Search PubMed⌕ Search

Biomedical subjects

K Hamaguchi

Publications and source records attributed to K Hamaguchi.

At least 37 records · Page 2Linked to original sources
PubMed1996

Monoclonal antibodies specific to the integral membrane protein P0 of bovine peripheral nerve myelin.

Two monoclonal antibodies (mAbs), 58A and 46E, were generated against the major protein P0 of bovine peripheral nervous system myelin (PNSM). The reactivities of the mAbs were assessed by enzyme-linked immunosorbent assay (ELISA), Western blot, and immunohistochemistry. Both mAbs, 58A and 46E, reacted to PNSM of bovine, human, rat and rabbit, but not to chicken PNSM or the brains of rat and rabbit. In the Western blot, these mAbs showed specific binding to bovine P0 as well as deglycosylated P0, but not to myelin-associated glycoprotein (MAG) of bovine spinal cord. The analyses of the lysylendopeptidase-digested peptides of bovine P0 revealed that the epitopes for the mAbs 58A and 46E were located on the amino acid residues 68-79 and 210-216, respectively. Since the mAbs 58A and 46E recognize the extracellular domain and the cytoplasmic domain of P0, respectively, they could be useful for studies on P0's role in myelin formation, its adhesive properties, and functions of the N-terminal extracellular and C-terminal cytoplasmic domains of the protein.

Amino Acid Sequence↗
PubMed1996

Different contribution of HLA-DR and -DQ genes in susceptibility and resistance to insulin-dependent diabetes mellitus (IDDM).

Previous studies have indicated that certain alleles of HLA-DR and -DQ genes were strongly associated with susceptibility and resistance to insulin-dependent diabetes mellitus (IDDM), and the role of DQ molecule in IDDM has been suggested. To further clarify the association of DQ alleles with IDDM, we determined the nucleotide sequences of full-length cDNA from 13 DQA1 alleles and 14 DQB1 alleles. The sequencing analysis revealed sequence polymorphisms outside the hypervariable region of DQ genes. We then analyzed the DQA1 and DQB1 polymorphisms along with that of DRB genes in 86 B-lymphoblastoid cell lines (B-LCLs) from various ethnic groups and in healthy unrelated Japanese and Norwegian individuals. The allelic and haplotypic distributions in each population revealed the characteristic haplotypic formation in the HLA class II region. HLA genes in 139 Japanese and 100 Norwegian IDDM patients were analyzed. DQB1*0301 was negatively associated with IDDM in both ethnic groups, irrespective of associated DRB1 and DQA1 alleles. In DQB1*0302 positive populations, which represented a positive association with IDDM in both ethnic groups, DRB1*0401, *0404, *0802 haplotypes increased in the patients, whereas DRB1*0406 haplotype decreased. Considering about the hierarchy in DRB1 alleles with IDDM susceptibility (DRB1*0401>*0404>*0403 in Norwegian and DRB1*0802>*0403>*0406 in Japanese), the genetic predisposition to IDDM is suggested to be defined by the combination of DR-associated susceptibility and DQ-associated susceptibility and by the DQ-associated resistance which is a dominant genetic trait.

Alleles↗
PubMed1996

PDX-1 induces insulin and glucokinase gene expressions in alphaTC1 clone 6 cells in the presence of betacellulin.

The pancreatic beta- and alpha-cells are developmentally related to each other but reveal diverse gene expression patterns. Among the two important transcription factors for insulin gene expression, IEF1 is present both in alpha- and beta-cells, but PDX-1/IPF1/STF-1/IDX-1, a homeodomain-containing transcription factor, is present in beta-cells but not in alpha-cells. To elucidate the function of PDX-1 in the expression of beta-cell-specific genes, we established stable alphaTC1 clone 6 (alphaTC1.6)-derived transfectants expressing PDX-1 and examined the changes in the gene expression patterns in them. The exogenous expression of PDX-1 in alphaTC1.6 cells alone could induce islet amyloid polypeptide (IAPP) mRNA expression in the cells but not the expression of insulin, glucokinase, or GLUT2 gene. However, when betacellulin was added to the medium, the PDX-1-expressing alphaTC1.6 cells, but not the control alphaTC1.6 cells, came to express insulin and glucokinase mRNAs. This did not occur with other growth factors such as epidermal growth factor, transforming growth factor alpha, and insulin-like growth factor I. GLUT2 mRNA remained undetectable in the PDX-1--expressing alphaTC1.6 cells. These observations demonstrate the potency of PDX-1 for the expression of the insulin, glucokinase, and IAPP genes and suggest that certain regulatory factors, which can partially be modified by betacellulin, also contribute to the beta-cell specificity of gene expression.

Amyloid↗
PubMed1996

[A case of familial amyotrophic lateral sclerosis with markedly decreased accumulation on 123I-MIBG myocardiac scintigraphy and atonic bladder].

A 63-year-old Japanese woman with familial amyotrophic lateral sclerosis (ALS) showed cardiac hypofunction and neurogenic bladder. Her autonomic function was evaluated by means of 123I-metaiodobenzylguanidine (MIBG) cardiac scintigraphy and urodynamic study. (1) MIBG scintigraphy: Both early and late imagings showed severe defects of myocardial 123I-MIBG accumulation despite the normal accumulation of 201thallium. (2) Urodynamic study: Atonic bladder was observed on cystometry. These data indicate that both sympathetic and parasympathetic nerve functions were disturbed, suggesting the possibility that autonomic disturbance in familial ALS may differ from those in sporadic ALS, in which increased sympathetic nervous function has been reported.

3-Iodobenzylguanidine↗
PubMed1996

[Rhabdomyolysis related-acute renal failure in a patient with hyperosmolar nonketotic diabetic coma (HNKC): demonstration of myoglobin casts after normalization of renal function].

We report a patient with rhabdomyolysis secondary to hyperosmolar nonketotic diabetic coma (HNKC), who progressed to acute renal failure. A 43-year-old male with diabetes mellitus for three years was admitted to our hospital because of loss of consciousness. The laboratory findings at admission were as follows: serum glucose 1792 mg/dl, serum Na 129 mEq/1, BUN 71 mg/d1, serum creatinine 3.3 mg/d1, CPK 715 IU/1, plasma osmolality 370 mOsm/1, and negative urine ketone bodies. A diagnosis of HNKC was made. On the 2nd day, he had oliguria and the serum creatinine increased despite adequate treatment of HNKC by the administration of intravenous fluid and insulin. On the 4th day, CPK reached 47,300 IU/1, and serum myoglobin was also increased, indicating rhabdomyolysis. His renal function improved gradually and was almost normalized on the 20th day. Renal biopsy on the 23rd day showed myoglobin at the distal renal tubules, which appeared to be involved in the pathogenesis of renal failure by rhabdomyolysis. However, we found little abnormality association with diabetic nephropathy in the renal tissue. Since HNKC is known to induce acute renal failure rarely without diabetic nephropathy, these findings suggested that the acute renal failure was caused mainly by the rhabdomyolysis. Acute renal failure induced by rhabdomyolysis in patients with HNKC is rare, but fatal. The present study showed that the measurement of serum CPK and urine myoglobin was helpful for early diagnosis. Only 12 cases have been reported to have developed renal failure due to rhabdomyolysis among patients with HNKC. To our knowledge, we demonstrated for the first time that myoglobin at the distal renal tubules after renal function was normalized.

Acute Kidney Injury↗
PubMed1996

[Idiopathic segmental anhidrosis].

We described two cases of idiopathic segmental anhidrosis. Case 1 was a 47-year-old man, who noticed anhidrosis on the right side of face and chest during body heating. Case 2 was a 54-year-old woman, who complained of anhidrosis on the left side of face and upper chest during exercise. Both cases had neither somatic neurological deficit nor autonomic failure except for anhidrosis pupil size and deep tendon reflexes were normal. Reflex sweating to pilocarpine was exaggerated in the anhidrotic areas in both cases, suggesting lesions in the preganglionic sudomotor nerves. Abnormal laboratory finding was elevated serum rheumatoid factor level in only case 2. Segmental anhidrosis was static for 1.5 year and one year, respectively. The previous literature contains similar four cases. Idiopathic segmental anhidrosis may be an abortive form of Ross' syndrome (tonic pupil, hyporeflexia and segmental anhidrosis).

Female↗
PubMed1996

[A case report of subacute panencephalitis associated with specific T cells sensitized to proteolipid protein (PLP) synthetic peptides identified with rubella virus].

A 37-year-old woman was admitted to the hospital on October 4, 1991 because of fever, headache, and abnormal behavior. Although she was treated with aciclovir, she developed encephalitis, which slowly manifested itself over the next month as meningeal irritation, loss of consciousness, partial seizure, and quadriparesis. Her cerebrospinal fluid showed mild lymphocytic pleocytosis without protein elevation. Serum IgG antibody titer to rubella virus was elevated, but the rubella virus could not be detected in the cerebrospinal fluid by PCR amplification. Her consciousness level improved slowly, and by the end of November she suffered only dystonic posture of her right arm and hand. By the middle of December, there were no abnormal neurological findings except some extrapyramidal tract signs and symptoms, such as tremor and rigidity. The serum rubella virus IgG titer had fallen back into the normal range. Her illness was diagnosed as subacute panencephalitis, and she recovered completely about 5 months after the onset of the disease. The lack of rubella virus in the cerebrospinal fluid suggests that panencephalitis may not be dependent on virus replication within the central nervous system. Specific T cells sensitized to proteolipid protein synthetic peptides (PLP158-166) identified with rubella virus were detected in this case during the active stage. These observations imply that subacute panencephalitis may be dependent on an immune-mediated mechanism and that PLP-specific T cells may play an important role in pathogenesis of the disease.

Adult↗
PubMed1996

[A case of sympathotonic orthostatic hypotension following herpes simplex encephalitis].

The etiology of sympathotonic orthostatic hypotension (SOH) is still unknown. We reported a 50-year-old male case of SOH associated with herpes simplex encephalitis. Eight days before admission to our hospital, he noticed fever, which was followed by intractable hiccup. He was admitted to a local hospital, where nuchal rigidity and mononuclear CSF pleocytosis were noted. On the 9th hospital day, he suddenly developed respiratory arrest, and his consciousness state deteriorated to coma. He was transferred to our hospital with artificial ventilation on the same day. The second CSF examination revealed pleocytosis and positive herpes-simplex-virus antibody. CAT scan showed diffuse high density areas in the bilateral temporal lobes. Intensive anti-herpetic therapy was started. On the 14th hospital day, spontaneous respiration came back and consciousness state was improved from coma to stupor. He gradually recovered to alert state and became ambulatory by the 30th hospital day. Seven weeks after the onset of his illness, he noticed orthostatic dizziness for the first time during his rehabilitation exercises. Blood pressure was 116/78mmHg at supine position and 82/62mmHg at standing position, and the heart rate was 83bpm, and 141bpm, respectively. Plasma noradrenaline concentration was 0.09 ng/ml (within normal range) at supine position, but increased to 0.29ng/ml upon standing. Catecholamine infusion tests revealed hyposensitivity in beta 2-receptors; decrease in blood pressure in response to isoprenaline was blunted, while increase of blood pressure to noradrenaline was not impaired. Nerve conduction studies and sweating tests were normal. When he was discharged from our hospital on the 87th hospital day, he still had orthostatic symptoms. His complete recovery took full one year. Some authors claimed that SOH is an abortive form of acute autonomic neuropathy, while others postulated that it was due to unbalanced cardiovascular alpha- and beta-adrenoceptor functions. SOH of the present case seems to be caused by the central nervous lesions; especially, the brain stem involvement due to herpes simplex encephalitis may well be causing SOH.

Autonomic Nervous System↗
PubMed1996

[Guillain-Barré syndrome and acute disseminated encephalomyelitis (ADEM)].

I would like to report the results of our immunological study on Guillain-Barré syndrome (GBS) and to consider the relationship between GBS and acute disseminated encephalomyelitis (ADEM). First of all, I referred to the historical view of the diagnostic criteria of GBS. Immunological study on GBS started after the report of experimental allergic neuritis (EAN) by Waksman and Adams (1995). We made EAN rabbits by immunization with peripheral myelin and observed the process of motor paralysis. In EAN, humoral and cellular immune responses to P2 protein and its synthetic peptides were obtained in accordance with the motor weakness. In patients with GBS we also investigated the humoral and cellular immune responses to P2 protein. Anti-P2 protein antibody and sensitized lymphocytes against P2 protein and its synthetic peptides were detected in GBS as well as in EAN. We also detected antineural antibodies such as anti-P0, anti-galactocerebroside and anti-GM1 ganglioside antibodies in GBS. And also anti-GQ1b antibody was detected in patients with Fisher syndrome and GBS with ophthalmoplegia. More than 50 years ago, Baker (1943) described 5 forms of GBS including 1) abortive or mononeuritic 2) polyneuritic 3) spinal, 4) bulbar and 5) cerebral forms. Guillain (1953) didn't deny the bulbar and cerebral forms, although he apparently denied the spinal form of GBS with Babinski's sign. According to "Merritt's Textbook of Neurology", lesions of ADEM (postinfectious and postvaccinal encephalomyelitis) involved not only the brain and the spinal cord but also the peripheral nerve. Guillain (1953) objected against "Landry-Guillain-Barré syndrome" proposed by Haymaker and Kernohan (1949). Guillain (1953) described that Landry's ascending paralysis was different from GBS and Landry's paralysis must belong to category of ADEM, as van Bogaert also commented. In our recent study for T cell subsets in GBS and ADEM, significant increase in activated CD4 and helper inducer cells were observed in both GBS and ADEM, which suggested the presence of a common pathogenic mechanism in these diseases. After considering the classification of immunological nervous diseases, we would propose a clinical entity "acute immuno-logical nervous diseases" including GBS, Fisher syndrome and ADEM.

Animals↗
PubMed1995

Regulation of synapse density by 5-HT2A receptor agonist and antagonist in the spinal cord of chicken embryo.

Identification of mechanisms that regulate the number of synapses in the brain has been a key issue for understanding the mechanism of plasticity. Here, we report that the density of synapses can be changed using an antagonist and/or an agonist of serotonin (5-HT) type 2A receptors in the chicken spinal cord. Because of the widespread distribution pattern of 5-HT fibers and 5-HT2A receptors in the central nervous system, 5-HT is thought to play a role in the formation and maintenance of synapses that are involved in normal brain function and mechanism of plasticity.

Amphetamines↗
PubMed1995

Stability of ribonuclease T2 from Aspergillus oryzae.

The stability of ribonuclease T2 (RNase T2) from Aspergillus oryzae against guanidine hydrochloride and heat was studied by using CD and fluorescence. RNase T2 unfolded and refolded reversibly concomitant with activity, but the unfolding and refolding rates were very slow (order of hours). The free energy change for unfolding of RNase T2 in water was estimated to be 5.3 kcal.mol-1 at 25 degrees C by linear extrapolation method. From the thermal unfolding experiment in 20 mM sodium phosphate buffer at pH 7.5, the Tm and the enthalpy change of RNase T2 were found to be 55.3 degrees C and 119.1 kcal.mol-1, respectively. From these equilibrium and kinetic studies, it was found that the stability of RNAse T2 in the native state is predominantly due to the slow rate of unfolding.

Aspergillus oryzae↗
PubMed1995

Cutaneous oxalate deposition in a hemodialysis patient.

We describe calcium oxalate and amyloid arthropathy with cutaneous calcinosis without vitamin C supplement. A 34-year-old woman developed glomerulonephritis requiring chronic hemodialysis. Seven years after beginning hemodialysis, multiple crystal deposits appeared in her skin; she also presented with arthralgia and gait disturbance. A skin biopsy was performed, which disclosed calcium oxalate deposition. In addition, a right femoral neck prosthetic replacement was performed. Pathologic examination of the hip synovia revealed diffuse calcium oxalate, amyloid, and iron deposition. Calcium oxalate and amyloid arthropathy with synovial hemosiderosis was diagnosed, and therapy with desferal and high-flux membrane dialysis was started. Clinical improvement occurred after 6 months.

Adult↗
PubMed1995

Secondary amyloidosis associated with Castleman's disease.

A rare case of secondary amyloidosis associated with Castleman's disease is reported. A 53-year-old woman was referred for investigation of proteinuria. Biopsy specimens from kidney and gastric mucosa revealed numerous amyloid deposits, defined as AA amyloidosis by immunohistological staining. Castleman's disease was found in the abdomen as the primary disease for the amyloidosis. Although the urinary protein was somewhat reduced and the inflammatory findings were improved after removal of the lymphoma, renal insufficiency progressed and hemodialysis was begun.

Amyloidosis↗
PubMed1995

[A case of nephrotic syndrome mimicking membranoproliferative glomerulonephritis (MPGN) and associated with reactive hemophagocytic syndrome after renal death].

We report a case of nephrotic syndrome which mimicked membranoproliferative glomerulonephritis (MPGN) and was associated with hemophagocytic syndrome after renal death. A 41-year-old Japanese man was referred to our hospital because of nephrotic syndrome in February 1979. He had no signs, symptoms nor laboratory data suggestive of liver damage. He was diagnosed as idiopathic MPGN and administered prednisolone and cyclophosphamide (total dose of about 50,000mg). He developed end-stage renal disease, and dialysis therapy was initiated in February 1992. Simultaneously, he was diagnosed as hepatitis C virus (HCV)-positive liver cirrhosis. In August 1994, he died because of reactive homophagocytic syndrome, which occurred in the setting of immunosuppression due to chronic renal failure, liver cirrhosis, and sesecondary diabetes. In this case, we can not deny the possibility that radical therapeutic intervention against "idiopathic MPGN" had a negative effect on the clinical course of chronic HCV infection.

Cyclophosphamide↗
PubMed1995

[Antineuronal autoantibody to a 40-kDa protein in a patient with cerebellar ataxia and breast cancer].

A 49-year-old woman was admitted to Utsunomiya Saiseikai hospital complaining of right breast swelling. There was half a year history of difficulty in walking. A diagnosis of breast cancer was made by biopsy. Neurological examination revealed scanning speech, nystagmus, intention tremor and ataxic gait, but brain CT scan and MRI showed neither metastatic, invasive lesions nor atrophy in the brain. Lumpectomy for breast cancer was performed. For immunocytochemical studies, the cytoplasm of neurons in sections of normal human cerebral cortex, cerebellum, spinal cord and dorsal root ganglia were stained by the patient's serum, but glial cells were not. Upon Western blot, the patient's serum reacted with a 40-kDa protein in extracts of both cerebrum and cerebellum obtained from normal rats. A diagnosis of paraneoplastic cerebellar degeneration (PCD) was made on the basis of clinical manifestations and detection of the antineuronal antibody. The antibody accompanying the breast cancer which stained neuronal cytoplasm and bound to a 40-kDa protein may be a subtype of antibody causing PCD.

Autoantibodies↗
PubMed1995

[A case of metamorphopsia caused by a very localized spotty infarct].

A 51-year-old woman complained that her right side of the face looked blurring and the right margin of all the objects in her visual field looked blurred. Neurological examination on admission showed no abnormalities including higher cortical function and visual fields except the metamorphopsia. In this case, a very localized spotty infarct caused no neurological symptoms other than the metamorphopsia. CT scan and MRI revealed a spotty lesion of infarct between retrosplenium and cingulate gyrus on the left side. This can be a breakthrough case to locate the exact anatomic pathology that causes metamorphopsia.

Cerebral Infarction↗