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Biomedical subjects

S Inui

Publications and source records attributed to S Inui.

At least 109 records · Page 6Linked to original sources
PubMed1981

Recrudescence of infectious bovine rhinotracheitis virus and associated neural changes in calves treated with dexamethasone.

Reactivation of infection bovine rhinotracheitis (IBR) virus in calves administered dexamethasone (DM) was studied in 2 experiments. At 2, 3, 5, 15, or 30 months after inoculation of the Los Angeles strain of IBR virus, IV injections of DM were given for 5 consecutive days to induce a recurrent infection (experiment 1). Three months after the 1st treatment, a 2nd recurrent infection was induced, using DM with the same doses as used in experiment 1. The virus was excreted from nasal secretions from the 4th to the 10th day after initial treatment with DM, and from the 6th to the 9th day after the 2nd treatment. On pathologic examination, trigeminal ganglionitis, consisting of many proliferated microglia and inflammatory cells, was observed in all DM-treated calves. Moreover, degeneration of the ganglion cells and neuronophagia were prominent features in the calves after the 2nd recurrent infection. These observations indicated that the trigeminal ganglion may be one of the latent sites of IBR virus in calves after intranasal infection and that calves can develop a recrudescent infection after DM treatment several times during their lifetime.

Animals↗
PubMed1980

Neural changes in vaccinated calves challenge exposed with virulent infectious bovine rhinotracheitis virus.

Recurrent infection in calves vaccinated with infectious bovine rhinotracheitis-(IBR) modified live virus was induced by dexamethasone (DM) treatment given 49 days after challenge exposure with virulent IBR virus. Nonchallenge-exposed IM and intranasally vaccinated calves did not excrete the virus after DM treatment; however, IM and intranasally vaccinated and subsequently challenge-exposed calves excreted the challenge-exposure virus into the nasal secretions 5 to 11 days and 6 to 10 days after the DM treatment, respectively. The calves were killed 15 to 18 days (experiment 1) and 14 days (experiment 2) and DM treatment was started and then were examined by histopathologic and fluorescent antibody techniques. All DM-treated calves that were inoculated with the vaccinal virus and challenge exposed with the virulent virus developed nonsuppurative trigeminal ganglionitis and encephalitis. On the contrary, the DM-treated nonchallenge-exposed vaccinated calves did not have lesions in the peripheral nervous system and CNS. Infectious bovine rhinotracheitis virus antigens were not observed in tissues of any of the calves examined (experiments 1 and 2) by fluorescent antibody techniques. These observations indicated that the modified live IBR virus neither produced lesions nor induced latent infection and that modified live IBR virus vaccination did not protect the calves against the establishment of a latent infection after their exposure to large doses of the virulent IBR virus.

Administration, Intranasal↗
PubMed1979

[Carcinogenic effect of the 3-di-(hydroxymethyl-)amino-6-(5-nitro-2-furylethenyl-)1,2,4-triazines in Panfuran-S on mice].

The carcinogenic activity of Panfuran-S containing 3-di-(hydroxymethyl-)amino-6-(5-nitro-2-furylethenyl-)1,2,4-triazine (DHNT) orally administered to mice for 35 weeks was studied. DHNT produced malignant tumors of the forestomach in the highest incidence and also, in decreasing order of frequency, of the duodenum and/or jejunum, esophagus and urinary bladder. Forestomach squamous cell carcinomas were produced dose-dependently in mice receiving more than 350 ppm DHNT and rose to 100% in mice receiving 3,500 ppm. The incidence of duodenal and/or jejunal adenocarcinomas were 8 of 28 mice (29%) receiving 1,750 ppm and 10 of 17 mice (59%) receiving 3,500 ppm. The incidence of esophageal squamous cell carcinoma was 3 of 11 mice (11%) receiving 1,750 ppm and that of urinary bladder transitional cell carcinoma was 2 of 28 mice (7%) receiving 1,750 ppm and 1 of 17 mice (6%) receiving 3,500 ppm DHNT.

Animals↗
PubMed1979

Neural changes in recurrent genital infection of infectious bovine rhinotracheitis virus in calves treated with dexamethasone.

Recurrent genital infection with infectious bovine rhinotracheitis (IBR) virus was induced in calves by dexamethasone (DM) treatment 3 months after primary infection. The virus was first recovered from vaginal secretions on the 3rd day after the initiation of DM treatment; however, the virus was not recovered at all from nasal secretions or from the cerebrospinal fluid of the DM-treated calves. The significant neural changes in all recurrent infected calves were nonsuppurative poliomyelitis in the lumbosacral spinal cords and their ganglia, and they were more severe in the sacrospinal cords than in other parts of the spinal cord. The virus antigen was detected in the sacrospinal ganglia and peripheral nerve fibres in the submucosa of the vagina by the fluorescent antibody technique on the 4th and 6th days after the start of DM treatment. These observations indicated that nonsuppurative poliomyelitis may be a characteristic lesion in recurrent genital infection of IBR virus. The sacrospinal cords and ganglia are considered as latent sites of IBR virus.

Animals↗
PubMed1979

Congenital cerebellar hypoplasia in newborn calves.

A sporadic outbreak of congential cerebellar ataxia (CCA) was seen in calves. The abnormality of this disorder of the central nervous system characteristic was cerebellar hypoplasia, which was observed in eight calves. The cerebellum was almost completely absent in some of these calves and approximately one-fifth of the normal size in some others. Six of the eight calves were also affected with hydrocephaly. The significant changes of the cerebellum were complete or partial destruction of the cortex, deficiency of granules and/or Purkinje cells, clumping of the remaining granule cells, and an irregular cavity formation in the terminal portion of the folium. The clinicopathological changes of CCA quite closely resembled those of the bovine viral diarrhea-mucosal disease virus infection.

Animals↗
PubMed1978

Production of pancreatic acinar cell carcinoma by combined administration of 4-hydroxyaminoquinoline 1-oxide and azaserine in partial pancreatectomized rats.

The effect of azaserine on the pancreatic tumorigenesis of 4-hydroxyaminoquinoline 1-oxide (4-HAQO) after partial pancreatectomy in rats was studied. Pancreatic acinar cell carcinomas were produced in 7 out of 10 rats (70%), which received 7 mg/kg body wt. 4-HAQO 3 days after partial pancreatectomy, followed by 10 weekly injections of 30 mg/kg body wt. azaserine. Partial pancreatectomy enhanced the carcinogenesis of 4-HAQO, which was further promoted by azaserine.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1978

Conversion of a poorly differentiated human adenocarcinoma to ascites form with invasion and metastasis in nude mice.

Cells (1 X 10(7)/0.5 ml) from a Borrmann type III poorly differentiated adenocarcinoma of the human stomach were injected ip into nude mice. The injection resulted in ascites carcinoma with invasion (carcinomatous peritonitis) and liver metastasis. The inoculum was obtained from subcutaneous tumors at passage 9 in nude mice that had received serial transplants from the patient with Borrmann type III poorly differentiated adenocarcinoma of the stomach. Serial transfers of 1.5 X 10(6) dispersed cancer cells/0.5 ml into the peritoneal cavity of nude mice converted this adenocarcinoma to an ascites form. Hemorrhagic ascites accumulated within 3 weeks at the first passage and 4-6 weeks in serial passages. Carcinomas peritonitis occurred consistently and was observed in the diaphragm, mesenteries, omentum, and pancreas; metastases were seen in the liver and spleen. Subsequently, iv injection of ascites at passage 3 (6 X 10(5) cells/0.2 ml) into nude mice produced metastatic lesions in the lung and the heart. The histology of the invasive and metastatic lesions in the nude mice was similar to that of the original tumor in the patient with stomach carcinoma.

Adenocarcinoma↗