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Biomedical subjects

F Furukawa

Publications and source records attributed to F Furukawa.

At least 361 records · Page 20Linked to original sources
PubMed1980

An ultrastructural study of precancerous and cancerous lesions of the pancreas in Syrian golden hamsters induced by N-nitrosobis(2-oxopropyl)amine.

Transmission electron microscopic studies of precancerous and cancerous lesions in the pancreas of hamsters induced by N-nitrosobis(2-oxopropyl)amine (BOP) are presented. BOP was injected subcutaneously once weekly for 10 weeks and hamsters were sacrificed every 5 weeks after initiation of the experiment. The ultrastructural findings indicated that serial changes occurred in the epithelium of the pancreatic duct. The epithelial cells became cuboidal and showed increased secretions at 5 weeks. Probably precancerous cells with prominent nucleoli and irregular rough endoplasmic reticulum were found in the main duct at 10 weeks. At 15 weeks, pancreatic tumors forming a duct arrangement were seen, in good accord with the histological appearance. Well differentiated adenocarcinoma cells showing a tubular pattern had oval nuclei with granular chromatin. Poorly developed rough endoplasmic reticulum was irregularly distributed throughout the cytoplasm and the cell surface was covered with microvilli. Poorly differentiated adenocarcinoma showed poor gland formation and had distorted nuclei with prominent nucleoli. These cells were loosely joined. Mitochondria and rough endoplasmic reticulum were poorly developed, and the tumor cells were devoid of secretory granules. The most characteristic and common change of the precancerous and cancerous lesions in this experiment was the appearance of numerous microvilli on the luminal surface and loss of cytodifferentiation. These findings were obviously different from those of normal epithelial cells or those seen in inflammation. The findings in this study confirm that the pancreatic carcinoma induced by N-nitrosobis(2-oxopropyl)amine in Syrian hamsters is of duct cell origin. No evidence of acinar cells was obtained.

Adenocarcinoma↗
PubMed1977

[A case of hypertensive intracerebral hemorrhage associated with cerebral arteriovenous malformation and aneurysm (author's transl)].

A 45-year-old man suddenly developed right hemiparesis and aphasia during work and lost conciousness next day, when he was admitted to us. Lumbar puncture showed bloody C.S.F. with the initial pressure of 220 mm H2O. Physical examination revealed hypertension and arteriosclerosis. Cerebral angiogram revealed an arteriovenous malformation in the left frontoparietal-parasagittal region and a saccular aneurysm at the left internal carotid-posterior communicating artery junction. In addition, the existence of putaminal hematoma was suspected on account of the displacement of the left anterior cerebral artery and the left lenticulostriate arteries. On the fourth day after admission his consciousness returned and the right hemiparesis gradually improved. One month later the disappearance of the displacement of the anterior cerebral artery was demonstrated by cerebral angiogram. A frontoparietal craniotomy was done and no hematoma was found around the arteriovenous malformation and the basis of the aneurysm did not adhere to the temporal lobe. Taking these findings into consideration, it is presumed that the hematoma in putaminal region was due to neither arteriovenous malformation nor aneurysm but was a hypertensive intracerebral hemorrhage.

Cerebral Hemorrhage↗
PubMed1977

[The relation of intracranial air to C.S.F. rhinorrhoea in the traumatic pneumocephalus (intracerebral and ventricular) (author's transl)].

The relation of intracranial air to C.S.F. rhinorrhoea in our four cases, one intracerebral and the others intracerebral-ventricular pneumocephalus, were investigated on their clinical course, operative findings and RI-cisternographic findings. In the occurrence of the pneumocephalus, it seemed important for the damaged brain to herniate into the defect of the bone and dura matar. Clinically in the stage of an intracerebral pneumocephalus, the C.S.F. rhinorrhoea was not recognized as a rule. And next stage, the sudden effusions of C.S.F. appeared when the intracerebral pneumocephalus developed to the intracerebral-ventricular pneumocephalus.

Adolescent↗
PubMed1975

[RI-cisternography of traumatic pneumocephalus (author's transl)].

A radionuclide, when injected intrathecally, normally does not enter into the ventricle system. In our three cases of intra cerebral-ventricular pneumocephalus the radionuclide entered into the ventricle and concentrated in the cyst. Such an abnormal movement of the radionuclide was generally caused by the obstruction of subarachnoid space and the increased C.S.F. absorption in the enlarged ventricle. Under consideration of the pre-and post-operative cisternograms of our three cases we examined the principal factor which brought on the abnormal movement of a radionuclide. Each principal factor was the excessive C.S.F. rhinorrohea in the first case, the increased C.S.F. absorption in the enlarged ventricle and the cyst in the third case. An analysis of our three cases shows that the accumulation of radionuclide into the ventricle system is not necessarily due to the obstruction of subarachnoid space, but also due to more C.S.F. absorption in the ventricle system than that in the subarachnoid space.

Adolescent↗
PubMedDate not supplied

Hyporesponsiveness of peripheral blood lymphocytes to streptococcal superantigens in patients with guttate psoriasis: evidence for systemic stimulation of T cells with superantigens released from focally infecting Streptococcus pyogenes.

Throat infection with Streptococcus pyogenes is the most important trigger for acute guttate psoriasis. We examined the in vitro responses of peripheral blood mononuclear cells (PBMC) to streptococcal superantigens, SPEA and SPEC, and staphylococcal superantigens, SEB and TSST-1, in patients with guttate psoriasis, in patients with chronic plaque psoriasis, and in healthy subjects. PBMC from patients with guttate psoriasis responded poorly to SPEA and SPEC at concentrations of 0.1 and 1 ng/ml as compared with those from patients with plaque psoriasis, but showed high responses to SEB and TSST-1. The hyporesponsiveness recovered after improvement of the skin eruption. There was no significant difference between guttate and chronic types of psoriasis in the percentage of circulating T-cell receptor BV2 or BV8-bearing T cells, responsive to streptococcal superantigens, indicating that T-cell clonal anergy was a mechanism underlying the hyporesponsiveness. Our results suggest that superantigens released from focally infecting S. pyogenes induce a transient activation of relevant T cells, leading to the development of skin eruption and, subsequently, temporary T-cell anergy to these toxins.

Adult↗
PubMedDate not supplied

Promotional effects of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) on N-nitrosobis(2-oxopropyl)amine (BOP)-initiated carcinogenesis in hamsters.

The effects of administration of low doses of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a tobacco-specific nitrosamine, were investigated in hamsters treated with N-nitrosobis(2-oxopropyl)amine (BOP). Female Syrian golden hamsters were given a single sc injection of BOP at a dose of 10 mg/kg and then administered 2 or 5 ppm NNAL in their drinking water for 52 wk. Additional groups of animals received the BOP injection alone, or only the 2 or 5 ppm NNAL treatments as BOP-negative controls. At wk 53 of the experiment, all surviving animals were killed and the development of proliferative lesions was assessed histopathologically. The total incidence of combined carcinomatous and dysplastic lesions of the exocrine pancreas was significantly higher (P < 0.05) in the BOP/NNAL 5 ppm group than in the BOP alone group, although there was no statistically significant influence of NNAL on the development of either pancreatic adenocarcinomas or dysplastic lesions viewed singly. The treatments with NNAL alone did not induce any proliferative lesions of the exocrine pancreas. No significant intergroup differences were found in either incidence or multiplicity of islet cell proliferative lesions. Immunohistochemical examination of islet cell proliferative lesions (hyperplasias and adenomas) found in the BOP-treated animals showed no significant differences in pancreatic hormone production between NNAL-treated and -untreated groups. The NNAL treatment did not exert any influence on lung, liver or kidney tumorigenesis. Thus, the results suggest that NNAL enhances BOP-induced exocrine but not endocrine pancreatic tumorigenesis in hamsters when given in the post-initiation phase.

Animals↗
PubMedDate not supplied

Induction of pancreatic islet cell tumors in rats by repeated intravenous administration of 4-hydroxyaminoquinoline 1-oxide.

The inducibility of pancreatic islet cell tumors by administration of 4-hydroxyaminoquinoline 1-oxide (4HAQO) was investigated in male 6-week-old Sprague-Dawley rats. Rats were given 4HAQO intravenously at a weekly dose of 5 mg/kg 4 times (group 1) or a single dose of 10 mg/kg (group 2). Control rats received the vehicle alone (group 3). Fifty-six weeks after the first 4HAQO administration, all surviving animals were killed and the pancreas was examined histopathologically, immunohistochemically and ultrastructurally. The incidences and multiplicities of islet cell tumors in groups 1, 2, and 3 were 52.3% (p < 0.05 vs group 2, p < 0.01 vs group 3), 19.2% and 0%, and 0.70/animal (p < 0.05 vs group 2, p < 0.01 vs group 3), 0.23 and 0, respectively. Islet cell carcinomas were induced only in group 1, accounting for 6/44 (26%) tumors. Islet cell hyperplasias were found in 61.4% (p < 0.05 vs group 3), 42.3% and 10.0% of groups 1, 2, and 3, with multiplicities of 0.95 (p < 0.05 vs groups 2 and 3), 0.54 and 0.20, respectively. As compared with normal islets from control subjects, islet cell tumors showed an increase in the number of insulin positive cells associated with cytological features indicative of enhanced insulin synthesis and secretion, and a decrease in the number of glucagon positive cells without ultrastructural signs of modified secretory activity. Thus our results indicate that repeated intravenous administration of 4HAQO to rats is useful for the induction of islet cell tumors at high incidence.

4-Hydroxyaminoquinoline-1-oxide↗
PubMedDate not supplied

Dual effects of prolonged ACTH stimulation on 4-hydroxyaminoquinoline 1-oxide-induced adrenocortical lesions in rats.

The effects of a long-acting synthetic ACTH on 4-hydroxyaminoquinoline 1-oxide (4HAQO)-induced adrenocortical lesions were investigated in female rats. A total of 140 6-week-old rats were divided into 4 equal groups, given a single s.c. injection of 7 mg/kg 4HAQO or vehicle, followed by repeated sc administration of the synthetic ACTH or no further treatment. Subgroups of 10 rats in each group were sequentially sacrificed at weeks 20, 30, and 40. Adenomas and adenomatous nodules developed in the adrenal cortex of animals receiving 4HAQO and the chronic ACTH stimulation. Both lesions were located in the deeper zones of the adrenal cortex adjacent to the medulla and were composed of large-sized, clear-type cells. From week 20, middle zone, cortical cystic degeneration, which mimics the age-associated degenerative change named adrenal peliosis, was frequently observed in the adrenal glands of animals treated with 4HAQO alone. Its development was inhibited by ACTH. In the control animals, peliotic changes occurred at low incidence and only at the termination of experiment. These results indicate that long-term stimulation of ACTH promotes the development of adrenocortical tumors but suppresses the occurrence of adrenal peliosis in rats treated with 4HAQO.

4-Hydroxyaminoquinoline-1-oxide↗
PubMedDate not supplied

Rothmund-Thomson syndrome with herpes encephalitis.

A 4-year-old Japanese boy with Rothmund-Thomson syndrome suffered from severe herpes encephalitis at 5 months of age. The serum level of immunoglobulin G was low and the responsiveness of peripheral blood mononuclear cells to bacterial superantigens was poor. It was suggested that these immunological abnormalities, possibly associated with Rothmund-Thomson syndrome, led to severe infection with herpes simplex virus in our patient.

Child, Preschool↗
PubMedDate not supplied

Psoriasis guttate acuta triggered by varicella zoster virus infection.

A 23-year-old man had small desquamative erythematous lesions, round or oval in shape, spread over his entire body, and diagnosed as psoriasis guttate acuta because of clinical and pathological findings. Three weeks before the lesions had started, he was diagnosed as having varicella by his family physician. The psoriatic lesions appeared at the same sites where previously lesions of varicella had appeared. Therefore, VZV infection was regarded as a trigger in this case. We speculate that genetic factors and the change of skin condition are basically involved in the pathogenesis of psoriasis guttate. In addition, one more factor as a trigger is needed to cause the lesions of psoriasis. VZV infection might change the skin condition and induce subsequent immunological disregulation.

Acute Disease↗
PubMedDate not supplied

Suppressive effects of Adenophora triphylla extracts on in vitro tumor cell growth and in vivo gastric epithelial proliferation.

Adenophora triphylla (AT), an oriental medicinal plant, was extracted using water and several organic solvents and each fraction was assayed for its tumoricidal effects on human Jurkat T cells with 3-(4,5-dimethylthiazolyl)-2,5-diphenyltetrazolium bromide (MTT). The influence on induction of apoptosis and G1 arrest was also examined. The ethyl acetate fraction showed the most pronounced inhibitory effects on proliferation of Jurkat T cells. Apoptosis was induced in line with up-regulation of FasL, tyrosine phosphorylation and c-fos mRNA levels. Arrest in G1 of the cell cycle was observed in A2780 cells with a wild type p53 gene but not HT-29 cells with a mutant p53 gene. Modifying effects of AT on cell turnover and glutathione(GSH) levels in vivo were also investigated in the stomach of rats given 150 mg/kg of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) by gavage and then fed a diet supplemented with 5% or 1% pulverized AT and 0.5% or 0.2% ethylacetate-extracted AT for 42 hours. The 5% AT and both of the ethylacetate fractions caused significant reduction in proliferating cell nuclear antigen (PCNA)-labeling in the glandular stomach epithelium as compared with the value for the MNNG alone group. In addition, the treatments significantly increased the gastric GSH levels. These results suggest that AT could be a chemopreventive agent against gastric cancer.

Animals↗
PubMedDate not supplied

Inhibitory effects of protocatechuic acid on the post-initiation phase of hamster pancreatic carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine.

The chemopreventive effects of protocatechuic acid (PCA) were investigated during the post-initiation stage of the N-nitrosobis(2-oxopropyl)amine (BOP)-initiated hamster pancreatic tumorigenesis model. Female 5-week-old hamsters were divided into 6 groups. Animals in groups 1-3, each consisting of 30 hamsters, were given two s.c. injections of 20 mg/kg body weight of BOP with a one week interval as an initiation treatment. After the BOP injection, hamsters in groups 1 and 2 were respectively fed diet supplemented with 1000 or 500 ppm of PCA for 49 weeks. The animals in group 3 were treated with BOP alone. The animals in groups 4-6, each consisting of 10 hamsters, were given 1000 or 500 ppm PCA, or basal diet alone without prior BOP injection. At the termination of experimental week 52, the incidences and multiplicities of neoplastic lesions in the pancreas were comparable among the BOP-treated groups. However, the incidence of pancreatic tumors larger than 3 cm was significantly lower in the PCA-treated high dose groups than in the control group (p < 0.05). Moreover the incidence of advanced pancreatic cancers which had directly invaded adjacent tissues such as the diaphragm, spleen and stomach was reduced by the PCA treatments, being significantly (p < 0.01) lower in group 2 than in group 3. Our results thus indicated that PCA can inhibit the late post-initiation or progression phase of BOP-induced pancreatic carcinogenesis in hamsters.

Adenocarcinoma↗