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Biomedical subjects

Y Ohyagi

Publications and source records attributed to Y Ohyagi.

47 records · Page 3Linked to original sources

Detection and quantitation of cellularly derived amyloid beta peptides by immunoprecipitation-HPLC-MS.

A quantitative method for detection of amyloid beta peptides using immunoprecipitation-HPLC-mass spectrometry (IP-LC-MS) is described. Comparison of IP-LC-MS with sandwich ELISA revealed comparable results in the analysis of A beta 1-40 and A beta 1-42 derived from fetal guinea pig cell media and cell lysates. The use of IP-LC-MS not only allows a quantitative method for A beta 1-40 and A beta 1-42 peptides present in Alzheimer's disease (AD), but allows detection of other A beta peptide species that may also play a role in the onset of AD in humans.

Amyloid beta-Peptides↗

[An adult case of Reye syndrome induced by diclofenac sodium, and recovered by plasma exchange].

Reye syndrome (RS) is an acute encephalopathy in childhood, and is very rare in adulthood. Here we report a 21-year-old woman with RS. Because of her dysmenorrhea, she took 3 tablets of diclofenac sodium (25 mg) per day in 3 divided doses for two days. Two days after the last intake of the medicine, she developed high fever, nausea, vomiting, and disturbance of consciousness with delirium, i.e., acute encephalopathy. She did not have seizure, hemiplegia, or other focal neurological manifestations. The serum GOT level was normal at onset, but in 12 hours dramatically increased up to 8,632 IU/L. The serum bilirubin level was normal. The cerebrospinal fluid revealed normal cell count, and protein. Although the liver biopsy was not performed because of thrombocytopenia, we diagnosed her as an adult case of RS according to the clinical criteria of the Center for Disease Control. In addition to treatment for the brain edema, plasma exchange was performed once treat the encephalopathy at the onset. The next day, her consciousness level and serum GOT level markedly improved. She completely recovered from acute encephalopathy in a week after her admission. In conclusion, diclofenac sodium, as well as aspirin, should be considered as a possible causal agent for RS, and early plasma exchange may be beneficial.

Adult↗

Hemoglobin as a novel protein developmentally regulated in neurons.

We have attempted to identify some novel genes which were found to be more highly expressed in the embryonic brain than in the adult brain. Consequently, one of these clones was identified as alpha-globin cDNA. Actually, alpha-globin mRNA was detected in the neurons. In addition, beta-globin mRNA was detected in the neurons as well. Both globin mRNAs were developmentally regulated in the same pattern. Subsequently, further examinations with antiserum to hemoglobin revealed the presence of hemoglobin in the neurons. Hemoglobin has, up to now, been known to be an important O2 transporter protein in erythrocytes. Moreover, hemoglobin is now considered to be also a very dangerous protein generating the toxic hydroxyl radical (.OH). We herein show the presence of hemoglobin and its regulation in the central nervous system, which may indicate the presence of a useful function regulating O2 homeostasis and a potential oxidative toxicity for neuronal cells.

Animals↗

Effect of growth factors and cytokines on expression of amyloid beta protein precursor mRNAs in cultured neural cells.

We analyzed the effect of several growth factors and cytokines on the expression of amyloid beta protein precursor (APP) mRNAs in cultured mouse neuronal and glial cells. In neuronal cultures from embryonic day-15 brain. Northern blotting revealed that APP mRNAs increased by 1.3- to 2.6-fold when treated with nerve growth factor, basic fibroblast growth factor, interleukin 1, interleukin 2, interleukin 3, interleukin 6 or granulocyte-macrophage colony-stimulating factor but not with tumor necrosis factor alpha. An S1 nuclease protection assay revealed that the enhanced APP mRNA in neuronal cultures was exclusively APP695 mRNA. On the other hand, astrocyte-enriched cultures prepared from postnatal day-2 brain did not show any significant alteration among these factors. We conclude that certain growth factors and cytokines could enhance APP 695 mRNA expression in neurons in vitro.

Amyloid beta-Protein Precursor↗

Cerebral cortical amyloid protein precursor mRNA expression is similar in Alzheimer's disease and other neurodegenerative diseases.

The expression of 3 beta-amyloid protein precursor (APP) mRNAs (695, 751, and 770) in the cerebral cortex in Alzheimer's disease and other neurodegenerative diseases was analyzed by the S1 nuclease protection assay. We found no significant Alzheimer's disease-specific alteration of APP mRNA expression when compared to the other neurological diseases as controls. Since the expression of this mRNA was not correlated with amyloid deposition, it is possible that gliosis/neuronal loss may secondarily alter APP mRNA expression. However, the current study revealed no significant correlation between them.

Adult↗

Developmental and differential expression of beta amyloid protein precursor mRNAs in mouse brain.

S1 nuclease analysis was used to determine the levels and patterns of three beta amyloid protein precursor (BPP) mRNAs in mouse developmental brain and in primary neuronal and glial cultures. BPP695 mRNA lacking the Kunitz proteinase inhibitor (KPI) domain was detected exclusively in neuronal cultures and increased considerably in late embryonic and early postnatal periods. On the other hand, BPP751 and 770 mRNAs with KPI domain were detected predominantly in astrocyte- and microglia-enriched cultures and increased slightly only in embryonic stages. These results suggest that the product of each BPP mRNA may play a different role in the brain.

Alzheimer Disease↗

[An adult case of primary antiphospholipid syndrome presenting recurrent anterior spinal artery syndrome].

A 50-year-old man suffered from sudden onset of paraplegia, sensory impairment of the lower extremities and difficulty urinating. These symptoms spontaneously resolved, and he was able to walk again within 10 days. After 2 months' observation, he experienced a relapse with identical symptoms. Neurological examination revealed paraplegia, hypalgesia and hypesthesia in the lower extremities and difficulty urinating. Position and vibration senses were preserved in the extremities. Knee jerk was mildly hyperreflexic on the left, but pathological reflexes were not present. He had such risk factors for arteriosclerosis as diabetes mellitus, hypercholesterolemia and smoking. Although antinuclear antibodies were negative, he repeatedly showed high anticardiolipin antibody titers. MRI showed a T2-hyperintense lesion of the anterior portion of the spinal cord at Th9-10 levels. Neither arteriovenous malformation nor fistula was found on MR angiography. Abdominal CT revealed no abnormality in the descending aorta. Cervical ultrasonogram showed arterioslerotic lesions on the right common carotid artery. This is the first report of recurrent spinal cord infarction in an adult patient associated with primary antiphospholipid syndrome. Recurrence of the spinal cord infarction in this case may have been facilitated by the presence of risk factors for arteriosclerosis.

Anterior Spinal Artery Syndrome↗

[A variant form of septo-optic-pituitary dysplasia (SOPD) complicated with acute optic neuritis].

We herein report a case of a variant form of septo-optic-pituitary dysplasia (SOPD). A 40-year-old man was admitted due to sudden occurrence of left blurred vision and lasting polyuria. He showed short statue of height of 144 cm and the neurological examination revealed hypesthesia of the left trigeminal nerve and temporal pallor in the left fundus oculi. Brain MR imaging demonstrated agenesis of the septum pellucidum and hypoplasia of the corpus callosum with subcortical spotty lesions, but optic nerve hypoplasia was not detected. The left eye showed a prolonged P100 latency of pattern reversal VEPs. He was diagnosed as having hypopituitarism since growth hormone-releasing factor did not stimulate growth hormone secretion and restriction of water-intake did not induce secretion of antidiuretic hormone. Thus we regarded this case as a variant form of SOPD. The mutation of HESX 1 gene, however, was not detected in the case. P100 of the left eye showed a reduction in latency four months after discharge. This case was considered to be a variant form of SOPD complicated by acute optic neuritis.

Acute Disease↗