Continuous infusion of prostaglandin E1 facilitates weaning from cardiopulmonary bypass

Vasodilators expedite the rewarming process and facilitate weaning from cardiopulmonary bypass (CPB). We continuously infused prostaglandin E1 (PG-E1) at 0.02-0.05 microgram.kg-1.min-1 (n = 11) or phentolamine (PHENT) at 5-10 micrograms.kg-1.min-1 (n = 13) during rewarming from mild hypothermic CPB. Rectal temperature was 33.3 +/- 1.7 degrees C in PG-E1 group vs. 31.3 +/- 1.3 degrees C in PHENT group at 30 minutes, and 34.0 +/- 1.2 degrees C vs. 32.7 +/- 1.1 degrees C at 40 minutes from the start of rewarming. There were significant differences (P less than 0.01 at 30 min, P less than 0.05 at 40 min) in rectal temperature between the two groups. There were no differences in perfusion index of CPB, arterial perfusion temperature, mean arterial pressure, systemic vascular resistance as well as esophageal, forehead or palm skin temperatures at any point between the two groups. The required time for weaning from CPB was significantly shorter in PG-E1 than in PHENT group (P less than 0.01, 36 +/- 8 min vs. 46 +/- 11 min). Our results also strongly suggest that PG-E1 preferentially improves splanchnic blood flow.     

A case of bilateral phrenic nerve paralysis following open heart surgery]

Coronary artery bypass surgery was performed on a 58-year-old female under cold cardioplegia with topical ice slush cooling. Bilateral phrenic paralysis was observed postoperatively, in spite of prevention with a mat during aortic cross clamp, cold injury owing to ice slush was thought to be causative. Mechanical ventilatory support continued for more than two months until her complete recovery of diaphragmatic function. She complained of sleeplessness besides respiratory symptoms, and felt uneasy. Although cold injury is mostly reversible, it is stressed that we must deliberately wean from mechanical ventilatory support, turning our attention to symptoms and blood gas analysis with as much mental assistance as possible.     

Electron microscopic observations of peripheral myelin in a central nervous system lesion

Summary After cyanide intoxication and after triethyltin implantation in the brain, cystic spaces were found in the forebrains, of two rats. Within these spaces, many examples of remyelinating axons were observed. Most of them displayed typical mature or developing central type myelin sheaths. Some, however, showed all the morphological features characteristic of mature or developing peripheral myelin. In both rats, the cavities of the cysts were open to the overlying subarachnoid spaces due to partial disruption of the subpial astrocytic layer. It was concluded that the myelin-forming cells responsible for the formation of the peripheral type myelin within the cyst were probably Schwann cells derived from peripheral nervous elements accompanying some subarachnoid blood vessels. It could not be determined whether the axons within the peripheral type sheaths were part of the central or peripheral nervous systems. These data might be relevant to the origin of central neurinomas.This investigation was supported by United States Public Health Service Research Grant No. B3533 from the National Institute of Neurological Diseases and Blindness, National Institutes of Health, and Grant No. 317-3 from the National Multiple Sclerosis Society.     

Advanced glycation endproducts are deposited in neuronal hyaline inclusions: a study on familial amyotrophic lateral sclerosis with superoxide dismutase-1 mutation

To determine the role of advanced glycation endproducts (AGE) in the pathogenesis of familial amyotrophic lateral sclerosis (ALS) with superoxide dismutase-1 (SOD1) mutation, we investigated the immunohistochemical localization of N(epsilon)-carboxymethyl-lysine (CML), one of the major AGE structures, in spinal cords from three familial ALS patients with a heterozygous Ala to Val substitution at codon 4 in the gene for SOD1. Neuronal hyaline inclusions (NHIs), the abnormal structures seen in some of the remaining lower motor neurons of familial ALS patients with SOD1 mutation, were intensely stained by a monoclonal antibody specific for CML in contrast to the only weakly stained cytoplasm. Immunoelectron microscopy depicted the CML determinants restricted to the granule-associated thick linear structures that mainly compose the NHIs. The NHIs were also recognized by antibodies to SOD1, phosphorylated neurofilament protein and ubiquitin. No focal collection of either CML or SOD1 was found in neurons of the control individuals. Our results indicate that CML is a component of the NHIs of familial ALS patients with SOD1 mutation, and suggest that the CML formation may be mediated by protein glycoxidation or lipid peroxidation in the presence of oxidative stress from mutant SOD1, in association with motor neuron degeneration.     

Studies on the occupational maladjustment syndrome (Part 2). In reference to relationship between psychophysiological characters and clinical features

In a previous report (Natsume et al., Jpn. J. Ind. Health, Vol. 24) on the occupational maladjustment syndrome (O.M.A.S.), on the basis of clinical data, we classified patients with O.M.A.S. into 5 subcategories; core, drop-out, transient reaction, special job maladjustment and other. The core and drop-out types are typical of O.M.A.S. In order to test our hypothesis regarding the clinical and psychophysiological character of patients with O.M.A.S., 39 subjects (25 core type and 14 drop-out type) were studied by polygraphic techniques such as EEG, EMG of facial muscles and electrooculogram, and the results were compared with those of 16 normal subjects. We were specifically interested in their behavior in mental arithmetic and at rest. The results are summarized as follows: At rest, less frequent irregular rapid eye movement (especially "r-type") and smaller amplitudes of the corrugator supercilii muscle characterized the patients compared to the normals. During mental arithmetic these two indicators showed a greater tendency to increase in the core type than in the normals, but they remained unchanged in the drop-out group. In the core type subjects, the increased levels in these indicators persisted briefly after the arithmetic sessions. We discuss the relationship between the clinical character of the two types and the above results. We consider that the psychophysiological character of the two types may play an important role in the pathogenetic mechanism of O.M.A.S.     

Effect of jasplakinolide on the growth,invasion, and actin cytoskeleton of Plasmodium falciparum

The effect of jasplakinolide (JAS), an actin-polymerizing and filament-stabilizing drug, on the growth, invasion, and actin cytoskeleton of Plasmodium falciparum was examined. Jasplakinolide markedly decreased the parasitemia in a synchronized culture of P. falciparum strain FCR-3 in a time- and concentration-dependent manner. The decrease became evident at day 2 at concentrations of 0.3 micro M and above, and parasites finally disappeared at day 4. Giemsa-stained smears of P. falciparum-infected erythrocytes demonstrated that there was no effect on the development of schizonts from ring forms. Merozoites were released from the infected erythrocytes in a normal manner with and without JAS. However, there were no ring form-infected erythrocytes when JAS was administered, even after the release of merozoites. This indicates that the merozoites exposed to JAS failed to invade erythrocytes. The inhibitory effect of JAS on the parasitemia was reversed by the removal of the drug after exposure to 1 micro M of JAS for 1 day. Electron microscopy revealed that the merozoites treated with JAS showed a protrusion of the apical end which contained the microfilament structure. Immunoblot analysis indicated that the JAS treatment increased F-actin filaments of merozoites but had no effect on those of the trophozoites and schizonts. Therefore, this study demonstrated that JAS has an antimalarial activity.     

Nucleotide sequences and characterization of haemolysin genes from Aeromonas hydrophila and Aeromonas sobria.

Extracellular haemolysin is thought to be one of the important virulence factors in Aeromonas infection. Two extracellular haemolysin genes (AHH3 and AHH4) from Aeromonas hydrophila strain 28SA, one (AHH5) from A. hydrophila strain AH-1 and one (ASA1) from Aeromonas sobria strain 33 were cloned into cosmid and plasmid vector DNA in Escherichia coli. The nucleotide sequences of the open reading frames of AHH3 and AHH4 are both 1476 basepairs (bp), whereas AHH5 and ASA1 are 1455 and 1467 bp in length, respectively. The deduced amino acid sequences of AHH3, AHH4, AHH5 and the previously reported aerolysin from A. hydrophila showed a significant degree of sequence homology of over 90% each. The amino acid identity of the ASA1 haemolysin and those from A. hydrophila and Aeromonas trota aerolysins ranged from 58-68%. From DNA hybridization analysis using our cloned haemolysin genes as probes, we found that the AHH5 and ASA1 DNA probes hybridized with about 31 and 75% strains of motile Aeromonas species, respectively. The activity of haemolysins of cloned genes were different in medium agar containing various erythrocytes.     

Different effects of cytochalasins on the growth and differentiation of<Emphasis Type="Italic"> Entamoeba invadens</Emphasis>

The effect of five different cytochalasins on the growth, encystation and excystation of Entamoeba invadens was examined. At 10 M, cytochalasins B, D, E and dihydrocytochalasin B markedly inhibited growth. Encystation was inhibited by cytochalasin D at 1 M but not by other cytochalasins at the same concentration, whereas it was inhibited by 10 M of cytochalasins B, E and dihydrocytochalasin B as well as cytochalasin D. Excystation, which was assessed by counting the number of metacystic amoebae after inducing excystation, was markedly enhanced by cytochalasin D as previously demonstrated, whereas the enhancing effect of cytochalasins A, B and dihydrocytochalasin B was weak. In contrast, cytochalasin E at 10 M inhibited excystation and metacystic development. These results indicate that there is a difference in the effect of different cytochalasins on the growth and differentiation of E. invadens, depending on differences in their chemical structure.