Biomedical subjects
Publications and source records attributed to M Miyamoto.
A case of extrahepatically growing hepatocellular carcinoma is reported, and the Japanese literature is reviewed. A 42-year-old man was admitted to our hospital on December 27, 1985 complaining of epigastralgia and nausea. Ultrasonography and computerized tomography showed a large tumor in the right hepatic lobe. This Was removed surgically and examined histologically.
Autoclave sterilization altered the leaching of plasticizer, CO2 gas permeability, surface area and the surface wettability of bag films. These changes affected granulocyte cell counts and functions during storage. Four types of polyvinyl chloride bags, with di-(2-ethylhexyl)phthalate (DEHP) or tri-(2-ethylhexyl)trimellitate (TOTM) as plasticizer, with or without treatment by glow discharge (H2), were sterilized with ethylene oxide (EO) or autoclaving (AC). The greatest amounts of plasticizer leached from DEHP-EO bags. TOTM plasticizer did not leach into plasma. CO2 gas permeability was greater with TOTM than DEHP. AC sterilization decreased the surface area of bags. Wettability of film surfaces was greatest with H2-TOTM-EO. After storage in these bags for 24 and 48 h at 22 degrees C, the granulocyte cell counts and functions were greatest in H2-TOTM-EO bags with the nonleaching plasticizer, higher CO2 gas permeability and higher wettable surface due to glow-discharge treatment. The H2-TOTM-EO bag was useful as a granulocyte storage container.
Adenosine is a potent vasodilator of the systemic circulation. Infusion of adenosine into the aorta causes water and sodium retention and a fall in glomerular filtration rate and renal blood flow. The effect of adenosine on medullary blood flow is unknown. Because systemic vasodilatory effects may confound its renal actions, adenosine was infused into the renal artery of anesthetized Munich-Wistar rats at doses of 2, 6, and 15 micrograms/min. A marked dose-dependent increase in urinary flow and sodium excretion was observed. Inulin and p-aminohippuric acid clearance did not change significantly. Blood flow in vasa recta in the exposed renal papilla, as determined by fluorescence videomicroscopy, increased significantly only with the highest dose of adenosine. In control animals infused with the vehicle only, there was no change in any of the above variables. These results indicate that direct intrarenal infusion of adenosine in the rat increases urinary flow and sodium excretion and at higher doses also increases vasa recta blood flow. The effects on urinary flow and sodium excretion were therefore mediated by a mechanism other than an increase in vasa recta blood flow.
CS-622 is a prodrug type ACE inhibitor with a thiazepin ring. Its active form, CS-622 diacid, was slightly more potent than enalaprilat in inhibiting ACE isolated from rabbit lung. The inhibitory potency of CS-622 diacid on isolated rat aorta was 3 times that of enalaprilat. The inhibitory action of enalaprilat was abolished quickly by washing the aortic strip with drug-free solution, whereas that of CS-622 diacid was abolished only slowly. This difference suggests that CS-622 diacid binds to vascular ACE more firmly than enalaprilat. By oral administration, CS-622 was 3 times more potent than enalapril, and its onset of action was faster than that of enalapril, suggesting that the conversion of CS-622 to its active diacid occurs faster than the conversion of enalapril. Although CS-622 diacid was only slightly more potent than enalaprilat by intravenous administration, it had a longer duration than enalaprilat. Elimination of renal excretory function potentiated the action of captopril but not that of CS-622, suggesting that unlike captopril, only a small portion of CS-622 is excreted through the kidney.
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In our previous study, we observed a tendency towards an age-related increase in the serum thyrotropin (TSH) concentration. Regulatory mechanisms of TSH secretion in elderly subjects were studied. In 43 elderly subjects, serum TSH did not correlate significantly with serum T4, T3 free T4 or rT3. Further, those with increased TSH (greater than 5 mU/l, 9 subjects) did not overlap with those with low T3 (less than 0.92 nmol/1, 8 subjects). Increases in serum TSH were not associated with the presence of circulating anti-thyroid autoantibodies. A TRH test using a 500 micrograms single bolus injection was performed in 15 subjects. TSH response (basal: 1.92 +/- 1.42 (s.d.) mU/1, peak: 11.25 +/- 5.33 mU/1, sigma: 26.74 +/- 12.89 mU/1, respectively) did not differ significantly from that of younger subjects. T3 response after TRH varied greatly and a close correlation was observed between basal T3 and peak T3 (r = 0.86), and also between peak T3 and delta T3 (r = 0.81). A significant correlation was observed between sigma TSH and basal T3 (r = 0.60). Neither plasma cortisol, epinephrine nor norepinephrine concentrations showed any significant correlation with basal and TRH-stimulated TSH or T3 concentrations. However, the plasma dopamine concentration correlated significantly with sigma TSH (r = 0.60) and basal T3 (r = 0.52), respectively. In conclusion, the increase in serum TSH observed in elderly subjects was felt to represent a physiological adaptation to maintain serum T3. Low T3 subjects appear to have a disturbance in this mechanism, with decreased TSH and T3 response to TRH stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Decreased serum T3 concentrations in elderly subjects and their possible relationship with the development of dementia have been indicated. To see the effects of a passive increase in the serum T3 concentration, low dose T3 administration was undertaken. Forty-four subjects from 65 to 93 years of age (average 81.0 +/- 7.8) were divided into 2 groups. The grade of dementia was determined by Hasegawa's dementia rating scale (DR score). In 22 subjects, 25 micrograms per day of T3 was administered for 4 W, while the control group was given a placebo. The DR score was measured before and immediately after the study. Changes in behaviour were monitored in a double-blind fashion. The administration of T3 induced a 0.65 nmol/l increase in serum T3 in 2 W and 0.36 nmol/l in 4 W. These T3 increases were not associated with significant changes in the DR score but 7 of 22 subjects showed apparent improvement in behaviour. TSH was suppressed to less than 1 mU/l in 2 W and then slightly increased by the 4th week, but T4, rT3 and fT4 all showed significant and progressive decreases. The DR score after T3 correlated significantly with the rT3/T4 ratio (before T3: -0.55, changes: +0.50) and also with changes in rT3 (r = 0.49). In conclusion, T3 administration to the elderly subjects was associated with behavioural improvement in some individuals, but the intellectual ability as assessed by the DR score in those with low T3 or elevated rT3 were hardly improved by passive T3 elevation.
A 47-year-old woman complaining of cold intolerance, general weakness and amenorrhea of 10 months duration was diagnosed, by endocrine examinations, as having panhypopituitarism. Skull x-ray films revealed a slightly enlarged sella with double floor sign and MRI showed a low intensity mass in the pituitary. Transsphenoidal exploration disclosed a degenerated pituitary gland, the histology of which showed a granulomatous lesion with moderate lymphocytic infiltration but containing no multinuclear giant cells. No caseous necrosis, causative microorganisms, or BCG antigen were noted. The present case is considered a variant form of lymphocytic adenohypophysitis.
Acute toxicity of cefodizime sodium (THR-221) was examined in mice of both sexes, rats of both sexes (including 5-day-old young), and male dogs. The LD50 values of THR-221 (mg/kg) were as follows: (1) mice: intravenous, 7200 for males and 5000 for females; intraperitoneal, 10500 for males and 11000 for females; subcutaneous, 17500 for males and 16500 for females; and oral, 28000 for males and 29000 for females. (2) rats (adult): intravenous, 7000 for males and 8200 for females; intraperitoneal, 9500 for males and 8800 for females; subcutaneous, 17000 for males and 15500 for females; oral, more than 20000 for both sexes; and intramuscular, more than 3200 for both sexes. (3) 5-day-old rats: subcutaneous, 5278 for males and 5314 for females. (4) male dogs: intravenous, more than 5000. Major changes in general conditions observed in mice and rats were decreased spontaneous activity, lying prone, respiratory changes, staggering gait, clonic or clonic-tonic convulsions, and cyanosis, and in the animals dosed orally, diarrhea or salivation was also noted. The changes in 5-day-old rats were respiratory changes, agony, loss of reflex to an external stimulus, and congestion at the injection site, and those in dogs were vomiting, dryness of the nose, and soft or mucous stools. Autopsies on the mice and rats which died revealed hemorrhage on the brain surface. In addition, the following were seen: intraperitoneal retention of fluid and dark red spots on the abdominal wall (i.p.), subcutaneous retention of fluid or jellylike material and hemorrhage at the injection site (s.c.), and retention of fluid and dark red spots on the mucosa in the digestive tract (mice p.o.). In 5-day-old rats which died, the subcutaneous tissue at the injection site showed hemorrhage macroscopically and inflammatory changes microscopically. Hematological and blood chemical tests performed in dogs showed an increase in white blood cells and changes suggesting anemia, increases in GOT, LDH and ALP activities, and slight changes in urea nitrogen and inorganic phosphorus. In one animal given a low dose of 2500 mg/kg, an increase in GPT activity was also seen. However, these changes were all transient. Microscopic findings in dogs were slight inflammatory changes in the subcutaneous tissue around the injection site.
One-month subacute intravenous toxicity study of cefodizime sodium (THR-221) in rats was carried out with dose levels of 2000, 1000 and 500 mg/kg/day. Sixteen males and 16 females were used per group (including the control group). THR-221 caused neither death nor change in general conditions at any dose level throughout the study, except that decreased spontaneous activity appeared only transiently in a part of the animals given 2000 mg/kg/day. Increases in water intake were observed in all compound groups, and transient decreases in food consumption were seen at an early stage of the administration period. However, the compound did not affect the body weight at any dose level. In urinalysis, the urine sediments in all THR-221 groups contained an increased number of epithelial cells as compared with the controls. At autopsy, dilation of the cecum was observed in all THR-221 groups, and in a part of the rats with this change, red spots or reddening of the serous membrane of the organ also appeared. Light microscopy revealed brown granules in the epithelium of renal tubules in all compound groups (with dose-dependent incidences) and congestion or hemorrhage in the cecum in some compound-treated animals. Electron microscopy on the kidney showed small bodies (considered to be lysosomes) in the tubular epithelium in all compound groups. No other changes related to THR-221 were observed. From the present results that no marked toxic signs were seen at any dose level, the toxicologically non-effective dose of THR-221 for rats of both sexes is considered to be more than 2000 mg/kg/day.
Six-month chronic subcutaneous toxicity study of cefodizime sodium (THR-221) in rats was carried out with dose levels of 3000, 1000, 300 and 100 mg/kg/day. The systemic change observed was slightly decreased spontaneous activity, which appeared only in a very few animals. At the injection site of the animals at 1000 and 3000 mg/kg/day, various cutaneous changes (subcutaneous retention of fluid, incrustation, loss of hair and perforation) were observed. The body weight gains of the males at 1000 and 3000 mg/kg/day were depressed from 1 month of administration onward, but the food consumption was not affected in any group. The water intakes at 1000 and 3000 mg/kg/day were increased. Hematological findings were signs of anemia, a slight decrease in red blood cell count or increases in platelet and/or reticulocyte counts in all THR-221 groups. At 3000 mg/kg/day, increases in white blood cell and neutrophil counts and a decrease in lymphocyte count were also observed. Plasma chemistry revealed decreases in total protein amount and, albumin (A) or globulin (G) amounts, and a decrease or increase in A/G ratio in all compound groups. Autopsy revealed dilation of the cecum and hematoma, dark red spots and yellowish brown spots in the subcutaneous tissue at the injection site in all THR-221 groups. Hypertrophy of the spleen was also noted at 300-3000 mg/kg/day. Changes in organ weights were a decrease in liver weight in all compound groups and an increase in spleen weight at 3000 mg/kg/day. Microscopically, the following were observed: brown granules or hyaline droplets in the epithelium of renal tubules; hemorrhage and inflammatory changes in the subcutaneous tissue at the injection site; and an increased number of lymphocytes or granulocytes in the spleen and bone marrow. Urinalysis and ocular and auditory tests showed no changes related to THR-221. From the present results, the toxicologically non-effective doses of THR-221 are considered to be 300 mg/kg/day for male rats and more than 1000 mg/kg/day for female rats.
The electrical impedance of the dog submandibular gland, as an indicator of changes in extracellular fluid (ECF) volume, was measured at 5 kHz, 500 kHz, and 5 MHz at intervals of 10 s during secretory stimulation, because the conductivity calculated from impedance at low frequencies reflected the ECF volume. The decrease in conductivity occurred in the first minute of stimulation. Its decrease was more marked during stimulation after circulatory arrest. Salivary secretion under intact circulation consists of two phases: an initial secretion occurring in the first minute of stimulation with a high secretory rate and a steady secretion continuing during stimulation at a constant rate. A decrease in conductivity occurred in the initial secretion. Within a few minutes following the cessation of stimulation, the conductivity increased to a level higher than the resting one with an intact circulation, while the blood flow remained several times higher than in the resting state. The conductivity of the gland slowly recovered to the prestimulation level over a 30-min period. The histological examination revealed that the main compartment of the ECF change was the interlobular space. Impedance and histological studies showed that the ECF volume of salivary glands changes dynamically during secretion. On the other hand, the cellular volume also increased in the initial secretion of an isolated gland. Its increase suggested that the fluid was transported to the lumen via a cellular pathway as well as a paracellular pathway in the initial secretion.
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