[Roentgenologic manifestations of primary macroglobulinemia (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Iijima.
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Specific histochemical techniques for the demonstration of noradrenaline and of acetylcholinesterase have been used to study the distribution of adrenergic and cholinergic nerves to the cerebral blood vessels of turtle, Geoclemys reevesii. The major and medium-sized cerebral arteries were supplied with dense adrenergic nerve plexuses, the plexuses were particularly dense in the medium-sized pial arteries of very thick vascular wall, indicating the functional significance of these arteries in the cerebral circulation. The parenchymal arterioles and capillaries were also supplied with adrenergic nerves. On the other hand, the cholinergic innervation was less dense than the adrenergic one and the acetylcholinesterase activity of the nerve fibres was remarkably weak. By contrast, the parenchymal small arterioles and capillaries exhibited heavy acetylcholinesterase activity on the vascular wall and, in addition, the capillaries were supplied with the well-stained acetylcholinesterase-positive nerve fibres. These fibres and also the adrenergic fibres associating with the capillaries appear to be of central origin. It is suggested that the cholinergic mechanisms in the parenchymal small vessels also play an important role in the cerebral circulation. The basophil leucocytes observed abundantly in the blood of turtle emitted an intensive greenish yellow fluorescence after formaldehyde gas-treatment.
Dual innervation of snake cerebral blood vessels by adrenergic and cholinergic fibres was demonstrated with the use of histochemical methods. Although the nerve plexuses are somewhat less dense, the essential features of innervation of the blood vessels are similar to those of mammals with the exception that the adrenergic plexuses are more prominent than the cholinergic plexuses. The major arteries of the cerebral carotid system have a rich nerve supply. However, the innervation is less rich in the basilar and poor in the spinal (vertebral) arteries. Although the arteries supplying the right side of head are poorly developed, three pairs of arteries, cerebral carotids, ophthalmics and spinals, supply the snake brain. The carotids and ophthalmics are densely innervated and are accompanied by thick nerve bundles, suggesting that the nerves preferentially enter the skull along those arteries. Some parenchymal arterioles are also dually innervated. Connection between the brain parenchyma and intracerebral capillaries via both cholinergic and adrenergic fibres was observed. In addition cholinergic nerve fibers, connecting capillaries and the intramedullary nerve fibre bundles, were noticed. Capillary blood flow may be influenced by both adrenergic and cholinergic central neurons. The walls of capillaries also exhibit heavy acetylcholinesterase activity. This may indicate an important role for the capillary in the regulation of intracerebral blood flow.
Most strains of Bacillus subtilis, dervied from the 168 (Marburg) strain, grow slowly on aspartate as sole carbon source. We isolated a mutant (aspH) that grows rapidly on aspartate because it produces aspartase constitutively. Thus, aspartase is needed for rapid growth on aspartate, whereas aspartate-alpha-ketoglutarate aminotransferase is not needed, as was demonstrated by a mutant lacking that enzyme activity. By two--and three-factor crosses using PBSl transduction, the aspH mutation was located between the aroD and the lys markers of the genetic map. Although sodium ions do not affect growth on glucose or L-malate, they specifically stimulate growth on aspartate in both the parent and the aspH mutant strains. Enzyme activities of crude aspartase and fumarase and of purified aspartase do not increase in the presence of sodium. These results show that stimulation by sodium involves some reaction other than the enzymes catabolizing aspartate. The ease of purification from the aspH strain and the stability of aspartase suggest that the B. subtilis enzyme is particularly useful for aspartate determinations.
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The distribution of adrenergic and cholinergic nerves in the arteriovenous anastomosis in the rabbit's ear was studied light microscopically using specific histochemical techniques for catecholamines and acetylcholinesterase. Histochemical observations was made with whole stretch preparations and cryostat or paraffin sections. Both kinds of nerves showed similar distribution, though the adrenergic innervation was denser than the cholinergic one. The intermediate segments of the anastomoses, which were characterized by a very thick wall, had the most dense innervation. The small arteries and arterial segments had a moderate innervation whereas most of the small veins and venous segments had few nerve fibers. The segmental variation in the vasomotor nerve supply clearly suggests that the intermediate segment has the most active contractility. An unusually rich innervation in the anastomosis, therefore, indicates the significance of the neurogenic mechanisms in the vasomotor control of the anastomosis.
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In isolated and cross-circulated canine A-V node preparations single injections of Mn2+ (1-30 mumol) and verapamil (0.3-10 nmol) into the posterior septal artery (PSA) caused a dose-dependent increase in the A-V conduction time and, in large doses, produced A-V conduction block. The A-V conduction time increased by Mn2+ and verapamil is resotred by 1-norepinephrine (1-NE) injected into the PSA. The A-V nodal tachycardia induced by 1-NE is suppressed by Mn2+ but not by verapamil. These indicate the following: (1) the slow Ca2+ channel plays an important role in A-V conduction; (2) the positive dromotropic response of the A-V node to 1-NE may have some relations to the Ca2+ channel; (3) the A-V nodal tachycardia induced by 1-NE may be mediated by the Ca2+ channel. Possible causes which produced differences between Mn2+ and verapamil in the effects in antagonizing the 1-NE-induced A-V nodal tachycardia are discussed.
The effects of neurotransmitters injected into the posterior and the anterior septal artery on the automaticity of the atrioventricular (AV) junctional area were examined in the excised, blood-perfused canine AV node preparation. An AV rhythm of 57.4 +/- 2.8 beats/min (N = 28) developed after the destruction of the sinoatrial node. l-Norepinephrine injected into the anterior septal artery increased the frequency of AV rhythm, but l-norepinephrine injected into the posterior septal artery caused a pacemaker shift from the anterior septal artery area to the posterior septal artery area. Acetylcholine injected into the posterior septal artery blocked retrograde conduction but did not decrease the frequency of AV rhythm; however, acetylcholine injected into the anterior septal artery decreased AV rhythm but did not affect retrograde conduction. Destruction of the posterior septal artery area failed to change AV rhythm. The surgically separated anterior septal artery preparation had the same rate as did the AV node preparation. The posterior septal artery preparation had a definitely lower rate and responded to smaller doses of l-norepinephrine than did the AV node preparation. The results of the present study indicate that AV rhythm in the AV node originates in the area supplied by the anterior septal artery and that the area supplied by the posterior septal artery, which has extremely low automaticity, is highly responsive to l-norepinephrine, resulting in nodal tachycardia.
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Salmonella typhimurium possesses at least three inducible transport systems for the tricarboxylic acids (citric, isocitric, cis-aconitic, and tricarballylic). The first system was induced by citrate, isocitrate, or cis-aconitate, and transported citric acid and isocitric acid. The second system was also induced by the same acids as in the first system and transported cis-aconitic acid. This system required Mg(2+) ions and was stable at pH 8.4 but unstable at pH 7.0. The metal ion was replaced with Sr(2+) or Ca(2+) ions but not with Ba(2+) ions. The third system was induced by tricarballylate and transported citric acid, cis-aconitic acid, and tricarballylic acid.
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