[Preoperative diagnosis of a case of biliobiliary fistula].
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Biomedical subjects
Publications and source records attributed to K Ohkubo.
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In order to give a neuroanatomical evidence to the mechanism of shifting from sucking to biting, we investigated in prenatal, newborn and postnatal mice whether there is a time difference in the neurogenesis of the neurons relative to sucking and biting or in the histogenesis of their peripheral effector organs by the HRP labeling technique and electron microscopy. The results obtained are as follows. (1) At birth the facial motoneurons exceed the trigeminal motoneurons in cell area and development. (2) After birth, the trigeminal motoneurons grow rapidly and outstrip the growth of the facial motoneurons at the age of 6 days. (3) Thereafter, the cell area of both neuron types continues to increase gradually. (4) The initial sign of the alpha motor end plates is found in the orbicularis oris muscle innervated by the facial nerve in 17-day-old fetuses, while that of the trigeminal nerve is delayed in the masseter muscle of 18-day-old fetuses. (5) The initial sign of the muscle spindle appears with the sensory terminals in the masseter muscle of 17-day-old fetuses and the fundamental structure of the muscle spindle is formed in 4-day-old youngs. (6) Myelination of the facial nerve begins in 3-day-old youngs, while that of the trigeminal nerve becomes apparent in 4- or 5-day-old youngs. From these bases, it is obvious that the facial nerve elements related to sucking are firstly developed at birth and that the differentiation of the trigeminal nerve elements related to biting is rapidly accelerated after birth.
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To obtain the neuroanatomical information on the role of the snout sensory input in mastication, the present study was conducted on young and adult mice, young Wistar rats and adult Japanese shrew-moles. The animals were subjected to unilateral and bilateral infraorbital nerve transection. Transganglionic degeneration was studied by the Nauta method and electron microscopy including HRP application to the neck muscles. Transganglionic degeneration was found in every experimental case. 1. Transganglionic degeneration of the fibers was found not only in the main sensory nucleus and spinal tract nucleus of the trigeminal nerve but throughout the cervical and the upper part of the thoracic spinal cord. 2. These transganglionically degenerated fibers descended bilaterally through the cuneate nucleus and then caudally through the posterior funiculus at the obex level. They then entered the dorsal and ventral horns to make a synaptic contact with the degenerated synapses on the dorsal horn cells and with the multipolar cells in the ventral horns. This neuroanatomical information suggests: 1) that the trigemino-neck muscle reflex will be generated monosynaptically by the primary neurons arising from the snout sensory organs and 2) that these primary neurons may play a large role as a neuronal bridge in connecting the masticatory reflex system and the cranio-neck reflex system.
The sensory input of the Vth cranial nerve might play a great role in the feeding activity of the mammals, especially of the Japanese shrew-moles. After the transection of the pure sensory infraorbital nerve, a drastic structural disorder was observed in the rat masseter muscle. In order to give anatomical evidence as to whether the interference of the sensory input affects the peripheral effector, electron microscopic investigations were performed on the primary axons and neurons of the Japanese shrew-moles. The results obtained are as follows: The preganglionic part of the transected nerves showed drastic degenerative changes of the myelinated fibers, characterized by a prominent decrease in the large- and medium-sized myelinated axon fibers, a gradual numerical increase of the clustered or isolated unmyelinated axons, and the frequent appearance of macrophages. The ganglion cells exhibited displacement of the nucleus with infolding of the nuclear membrane, the appearance of a large amount of lipofuscin granules, and an increase of neurofilaments and reduced Nissl bodies. The transganglionic part of the sensory root exhibited mainly a predominant axonal destruction, accompanied by myelinated disintegration.
Each muscle of the extraocular muscles, containing abundant muscle spindles, was exposed to horseradish peroxidase (HRP) on 8 young pigs (2-month-old, 20-30 kg in body weight, both sexes). The results obtained are follows: The HRP-labelled neurons innervating the superior rectus muscle were always found in a crescent ventro-medio-dorsal fashion in the most medial position of the contralateral oculomotor nucleus. The HRP-labelled cells for the medial rectus muscle appeared close to the superior rectus group in the ipsilateral nucleus. The labelled cells for the inferior rectus muscle appeared in the ventrolateral position of the ipsilateral nucleus and those for the inferior oblique muscle in the area between the medial rectus and inferior rectus muscle groups. The labelled cells for the superior oblique muscle were found in the contralateral trochlear nucleus and those for the lateral rectus muscle bilaterally in the abducens nuclei, predominantly on the ipsilateral side and poorly on the contralateral side. The HRP-labelled cells were composed of large (alpha) and small (gamma) multipolar cells and of bipolar, oval or round (proprioceptive) cells, all intermingled together within the nucleus. The bipolar cells have been also identified in the 3 nuclei by means of Nissl staining technique. On this basis, they should be considered as the proprioceptive neurons. In the shrew-moles, the cell bodies of the proprioceptive neurons innervating the snout muscle spindles have been found close to the ipsilateral glossopharyngeal ganglion and those of the somatic sensory neurons in the ipsilateral trigeminal ganglion. In the pigs, no HRP-labelled cells were found in the trigeminal mesencephalic tract nucleus, but the HRP-labelled cells were found in the ipsilateral trigeminal and the superior cervical sympathetic ganglia. From the results, it could be emphasized that the proprioceptive neurons innervating the pig extraocular muscle spindles are located within the nuclei of the IIIrd, IVth and VIth cranial nerves.
In summarizing the present experimental results of tooth extraction, it can be emphasized that the disturbance of the sensory input units from the teeth resulted in a definite degeneration of the primary neurons. On this ground, it is suggested that the lesion of the sensory input units in the masticatory computer system, according to the individual age affected, may become a large factor in impeding the masticatory activity and accelerating the aging of the masticatory function.
20 ICR mice (adult females) were used for analyzing the axonal projection of the trigeminal mesencephalic tract neurons and 10 Japanese shrew-moles for analyzing that of the snout proprioceptive neurons. The HRP-labeled axons were found to be ipsilaterally terminated in the trigeminal motor nucleus, supratrigeminal nucleus and trigeminal main and spinal tract nuclei, lateral pontine-medullary reticular formation, vagal dorsal motor and hypoglossal nuclei and the lamina V of the C2 spinal cord segments. No HRP-labeled axons were found in the facial and solitary nuclei and the cerebellum. Also, the functional localization of the trigeminal mesencephalic tract neurons was analyzed with the retrograde tracers of fluorescent compounds injected into the jaw-closing muscles having spindles. The fluorescent-labeled neurons were found to be intermingled throughout the nucleus and clustered at the caudal level of the nucleus. Also, double or triple fluorescent-labeled neurons were not observed in the nucleus. The HRP-labeled axon bundle of the facial proprioceptive neurons are divided rostro-caudally into the shorter ascending and the longer descending roots, both running closely dorsal to the trigeminal spinal tract nucleus. The ascending root lies adjacently dorsal to the spinal tract nucleus, giving off the terminal fibers to it, to the wider area of the dorso-medial pontine nuclei and finally to the cerebellar nuclei. At the level of the facial inner genu, it turns medially to meet the facial nerve root, giving off the terminal fibers to the facial motor nucleus and to the raphe nuclei and to the opposite nuclei bilaterally. The HRP-labeled descending root takes the course caudally at least down to the C3 segment of the spinal cord, giving off the terminal fibers to the spinal tract nucleus, the nuclei of the IXth, Xth and XIIth cranial nerves and the pontine-medullary reticular formation. In the spinal cord, it descends bilaterally through the posterior fascicles, giving off the terminal fibers to the dorsal and ventral horns.
The relationship between chemical modifications of arginine derivatives and inhibitory activity to trypsin, plasmin and glandular kallikrein was investigated comparing with that of thrombin and concluded as follows: The hydrophobic binding pocket, which has been reported previously to be stereogeometrically very similar in trypsin and thrombin, corresponded to the length of ethylpiperidine. Concerning the site (termed the P site) next to the hydrophobic binding pocket, there were large differences in stereogeometry between trypsin and thrombin; the binding site of trypsin extended further to allow propyl and phenyl group attached to piperidine, while that of thrombin would be much narrower and unable to allow them. The P sites of plasmin and glandular kallikrein resembled that of trypsin in being able to allow phenyl group. To substantialize the hydrophobic binding pocket and the P site, a (2R, 4R)-MQPA-trypsin complex model was generated using the results of X-ray crystallography of (2R, 4R)-MQPA and BPTI-trypsin complex by calculation to minimize van der Waals contacts, and it was of great use for understanding the geometry of the active sites of trypsin, thrombin, plasmin and glandular kallikrein.
The morphogenesis of the muscle spindles of the masseter muscle was investigated by electron microscopy. The mice used in this study were those from the 16-day-old fetuses to the four-day-old young, and the three-month-old adult ICR mice. At the time of observation the formation of the masseter muscle spindle had already started in the 16-day-old fetus. In the 17-day-old fetus, the sensory nerve terminated not only in the myotube but also in the myoblast in which no myofilaments were yet formed. From the observations on the 16-day-old and 17-day-old fetuses, it is suggested that the myotubes of the intrafusal muscle fibers are formed by the fusion of the myocytes already containing the myofilaments. The gamma motor end-plate appeared two days later than the sensory nerve terminal formation in the muscle spindle. The initial inner capsule of the spindle was observed in the four-day-old young. The cell without the myofilaments appeared amidst the cluster of the intrafusal muscle fibers in the three-day-old young. It is considered that this cell may be the origin of the inner capsule cell. The periaxial space formation and the myelination of the masseteric nerve fiber occurred in the four-day-old young. The formation of the postsynaptic folds was observed in the extrafusal muscle fiber at the same stage. Thus, the muscle spindles, nerve fibers and the extrafusal muscle fibers showed a remarkable development at the same time in this early postnatal stage.
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Eight pediatric patients with acute lymphoblastic leukemia (ALL) were treated with intermediate-dose cytosine arabinoside (ID-AraC, 1 g/m2) in combination with adriamycin except one patient. Of the eight patients, four refractory to the initial induction therapy and one in bone marrow relapse gained complete remission with two to three cycles of this therapy. Four of the five patients have been in continuous remission for 4 to 24 months with the maintenance therapy of monthly administration of ID-AraC. One patient in central nervous system (CNS) relapse has continued in remission from CNS leukemia after two cycles of the therapy. Side effects of ID-AraC and adriamycin were generally mild to moderate and tolerable in all children. These results suggest that the use of ID-AraC and adriamycin might prove effective in the treatment of ALL refractory to other regimens.
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The effects of sodium salicylate (SS) on ADP-induced platelet aggregation and on a metabolism of calcium in platelets were studied, using gel-filtrated platelets (GFP). SS inhibited dose-responsively ADP-induced aggregation in the presence of fibrinogen and Ca2+. It was found that extracellular 45Ca2+ was rapidly taken up into platelets after stimulation by ADP, while SS significantly inhibited this activity. On the other hand, SS had no effect on platelet aggregation induced by 0.11-1.0 microM ionophore A23187. Therefore, it was found that the inhibitory effect of SS on ADP-induced platelet aggregation may be due to the inhibition of the active influx of extracellular Ca2+ into platelets during aggregation.