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M Sakuta

Publications and source records attributed to M Sakuta.

At least 91 records · Page 5Linked to original sources
PubMed1984

Collateral reinnervation of sweat glands.

The collateral reinnervation of mouse sweat glands has been studied by a method that allows serial evaluation of the course of reinnervation in intact animals. The method is based on the finding that the activation of secretion from newly denervated sweat glands by pilocarpine or nerve stimulation is completely absent seven days after nerve section but returns with reinnervation. These characteristics allowed serial detection of footpad sweat glands newly reinnervated by collateral sprouting of the remaining intact saphenous nerve after section of the sciatic nerve. The number of saphenous innervated glands increased five- to sevenfold and the total saphenous sweat territory was greatly expanded across the volar surface of the hind paw. There was less enlargement when the sciatic nerve was allowed to regenerate and participate in reinnervation of sweat glands. None of the reinnervated glands were dually innervated by saphenous and sciatic nerves, as is the case in normal glands. When the saphenous nerve was sectioned after saphenous collateral sprouting was complete and after sciatic regeneration had innervated an apparent maximal number of glands, the sciatic nerve reacted by advancing farther into the formerly enlarged saphenous territory and re-reinnervated many of the glands. Collateral sprouting by sudomotor axons is more abundant and more widely dispersed than reported for larger nerve fibers to skeletal muscle and to low-threshold mechanoreceptors. It more closely resembles sprouting of nociceptive axons.

Animals↗
PubMed1984

Quantitation of the sweating deficiency in diabetes mellitus.

This report introduces quantitative tests for the evaluation of sweating and the results obtained in 81 diabetic and 30 control subjects. The tests rely on the ability of pilocarpine, introduced into the skin by iontophoresis, to stimulate sweating from fully or partially innervated sweat glands but not from denervated glands. Many diabetic patients had a reduced number of excitable sweat glands and a low volume of sweat per square centimeter of skin. The results of the sweat tests correlated best with the clinically determined perception of pain from pinprick. The similar degree of involvement of sudomotor axons and pain-conveying axons may be related to the known similarity in size and reinnervation patterns. There was poor correlation of the sweating deficiency with alpha motor conduction velocity and with denervation of foot muscles as determined by the evoked muscle action potential. The number of excitable sweat glands was usually normal if the muscle action potential was above 0.5 mv, and often normal even when a muscle action potential was unobtainable. Every diabetic patient with abnormal sweating and several with normal sweating had reduced heart rate fluctuation during a standard Valsalva maneuver or during slow respiration.

Adult↗
PubMed1984

Rodent eccrine sweat glands: a case of multiple efferent innervation.

The sweat territories of peripheral nerves to the hind-paw of the mouse were defined by a silastic impression mold method that allowed identification of every secreting sweat gland. It was found that the tibial, sural, saphenous and peroneal nerves all contribute to the innervation of foot pad sweat glands, and there is extensive overlapping of the sweat territories of the different peripheral nerves. Most sweat glands could be activated by electrical stimulation of axons in two or three peripheral nerves or in separate fascicles of one nerve. This was interpreted to indicate that these sweat glands receive multiple innervation and that sweat glands in the overlap regions between autonomous zones of adjacent cutaneous nerves can receive axons from each nerve. Partial denervation of sweat glands by section of one source of innervation did not prevent the gland from sweating during stimulation of intact axons to the gland, or after pilocarpine treatment. Totally denervated glands did not exhibit denervation hypersensitivity; they became unresponsive to pilocarpine, acetylcholine and adrenaline. These characteristics allowed detection of the appearance and progression of reinnervation (and reactivation) of denervated sweat glands by collateral branching from sudomotor fibers. Not only do these results increase our basic understanding of the anatomical relations between peripheral nerves and the sweat glands they innervate, but they also demonstrate that the mouse sweat gland provides a useful model system for studying neuropathology of the sympathetic nervous system.

Animals↗
PubMed1984

The sweating deficiency in diabetes mellitus: methods of quantitation and clinical correlation.

A method that measures the amount of sweat evaporating from the skin was used to quantitate the sweating deficiency that accompanies diabetic neuropathy. The decreased amount of sweat secreted after pilocarpine stimulation was proportional to the reduction in number of excitable sweat glands, and to the decrease in water measured by the summed volume of all sweat droplets secreted. The results also correlated favorably with the degree of sensory loss to painful stimuli, but not to the alpha motor nerve conduction velocity or motor axon loss evaluated by muscle action potentials evoked from foot muscles. Respiratory-cardiovascular reflexes, as measured by the Valsalva ratio, were always abnormal in patients with demonstrated sweating deficiency and often in patients with normal sweat function.

Adult↗
PubMed1984

Neuropathological study of chorea-acanthocytosis.

Neuropathological studies of a woman with chorea-acanthocytosis were reported. The patient clinically showed generalized epileptic seizures, choreatic involuntary movements, hypotonia , areflexia, neurogenic muscular atrophy, tongue-biting and acanthocytosis of the peripheral blood and died from asphyxia at the age of 34. Autopsy revealed atrophy of the caudate nucleus but the cerebral cortex was well preserved. Histological examination showed severe neuronal loss associated with moderate fibrous gliosis of the caudate. The putamen was similarly but less markedly affected. The small striatal neurons were more severely depopulated than the large neurons, although the latter were not spared. Cytometrical study of the caudate head revealed that the remaining small neurons were significantly larger in size than the normal small neurons of the same area. The anatomical substratum of the choreatic involuntary movements in chorea-acanthocytosis is thought to be the degeneration of the striatum, especially the caudate nucleus. Neuropathological differentiation of chorea-acanthocytosis from Huntington's chorea which shows similar pathology was discussed.

Acanthocytes↗
PubMed1983

Immunobiological activities of synthetic lipid A analogs and related compounds as compared with those of bacterial lipopolysaccharide, re-glycolipid, lipid A, and muramyl dipeptide.

Thirteen acylated and phosphorylated derivatives of beta-1,6-linked glucosamine disaccharide (lipid A analogs), which were synthesized after the structural model of Salmonella-type lipid A, and seven similar derivatives of glucosamine monosaccharide (lipid A-related compounds) were studied for their immunobiological activities. These included mitogenicity and polyclonal B cell activation enhancement of migration of monocytes and polymorphonuclear leukocytes derived from human peripheral blood, stimulation of guinea pig peritoneal macrophages, activation of human complement, and stimulation of serum antibody production and induction of delayed-type hypersensitivity against ovalbumin in guinea pigs. Comparisons were made with lipid A, RE-glycolipid, lipopolysaccharide of natural sources, and a well-known synthetic adjuvant, N-acetylmuramyl-L-alanyl-D-isoglutamine. Some of the lipid A analogs were found to manifest the mitogenic, polyclonal B cell-activating macrophage-stimulating, complement-activating, and immunostimulating activities, although the observed activities were generally far less than those of natural products in intensity and efficiency. Other immunobiological effects exhibited by most of the synthetic lipid A analogs were the enhancement of migration of monocytes and polymorphonuclear leukocytes. It is premature to draw definite conclusions on structure-activity relationships, since a few compounds which were active in some assay systems were scarcely active in other assays. However, an indisputable fact was that beta-1,6-glucosamine disaccharide 1 alpha,4'-diphosphate, which carries two amide-bound (R)-3-hydroxytetradecanoyl and three ester-bound tetradecanoyl residues, and thus has the structure most closely resembling natural lipid A among test compounds in this study, was definitely active in all of the present assay systems. However, its potency was generally much less than natural products. Some of glucosamine monosaccharide derivatives, especially N-(R)-3-[(R)-3-hydroxytetradecanoyloxy]tetradecanoyl glucosamine, also exerted all of the in vitro activities described above. This fact suggests that a glucosamine disaccharide structure may not necessarily be a prerequisite as far as the in vitro immunobiological activities tested are concerned.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1980

Dissociated nystagmus in a comatose patient. A clinicopathological study.

Electro-oculographic recordings of dissociated vertical (oblique and upbeat) nystagmus were carried out in a patient in coma due to vascular lesions. Based on the clinical and neuropathological findings, it was suggested that dissociated vertical (oblique and upbeat) nystagmus in a patient in coma can be caused by bilateral lesions in the brachium pontis.

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