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Biomedical subjects

A Shimada

Publications and source records attributed to A Shimada.

At least 163 records · Page 9Linked to original sources
PubMed1997

Enhanced neuropathogenicity of avian influenza A virus by passages through air sac and brain of chicks.

Three-day-old, specific-pathogen-free (SPF) chicks were inoculated with the strains of influenza A/whistling swan/Shimane/ 499/83 (H5N3) via the air sac route. The strains had been passaged through air sacs or air sacs and brains of SPF chicks. Two experiments were undertaken to examine the pathogenicity of these strains and the development of brain lesions based on time-interval changes. In experiment 1, original strain (4e) showed low pathogenicity with mild respiratory signs and zero mortality. Air sac passaged strains (18a and 24a) of 4e demonstrated mortalities of 50% and 67%, respectively, and inoculated chicks showed hemorrhages and necrotic lesions in major organs. Air sac-brain passaged strain (24a5b) of 4e produced 100% mortality and severe nervous signs. Severe circulatory disturbance with multiple foci of necrosis in major organs including the brain was found in chicks inoculated with 24a5b. The 24a5b was analogous to highly pathogenic avian influenza virus in regard to its pathogenicity to chicks. Hence, low pathogenic influenza virus (4e) gradually aggravated its pathogenicity to highly pathogenic virus (24a5b) by air sac and brain passages. In experiment 2, chicks were inoculated with 24a5b, and the earliest histological lesion was the enlargement of the vascular endothelial cells at 18 hr post-inoculation (PI) followed by necrotizing encephalitis at 24 to 48 hr PI. Immunohistological staining revealed avian influenza virus antigen initially in the vascular endothelial cells and then in the astrocytes, neurons and ependyma.

Air Sacs↗
PubMed1997

Avian influenza A virus induced stunting syndrome-like disease in chicks.

Two-day-old specific-pathogen free chicks were inoculated with type A influenza virus (A/whistling swan/Shimane/499/83 (H5N3) through the air sac. Inoculated chicks showed mild to severe diarrhea and lesions of pancreatitis and atrophy of the pancreas, thymus and bursa of Fabricius. One chick died on each of days 4, 6 and 14 postinoculation (PI). Reduced weight gain was conspicuous from day 22 PI. Positive immunoreaction to the virus antigen was detected in the pancreas, kidneys, liver, lungs and air sacs, and cecal lamina propria. Virus recovery persisted longer in the pancreas. Some of these findings conformed to those of stunting syndrome.

Air Sacs↗
PubMed1997

Molecular cloning of a canine metallothionein cDNA.

A canine metallothionein cDNA obtained from the liver of a cadmium-treated beagle was cloned and sequenced. Asn at position 4 conserved among all mammalian metallothionein-1 and metallothionein-2 is replaced by Asp in the canine metallothionein cDNA clone. Because the acidic amino acid doesn't exist at either position 10 or 11 in the deduced amino acid sequence, it is supposed that this cDNA is derived from canine metallothionein-1 mRNA. Northern blot analysis using the cDNA as a probe revealed the induction of the canine metallothionein mRNA expression in the liver and kidney of a cadmium-treated beagle. Thus, the canine metallothionein cDNA obtained in the present study should provide an useful tool for the molecular investigation of metallothionein in dog.

Amino Acid Sequence↗
PubMed1997

Pathological findings of nude mice inoculated with bovine Neospora.

Nude mice were infested with bovine Neospora by intraperitoneal inoculation of the brain and spinal cord from an aborted bovine fetus due to neosporosis. Inoculated mice showed severe emaciation and tetraplegia at about 2 to 4 months post-inoculation. Histopathologically, polyradiculoneuritis and peripheral neuritis were the major findings, and lesions in the central nervous system were located at periventricular and submeningeal areas of the cerebrum or at the white matter around the roots of radices of the spinal cord. These findings may suggest the protozoa inoculated into the abdominal cavity invaded the spinal cord via the spinal nerve and later reached the brain through the cerebrospinal fluid.

Animals↗
PubMed1997

Diabetes associated with a novel 3264 mitochondrial tRNA(Leu)(UUR) mutation.

OBJECTIVE: To present a novel mitochondrial DNA mutation in a diabetic family RESEARCH DESIGN AND METHODS: The proband was a 64-year-old man. In the family, diabetes was maternally inherited. He had diabetes, cerebellar ataxia, cervical lipoma, hearing loss, olfactory dysfunction, ophthalmoplegia, and facial nerve bilateral palsy. On examination, early insulin secretion was blunted, and the M value on glucose clamp test was low. In muscle, ragged red fibers were not found. T-to-C mutation at position 3264 was detected in the proband (0.5% mutant DNAs in leukocyte and 30% in muscle), but was not detected in 201 normal individuals. RESULTS: Heteroplasmy of mutation, maternal inheritance of diabetes, and symptoms related to mitochondrial dysfunction suggest the pathogenecity of this 3264 mutation. As for diabetes etiology, both impaired insulin secretion and decreased insulin sensitivity seem to be important. In phenotypic characteristics, the combination of cerebellar ataxia and lipoma is a symptom sometimes found in myoclonic epilepsy and ragged red fibers (MERRFs). Ophthamoplegia is a symptom of chronic progressive external ophthalmoplegia (CPEO). These suggest that our proband had phenotypic overlap with MERRF and CPEO. Conversely, facial nerve bilateral palsy is a rare finding. The pictures that focused on his cranial nerves were thus unique, suggesting the heterogeneity of mitochondrial DNA (mtDNA)-related diabetes. CONCLUSIONS: A novel 3264 mitochondrial DNA mutation in diabetes gives new insight to the etiology of mitochondrial diabetes. Its pathogenecity supports the belief that the tRNA(Leu)(UUR) gene is an etiological hot spot of mitochondrial diseases.

DNA, Mitochondrial↗
PubMed1997

99Tcm-MAG3: a sensitive indicator for evaluating perfusion and rejection of renal transplants.

Radionuclide renography has a role in evaluating perfusion of transplanted kidneys. In the course of rejection, cortical perfusion decreases before urinary excretion changes. Based on the facts that 99Tcm-MAG3 has different pharmacokinetics and shows a higher kidney-to-background count ratio than 99Tcm-DTPA, we postulated that 99Tcm-MAG3 was a sensitive and reproducible agent to measure cortical perfusion of transplanted kidneys. To clarify the feasibility of using 99Tcm-MAG3 to measure the cortical perfusion index (CPI), sequential renography was performed using 99Tcm-DTPA and 99Tcm-MAG3 in 14 patients with stable renal transplants, who had changes in serum creatinine concentration of less than 50% between the two studies. The CPI was calculated with 99Tcm-DTPA and 99Tcm-MAG3 and these were then compared and correlated with concurrent serum creatinine concentration. The CPI with 99Tcm-MAG3 was 1.43 times that with 99Tcm-DTPA in patients with changes in serum creatinine concentration equal to or less than 20%, and regression analysis revealed that the difference in CPI was larger in patients with more severely decreased renal perfusion than in patients with normal or mildly decreased renal perfusion. This preliminary study has indicated that the CPI with 99Tcm-MAG3 is a sensitive index for detecting changes in renal function, and thus is a feasible indicator of cortical perfusion when evaluating the rejection of transplanted kidneys.

Adult↗
PubMed1996

Neurochemical analysis of the psychotoxicity of methamphetamine and cocaine by microdialysis in the rat brain.

To examine the neurochemical mechanism underlying the development of psychotoxicity by methamphetamine and cocaine, the levels of dopamine, serotonin and their metabolites were determined by in vivo microdialysis in the brains of freely moving rats. Methamphetamine (0.5 mg/kg, s.c.) or cocaine (10 mg/kg, i.p.) was repeatedly administered for 8 to 21 experiment days, and after confirming the development of sensitization to the stimulating effect of the drugs on spontaneous motor activity, a microdialysis probe was implanted into the nucleus accumbens (N.Acc.) or striatum of the brain of the treated rats. Then, each test drug was readministered to the rats and dopamine and DOPAC or serotonin and 5-HIAA concentrations were determined. In the N.Acc. of untreated control rats, methamphetamine increased dopamine to about 4 times the preadministration value along with a decrease of DOPAC. Methamphetamine also increased serotonin to about twice the preadministration value along with no change in 5-HIAA. Cocaine increased dopamine to about 4 times along with a slight decrease in DOPAC. In the treated rats as compared with the untreated rats, the increasing effect of methamphetamine on dopamine in the N.Acc. was enhanced but that of cocaine was not. Also, the serotonin levels were lower than in the untreated rats and 5-HIAA was unchanged. In the striatum of untreated rats, methamphetamine increased dopamine to about 3 times the preadministration value along with a slight decrease in DOPAC. In the treated rats, the increasing effect of methamphetamine on dopamine in the striatum was enhanced, and the DOPAC level was higher than in the treated rats. The present study suggests that the dopamine level at the N.Acc. does not necessarily reflect the sensitization to spontaneous motor activity, and that enhancement of the motor activity does not seem to be the best model for psychotoxic manifestation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Ser-27, Tyr-10 and Tyr-7 in the alpha-chain of pig stomach H+,K(+)-ATPase as Ca(2+)-dependent phosphorylatable sites by intrinsic and extrinsic protein kinases.

When pig stomach membrane H+,K(+)-ATPase preparations were incubated with [gamma-32P]ATP, Mg2+ and Ca2+, reversible phosphorylation of specific Tyr and Ser residues in the N-terminal alpha-chain of H+,K(+)-ATPase occurred without any detectable phosphorylation in other regions of the alpha-chain. Mild tosylphenylalanyl chloromethyl ketone trypsin treatment followed by reverse-phase column chromatography yielded three radioactive peptide peaks. The first peak contained both Tyr10(32P) and Tyr7(32P) and the second peak contained Tyr10(32P). The third peak contained Ser27(32P) which was also obtained after trypsin treatment of partially purified H+,K(+)-ATPase preparations phosphorylated with protein kinase-C + Ca2+ or protein kinase-A. This is the first demonstration of Ca2(+)-dependent phosphorylation of the alpha-chain of H+,K(+)-ATPase by protein kinases.

Amino Acid Sequence↗
PubMed1996

Cognitive enhancement. New strategies for stimulating cholinergic, glutamatergic, and nitric oxide systems.

The development of treatments for AD is being pursued along many diverse lines. While the ACh hypothesis has generated abundant development efforts, little clinical progress has been achieved to date. Recent efforts aimed at developing more potent, more specific, and safer ChE inhibitors appear to offer greater potential for therapeutic success than achieved to date. Treatments aimed at the NMDA Glu system lag much further behind in their development. Progress in this area must be tempered by the potential for glutamate excitotoxicity mediated through this neurotransmitter system. Development of indirect agonists operating at the glycine and polyamine modulatory sites on the NMDA receptor might offer the safest alternative to applying more direct agonists. While a great degree of interest had been generated by the reports of NO involvement in signal transduction through the NMDA system, this area of research has been complicated by conflicting reports regarding NO involvement in learning and LTP. Moreover, the interaction of drugs acting on NOS with the vascular effects mediated by eNOS has also complicated development of drugs that act specifically on the neural actions of NO. This area will continue to receive extensive research attention; but similar to the development of Glu agonists, attention must be given to the potential neurotoxic effects of overstimulating this system. Perhaps targeting other presynaptic mechanisms that effect glutamate release might be a safer strategy to pursue. Considerable progress has been made over the last two decades in identifying the genetic and neural mechanisms involved in AD. Progress in developing treatments will remain highly correlated with this effort, and with basic research geared to comprehending how memories are formed and why neurons degenerate and regenerate.

Animals↗
PubMed1996

Immune regulation in type 1 diabetes.

The non-obese diabetic (NOD) mouse is an animal model of insulin-dependent diabetes mellitus (IDDM) that shows many of the characteristics of human IDDM. In the NOD model, there exists a discrepancy between the onset of insulitis and diabetes suggesting the potential existence of some form of immune regulation that delays beta cell destruction. Our transfer system using NOD-scid/scid (NOD-scid) mice as recipients of donor NOD cells suggested that immune regulatory cells exist in the periphery of NOD mice, not in the islets. These regulatory cells are considered to be memory CD4+ cells which show a Th2 (or Th zero) type cytokine profile following activation in vitro. The function of the memory CD4+ cells seems to change from protective to pathogenic as the disease progresses. Moreover, cytokine profiles of this CD4+ CD45RBlow (memory) population shifted from a Th2 (or Th zero) to a Th1 type response coincident with the onset of hyperglycaemia. These data suggest that the progression of NOD disease from insulitis to frank hyperglycaemia is under the control of CD4+ CD45RBlow immune 'regulatory' cells.

Animals↗
PubMed1996

Detection of autoantibodies to the pancreatic islet heat shock protein 60 in insulin-dependent diabetes mellitus.

Autoantibodies against heat shock protein (hsp) 60 have been reported to be detected in sera of non-obese diabetic mice, in an experimental model of IDDM. However, there are only a few studies which have examined IDDM patients for antibodies against mammalian hsp60. We produced murine hsp60 derived from pancreatic beta cells which has high homology to human hsp60 and examined antibodies against the hsp60 in IDDM patients using an enzyme-linked immunosorbent assay. We extended the analysis to patients with other immune-mediated diseases and non-insulin-dependent diabetes mellitus (NIDDM). Positive sera for hsp60 antibody were more frequently detected in 13 out of 84 IDDM (15.5%) and 5 out of 25 rheumatoid arthritis patients (20%), when compared to healthy subjects (1/85; 1.2%, P < 0.001 and P < 0.01, respectively). The levels of hsp60 antibodies of IDDM (0.218 +/- 0.227) and rheumatoid arthritis patients (0.259 +/- 0.191) were significantly higher than those of healthy subjects (0.076 +/- 0.131, P < 0.001, P < 0.01, respectively). Patients with slowly progressive IDDM (n = 26), autoimmune thyroid disease (n = 42), or NIDDM (n = 40) had levels of hsp60 antibodies similar to those in healthy subjects. We found no relationship between the levels of hsp60 antibodies and islet cell antibodies (ICA) or antibodies to glutamic acid decarboxylase (GAD65) in IDDM patients. In conclusion, hsp60 antibodies were detected in Japanese IDDM as well as in rheumatoid arthritis patients. Although the positivity was low, the detection of hsp60 antibodies may be helpful for diagnosis of IDDM especially in GAD65 Ab- or JCA-negative Japanese patients.

Autoantibodies↗
PubMed1996

Non-functional pituitary chromophobe adenoma in a calf.

A 5-month-old male calf showed neurological signs, including circling, in-co-ordination, depression, blindness and eventual recumbency. On necropsy, a mass measuring 3.5 x 4.5 x 5 cm was found at the base of the brain, at the level of the pituitary gland. The hypothalamus and optic nerves were compressed by the dorsally expanding mass. Non-functional pituitary chromophobe adenoma was diagnosed from histochemical, immunohistochemical and electron microscopical findings.

Adenoma, Chromophobe↗
PubMed1996

Monoclonal T cells identified in early NOD islet infiltrates.

To examine the hypothesis that a single initiating antigen was recognized by a monoclonal T cell population leading to subsequent inflammatory insulitis in non-obese (NOD) mouse islets, we examined the T cell receptor TCR V beta repertoire of islet-infiltrating T cells in very young (2-week-old) NOD mice. In independent experiments, we repeatedly identified one monoclonal TCR V-beta 8.2 gene product expressed by T lymphocytes infiltrating the islets of NOD mice at 2 weeks of age. The resultant inflammatory response quickly obscures the monoclonal nature of the initiating event. These data suggest that autoimmune diabetes in NOD mice may be initiated by recognition of a single autoantigen.

Age Factors↗
PubMed1996

Age-related changes in the olfactory system of dogs.

Age-related changes in the olfactory system were examined in 22 dogs ranging in age from 10 to 19 years old. Atrophic changes with degeneration were observed in the olfactory epithelium of dogs older than 14 years; the changes were prominent in the dogs over the age of 17 years. Immunohistochemistry using an anti-carnosine antibody, which is a marker for the olfactory cells, demonstrated a decrease in the number of olfactory cells. Electron microscopy also showed a decrease in the number of cilia of olfactory cells and microvilli of supporting cells. Atrophic changes with the features of regeneration were rarely observed in the aged animals. Lipofuscin-like granules in the olfactory epithelium became prominent with age. These age-related changes were similar to those reported in the olfactory epithelium of man and rats. Dystrophic neurites were not detected by a modified Bielschowsky stain or by neurofilament, synaptophysin and tau immunohistochemistry in the olfactory mucosa. There was no beta-amyloid- and ubiquitin-immunostaining in the olfactory mucosa. Senile brain changes, including cerebrovascular amyloidosis, age-related astrocytic gliosis and ubiquitin deposits were found in the olfactory bulb, although neurofibrillary tangles and senile plaques were not detected either by a modified Bielschowsky stain or by beta-amyloid immunohistochemistry. These results indicate that dog may be a useful animal model to study the age-related changes in the olfactory system in man.

Age Factors↗
PubMed1996

Aneurysmal bone cyst in a dog.

A one-year-old male mongrel dog was referred to the Veterinary Clinic with a several-week history of lameness and pain of the right front leg. Radiological examination of the right humerus revealed a cystic lesion at the distal end of the bone; the lesion was nodular in a gross appearance. Histologically, the nodular lesion consisted of large areas of haemorrhage and thick fibrous trabeculae mixed with a variably dilated cavernous structure of blood vessels attributed to haemangiosarcoma. Based on these findings, aneurysmal bone cyst secondary to the tumour was diagnosed.

Animals↗