oriens of CA1, but not with HRP injected into other CA1 strata. Thus the medial septal nucleus was indicated to send excitatory inputs to basal dendrites of CA1 pyramidal cells.
Transcatheter arterial embolization (TAE) for unresectable hepatocellular carcinoma (HCC) was performed in cirrhotic patients with nonoccluded main portal trunk and total bilirubin levels less than 5 mg/dl. In 48 patients with tumor response to TAE, its benefit was evaluated by comparing their survival with that in 28 patients after conservative treatments, matched by clinical data. In TAE-treated patients, tumor findings on computerized tomography and angiogram were significantly different between those dying within 3 months and those surviving over 18 months. In cases of tumors occluding the first- or second-order portal branches or occupying more than 20% of the liver, or relatively hypovascular tumors with unclear boundaries, survival was not different between TAE- and non-TAE-treated patients, whereas it was significantly improved by TAE in cases without these findings. These results suggest that TAE is beneficial in cases of unresectable HCC complicating liver cirrhosis, but its benefit is limited under certain conditions.
Morphological analysis of 77 neurons in the ventroanterior (VA), ventrolateral (VL), ventromedial (VM), and central lateral (CL) nuclei was performed by intracellular HRP staining in combination with electrophysiological studies. The neurons were classified into four groups according to either electrophysiological or morphological criteria, i.e., 20 relay neurons (18 thalamocortical (T-C) and two thalamocaudate (T-Cd) relay neurons), 17 projection neurons, 36 unidentified neurons, and four presumed interneurons. All 36 unidentified neurons had morphological features similar to those of relay and projection neurons. All neurons except four presumed interneurons had dendrites sparsely covered with spinelike appendages. Most of their dendrites displayed a spherically radiating branching pattern, and a few showed a tufted or linearly oriented pattern. Sizes of somata and dendritic radii were compared in entopeduncular (Ent)-responsive (n = 25) and cerebellar (CN)-responsive groups (n = 37) in VA, VL, and VM nuclei. The soma size was similar in VL (18-21 X 29-34 micron) and VM (15-19 X 29-31 micron), but in VA, CN-responsive neurons (15 X 30 micron) seemed to be smaller than Ent-responsive ones (22 X 36 micron). The largest dendritic field of neurons in each thalamic nucleus was similar in both groups. They were about 250-320 micron in radius. Diameters of axons were also compared but no statistically significant difference was detected (i.e., 1.5 +/- 0.3 (mean +/- S.D.) micron for the Ent group and 1.7 +/- 0.5 micron for the CN group). Three types of axonal trajectories were noted, i.e., neurons projecting their axons dorsolaterally, ventrolaterally, or horizontally. Fourteen neurons out of 37 relay and projection neurons gave off several fine distal axon collaterals in the thalamic reticular nucleus, and one T-Cd, three projection, and one unidentified neurons gave off proximal axon collaterals near the soma-dendritic domain in addition to those in the thalamic reticular nucleus. Four neurons classified as presumed interneurons had smaller somata (9-13 X 18-23 micron) and varicose dendrites. Three of them received Ent-induced inhibitory postsynaptic potentials (IPSPs) or CN-induced excitatory postsynaptic potentials (EPSPs). Several presumed axon terminals were found to cover the soma of an adjacent neuron, which seemed to indicate their inhibitory nature. The proximal axon collaterals in the ventral thalamic nuclei may consist of local inhibitory circuits with presumed interneurons in addition to other inhibitory circuits with thalamic reticular neurons.
A simple, rapid and precise analytical method for tetracycline (TC) residues in the liver of slaughtered animals has been established. The recoveries of oxytetracycline (OTC), TC, chlortetracycline (CTC) and doxycycline (DC) from beef liver spiked at the level of 1.0 ppm were 87.7, 87.5, 79.6 and 67.5% with coefficients of variations of 1.01-2.87%. Detection limits in beef liver were 0.05 and 0.1 ppm for OTC and TC and for CTC and DC, respectively. It is also possible to apply this method to the analysis of residual TCs in various foods with the same recovery, accuracy and detection limits as in the case of beef liver.
Electrical stimulation of the thalamic ventromedial nucleus (VM) produced surface-negative field potentials in the insular cortex of the cat. Laminar field potential analysis revealed that the VM-evoked potentials showed the same depth profile as the potentials evoked by stimulation of the cerebellar fastigial nucleus (FN). The active synaptic site for both evoked potentials is indicated to be located in layer I of the insular cortex. These results suggest that the VM mediates the FN projections onto layer I of the insular cortex.
In human platelets, wheat germ agglutinin (WGA) induced serotonin release without cell agglutination. WGA induced the phosphorylation of both 40-kDa and 20-kDa proteins in a parallel manner, and at least, the phosphorylation of 40-kDa protein was preceded by transient formation of endogenous diacylglycerol (DG) accompanied by a decrease in phosphatidylinositol (PI). Both phosphorylation of these two proteins and serotonin release were inhibited by prior treatment of platelets with dibutyryl cyclic AMP, W-7, or TMB-8. These results suggest that both phosphatidylinositol turnover and Ca2+ mobilization play an essential role in WGA-induced platelet activation.
Electrical stimulation of the fastigial nucleus provoked surface-negative field potentials bilaterally in the cerebral cortical regions around the anterior ectosylvian sulcus (AES) in the cat anesthetized with pentobarbital. Laminar field potential analysis revealed that the active locus for the negative potentials is located within the cortical layer I of the lower bank of the AES, i.e. the insular cortex.