Biomedical subjects
Publications and source records attributed to K Tashiro.
A rare case of cerebral alveolar hydatid disease in a 41-year-old female is presented. The larval mass was subtotally removed and the presence of alveolar hydatid cysts established histologically. Postoperatively, slight mental disturbance persisted but paresis did not develop.
Retrospective study on the frequency of associated bladder cancer and the influence on the prognosis was carried out in 170 cases of renal pelvic and ureteral cancer. The number of cases of associated bladder cancer coexistent with renal pelvic and ureteral cancer was 31 (18.2%), and the number of subsequent cases 3 (19.4%). The frequency of occurrence of the primary tumor site was 27.2% in the renal pelvis, 45.6% in the ureter and 58.3% in both renal pelvis and ureter. Multiple tumors occurring in the renal pelvis and ureter occupy a high percentage. As for the degree of differentiation, many cases were subsequent to G1. As for the stage, a few cases with bladder cancer were subsequent to T4, but there was no definite tendency in the occurrence of bladder cancer. The prognosis of renal pelvic and ureteral cancer: the 10-year survival rate was 93.3% for G1, 66.6% for G2 and 12.4% for G3. As can be seen, there was good correlation with the pathological gradings. It must be remembered, however, that 5-year survival rates in cases of associated bladder cancer of coexistent type, in cases of subsequent type and in cases without associated bladder cancer were 56.2%, 72.7% and 64.8%, respectively: there was no significant difference. Bladder cancer associated with renal pelvic and ureteral cancer makes the therapy troublesome, but no influence on the prognosis was observed. Therapy in conformity with the pathological grading and stage is regarded as particularly important in cases of associated bladder cancer.
We reported a 29-year-old woman who had chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with multifocal nerve hypertrophy. She developed chronic progressive muscular weakness of distal part of her extremities and sensory ataxia of limbs and trunk for five years. Steroid therapy improved most of her signs and symptoms. No recurrence has occurred for the subsequent four years until present time. Magnetic resonance imaging (MRI) revealed multifocal and nodular hypertrophy of her peripheral nerves in the extremities. MRI also detected the hypertrophy of posterior nerve ganglia and extradural nerve roots. Hypertrophic nerve trunk comprised of multifocal and nodular hypertrophy of the nerve fiber fascicles which were detected as abnormal high signal intensity area in MR T2-weighted images. Her sural nerve contained no onion-bulb formations and presented normal low signal in MR T2-weighted images. We concluded that the hypertrophic changes occurred multifocally in and among nerve fascicles predominantly at the proximal part of the nerves of the extremities. MRI is useful method to detect the hypertrophic change of peripheral nerves deep in the trunk and the extremities in CIDP.
We have established a new in situ hybridization method utilizing non-radiolabeled probes. Using this technique, we have attempted to detect the choline-acetyltransferase (ChAT) gene expression in rat spinal cord. It was revealed that the ChAT gene was expressed mainly in the cytoplasm of motor neurons and para-central cells. On the other hand, ChAT protein has already been reported to exhibit a diffused distribution in the cholinergic fibers. Comparing the localization of the ChAT gene with that of the ChAT protein, the ChAT gene was shown to exist only in the cytoplasm surrounding the nuclei. However, the ChAT gene was not expressed in axon terminals where ChAT protein synthesized acetylcholine. This result indicates that the ChAT gene is translated into protein around the nuclei and is thereafter transported toward the action site. We now think that there are two different patterns of neurotransmitter gene distribution. After mRNA is translated into protein, this protein is carried to the action site. On the other hand, mRNA itself is delivered to the action site and translated into protein. After the translation, this protein form exerts its own function. The ChAT gene is suspected as belonging to the first category of gene distribution. In Alzheimer disease, not only the acetylcholine system but also its biosynthetic enzyme, ChAT, system are supposedly destroyed by an unknown factor. If we can clarify the regulatory mechanism of the ChAT gene, this will lead us to the molecular pathogenesis of Alzheimer disease. Additionally, this new in situ hybridization technique should shed some light on the complex brain networks.
The pathogenic relation of chronic mercurialism and amyotrophic lateral sclerosis (ALS) was evaluated clinically on 83 ex-mercury workers who were poisoned or exposed to mercury vapor about 18 years ago at one of the biggest mercury mines in Hokkaido, as well as on the causes of 65 expired workers in the cohort. The 83 ex-mercury workers were subdivided into two groups according to severity of mercury poisoning: 31 ex-workers who had been hospitalized for treatment of mercury poisoning and the remaining 52 ex-workers severely exposed to mercury vapor but not hospitalized. Neurologic examinations and measurements of mercury contents in the blood, urine, and hair samples in the 83 cases, failed to disclose any pathogenicity of mercury to ALS. Among these 148 including the 65 deceased cases, no ALS cases were found. Further clinical and epidemiological studies should be required on mercury poisoning as one of the risk factors in the development of ALS, especially in relation to selenium.
Benign intracranial hypertension or pseudotumor cerebri is an collective term for a number of diverse syndromes characterized by increased intracranial pressure. Neither intracranial mass nor ventricular dilatation is observed in this disorder. Moreover, the pathogenesis of this syndrome has yet to be determined. We report a case of 36-year-old female diagnosed as benign intracranial hypertension, who has developed superior sagittal sinus thrombosis and dural AV fistula during the follow up period. The patient was pointed out to have papilledema and elevated intracranial pressure six years ago. Although she was examined by both DSA and CT scan, no abnormal intracranial lesions were observed. Consequently, she was diagnosed as the benign intracranial hypertension and had been followed as an out patient. Three years later, lumboperitoneal shunting was performed because of severe headache and visual impairment. Postoperatively, the patient had been well for two years. Recently, occipital headache recurred and she was readmitted to our hospital. MRI studies demonstrated dilated vessels in the right occipital area. Additionally, angiograms revealed not only the superior sagittal sinus thrombosis but also the rich network of dural AV fistula adjacent to the occlusion. According to those results, the superior sagittal sinus was supposed to have the incomplete occlusion or delayed blood flow that were not observed by DSA, MRI and CT scan performed previously. Those occlusive change in the superior sagittal sinus impeded the CSF absorption and elevated the pressure of venous inflow, then the arterio-venous communication has been developed.(ABSTRACT TRUNCATED AT 250 WORDS)
A 63-year-old man developed muscular atrophy and weakness in his four extremities since 1983, and was pointed out to have smoldering ATL by elevated HTLV-1 antibody titers in the serum (x 2,500) and CSF (x 32) in 1985. Neurological examinations revealed proximal muscular weakness and atrophy of four extremities, and mild spasticity of both legs. Deep tendon reflexes were hypoactive in both arms and hyperactive in both lower extremities with ankle clonus and bilateral positive Babinski and Chaddock reflexes. These findings were compatible with HAM. His gait, however, was markedly waddling, requiring support. Muscle biopsy at left biceps muscle revealed inflammatory change with rimmed vacuoles, small group atrophy, and marked type 1 fiber predominance. These findings on muscle biopsy are different from those of previously reported cases with HAM, showing some similarities to inclusion body myositis or distal myopathy with rimmed vacuole.
From the linkage study of D6S89, we previously reported that hereditary OPCA in Japan is genetically heterogenous. Two pedigrees, P2 and P35, reported in this report, were not linked to D6S89. In order to examine possible correlation between OPCA genotypes and disease phenotypes, we studied clinically eight cases in these two pedigrees. One autopsied case in pedigree P2 was proven to have marked neuronal degeneration in the inferior olivary nuclei, pontine nuclei, cerebellar cortex, and substantia nigra. Dentate nucleus and oculomotor nuclei were free from neuronal degeneration. Clinical features of those 8 patients were fairly uniform, characterized by cerebellar ataxia, hypoactive DTR, and slow eye movement. Parkinsonism or choreiform movements were observed in one patient, respectively. Pupillary dilatation, twitching of face and tongue, limb amyotrophy were observed in patients of advanced stages. However, these signs were not dominating nor common throughout clinical course. None of our cases showed hyperactive DTR, limb spasticity, or external ophthalmoparesis. On the other hand, these latter signs were popular in SCA1 so far as reviewing the literature. The present study showed that there was possible correlation between genotypes and phenotypes in hereditary OPCA.
A 57-year-old man of Kennedy-Alter-Sung syndrome (K-A-S) with type IIa hyperlipidemia was reported with studies of several sex hormone receptors. He noticed tremulous movements of hands on gripping at age 40 and gynecomastia at age 46. He had been pointed out to waddle since 52 years old, and also noticed difficulty in going up stairs and standing up at age 54. He was admitted to our Neurology Service on June 5, 1989. On general physical examinations, gynecomastia, eyelids xanthomas and hypertrophy of Achilles tendons were found. Neurologic examination revealed clear consciousness and slight dysarthric speech with nasal voice. Cranial nerves showed mild bilateral facial weakness, poor uvula and soft palatal movements, atrophy and weakness of bilateral sternocleidomastoid muscles, and atrophy of tongue with fasciculation. The four extremities were hypotonic, and proximal muscular atrophy and weakness of four extremities were seen. Deep tendon reflexes were absent in four extremities and fasciculation on both thighs was noted on contraction. Sensory and cerebellar functions were intact. Waddling gait and Gowers' sign were present. In K-A-S syndrome, abnormal lipid metabolism such as a family of type IIa hyperlipidemia, or familial and sporadic cases of type IV hyperlipidemia has been documented. In the family of our cases, his elder sister was found to have type IIa hyperlipidemia, while his son had type IV hyperlipidemia. The coexistence of these two types of hyperlipidemia in the same family of K-A-S syndrome has not been reported so far to our knowledge.(ABSTRACT TRUNCATED AT 250 WORDS)
A 26-year-old woman developed two separate episodes of myelopathy mainly presenting paraparesis. Neurologic examination disclosed flaccid paraparesis associated with slight spasticity of the right arm. Deep tendon reflexes were generally hyperactive with positive bilateral Babinski and Chaddock reflexes. Arm pronation sign and Barré leg signs were bilaterally positive. Sensory disturbance below T6, and diminished vibration and position sense in both legs were seen. Urinary and fecal disturbances were also present. She could walk, but her gait was unsteady. Brain MRI showed abnormal high signal intensity areas on T2-weighted image at the left fronto-parietal lobe and right temporo-parietal lobe. Spinal MRI disclosed a cavity formation which was delineated low signal intensity on T1-weighted image through T4 to T8 and high signal intensity on T2-weighted image through T3 to T10. From these clinical manifestations and radiological findings, she was able to be diagnosed to have definite MS. The coexistence of syrinx formation in MS has rarely been reported, and only 5 cases including our case were found. These cases are characterized by the central localization of syrinx, and fair prognosis in their neurological features.
A 41-year-old man was doing well until July 1989, when he noted numbness over soles, followed 4 months later by difficulty in walking. These symptoms were progressively getting worse, and he was admitted to our department on June 12, 1990. General physical examination was unremarkable. Neurologically cranial nerves were intact except old right, traumatic strabismus. Muscle tone and deep tendon reflexes were normal throughout, but bilateral Babinski and Chaddock reflexes were present. Mild weakness of lower extremities were found on muscle testing (4/5). In sensory system, superficial sensory disturbance below T10 was seen, and markedly diminished vibration and position senses of lower extremities were noted. Cerebellar test was intact, although unsteadiness was found on heel-shin test. Romberg sign was definitely positive. His gait was wide-based and ataxic. Laboratory data showed no abnormalities in CBC, chemistry, urinalysis, serological tests and endocrinological examinations. Spinal MRI (Siemens 1.5 Tesla) showed abnormal deposition of epidural fatty tissues compressing spinal cord with flattening of cord from T4 to T8. Spinal ataxia as compressive myelopathy due to epidural lipomatosis was considered and he underwent laminectomy from T4 to T8 with improvement in walking. Epidural lipomatosis is an unusual cause of spinal cord compression, presenting compressive myelopathy, radiculopathy, cauda equina syndrome, intermittent claudication, or back pain. Most of cases were associated with long-term administration of adrenocortical steroid hormone, or underlying diseases, except only 3 cases including ours. This is the first case of spinal epidural lipomatosis presenting progressive gait disturbance due to spinal ataxia.
Hepatocyte growth factor (HGF) has been demonstrated to be synthesized and secreted by non-parenchymal liver cells for liver regeneration after hepatic injury. We performed in situ hybridization to identify HGF-producing cell types in rat liver hepatitis induced by administrating carbon tetrachloride as a hepatotoxin. We found that transcripts of the HGF gene are localized in the Kupffer and endothelial cells in normal livers and increased remarkably in the Kupffer cells of the damaged livers. Thus, HGF is concluded to be synthesized in the Kupffer and endothelial cells to repair the liver tissue in paracrine fashion. No significant increase in the transcripts of the HGF gene was observed in livers after partial hepatectomy, indicating that a mechanism on liver regeneration after the hepatectomy differs from that on liver repairs. Since the HGF gene expression was also found in lung and kidney, HGF may be a ubiquitous factor for tissue repairs.
The binding sites of TFID, a species-dependent transcription factor, on the mouse ribosomal RNA gene (rDNA) have been analyzed by DNase I footprinting using partially purified TFID. The region -12 to -140 spanning over the upper half of the core promoter (-12 to -40) and an upstream sequence (-40 to -140) was protected. Human fraction D could not protect corresponding regions of mouse rDNA indicating that the protection was indeed caused by TFID. This was corroborated by a competition experiment using point mutants having different affinities to TFID. The analysis with deletion mutants of upstream sequence together with the competition data indicates that the binding of TFID to the core sequence is required for the binding of TFID or some co-purified proteins to the upstream sequence, while the presence of upstream sequence stabilizes the TFID binding to the core sequence. The pattern of protection of the upstream sequence suggests that at least a part of the upstream binding does not require a specific DNA sequence there but rather is caused by protein-protein interaction involving TFID bound with the core sequence. These protection patterns did not change with TFID highly purified by sequence-specific DNA affinity chromatography.
The complete amino acid sequence of the tryptophan 2,3-dioxygenase (TO) of rat liver was determined from the nucleotide sequence of a full length TO cDNA isolated from a rat liver cDNA library and determined its primary structure. TO was encoded in a mRNA of about 1.7 kb containing an open reading frame of 1218 bp. According to the deduced amino acid sequence, the monomeric polypeptide of TO consisted of 406 amino acid residues with a calculated molecular weight of 47,796 daltons. It has twelve histidine residues around its hydrophobic region, which has homology with some heme proteins and oxygenase, suggesting that this hydrophobic region might to be the core of TO for the activity.
We report here that an interleukin-3-dependent precursor B-cell line, LyD9, differentiated in vitro into mature B cells, producing immunoglobulin (Ig)M and IgG by co-culture with bone marrow stroma cells. Induced LyD9 cells underwent heterogenous immunoglobulin gene rearrangement and synthesized mRNAs encoding immunoglobulin mu (mu), gamma (gamma) and kappa (kappa) chains. LyD9 was also shown to differentiate into myeloid cells. We have established an interleukin-4-dependent derivative clone K-4 that is an intermediate between myeloid-lymphoid cells and the LyD9 clone. This differentiation required direct contact between LyD9 and stromal cells.
An interleukin-5 (IL-5)-dependent subclone, K-5, was established from an IL-3-dependent murine hemopoietic progenitor cell line by co-culturing with bone marrow stroma cells. K-5 cells were induced to differentiate into myeloid lineage cells by co-culturing with cloned PA6 stroma cells. By co-culturing with another cloned stroma cell (ST-2s10), K-5 cells gave rise to a factor-independent transformant cell line LT-5 which proliferated in an autocrine manner by secretion of IL-5 and produced tumors in nude mice. Molecular cloning of the IL-5 gene of LT-5 cells and the nucleotide sequencing of its 5' flanking region indicate that a transposition of an intracisternal A-particle (IAP) element to the 5' flanking region of the IL-5 gene is responsible for the constitutive expression of IL-5 mRNA of an aberrant size in LT-5 cells.
Twelve patients with discharge of clear colorless fluid during percutaneous transhepatic gallbladder drainage (PTGBD) were encountered during a period of 4.5 years. On the average, the fluid appeared on the 12th day after PTGBD and continued to flow until the completion of observation. The volume was usually less than 60ml per day. It flowed in an alternating pattern with normal yellow color bile each day. The fluid was observed in patients in whom satisfactory patency of the biliary system was confirmed by cholangiography and/or cholangio-fiberscopy. Biochemical examinations of the fluid revealed lower biliary lipids but a similar electrolyte composition compared to bile of normal color. It was alkaline. These observations indicate that the clear colorless fluid is different from what is known as "white bile", which is produced when there is an obstruction of the biliary tree. The fluid may be secreted from the gallbladder epithelium or the bile duct epithelium. The significance was not clarified in this study. Further investigation is necessary to elucidate the clinical implications of the clear and colorless fluid secretion.
Sixty-two consecutive patients with clinically definite multiple sclerosis (MS) were classified into 2 subgroups: group A, consisting of 16 patients who had shown acute transverse myelopathy (ATM) during the course of illness; and group B, 46 patients without ATM. The clinical features of these 2 groups were analysed prospectively for certain periods, and some significant differences were found. There was (1) later onset, (2) less frequent occurrence of brain stem, cerebellar and cerebral symptoms, (3) more frequent and severe involvement of the optic nerve, (4) a smaller proportion of patients with abnormal findings on brain MRI in group A compared with group B. The clinical features of group B were quite similar to those of previous Western series, while group A seemed to constitute a distinct clinical subgroup in patients with MS.