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Biomedical subjects

C Ito

Publications and source records attributed to C Ito.

At least 163 records · Page 9Linked to original sources
PubMed1988

A novel endogenous sugar acid depolarizes ventromedial hypothalamic neurons in vitro.

2-Buten-4-olide (2-B-4-O) has been identified in the serum of fasted rats and proved to act as a feeding suppressant. The effect of 2-B-4-O on neurons in the ventromedial hypothalamic (VMH) nucleus was investigated with intracellular recordings in brain slice preparations of rats. 2-B-4-O, applied by perfusion (0.1-10 mM) or drops (50-100 mM), dose dependently depolarized 30% of the VMH neurons tested. The depolarization by 2-B-4-O application persisted after complete elimination of synaptic inputs during perfusion with Ca2+-free/high-Mg2+ solution. The depolarization, accompanied by a decrease in membrane conductance, reversed polarity around -95 mV and was dependent on extracellular K+ concentration. The VMH neurons depolarized by 2-B-4-O had some specific electrophysiological properties corresponding with those of glucoreceptor neurons. The results suggest that 2-B-4-O directly excites VMH neurons, presumed to be glucoreceptor neurons, by decreasing K+ conductance, and this effect may participate in the feeding suppressive action of 2-B-4-O.

4-Butyrolactone↗
PubMed1988

Relationship between the occurrence of late potential on the body surface ECG and cardiac performance in myocardial infarction.

Comparative evaluations of the percent of the perimetric circumference of infarction and cardiac performance for the occurrence of late potential were performed in 12 normal subjects and 22 patients with old myocardial infarction (MI). All patients were in normal sinus rhythm without bundle branch block. Bipolar X, Y, and Z leads were signal-averaged using a bandpass filter with a low-cut frequency of 100 Hz and a high-cut frequency of 300 Hz. The filtered signals for the three leads were displayed and combined into a vector magnitude, square root of X2 + Y2 + Z2. The percent ratio of the root mean square voltage in the last 40 msec of the QRS complex was calculated against that of the total filtered QRS (%RMS40). The value of the standard deviation (SD) in the phase distribution was obtained by the Fourier analysis of multi-gated blood pool images. Significant differences were observed among MI with late potential, MI without it and the normal subjects for %RMS 40 (5.7 +- 2.8% vs 26.9 +- 8.1, 37.5 +- 10.8%). Left ventricular ejection fraction was lower in MI with late potential (19.7 +- 7%) compared to that of MI without it (33 +- 18%) and the normal subjects (60 +- 4%); the value of SD was higher in MI with late potential (64 +- 21 degrees), compared to that of MI without it (43 +- 20 degrees) and the normal subjects (9 +- 4 degrees). These findings showed that the percent ratio of the last 40 msec RMS voltage (%RMS 40) was found to discriminate effectively among MI with and without late potential and normal subjects. It was suggested that the amount and structure of the infarcts may be important factors in the occurrence of late potential.

Adult↗
PubMed1988

[Detection of late potentials on the signal averaged body surface ECG using X, Y, Z and anterior chest leads].

We developed the system of high-frequency analysis of the signal-averaged body surface ECG to detect low amplitude signals in the terminal portion of the QRS. Thirty-five patients four or more weeks after transmural myocardial infarction (MI) and 30 normal volunteers were studied. All patients were in normal sinus rhythm and did not have bundle branch block. Body surface ECG recording using bipolar X, Y, and Z leads was performed in a shielded room. One lead served as the reference. The three-channel amplifier was a commercially-available ECG system. The common mode rejection ratio was 120 dB. The signal from each lead was amplified and passed through an analogue filter (NF FV 624) with a low-cut frequency of 100 Hz and a high-cut frequency of 300 Hz. Then AD conversion was performed with 12-bit accuracy, 1024 samples/sec. The filtered signals for the three leads were displayed separately for each channel and were combined into a vector magnitude, square root of X2+Y2+Z2. The percent ratio of the root mean square voltage in the last 40 msec of the QRS complex to that of the total filtered QRS (%RMS40) and the duration of the filtered QRS were automatically calculated. These parameters obtained from the three groups were compared. Signal-averaged, non-filtered and filtered body surface ECGs were recorded using 25 (5 x 5 array) anterior chest unipolar leads in 20 normal volunteers and in patients with late potential. The departure index was calculated as the voltage differences between the mean value (M) in normal persons and the value in patients (Xi) with MI using the formula (Xi-M/SDi) at intervals every four msec. The departure maps, capable of identifying the location of the MI, were made from the departure index at four msec intervals; then the late potential (LP) area maps were superimposed on the departure maps. To determine the late potential, we used the filtered ECG of X, Y, and Z leads and quantitative values (%RMS 40) obtained from a vector magnitude incorporated in these three leads. Six MI patients, four anterior and two inferior, with the late potential had low amplitude signals at the end of the filtered QRS complex. The %RMS 40 was 6.8 +/- 2.9% (p less than 0.001) in MI patients with the late potential, 2.8 +/- 8.5% (p less than 0.01) in MI patients without the late potential, and 37 +/- 11% in normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

Electrocardiography↗
PubMed1987

Epidermal growth factor has a unique effect in combination with fetal bovine serum to bypass the ts-block of G0-specific ts mutant tsJT60.

tsJT60 cells are G0-specific temperature-sensitive mutants of the cell cycle from Fischer rats i.e., they grow exponentially at both 34 degrees and 39.5 degrees C, but when stimulated with fetal bovine serum (FBS) from the resting state (G0) they enter S phase at 34 degrees C but not at 39.5 degrees C. Epidermal growth factor (EGF) also induced DNA synthesis, although weakly, in G0-arrested tsJT60 cells at 34 degrees C but failed at 39.5 degrees C. When G0-arrested tsJT60 cells were stimulated at 39.5 degrees C with FBS plus EGF, they entered S phase and divided. Somatomedin C, insulin, or transferrin had a weak effect in inducing DNA synthesis in G0-arrested cells when applied at 34 degrees C or with FBS at 39.5 degrees C. Fibroblast growth factor, platelet-derived growth factor, or 12-O-tetradecanoylphorbol 13-acetate had no such stimulatory effect at 39.5 degrees C. Binding of 125I-somatomedin C was not temperature-sensitive. Several other ts mutant cells that were blocked at 39.5 degrees C from entering S phase from the resting state following FBS addition were stimulated by FBS plus EGF at 34 degrees C but not at 39.5 degrees C.

Animals↗
PubMed1987

Bypass of the ts block of tsJT60, a G0-specific ts mutant from rat fibroblasts, by fetal bovine serum and epidermal growth factor.

tsJT60, a temperature-sensitive (ts) G0-mutant cell line from a Fischer rat, grows normally in the exponential growth phase at 34 degrees C and 39.5 degrees C, but when stimulated with fetal bovine serum (FBS), from the G0 phase they reenter the S phase at 34 degrees C but not at 39.5 degrees C. The ts-block was bypassed when G0-arrested tsJT60 cells were stimulated at 39.5 degrees C with FBS plus epidermal growth factor (EGF). The presence of EGF for the first 6 h after serum stimulation caused tsJT60 cells to enter the S phase in the presence of FBS at 39.5 degrees C. When EGF was added 6 h after serum stimulation, entrance into the S phase was delayed by about 6 h. The sequential presence of two growth factors, EGF without FBS for 6 h then FBS without EGF, or the reversed sequence, failed to initiate DNA synthesis at 39.5 degrees C. The binding of EGF was not temperature sensitive. The amounts of RNA and protein present doubled after stimulation with both FBS and EGF at 39.5 degrees C. These and other findings suggest that EGF bypasses only some specific event in the entire prereplicative process that operates operating in serum-stimulated cells at 39.5 degrees C.

Animals↗
PubMed1986

[Pharmacological properties of MO-8282, a novel antidepressant].

The pharmacological properties of MO-8282 (1,2,3,4-tetrahydro-2-methyl-9H-dibenzo [3,4: 6,7]cyclohepta [1,2-c]pyridine maleate) as an antidepressant were investigated. At doses 10 times less than those of amitriptyline, MO-8282 showed similar potencies in reducing the duration of immobility during forced swimming in rats and in potentiating stereotype induced by L-DOPA. Intermediate doses of MO-8282 reduced the duration of immobility during forced swimming, in mice as well, suppressed muricide behavior of olfactory-bulbectomized rats and antagonized clonidine-induced suppression of exploratory activity in mice. MO-8282 moderately antagonized the ptosis but not the hypothermia induced by reserpine in mice. MO-8282 exhibited weak antagonism against the tremor, lacrimation and diarrhea induced by tremorine, but its activity was milder than that of amitriptyline. The uptake of noradrenaline into rat hypothalamic synaptosomes was inhibited by MO-8282 at concentrations 20 times less than equally effective doses of amitriptyline, but the uptake of dopamine or serotonin was unaffected by MO-8282. A single oral administration of MO-8282 at a dose of 30 mg/kg accelerated noradrenaline turnover, but did not affect dopamine and serotonin turnover in the rat brain. MO-8282 strongly inhibited noradrenaline-, histamine- or adenosine-sensitive adenylate cyclase activity of guinea pig brain. Its mode of action differed from that of imipramine, rather resembling that of mianserin. MO-8282 did not affect monoamine oxidase activity of rat liver. These results suggest that the pharmacological characteristics of MO-8282 are different from those of tricyclic antidepressants and rather similar to those of mianserin, but more potent. The results, therefore, indicate that MO-8282 is possibly a novel antidepressant.

Aggression↗
PubMed1985

Protective effects of urinary trypsin inhibitor in experimental shock.

The effects of human urinary trypsin inhibitor (UTI) were studied in experimental shock models. Administration of 50,000 U/kg, i.v., of UTI protected against mortality from shock induced by burn, endotoxin or trauma. Aprotinin at a dose of 50,000 U/kg improved only endotoxin shock and showed a moderate but not significant effect on burn and traumatic shock. Administration of 50,000 U/kg, i.v., of UTI protected against the aggravation in systemic hemodynamics in canine hemorrhagic shock. Furthermore, in rat traumatic shock, 50,000 U/kg, i.v., administration of UTI significantly reversed the increased serum beta-glucuronidase and trypsin activities and the decreased hepatic ATP level, and it moderately suppressed the increased serum uric acid level. Aprotinin failed to affect all these biochemical changes induced by drum trauma. These results suggest that the protective effect of UTI against experimental shock is possibly exerted through lowering the elevated enzyme activities in the serum during shock.

Animals↗