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Biomedical subjects

Y Teraki

Publications and source records attributed to Y Teraki.

47 records · Page 3Linked to original sources
PubMed1989

Immunocytochemistry of neuron-specific proteins and neuropeptides in taste buds and associated nerves.

The taste buds and associated nerves in the guinea pig, rat, cat, and mouse were investigated by immunocytochemistry and formaldehyde-induced fluorescence histochemistry. The antisera used were against spot 35 protein, neuron-specific enolase (NSE), neurofilament protein (NFP), and substance P. The spot 35 protein immunoreactivity was confined to taste bud cells in the guinea pig and rat; the immunoreactive cells, slender in shape, comprised half the number of the total taste bud cells in the guinea pig but were fewer in the rat. For NSE, on the other hand, taste bud cells as well as neural elements localized in both the taste bud and the subepithelial connective tissue were immunoreactive in all the species investigated. Furthermore, all of the spot 35 protein-immunoreactive cells proved to be NSE-immunoreactive in the guinea pig and rat. For NFP, neither the bud cells nor the nerves in the taste bud were reactive, whereas a part of nerves in the connective tissue was immunostained in all the species. The antiserum against substance P exclusively detected some parts of nerves in and out of the taste buds in the cat, rat, and mouse. The aminergic innervation was rather meager and appeared in the nerve fibers localized in the taste buds and connective tissue of the cat and mouse.

Animals↗
PubMed1989

Effects of prostaglandins and several vasoactive substances on blood pressure, respiration and blood flow by intra-ventricular, intra-arterial and intravenous routes.

Differences by routes of administration of the effects of prostaglandins and vasoactive substances on blood pressure, peripheral blood flow and respiration were investigated. Intravenous prostaglandins evoked respiratory excitation in rabbits, and lowered blood pressure more prominently and longer after intracarotid injection than after the intrajugular administration. The effects of prostaglandins were apparently more conspicuous after vertebral artery than via carotid artery. In rats, 1 microgram/kg i.v. of PGE1 and PGE2 caused a fall of blood pressure but 1 microgram/kg i.v. of PGF2 alpha caused a rise. PGF2 alpha produce a decrease of blood pressure when injected 10 micrograms/kg i.v.. A remarkable elevation of blood pressure occurred in rats following injection into the lateral cerebral ventricle of 0.1 microgram/kg of PGE1 or PGF2 alpha or of the same dose of 5-hydroxytryptamine (5-HT). Intra-arterial injection of PGE1 gave rise to an increase in blood flow of rabbit dorsal skeletal muscle whereas that of PGF2 alpha resulted in blood flows. The above results indicate that the effects of prostaglandins on these parameters essentially vary to slight extents with the species of animals and differ in intensity with routes of administration.

Animals↗
PubMed1988

Immunocytochemical localizations of neuron-specific proteins in the taste bud of the guinea pig.

The taste buds and their nerves in the guinea pig were immunocytochemically investigated with regard to the localization of spot 35 protein, neuron-specific enolase (NSE), neurofilament protein (NFP), and S-100 protein. The spot 35 protein-like immunoreactivity was confined to slender cells comprising half the number of taste bud cells. NSE-like immunoreactivity was recognized in some taste bud cells as well as nerve fibers both within the taste bud and in the subepithelial connective tissue. The NSE-immunoreactive cells were divided into two cell populations: one weakly and the other intensely immunoreactive. The former cells proved to be spot 35 protein-immunoreactive. Moreover, the cells immunoreactive for both spot 35 protein and NSE were frequently associated with nerve fibers immunostained intensely for NSE. The NFP- and S-100 protein-like immunoreactivities were found in none of cells in the taste bud, but exclusively in the subepithelial neural elements.

Animals↗
PubMed1982

A morphologic study of the behavior of biogenic amines in experimental acetic acid gastric ulcer.

Morphological observations were made of the behavior of biogenic amines in the gastric wall of rats with acetic acid-induced ulcer. In the normal rat stomach, abundant adrenergic fibers were seen in the adventitia of arteries and arterioles, with frequently distributed mast cells in their environs, in all gastric wall layers. Mast cells had a more frequent distribution in the antral region than in the corpus ventriculi while enterochromaffin-like cells (EC-like cells) were found with greater frequencies in the latter region of gastric wall. Adrenergic fibers were abundant around blood vessels in perilesional area of the gastric wall of rats with acetic acid ulcer. Mast cells, seen more frequently in the antral region as in the normal rats, showed degranulation in these rats. The population of PAS-positive mucous cells reached its peak in 10 days after injection of acetic acid and subsequently declined with healing of the ulcer, thus remarkably concordant with the ulcer index. Local administration of serotonin produced angiospasm in the greater omentum. The finding indicates a possible participation of arteriospasm by adrenergic nerve fibers in the pathogenesis of gastric ulcer. The results of the present study strongly suggest that biogenic amines have bearing as an aggressive factor upon the angiospasm theory of ulcerogenesis.

Acetates↗
PubMedDate not supplied

Apoptosis and the skin.

In multicellular organisms, homeostasis is maintained by a balance between cell proliferation and cell death. Two common forms of cell death, called apoptosis and necrosis, have been described. Apoptosis, which is often equated with programmed cell death, is a physiological form of cell death that is responsible for the deletion of cells. Apoptosis is morphologically and biochemically characterized by cell shrinkage, dense chromatin condensation, cellular budding, fragmentation, rapid phagocytosis by nearby cells, and DNA fragmentation into units of approximately 200 base pairs. Apoptosis can be triggered by a wide variety of stimuli such as cytokines, hormones, drugs, and viruses, and their signal transduction tightly regulated by genes such as Bcl-2. Effector caspases are finally activated, resulting in apoptotic cell death. In the skin, there is considerable evidence that apoptosis plays an important role in the pathogenesis of a wide variety of skin diseases. In lichenoid tissue reactions, the Civatte body or colloid body is a form of apoptotic keratinocytes which is mediated by T lymphocytes via Fas-FasL interaction or through the perforin-granzyme B pathway. In several skin tumors, Bcl-2 or FasL expression is involved in the proliferation or regression of the tumors, or in the escape from immune attack by T cells. Moreover, apoptosis is also responsible for the homeostasis of skin, such as the keratinocyte differentiation and hair cycle. In this review, we describe the basic concept of apoptosis and its relevance to skin diseases.

Apoptosis↗