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Biomedical subjects

Takashi Inuzuka

Publications and source records attributed to Takashi Inuzuka.

6 recordsLinked to original sources
PubMed2003

Growth inhibitory factor prevents degeneration of injured adult rat motoneurons.

We examined neuroprotective effects of growth inhibitory factor (GIF) on injured adult rat facial motoneurons. The right facial nerves of adult rats were avulsed and removed from the stylomastoid foramen, and an adenoviral vector encoding rat GIF and Myc epitope (AxCArGIFM) were injected into the facial canal. Animals treated with AxCArGIFM showed intense immunolabeling for GIF/Myc in injured facial motoneurons. Treatment with AxCArGIFM after avulsion significantly prevented the loss of injured facial motoneurons, improved choline acetyltransferase immunoreactivity and prevented the induction of nitric oxide synthase activity in these neurons. These results indicate that GIF may have therapeutic potential against degeneration of motoneurons in adult humans with motoneuron injury and motor neuron diseases.

Adenoviridae↗
PubMed2003

A novel insertion mutation of acetazolamide-responsive episodic ataxia in a Japanese family.

We report a Japanese family with acetazolamide-responsive episodic ataxia. The proband was a 41-year-old woman with interictal nystagmus. She experienced recurrent attacks of loss of equilibrium and loss of coordination of the extremities accompanied by dysarthria and nausea beginning at about 10 years old. These episodes usually lasted for several hours two or three times a week. Direct sequence of CACNA1A demonstrated a novel insertion mutation in the patient and her father. This mutation is estimated to cause early stop of the gene transcription, producing a truncated protein. This is the first report of episodic ataxia type 2 of which the mutation was identified in a Japanese family.

Acetazolamide↗
PubMed2003

Regulation of gene expression in response to brain injury: enhanced expression and alternative splicing of rat prosaposin (SGP-1) mRNA in injured brain.

Prosaposin, the precursor of saposins or saps, is an injury-repair protein that acts on both neurons and glia. Previous studies identified the prosaposin gene as one of differentially expressed genes following nerve injury. In the present study, we investigated expression of prosaposin mRNA in injured brain utilizing rat models of focal cerebral ischemia and cortical stab wound in order to explore the significance of prosaposin in nerve injury. In ischemic brain, the level of prosaposin mRNA was elevated greater than 400% over controls within 5 days after ischemic insults. Importantly, this induction was accompanied by a 9-base splicing consistent with the alternative Exon-8 splicing of human prosaposin mRNA. In normal brain, two prosaposin mRNA species with and without the 9-base insertion were expressed at a ratio of 85:15; however, this equilibrium reverted to 5:95 following ischemic injury. Similar inductions were observed in stab wound brains. Immunohistochemical staining and in situ hybridization demonstrated an enhanced signal distribution of prosaposin mRNA and injury-induced prosaposin protein around the lesion. The data suggest the expression and processing of prosaposin mRNA may be crucially regulated not only for cerebral homeostasis but also during nerve regenerative and degenerative processes.

Alternative Splicing↗
PubMed2003

Steroid-responsive limbic encephalitis.

A 71-year-old man presented with gradually progressing cognitive decline following acute febrile exanthematous disorder. The MRI showed an abnormality in the bilateral limbic systems. An elevation of cerebrospinal fluid (CSF) protein with lymphocyte pleocytosis was noted. Immunoblot of the CSF revealed the presence of anti-white matter antibodies that mainly recognized astrocytes. Intravenous steroid followed by oral steroid reduced the symptoms to a remarkable degree. The patient has now been successfully sustained with steroid for more than two years. We considered that this case is classified as non-paraneoplastic limbic encephalitis, and acquired autoimmunity played a major role in the pathogenesis of this case.

Aged↗
PubMed2002

A clinicopathological study of a patient with anti-Hu-associated paraneoplastic sensory neuronopathy with multiple cranial nerve palsies.

Only a few cases of paraneoplastic neurologic syndrome with multiple cranial palsies have been reported. This is the case report of a patient with small-cell lung cancer and a high titer of anti-Hu antibodies who developed a tonic left pupil and multiple cranial nerve palsies, including palsies of the left fifth through tenth nerves and both twelfth nerves, as in Garcin syndrome showing at least more than seven ipsilateral cranial nerve palsies, in the course of paraneoplastic sensory neuronopathy (PSN). Pathologic examination revealed no metastasis or direct invasion of malignancy with gliosis and perivascular inflammation throughout the brainstem, indicating paraneoplastic encephalomyelitis (PEM). The numbers of EBM11+ cells (probably reactive microglia), CD8+ cells, and CD4+ cells increased. Intracellular adhesion molecule-1 and lymphocyte function associated molecule-1 were expressed intensely on the endothelia of microvessels and were found to have infiltrated mononuclear cells around microvessels in the brainstem. Multiple cranial nerve palsies and their effects including the tonic pupil are likely due to the paraneoplastic effect of the primary systemic malignancy.

Aged↗