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Biomedical subjects

Y Minowa

Publications and source records attributed to Y Minowa.

At least 19 recordsLinked to original sources
PubMed2002

Effects of inhaled furosemide on CO(2) ventilatory responsiveness in humans.

We previously showed that inhaled furosemide improves experimentally induced dyspnea. In order to test the possibility that inhaled furosemide may alter the CO(2) chemosensitivity and thereby reduce the dyspneic sensation, the effect of inhaled furosemide on CO(2) chemosensitivity was evaluated with a double-blinded, randomized crossover design in 10 healthy subjects. The CO(2) chemosensitivity was measured by the steady-state and rebreathing methods before and after the inhalation of placebo (normal saline) and furosemide aerosols (40 mg). In addition, subjects were asked to rate their sensation of respiratory discomfort using a visual analog scale (dyspneic VAS) during the measurement of CO(2) chemosensitivity with the steady-state method. Our results showed that (1) inhaled furosemide does not affect the breathing patterns of resting breathing, (2) inhaled furosemide does not affect the slope and intercept of the CO(2) response curve, regardless of whether the CO(2) chemosensitivity is measured by the steady-state technique or rebreathing technique and (3) inhaled furosemide improves the dyspneic sensation produced during hypercapnic hyperpnea. These results suggest that the mechanism of the improvement of dyspnea by inhaling furosemide is not associated with the decrease in the ventilatory drive to CO(2).

Administration, Inhalation↗
PubMed2001

Ethanol and oxidative stress.

This article represents the proceedings of a workshop at the 2000 ISBRA Meeting in Yokohama, Japan. The chair was Albert Y. Sun. The presentations were (1) Ethanol-inducible cytochrome P-4502E1 in alcoholic liver disease, by Magnus Ingelman-Sundberg and Etienne Neve; (2) Regulation of NF-kappaB by ethanol, by H. Matsumoto, Y. Nishitani, Y. Minowa, and Y. Fukui; (3) Chronic ethanol consumption increases concentration of oxidized proteins in rat liver, by Shannon M. Bailey, Vinood B. Patel, and Carol C. Cunningham; (4) Antiphospholipids antibodies and oxidized modified low-density lipoprotein in chronic alcoholic patients, by Tomas Zima, Lenka Fialova, Ludmila Mikulikova, Ptr Popov, Ivan Malbohan, Marta Janebova, and Karel Nespor; and (5) Amelioration of ethanol-induced damage by polyphenols, by Albert Y. Sun and Grace Y. Sun.

Alcoholism↗
PubMed2000

Mutagenicity of cooked hamburger is controlled delicately by reducing sugar content in ground beef.

Effect of sugars added to ground beef on the generation of mutagenicity of cooked hamburger was investigated. Mutagenicity of hamburger was assayed by the Ames test using Salmonella typhimurium TA98 strain with metabolic activation after the mutagens were purified by use of blue rayon. Intrinsic reducing sugar content in ground beef was estimated to be 0.07% (w/w). Mutagenicity of hamburger was sharply or delicately controlled by the amount of a reducing sugar added to ground beef. Mutagenicity was increased more than 2-folds by addition of 0.08% (w/w) glucose, fructose or lactose but decreased to about a half by addition of more than 0.67% (w/w) each of the reducing sugars. Mutagenicity of cooked hamburger was not influenced by addition of sucrose at the ranges between 0.08 and 0.67% (w/w). When red wine with 0.10% (w/w) equivalent amount of reducing sugars or white wine with 0.13% (w/w) equivalent amount of reducing sugars were added to the ground beef, mutagenicity of cooked hamburger was similarly increased 1.6-1.8-fold. Controlling the reducing sugar content in ground beef would be a simple way to regulate the mutagenicity of cooked hamburgers.

Animals↗
PubMed2000

Role of Kupffer cells in the release of nitric oxide and change of portal pressure after ethanol perfusion in the rat liver.

The objective of this study was to elucidate the role of Kupffer cells during the increase of portal vein pressure caused by ethanol. We measured nitric oxide (NO) in the perfused rat liver using a commercial NO meter. Ethanol perfusion increased NO release and portal vein pressure. Gadolinium chloride pretreatment reduced the increase in portal vein pressure during the early phase of ethanol perfusion, but did not affect the release of NO after ethanol infusion. These findings suggest that Kupffer cells play an important role in liver microcirculation during the early stage of ethanol intake, but that the mechanism may not be regulated by NO.

Animals↗
PubMed1999

An allometric model for predicting blood ethanol elimination in mammals.

The relationship of ethanol elimination kinetics in mammals was estimated using the allometric principle. The hypothesis of relationships between parameters obtained from the compartment model with Michaelis-Menten elimination kinetics and body weight can lead to common equations of blood ethanol elimination in mammals. The maximum elimination velocity (g/hr) and the apparent volume of distribution (L) were significantly proportional to the 0.71 and 0.93 powers of body weight (r = 0.994, P < 0.01 and r = 0.998, P < 0.001), respectively. There was no significant relationship between the Michaelis constant and body weight. In the differential equations of the two-compartment model, the kinetics parameters were substituted for the obtained power functions. Good fitting of these equations for the real data showed that ethanol elimination kinetics in mammals can be predicted quantitatively.

Computer Simulation↗
PubMed1998

Mutagenicity of cooked hamburger is reduced by addition of onion to ground beef.

Addition of onion effectively reduced mutagenicity of cooked hamburger when tested on Salmonella typhimurium TA98 strain with metabolic activation. The components of onion that participated in the reduction of mutagenicity were sugars. Addition of starch or glucose to ground beef the amount equivalent to that in onion reduced the mutagenicity of cooked hamburger. Addition of onion may cause imbalance of the sugar content of ground beef that effectively produces mutagenicity. Mutagenicity of the heated model mixture of glucose/glycine/creatinine in diethyleneglycol-water was reduced by an excessive amount of glucose. Hence, Japanese cooking-style with addition of onion can reduce mutagenicity of hamburger.

Animals↗
PubMed1997

A case of homosexual murder: a victim with testicular regression syndrome.

A 25-year-old male was killed with a survival knife by his business and homosexual partner. In addition to 22 wounds on the extremities, 16 wounds were found on the neck, chest and abdomen. The heart and lungs were penetrated, and three wound tracks reached the back of the body. The cause of death was diagnosed as hemorrhage. The genitalia of the victim was anomalous: the pubic hair pattern was that of a female, the penis was small and no testes were identified in the scrotal sac. According to his medical records, micropenis and bilateral cryptorchidism were present at birth, and neither hormonal treatments nor bilateral orchidopexy could enlarge his penis size. At the age of 17, his condition had been diagnosed as hypergonadotropic hypogonadism. His genital anomalies were considered due to embryonic testicular regression syndrome, and his micropenis a possible cause of his homosexual orientation. Judging from the patulous anus with thickened margins, he was probably a passive homosexual. The motive of the murder was not monetary, but rather emotional entanglement. The court judged that the case was one of premeditated murder with a short-circuited motive, and sentenced the defendant to ten years imprisonment.

Adult↗
PubMed1997

A case of disseminated intravascular coagulation probably arising from sudden infant death syndrome.

The cause of death in a 45-day-old male infant who was found apneic at home and died 21 hours later was disseminated intravascular coagulation (DIC). The patient was admitted to a hospital in a state of cardio-respiratory arrest. The initial diagnosis was interrupted sudden infant death syndrome. The patient remained apneic, and recurrent discharge of bloody stool was the dominant clinical findings. He died without spontaneous respiration being restored. The autopsy revealed hemorrhages in the lungs and the ventricular septum and the free wall of the left ventricle of the heart. Microscopically, fibrin thrombi were noted in the large intestine and heart. The DIC was probably triggered by a widespread endothelial injury caused by severe hypoxia and acidosis originating from the apnea and cardiac arrest lasting longer than 30 min.

Disseminated Intravascular Coagulation↗
PubMed1996

[Palliative radiation therapy for multiple myeloma].

PURPOSE: Radiation therapy is a useful palliative modality for refractory lesions of multiple myeloma. It has been reported that total doses of 10 to 20 Gy are usually adequate to obtain some degree of pain relief. However, there are many patients who need additional doses to obtain sufficient pain relief. In this study, we retrospectively analyzed the records of patients with multiple myeloma irradiated at our department, in an attempt to develop an effective treatment policy for this disease. MATERIALS AND METHODS: Twenty-nine patients with 53 lesions were treated between 1968 and 1993. Total irradiation doses were 4 to 60 Gy(median 40 Gy) with daily fractions of 2 Gy or less, and 16 to 51 Gy(median 30 Gy) with daily fractions greater than 2 Gy. Evaluated were 59 symptoms, including pain (68%), neurological abnormalities (15%), and masses (28%). RESULTS: Symptomatic remission was obtained in 33 of 36 (92%) lesions with pain, 6 of 8(75%) with neurological abnormalities, and 13 of 15(87%) mass lesions. Pain was partially relieved at a median TDF of 34, and completely at a median TDF of 66(equivalent to 40-42 Gy with daily fractions of 2 Gy). CONCLUSIONS: Radiation therapy is an effective and palliative treatment method for symptomatic multiple myeloma. However, the treatment seems to require higher radiation doses than those reported to obtain adequate relief of symptoms.

Adolescent↗
PubMed1991

Evoked otoacoustic emissions from ears with idiopathic sudden deafness.

Evoked otoacoustic emissions (EOEs) were examined in ears with idiopathic sudden deafness (ISD) at an early stage after onset and were compared with those in ears with long-standing sensorineural hearing losses of unknown etiology (SHLUE). In ears with SHLUE, EOEs were not recordable from ears with a hearing loss exceeding 35 dB at minimum hearing level of 4 audiometric frequencies: 500, 1,000, 2,000 and 4,000 Hz (4 MHL). On the other hand, although 4 MHLs were greater than 35 dB in most of the ears, EOEs could be detected in about one-half of the ears with ISD, and, moreover, the majority of these EOE detectable ears showed a good hearing prognosis in spite of the degree of hearing loss. There was, however, no correlation between EOE threshold and degree of hearing recovery. From these results it seems that EOE testing might be clinically applicable for predicting whether or not hearing loss due to ISD can be recovered.

Acoustic Stimulation↗
PubMed1991

Frequency analysis of evoked otoacoustic emissions.

Evoked otoacoustic emissions (EOEs) were examined in 8 normal hearing ears without spontaneous otoacoustic emissions (SOEs), and the frequency of the first 10 ms after appearance of the EOE response wave was analyzed, dividing it into the first 5 ms half (First half A) and the last 5 ms half (Last half B). In the First half A, the peak frequency of the power spectrum tended to match the stimulus frequency, but in the Last half B, the peak frequency tended to be constant and moreover, it tended to match the frequency at which EOE can best be recorded. These findings suggest that each ear has its own characteristic EOE frequency.

Cochlea↗
PubMed1990

Purification and characterization of a novel intracellular acid proteinase from the plasmodia of a true slime mold, Physarum polycephalum.

An acid proteinase was purified to apparent homogeneity from the plasmodia of a slime mold, Physarum polycephalum, by a combination of detergent extraction, acid precipitation, and column chromatographies on DEAE-Sephadex, hydroxylapatite, CM-Sephadex, and Sephadex G-100. The enzyme was shown to be composed of two polypeptide chains (a 31-kDa heavy chain and a 23-kDa light chain) cross-linked by disulfide bond(s). The NH2-terminal amino acid sequence of the heavy chain was determined to be Ala-Gly-Val- Asp-Gly-Tyr-Ile-Val-Pro-Tyr-Val-Ile-Phe-Asp-Leu-Tyr-Gly-Ile-Pro-Tyr and that of the light chain to be Ala-Glu-Pro-Pro-Ile. The heavy chain contained carbohydrate moiety composed of mannose, glucosamine, fucose, and glucose. The enzyme was optimally active at pH 1.7 toward hemoglobin as a substrate. Among the proteinase inhibitors tested only diazoacetyl-D,L-norleucine methyl ester, a typical aspartic proteinase inhibitor, inhibited the acid proteinase in the presence of cupric ions. It was insensitive to the other typical aspartic proteinase inhibitors, pepstatin A and 1,2-epoxy-3-(p-nitrophenoxy)propane. The enzyme hydrolyzed Lys-Pro-Ile-Glu-Phe(4-NO2)-Arg-Leu at the Phe-Phe(4-NO2) bond, but could not hydrolyze another synthetic pepsin-substrate, N-acetyl-L-phenylalanyl-3,5-diiodo-L-tyrosine. The enzyme showed a unique substrate specificity toward oxidized insulin B chain. The major cleavage sites were the bonds Gly8-Ser9, Leu11-Val12, Cya19-Gly20, and Phe24-Phe25, and the Gly8-Ser9 bond was most susceptible. These results indicate that the enzyme is a novel type of intracellular acid proteinase with a unique substrate specificity.

Amino Acid Sequence↗