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Biomedical subjects

N Sumi

Publications and source records attributed to N Sumi.

At least 73 records · Page 4Linked to original sources
PubMed1995

[Mutagenicity studies of montirelin hydrate (NS-3)].

Montirelin hydrate (NS-3), a new drug for the treatment of disturbance of consciousness, was examined for mutagenicity in the reverse mutation test, the chromosome aberration test in vitro, and the micronucleus test in mice. The reverse mutation test was performed at dose range of 156.25-5,000 micrograms/plate using Salmonella typhimurium strains, TA1535, TA100, TA1537, and TA98, and Escherichia coli WP2uvrA. The drug did not increase revertant colonies significantly in any of the test strains with or without metabolic activation system (S-9mix). The chromosome aberration test was carried out at dose range of 300-4,800 micrograms/ml using cultured Chinese hamster lung cells (CHL/IU). No significant increases of the frequencies of cells with chromosomal aberrations were observed with or without metabolic activations. The micronucleus test was conducted in the bone marrow cells of Slc:ddY male mice. Mice were given the drug by a single intraperitoneal administration at doses of 0, 250, 500, 1,000, and 2,000 mg/kg. There were no significant increases in the frequencies of micronucleated polychromatic erythrocytes at any dose levels. These results show that montirelin hydrate has no mutagenic activity in vitro or in vivo.

Animals↗
PubMed1995

[Vascular irritability study of montirelin hydrate (NS-3) injection in rabbits].

A vascular irritability study of montirelin hydrate (NS-3) injection, a new drug for the treatment of disturbance of consciousness, was conducted in Japanese white rabbits. The concentration of montirelin hydrate was 4 mg/ml. Saline and 0.75% acetic acid were used as negative and positive control, respectively. In a part of the ear vein, 0.05 ml of each compound was allowed to remain for 3 min after intravenous injections once a day for 8 days. Inflammation in peri-venous region and thrombus were macroscopically observed in injection sites of rabbits with the montirelin hydrate injection group. However, no changes were seen with the negative control group. Histopathological examination revealed periphlebitis, desquamation of endothelial cells and thrombus in rabbits given montirelin hydrate injection or saline. But incidence and degree of periphlebitis caused by montirelin hydrate injection were higher than those caused by saline. On the other hand, the irritating changes caused by 0.75% acetic acid were severer than those by montirelin hydrate injection. These results show that montirelin hydrate injection has a very weak vascular irritability in the ear of rabbits.

Animals↗
PubMed1994

[Single dose toxicity studies of lactitol (NS-4) in mice and rats].

The single dose toxicity studies of lactitol, a hepatic encephalopathy drug, were performed in ddY mice and SD rats of both sexes by administering the drug orally, intravenously or subcutaneously. The drug was administered as a single dose followed by a 14-day observation. Oral LD50 values of lactitol were estimated to be between 23 and 30 g/kg in male mice, approximately 30 g/kg in female mice, and more than 30 g/kg in male and female rats. Lethal dose was more than 10 g/kg intravenously and subcutaneously in mice and rats of both sexes. The signs of toxicity in mice and rats observed following the administration of this drug included the following: decreased spontaneous movement [p.o., i.v., s.c.]; diarrhea, oligopnea or prone position, transient decreased body weight [p.o]. There were no treatment-related changes in gross examination. Based on these results, it was found that lactitol had a very low acute toxicity when administered by a single dose method in mice and rats.

Administration, Oral↗
PubMed1994

[Single dose toxicity study of lactitol (NS-4) in dogs].

Male beagle dogs were orally given lactitol, a hepatic encephalopathy drug, in a single dose of 7.5, 15.0 or 30.0 g/kg. Vomiting was seen within 30 minutes after dosing in all treated groups. Diarrhea was observed 3 or 5 hours after dosing in the 15.0 and 30.0 g/kg dose groups. There were no drug related effects on survival, food and water consumption, body weight gain or tissues and organs.

Administration, Oral↗
PubMed1994

[13-week oral toxicity study of lactitol (NS-4) in rats followed by 5-week recovery test].

Twenty male and 20 female Slc : SD rats were orally given lactitol, a hepatic encephalopathy drug, for 13 weeks at doses of 0, 0.625, 2.5 or 10 g/kg/day. A 5 week recovery test was conducted after the discontinuation of the drug treatment. Soft stool and decreased food consumption were seen in the 2.5 and 10 g/kg groups. In the 10 g/kg group, there were diarrhea, soiled fur, abdominal distention, salivation, piloerection, decreased body weight gain and increased water consumption. Urinalysis showed decreased urine volume and K+ excretion in the 10 g/kg group. In this dose group, biochemical examination showed decreased ALP, total cholesterol, triglyceride, glucose, Ca, Na+, Cl- and total protein. In the pathological examination, the cecum weight was increased in all dose groups. In the 2.5 and 10 g/kg groups, cecum distention with mucosal hyperplasia was observed. The adrenal weight was increased in the 10 g/kg group and hypertrophy of zona fasciculata of adrenal gland were seen in the 2.5 and 10 g/kg groups. The thymic weight was decreased in the 10 g/kg group. Ophthalmoscopic and hematologic examinations failed to reveal any drug induced changes. The increased cecum weight in the 0.625 g/kg group was regarded as toxicologically insignificant because of the failure of the association with any clinical or morphological findings. The above mentioned changes were satisfactorily reversible except for those in the cecum. Based on the results obtained, the NOAEL of this study was suggested to be 0.625 g/kg/day.

Administration, Oral↗
PubMed1994

[13-week oral toxicity study of lactitol (NS-4) in dogs followed by 4-week recovery test].

UNLABELLED: 13-week repeated dose toxicity studies were conducted on lactitol, a hepatic encephalopathy drug. In the experiment I, male and female dogs were orally treated with lactitol at doses of 0, 1.0, 2.5 and 6.25 g/kg/day for 13 weeks, followed by 4 weeks recovery period. In the experiment II, male and female dogs were orally treated with lactitol at doses of 0, 0.25, 0.50 and 1.0 g/kg/day for 13 weeks in order to require the no-toxic dose. RESULTS: 1. Soft stool and diarrhea were observed at the 0.50 g/kg group and above, and vomiting was observed at the 1.0 g/kg group and above. Increased water consumption was observed at the 6.25 g/kg group. No deaths occurred at all groups. 2. In urinalysis, increased urine volume was observed at the 6.25 g/kg group. 3. Blood chemistry showed decreased BUN at the 6.25 g/kg group. 4. There were no drug-related changes in body weight, food consumption, ophthalmological examination, electrocardiography, hematology and pathology. 5. At the end of the recovery period, all these changes observed at the end of the administration period were disappeared. Based on these results, it was considered that the no-toxic dose of lactitol is 0.25 g/kg/day.

Administration, Oral↗
PubMed1994

[52-week oral toxicity study of lactitol (NS-4) in rats followed by 9-week recovery test].

Twenty five male and 25 female Slc:SD rats were given orally lactitol, a hepatic encephalopathy drug, for 52 weeks at doses of 0, 0.4, 2 or 10 g/kg/day. A 9 week recovery test was conducted after the discontinuation of the drug treatment. Treatment related death, soft stool, diarrhea, decreased body weight gain and food intake and increased water consumption were observed in the 10 g/kg group. Urinalysis showed increased Ca excretion in the 2 and 10 g/kg groups. In the 10 g/kg group, there were increased Ca++ excretion and urine specific gravity and decreased K+ and Na+ excretion and urine volume. Hematologic examination showed decreased platelet count in the 10 g/kg group. Biochemical examination revealed higher A/G ratio in the 2 and 10 g/kg groups. In the 10 g/kg group, there were lowered level of total cholesterol, triglyceride, phospholipid, Na+, Cl- and total protein. Distention of the cecum with increased organ weight was seen pathologically in the 2 and 10 g/kg groups. In the 10 g/kg group, cecal mucosa was hyperplasic. The adrenal gland was hypertrophic in the zona glomerulosa in the 2 and 10 g/kg groups. In the 10 g/kg group, the adrenal weight was increased. Dilatation of renal tubules was also found in the 10 g/kg group. The above mentioned changes were satisfactorily reversible except for the increased cecum weight in the 10 g/kg group. Based on the results obtained, the NOAEL of this study was suggested to be 0.4 g/kg/day.

Administration, Oral↗
PubMed1994

[52-week oral toxicity study of lactitol (NS-4) in dogs followed by 9-week recovery test].

Five male and 5 female beagle dogs were orally given lactitol, a hepatic encephalopathy drug, for 52 weeks at doses of 0, 0.25, 1.25 or 6.25 g/kg/day. A 9 week recovery test was conducted after the discontinuation of the drug treatment. Soft stool, diarrhea, and vomiting were seen in the 1.25 and 6.25 g/kg groups. In the 6.25 g/kg group, bloody stool and increased water consumption were also observed. Urinalysis showed larger amount of the urine volume in the 6.25 g/kg group. The cecum weight of this group was increased without any morphological changes. There were no drug related effects on survival, body weight gain and food consumption. Electrocardiographic, ophthalmoscopic, hematologic and biochemical examinations failed to show any abnormalities related to the drug treatment. The above mentioned changes were satisfactorily reversible. Based on the results obtained, the NOAEL of this study was suggested to be 0.25 g/kg/day.

Administration, Oral↗
PubMed1994

[Reproductive and developmental toxicity studies of lactitol (NS-4) (1)--Fertility study in rats by oral administration].

A study of fertility and fetal development was conducted in Sprague-Dawley rats. Male rats were given lactitol, a hepatic encephalopathy drug, orally from 63 days before mating to the end of mating period. Female rats were given from 14 days before mating to day 7 of pregnancy. The dose levels for both males and females were 0 (control), 0.7, 2.65 and 10 g/kg. The females were sacrificed on day 20 of pregnancy for examination of their fetuses. The decrease in food consumption in either male or female was observed in the intermediate and high dose groups. The high dose caused soft stool, diarrhea and increase in water consumption in either male or female. Moreover, the high dose caused salivation and suppression of body weight gain in male. In the pathological examination, the enlargement of cecum were observed in male of the intermediate and high dose groups. The increase in cecum weight were observed in male in all lactitol groups, and in female of the high dose group. Lactitol did not affect on copulation and fertility indexes in either male or female rats. Lactitol failed to affect on estrous cycle in female rats, and number of corpora lutea, implantations and preimplantation egg losses. In the fetal examination, lactitol did not affect on the development of live fetuses. The results show that no-effect dose levels of lactitol are less than 0.7 g/kg in male rats and 0.7 g/kg in female rats for general toxicity, and 10 g/kg for reproductive function in parent animals and fetuses.

Administration, Oral↗
PubMed1994

[Reproductive and developmental toxicity studies of lactitol (NS-4) (2)--Teratogenicity study in rats by oral administration].

A teratogenicity study of lactitol, a hepatic encephalopathy drug, was conducted in Sprague-Dawley rats. Female rats were given lactitol orally at dose levels of 0 (control), 0.7, 2.65 and 10 g/kg from day 7 to day 17 of pregnancy. Twenty-two female rats per dose level were sacrificed on day 20 of pregnancy for examination of their fetuses, and thirteen pregnant rats per dose level were allowed to deliver naturally for postnatal examination of their offspring. The high dose of lactitol caused diarrhea or soft stool in pregnant rats. The food consumption of female rats decreased in the intermediate and high dose groups. The water consumption of female rats increased in the high dose group. The drug failed to alter the body weight of female rats. The weights of cecum of dams increased in the intermediate and high dose group. The high dose caused enlargement of cecum in dams. The drug failed to alter the numbers of corpora lutea and implantations, fetal mortality, the number of live fetuses, body weight of live fetus, sex ratio, and external, visceral and skeletal development of fetuses. Lactitol did not affect the delivery of dams, the number of live newborns, birth index, external development, body weight, viability index, weaning index, and sex ratio of weanlings. Nor did lactitol have any adverse effect on the postnatal development of the first (F1) generation offspring, such as differentiation, emotionality, motor ability, learning ability or reproductive performance. Nor did lactitol have any adverse effect on the second (F2) generation offspring. The results show that no-effect dose levels of lactitol are 0.7 g/kg for general toxicity in mother animals, 10 g/kg for reproductive function in mother animals and their offspring.

Abnormalities, Drug-Induced↗
PubMed1994

[Reproductive and developmental toxicity studies of lactitol (NS-4) (3)--Teratogenicity study in rabbits by oral administration].

Lactitol, a hepatic encephalopathy drug, was administered by oral gavage to pregnant New Zealand White rabbits during organogenesis from day 6 to day 18 of gestation inclusive, at dosages of 0, 0.25, 0.75 or 4.5 g/kg/day. On day 29 of gestation, females were killed to allow examination of their uterine contents. There was a slight reduction in food intake and faecal output among females receiving 4.5 g/kg. One female receiving 4.5 g/kg aborted following a prolonged period of weight loss. No adverse effects on litter parameters were recorded that could be attributed to treatment. Foetal morphogenesis was unaffected by treatment with lactitol. The results show that no-effect dose levels of lactitol are 0.75 g/kg in mother rabbits for general toxicity and for reproductive functions, and 4.5 g/kg for their fetuses.

Abnormalities, Drug-Induced↗
PubMed1994

[Reproductive and developmental toxicity studies of lactitol (NS-4) (4)--Perinatal and postnatal study in rats by oral administration].

A perinatal and postnatal study of lactitol, a hepatic encephalopathy drug was conducted in Sprague-Dawley rats. Female rats were given lactitol orally at dose levels of 0 (control), 0.7, 2.65 and 10 g/kg from day 17 of pregnancy to day 21 after delivery. All pregnant rats per level were allowed to deliver naturally for postnatal examination of their offspring. The high dose caused diarrhea or soft stool in dams. The high dose suppressed the body weight of dams during the perinatal period. The food consumption of dams decreased in the intermediate and high dose groups. The water consumption of dams increased in the high dose group. The high dose caused enlargement of cecum and increase of weights of cecum in dams. The drug failed to affect the delivery of dams and gestation index. However, high dose caused prolongation of gestation period. Two dams in the high dose group failed to nurse their all newborns during early lactation. The drug did not affect the number of live newborns, birth index, external appearance, body weight, viability index, weaning index, and sex ratio of weanlings. Nor did lactitol have any adverse effect on the postnatal development of the first (F1) generation offspring, such as differentiation, emotionality, motor ability, learning ability or reproductive performance. Nor did lactitol have any adverse effect on the second (F2) generation offspring. The results show that the no-effect dose levels of lactitol are 0.7 g/kg for general toxicity in mother animals, 2.65 g/kg for reproductive function in mother animals, and 10 g/kg for their offspring.

Administration, Oral↗
PubMed1994

[Mutagenicity studies of lactitol (NS-4)].

Lactitol (NS-4), a hepatic encephalopathy drug, was examined for mutagenicity in the reverse mutation test in bacteria, the chromosome aberration test with cultured mammalian cells, and the micronucleus test in mice. 1. In the reverse mutation test using Salmonella typhimurium (TA1535, TA100, TA1537, and TA98) and Escherichia coli (WP2uvrA), the drug did not significantly increase revertant colonies in any of the test strains with or without metabolic activation system (S-9mix). 2. In the chromosome aberration test with cultured Chinese hamster lung cells (CHL/IU), the drug did not significantly increase aberrant cells in the direct method or in the metabolic activation method. 3. In the micronucleus test with Slc:ddY male mice, the drug did not significantly increase micronucleated polychromatic erythrocytes in the bone marrows. These results suggest that lactitol has no mutagenicity in vitro or in vivo.

Animals↗
PubMed1993

An analysis of sit-to-stand movements.

We analyzed the movements involved in rising from a knee-high chair in 12 healthy men weighing within +/- 10% of standard body weight. A regular series of transition points was observed in the angles of the hip, knee, and ankle joints throughout the sit-to-stand movement, which was classified into six stages. As the duration of sit-to-stand movements increased, the duration of Stage 2 decreased, whereas Stage 3 grew longer. The durations of stages 4 and 5 remained constant. We also calculated the minimum unilateral hip and knee extension torque per weight in kilograms required for natural sit-to-stand movements, or N-Stand (1.7-2.3 seconds), and found that minimum hip extension torque was 0.7Nm and minimum knee extension torque was 0.9Nm. The minimum hip and knee extension torque required for N-Stand corresponds to a mean 27% and 30%, respectively, of the actual maximum hip and knee extension torque.

Adult↗
PubMed1992

[Food poisoning caused by enteroinvasive Escherichia coli (O164:H-)--a case in which the causative agent was identified].

Food poisoning due to "Godofu (Sasayuki tofu)" as a main causative foodstuff which broke out on July 14, 1988. There were 670 out of 918 persons who ingested this food who became ill (incidence 73.0%). The main symptoms were diarrhea (93.4%), fever (77.5%), abdominal pain (64.5%), and vomiting (19.9%). A high degree of fever and watery diarrhea were characteristic of this poisoning. The average latent period was 35 hours with a range of one to 156. The O164:H- strains of enteroinvasive Escherichia coli (EIEC) were detected from 22 of the 32 fecal samples collected from the patients, five of ten samples collected from workers engaged in tofu making, and one sample of left-over Godofu. The virulence of EIEC strains isolated from the patients, workers, and left-over food was confirmed by invasion into HeLa and HEp-2 cells, Sereny test, and ELISA test to detect invasive plasmid-derived protein of the organism (conducted at Tokyo Metropolitan Research Laboratory of Public Health). These EIEC strains were sensitive (less than or equal to 0.19 to 6.25 micrograms/ml) to GM, ABPC, CBPC, CER, CET, NA, PB, MINO, TC and CP as well as KM and OFLX which were used for treatment. However, their susceptibility to FOM varied to some extent (6.25 to 25.0 micrograms/ml) and one strain isolated from a tofu worker was resistant to MINO, TC, FOM and CP (25 to greater than or equal to 100 micrograms/ml). Since investigation revealed that Godofu was left at room temperature about 29 degrees C until ingested, we did a experiment to check the bacterial growth in Godofu under similar conditions at the time of outbreak.(ABSTRACT TRUNCATED AT 250 WORDS)

Escherichia coli↗
PubMed1991

A case of multiloculated, intracranial epidermoid cyst in a beagle dog.

An intracranial epidermoid cyst was identified within the fourth ventricle of a male 10-month-old beagle dog. The cyst, which exhibited a multilocular structure, was lined by a stratified squamous epithelium and filled with desquamated keratin. In the region of the roof of the fourth ventricle, choroid plexus adherent to the cyst wall and secondary compression of the cerebellum were also seen.

Animals↗
PubMed1988

A study of the central cavity in the bovine corpus luteum.

Seven hundred and six bovine corpora lutea in various luteal stages were examined morphologically and endocrinologically to discover whether there is a relationship between the presence of a central cavity in the corpus luteum and infertility in cows. A central cavity was found in 42.1 per cent (80/190) of developing corpora lutea, 33.7 per cent (126/374) of fully developed corpora lutea, 11.1 per cent (7/63) of corpora lutea in regression and in 5.1 per cent (4/79) of corpora lutea in pregnancy. There was no significant difference between the rates of appearance of midcycle follicles in corpora lutea either with or without a central cavity. The proportion of luteal cell type 1 was higher in fully developed corpora lutea with a central cavity than without, but the reverse was found with luteal cell type 2. In fully developed corpora lutea the concentration of progesterone in the luteal tissue was significantly higher in corpora lutea with a central cavity. These results suggest that there are some differences in luteal function between corpora lutea with and without a central cavity, but that the presence of a central cavity in a corpus luteum cannot be described as a pathological condition.

Animals↗