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Biomedical subjects

M Yoshimura

Publications and source records attributed to M Yoshimura.

At least 703 records · Page 39Linked to original sources

Participation of extracapillary lesions (ECL) in progression of IgA nephropathy.

To clarify long-term prognosis and risk factors of IgA nephropathy, 205 patients with the disease were followed up for a period of 1 to 22 years with a mean of 7.9 years. According to the percentage of glomeruli involved with extracapillary lesions (ECL), which were defined by crescents and fibrous adhesion of glomerular tufts to Bowman's capsule, the patients were divided into four groups: group 1-absence of ECL; group 2-less than 25%; group 3-25-50%; group 4-more than 50%. During the follow-up period, 26 patients progressed to chronic renal failure requiring hemodialysis, and one patient died of acute peritonitis. The actuarial kidney survival rate was 90.4% for 5 years and 86.0% for 10 years. Ten-year survival rates were 100% in group 1, 94.3% in group 2, 81.8% in group 3 and 25.5% in group 4. Re-biopsy specimens, observed in 31 patients after intervals of 1.4 to 13.4 years, revealed an increase of ECL in 20 patients concomitant with an apparent reduction of renal function in 13, whereas in the other 11 patients with no increase, renal function remained unchanged. These results strongly suggest that ECL plays an important role in the progression of IgA nephropathy, and renal function could be impaired by repeated formation and accumulation of these lesions.

Adolescent↗

Noradrenaline mediates slow excitatory synaptic potentials in rat dorsal raphe neurons in vitro.

Repetitive focal stimulation to the slice surface within the region of the dorsal raphe (DR) nucleus of rat brain elicited a slow excitatory synaptic potential (slow EPSP), which followed a slow inhibitory synaptic potential (slow IPSP) in a majority of the DR neurons. The slow EPSPs were associated with either an increase of a decrease in membrane resistance. Noradrenaline (NA) application caused a membrane depolarization in most of the DR neurons. The NA-induced depolarization was also accompanied by either an increase or a decrease in membrane resistance. Both the slow EPSP and NA-induced depolarization were inhibited by phentolamine and prazosin but not by yohimbine and propranolol. The result suggests that slow EPSPs in rat DR neurons are mediated by NA interacting with an alpha 1-adrenoceptor.

Animals↗

Selective depression of hippocampal inhibitory postsynaptic potentials and spontaneous firing by volatile anesthetics.

The effects of halothane, isoflurane and enflurane on the rat hippocampal CA1 neurons in in vitro preparations were studied by intracellular recordings. All volatile anesthetics, at the concentrations which are likely to be in the range of clinical doses, depressed the IPSPs and the spontaneous firing without affecting the resting membrane properties and the EPSPs. The results suggest that the simultaneous blocking effects of the anesthetics on both the spontaneous firing and IPSPs are responsible for production of general anesthesia rather than their blocking actions on the EPSPs in terms of behavior of hippocampal neurons.

Anesthetics↗

5-Hydroxytryptamine mediates inhibitory postsynaptic potentials in rat dorsal raphe neurons.

In rat dorsal raphe neurons, focal electrical stimulation elicited a slow inhibitory postsynaptic potential (IPSP) associated with increased membrane conductance. On the basis of data in the literature this IPSP is presumably caused by a recurrent inhibitory circuit. 5-Hydroxytryptamine (5-HT) application caused a hyperpolarization of the cell membrane, also associated with increased membrane conductance. Both responses could be abolished by lysergic acid diethylamide or methysergide, and enhanced by imipramine. The reversal potentials for the responses were at the same level of - 95 mV which suggests an increase in membrane potassium conductance as the mechanism of both responses. These data suggest that 5-HT may be the mediator of the IPSP evoked by focal stimulation.

Animals↗

A new method of electrodiagnosis during operations on the brachial plexus and peripheral nerve injuries. The value of motor nerve action potentials evoked by trans-skull motor area stimulation.

A method is described which records efferent motor nerve action potentials (MNAPs), evoked by trans-skull motor area stimulation, directly from a nerve root or peripheral nerve fibres during operation. The records of MNAPs from the root show whether function of the anterior root is intact and its continuity retained. When recorded from the proximal stump of a divided nerve at the wrist the motor funiculus can be identified, enabling funicular nerve suture to be carried out more easily.

Action Potentials↗

Change of hyaluronic acid synthesis during differentiation of myogenic cells and its relation to transformation of myoblasts by Rous sarcoma virus.

Hyaluronic acid synthesis was examined in cultures of differentiating chick embryo muscle cells before, during and after fusion. Prior to fusion, hyaluronic acid was synthesized and secreted into the medium, but once fusion began this synthesis was reduced significantly. Synthesis then increased again after completion of fusion. Thus, production of hyaluronic acid was lowest at the time of or right before cell fusion. When myoblasts were transformed by Rous sarcoma virus (RSV), a higher amount of hyaluronic acid was synthesized, and cells were not able to fuse. The turnover rate of hyaluronic acid might be different between myotubes and RSV-transformed myoblasts. The addition of exogenous hyaluronic acid to myoblast cultures resulted in the partial inhibition of fusion. The effect was reversible because fusion took place after removal of the exogenous hyaluronic acid. These observations suggest that hyaluronic acid plays an important role in the differentiation of myogenic cells, and that elevated hyaluronic acid synthesis may partly be the reason for inhibition of myotube formation upon transformation by Rous sarcoma virus.

Acetates↗

Centrally-induced vasodepressor responses to diltiazem, a calcium channel blocker, in rats.

The effects of a calcium channel blocker, diltiazem, on central cardiovascular regulation were investigated by injecting it intracerebroventricularly (i.c.v.) in urethane-anaesthetized rats. The blood pressure decreased immediately after the injection returning to baseline level 20-30 min later. Both heart rate and abdominal sympathetic nerve activity decreased correspondingly. Diltiazem injected intravenously (i.v.) decreased both blood pressure and heart rate without affecting sympathetic nerve firing. Although the central pressor responses to carbachol and prostaglandin E2 were not affected by i.c.v. pretreatment with diltiazem, diltiazem attenuated the pressor responses to angiotensin II. Furthermore, electrical lesioning of the anteroventral third ventricle (AV3V) area significantly attenuated the depressor responses to diltiazem injected i.c.v. These results suggest that diltiazem injected i.c.v. affects the central nervous system to decrease sympathetic outflow, and thereby to attenuate the central vasopressor effects of angiotensin II in the brain AV3V area.

Angiotensin II↗

Noradrenaline hyperpolarization and depolarization in cat vesical parasympathetic neurones.

Responses to noradrenaline (NA) applied by superfusion, ionophoresis or pressure pulse were analysed using conventional intracellular recording and voltage-clamp methods in cat vesical parasympathetic ganglia. NA (1 microM) hyperpolarized 60% of the neurones, depolarized 25%, and produced a biphasic potential, which comprised a membrane hyperpolarization followed by a membrane depolarization, in 10%. About 5% of the neurones did not respond to NA. The NA hyperpolarization was blocked by yohimbine (1 microM), an alpha 2-adrenoceptor antagonist, whereas the NA depolarization was blocked by prazosin (0.1-1 microM), an alpha 1-adrenoceptor antagonist. These data indicated that the NA hyperpolarization was mediated through alpha 2-adrenoceptors and the NA depolarization through alpha 1-adrenoceptors. The NA hyperpolarization was accompanied by an increase in conductance, while the NA depolarization was associated with a decrease in conductance measured under manual-clamp conditions. Similar conductance changes were observed under voltage clamp. NA hyperpolarizations became smaller as the membrane was hyperpolarized and reversed polarity beyond -100 mV. NA depolarizations also became smaller at hyperpolarized membrane potentials and reversed polarity around -90 mV. The NA responses were enhanced in low-K media and depressed in high-K Krebs solution. The NA hyperpolarization was blocked by the Ca antagonists, Cd, Mn and Co. Intracellular injection of EGTA caused a slowly developing, progressive block of the NA hyperpolarization. The NA depolarization was not affected by low Ca concentrations, Ca antagonists or intracellular injection of EGTA. In some neurones the NA depolarization was unmasked in solutions containing Ca antagonists and after intracellular EGTA injection. The NA hyperpolarization was depressed by intracellular injection and extracellular superfusion of Cs but not by TEA. Ba (10-100 microM) depressed the NA hyperpolarization by 30%. The NA depolarization persisted in the presence of muscarine (10 microM) and was not blocked by Cs or TEA but was depressed 70% by Ba (10 microM). These data are consistent with the hypotheses that alpha 2-adrenoceptor activation produces a membrane hyperpolarization that is mediated through a Ca-dependent K conductance, and that alpha 1-adrenoceptor activation produces a membrane depolarization through closure of a voltage-insensitive K channel.

Action Potentials↗

Alpha mating type-specific expression of mutations leading to constitutive agglutinability in Saccharomyces cerevisiae.

Two mutants of Saccharomyces cerevisiae have been isolated and characterized. The mutants were constitutively agglutinable at 36 degrees C, the temperature at which wild-type cells agglutinate only after induction by mating pheromone. The mutant cells had other properties specific for the normal alpha cell type, i.e., conjugation with a cells, response to a mating pheromone, and production of alpha mating pheromone. The two mutations, cag1 and cag2, were recessive and expressed only in alpha cells. cag1 is linked very closely to the MAT locus, but cag2 is unlinked to the MAT locus. These cag mutations complemented ste3-1. These results indicate that CAG genes are novel alpha-specific genes involved in the regulation of sex agglutinin synthesis.

Agglutination↗