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Biomedical subjects

G Hirose

Publications and source records attributed to G Hirose.

At least 55 records · Page 3Linked to original sources
PubMed1994

A hippocampal protein associated with paraneoplastic neurologic syndrome and small cell lung carcinoma.

A hippocampal 38 kd autoantigen recognized by an autoantibody from the serum of a patient with paraneoplastic limbic encephalitis (PLE) and small cell lung carcinoma (SCLC) was isolated by screening a human hippocampal cDNA library. The 1,991-nucleotide ple21 clone was obtained and the deduced 350-residue protein encoded by the ple21 cDNA clone was found to be highly homologous to the neuron-specific RNA recognition motifs (RRMs)-containing proteins. The homologies were confined to the RRMs and the RRM connecting region. The presence of RRM in the antigenic protein may be important in the pathogenesis of SCLC-associated paraneoplastic neurologic syndrome.

Amino Acid Sequence↗
PubMed1993

Analysis of autoantibody binding to 52-kd paraneoplastic cerebellar degeneration-associated antigen expressed in recombinant proteins.

A 52-kd neural antigen was reported to be recognized by anti-Purkinje cell antibodies in serum of a patient with paraneoplastic cerebellar degeneration associated with uterine carcinoma. In this study, we demonstrate that this neural antigen is recognized by antibodies known as anti-Purkinje cell antibody type I (PCAb Type I) and anti-YO. The latter's antigen is reported to be specific for the 62- to 64-kd antigen CDR62. Assuming that the 52-kd and 62- to 64-kd antigens share a common epitope(s) recognized by all of these antibodies, we examined the antigenic region on the 52-kd protein by immunoblots with deletion fragment proteins of the recombinant 52-kd protein. A major epitope was localized in the region of amino acid residues 94 to 133 of the 52-kd protein, which is the site of a leucine zipper motif. The potential pathogenicity of PCAb Type I is discussed.

Amino Acid Sequence↗
PubMed1993

Neuropathological studies of the spinal cord in early stage HTLV-I-associated myelopathy (HAM).

Necropsy findings for a patient with HTLV-I-associated myelopathy (HAM) of 9 months clinical duration are reported. Loss of myelin sheaths and axons together with perivascular lymphocytic infiltration was seen in the lateral and posterior columns of the spinal cord from the cervical to the lumbar region where vacuolar changes caused by the splitting of myelin sheaths were prominent. Immunohistochemical analyses revealed CD8+ cytotoxic T cell infiltration predominated in the absence of HTLV-I core protein antigen bearing-cells in the brain and spinal cord. Myelin sheath damage and predominant CD8+ cytotoxic T cell infiltration are thought to be the main neuropathological findings in the spinal cord in early stage HAM.

Aged↗
PubMed1993

[Clinical neurological findings in brain-dead patients].

Most of university hospitals have their own criteria for brain death, based on the national criteria. Here the term "brain death" has been restricted to cases with irreversible deep coma and lack of spontaneous respiration secondary to "total destruction of the brain" for which the cause of the primary brain disease should be known and the most vigorous treatments have been given in vain. In evaluating patients with brain death, careful and accurate neurological examinations are mandatory. The level of consciousness should be in deep coma even after deep painful stimuli, without any movements including decorticate and decerebrate postures. The absence of spontaneous respiration is a crutial determinant for the diagnosis. The more sophisticated apnea testing has been standardized for clinical use. This will be discussed by another speaker. However, unusual spontaneous upper limb movements, called "Lazarus' sign", should be appreciated by examiners. This complex spinal movements need not exclude brain death. Brainstem functions such as reactivity of pupils, corneal reflex, ocular motility, pharyngeal reflex and cough reflex should be totally absent for the diagnosis. The isoelectric EEG is a predictor of brain death, if the technical requirements are carefully followed. But according to our experiences, brain-dead patients may have several waves on BAEP recordings even after obtaining a flat EEG. Because of this, BAEP examination and absence of the cerebral circulation were included in our criteria for brain death.

Brain Death↗
PubMed1993

[Benign non-progressive familial chorea].

Benign non-progressive familiar chorea is a chronic childhood (less than 5 years) choreatic disorder inherited as an autosomal dominant trait but not associated with dementia or progressive motor dysfunction. The major feature of this disease is chorea with early insidious onset and an arrested progression. The lack of mental retardation, mental deterioration or convulsion is the other significant aspects of this disorder. The chorea usually involves the distal limbs, face and trunk. This does not progress to a profound degree throughout the life. There is a controversy regarding whether this benign disorder might be a subtype variant of Huntington's disease. This should be clarified by more extensive molecular genetic studies of this disease.

Age of Onset↗
PubMed1993

[A clinicopathological study of a patient with paraneoplastic limbic encephalitis, myelitis, sensory neuropathy and cerebellar degeneration, associated with a unique antineuronal antibody].

Clinicopathological and immunohistochemical studies were performed in a patient with paraneoplastic limbic encephalitis, myelitis, sensory neuropathy and cerebellar degeneration secondary to small cell lung cancer. A 67-year-old male smoker developed orthostatic dizziness 6 months prior to admission. Over the following months, his wife noticed that he became forgetful and confused. Over the next three weeks, he became unable to sit or stand unaided and admitted to our service. On admission, he was lethargic and disoriented in time and place. Neurological examination revealed marked limb weakness with distal dominant muscle atrophy. A chest radiograph demonstrated a mass in the right middle lobe and a bronchial biopsy revealed a small cell carcinoma. CT scan and MRI of the brain revealed abnormalities in the bilateral medial temporal lobes and putamen. He was treated with anti-cancer chemotherapy, but died of respiratory failure after 13 months illness. Postmortem examination showed a mass in the right middle lobe of the lung. No tumor metastases were noted in the nervous tissue. Microscopical examinations of the nervous system revealed neuronal loss, astrogliosis and perivascular and parenchymatous lymphocytic infiltration in the hippocampus, subiculum, amygdala, putamen, medulla oblongata, spinal cord and dorsal root ganglia. Loss of Purkinje cells was also seen in the cerebellum without lymphocytic infiltration. Immunohistochemical analysis of the patient's serum and CSF by the use of adult rat brain revealed immunoreactivity at the hippocampal pyramidal neurons CA3 and CA4. At the higher dilution, neuronal nuclei were specifically stained.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Unilateral conjugate gaze palsy due to a lesion of the abducens nucleus. Clinical and neuroradiological correlations.

We report a case of left-sided horizontal gaze palsy, ipsilateral adduction weakness, and left peripheral facial weakness, all of which indicate the lesion in the left median pontine tegmentum. The enhanced MRIs revealed a discrete left median pontine tegmental lesion, involving the abducens nucleus, MLF, and facial nerve knee. This lesion spared the area of the left PPRF. Among these structures, the area of the abducens nucleus seems to be responsible for the unilateral horizontal gaze palsy. We are not aware of any previous precise neuroradiological documentation of unilateral paralysis of conjugate gaze due to a lesion of the abducens nucleus by sagittal and horizontal MRIs.

Aged↗
PubMed1992

The expression of a cerebellar degeneration-associated neural antigen in human tumor line cells.

We examined the expression of the paraneoplastic cerebellar degeneration-associated autoantigen (PCD-AA) protein in human tumor lines of different origins by using an immunoaffinity-purified antibody from a patient with paraneoplastic cerebellar degeneration (PCD) and uterine adenocarcinoma. Immunocytochemical studies revealed that this antigen is expressed in the cytoplasm of two different uterine carcinoma lines and the tumor lines of neural origin as well as in the cytoplasm of a normal skin fibroblast line. By immunoblot analysis, we detected a 52-kd antigen identical to the PCD-AA protein in all the cell lines studied, including a colon adenocarcinoma line, a small-cell lung carcinoma line, and a squamous cell lung carcinoma line. These results indicate that the PCD-AA protein is expressed in a wide range of tumor cells. In this respect, this antigen is distinguishable from the cerebellar degeneration-related--34 antigen, of which expression is confined to tumor lines of neuroectodermal origin and not detected in colon, breast, or ovarian carcinoma lines derived from patients without PCD. These findings suggest the variability of the immune response to antigens in PCD.

Antigens, Neoplasm↗
PubMed1992

[Immunohistochemical studies of paraneoplastic subacute sensory neuropathy--an analysis of antineuronal antibody and infiltrated lymphocytes].

In order to clarify the pathogenesis of paraneoplastic syndrome, immunohistochemical studies were performed in a patient with subacute sensory neuropathy secondary to a small cell lung cancer. The case was a 73-year-old ex-farmer, whose chief complaints were pins and needles sensation of distal limbs and gait difficulty. After 6 weeks prodromata of pain in the upper limbs and numbness in all the limbs, he became unable to stand up without assistance. Neurological examinations on admission revealed marked sensory disturbances with glove and stocking type hypalgesia to pin prick and the loss of position and vibration senses in the distal extremities. His deep tendon reflexes also decreased in all the limbs. A chest X-ray showed a mass in the left upper lung field. A transbronchial lung biopsy of the mass revealed a small cell carcinoma. He was treated with anti-cancer drugs and radiation but he died of pneumonia after 8 months illness. Autopsy revealed a marked demyelination of the entire posterior column of the spinal cord. Dorsal root ganglia were infiltrated by lymphocytes with significant neuronal loss. Immunohistochemically, most of the infiltrated cells around the neurons were classified as CD8+ with fewer CD4+ lymphocytes. No B-lymphocytes were detected in the ganglia. The HLA-ABC and HLA-DR positive cells were found only among the satellite cells, not in the neurons. The serum and CSF from the patient were immunohistologically reacted with the nuclei and cytoplasm of all neurons of human as well as of rats, indicating the presence of anti-Hu type antineuronal antibody in the patient's CSF as well as serum.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Delayed postanoxic encephalopathy after strangulation. Serial neuroradiological and neurochemical studies.

A 13-year-old boy was the victim of attempted strangulation. His condition had returned to normal by the sixth day after the assault; however, from the seventh day, choreoathetosis, dystonia, and marked pseudobulbar paralysis developed in the boy. The computed tomographic scans and T2-weighted magnetic resonance images that were obtained at this time revealed low-density and high-signal intensities in the region of the bilateral putamen and caudate nucleus. These symptoms and the changes in his computed tomographic scans and magnetic resonance images subsided gradually during a 2-month period. Sequential analysis of the cerebrospinal fluid for gamma-aminobutyric acid and dopamine concentrations during his illness revealed reciprocal changes with normal recovery. Because of the delayed onset of neurological changes and the cerebrospinal fluid showing reversible symptoms, the delayed encephalopathy after strangulation had been related to the biochemical alterations that followed anoxia in the vulnerable basal ganglia.

Adolescent↗
PubMed1991

Upbeat nystagmus: clinicopathological and pathophysiological considerations.

We describe an electro-oculographic study of upbeat nystagmus in 4 patients, with neuropathological correlation in one. All patients had lesions in the pontine tegmentum. The electro-oculographic data may be explained by imbalanced vertical vestibular or smooth pursuit eye movement control. The nystagmus stopped or reversed direction during convergence or in supine head positions. We propose that changes in the intensity or direction of upbeat nystagmus that are induced by convergence or changes in head position, are caused by vertical imbalance in the otolithic-ocular reflex, when superimposed on an imbalanced vestibulo-ocular reflex (VOR). Imbalance of the otolithic-ocular reflex and the vertical VOR are caused by damage in the pontomedullary tegmentum.

Adult↗
PubMed1991

Primary position upbeat nystagmus. Clinicopathologic study of four patients.

We report an electro-oculographic study (EOG) of upbeat nystagmus and neuroradiological correlations in 4 patients and neuropathological findings in 1 patient. All 4 patients revealed responsible lesions in the lower pontine tegmentum. The EOG data suggest that our patients had a deficit in vertical smooth eye movement balance. The nystagmus stopped or reversed direction during convergence or changes of head position. These EOG findings might be caused by vertical imbalance in the otolithic ocular reflex, superimposed on an imbalanced vestibulo-ocular reflex (VOR), secondary to a damage to the pontomedullary tegmentum.

Adult↗
PubMed1990

Acute effects of anticonvulsants on brain-stem auditory evoked potentials in rats.

Acute effects of various anticonvulsants on brain-stem auditory evoked potentials (BAEPs) in rats were tested. A high dose of phenytoin abolished all BAEP waves. Carbamazepine increased all 4 wave latencies. Phenobarbital and clonazepam increased the latencies of waves IV and III. Therefore, if BAEPs are to be used as an ancillary test for brain death, the possibility of significant effects of high dosages of anticonvulsants on BAEPs must be considered.

Acoustic Stimulation↗
PubMed1990

Phosphorylated and dephosphorylated myosin light chains of Drosophila fly and larva.

1. The present study confirmed that light chains of Drosophila adult fibrillar (flight) muscle myosin consist of Lf1, Lf2, Lf2' and Lf3, and tubular muscle myosin light chains contain Lt1, Lt2, Lt2' and Lt3, as revealed by two-dimensional (isoelectric focusing and SDS-gel electrophoresis) gel electrophoresis. 2. Larva myosin light chains were of all the tubular type. However, it was found that Lt1 and Lt2' are produced by phosphorylation of Lt2, and Lf1 is produced by phosphorylation of Lf2'. 3. Injection of radioactive phosphate into Drosophila fly resulted in phosphorylations of Lf1 and Lt1. When larva or late pupa myosin was incubated with myosin light chain kinase from chicken gizzard or adult flies, phosphorylation of Lt1, Lf2' and Lt2' occurred. Drosophila myosin light chain kinase phosphorylated Lf1 in addition to Lt1 and L2' (Lf2' + Lt2') of adult myosin. 4. Dephosphorylation of adult myosin by potato acid and calf intestine alkaline phosphatases led to the shift of Lf1 (34,000), Lt1 (31,000) and L2' (Lf2' + Lt2') (30,000) to L2 (Lf2 + Lt2) positions (30,000). 5. Peptide mapping analyses revealed that larva Lt1, Lt2', Lt2 and adult Lt1 were all the same; therefore, it is thought that a single species of Lt2 specific to the tubular type of myosin and its phosphorylated isoforms (Lt1, Lt2') exist. 6. The peptide map of Lf1 was slightly different from that of Lt1, but very similar to that of L2' in adult myosin. L2 and L2' of adult myosin showed very similar peptide maps, but there were several different peptide fragments.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

[Delayed postanoxic encephalopathy after strangulation--the serial neuroradiological and neurochemical studies].

A 13-year-old boy was the victim of a strangulation attempt. His behavior was normal by the 6th day after the assault. However, from the 7th day, he developed choreoathetosis, dystonia and marked pseudobulbar palsy. CT and T2-weighted MRI at this time revealed a low density and high signal intensity in the region of the bilateral putamen and caudate respectively for the first time. Thereafter, these symptoms and changes in CTs and MRIs subsided gradually over two months. Sequential analysis of CSF for GABA and dopamine during illness revealed reciprocal changes each other with normal recovery. Because of delayed onset of neurological changes, and findings of CSF with reversible symptoms the delayed encephalopathy after strangulation is probably related to biochemical alteration secondary to anoxia in vulnerable basal ganglia.

Adolescent↗
PubMed1990

[A case of unilateral VIIIth, IXth and Xth cranial nerve involvement with herpes zoster].

A 46-year-old healthy man suffered from sore throat, fever and right otalgia. On the next day, he developed hoarseness and difficulty in swallowing. On the 6th day, he suffered from vertigo, nausea and vomiting associated with unsteady gait. He was admitted to the otorhinolaryngology department in our hospital and pointed out to have vesicles at his right ear. On the 13th day, he was referred to our service. On admission, no vesicles were noted at the right ear or pharynx. Neurological examination revealed mild nuchal rigidity and marked hoarseness, associated with poor elevation of soft palate and loss of pharyngeal reflex on the right side. He also had horizontal-clockwise rotatory nystagmus in primary gaze and ataxic gait. There was no hearing loss nor facial palsy. No other abnormal neurological findings were noted. The cerebrospinal fluid showed pleocytosis associated with increased protein. The viral antibody titre for herpes zoster was significantly elevated on 18th day in serum as well as in cerebrospinal fluid. Vertigo, nausea, vomiting, ataxia and difficulty in swallowing were all disappeared by the 25th day, whereas hoarseness was improved but still noted 6 months later. Among cranial nerves, trigeminal and facial nerves are the most commonly affected in patients with herpes zoster, but there have been a few reported cases of the 9th and 10th cranial nerve involvement in the literature. In these previously reported cases, all were written before the era of serological diagnosis, and herpes zoster was diagnosed by the vesicles at the ear or pharynx.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Viral↗
PubMed1990

[Intramedullary spinal cord metastasis documented by MR imaging].

A 63-year-old woman with progressive paraparesis was found to have an intramedullary spinal cord metastasis from the primary rectal cancer. Myelography and post myelography CT showed an enlargement of the spinal cord at level of the sixth to seventh thoracic vertebra. MR imaging disclosed a localized mass in the spinal cord at the same level. T2-weighted images showed an oval high signal intensity area with central low intensity, and gadolinium-DTPA-enhanced T1-weighted images demonstrated a ring enhancement. Histological examination of the spinal cord revealed an intramedullary spinal cord metastasis with intra-tumorous necrosis at T7 to T8 cord level.

Adenocarcinoma↗