Forward-backward charge asymmetry of quark pairs produced at the KEK TRISTAN e+e- collider.
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Biomedical subjects
Publications and source records attributed to R Tanaka.
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Effects of voluntary rapid head rotation movement in horizontal plane on EMG activities of tonically contracting elbow extensor and flexor muscles were studied in five healthy subjects. Arm EMGs were averaged in relation to the EMG onset of the prime mover. M. sterno-cleidomastoideus (SCM). EMG variations could occur before SCM-EMG onset. Facilitatory and inhibitory effects were observed. They were not necessarily organized in reciprocal fashion but varied in every subject. We interpret the present findings as resulted from an incorporated part of the central motor program for head rotation which was specific to each subject.
2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is the most abundant mutagenic heterocyclic amine in cooked foods. Two mouse tumor cell lines, BMT11 and FM3A, were exposed to its proximate form, 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]pyridine (N-OH-PhIP). Fifty-six subclones of BMT11 and 39 subclones of FM3A were isolated and analyzed by DNA fingerprinting. Treatment with 10-20 microM N-OH-PhIP gave rise to extra bands or shifted bands, but treatment without N-OH-PhIP did not. This suggests that mutations resulting from recombination were induced. The mutation frequencies were 21-53% and 22-35% for BMT11 and FM3A, respectively. These findings suggest that PhIP induces recombinational mutations.
Gelatinase activity and inhibitory activity against collagenase were measured in serum-free medium conditioned by murine colonic carcinoma cells with different spontaneous metastatic potentials to the lung. The medium conditioned with poorly metastatic NM11 cells gave higher inhibitory activity than that conditioned with highly metastatic LuM1 cells, while the level of secreted gelatinases in the same medium was lower in NM11 medium than in LuM1 case. Northern analysis showed the higher gene expression of both tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 in NM11 cells than in LuM1 cells, suggesting that both TIMPs are responsible for the increase of inhibitory activity in NM11 conditioned medium. Examination of the balance of gelatinases and inhibitor revealed that the amount of inhibitor exceeded that of gelatinases in the medium conditioned with NM11 cells. In contrast, the medium conditioned with LuM1 cells contained excess amounts of gelatinases. The results indicated a close correlation between the balance of gelatinases and inhibitors and the metastatic behavior of murine tumor cells.
Using polymerase chain reaction-assisted single-strand conformation polymorphism (PCR-SSCP) and immunohistochemical analyses, mutations in the p53 tumor suppressor gene were examined in 19 low- and high-grade gliomas. By PCR-SSCP and nucleotide analyses, p53 gene mutation was seen in 7 gliomas. Out of the 7 mutations, 3 were located at the CpG site of the previously proposed hot-spot codons 248 and 273, 2 were at codons 171 and 214 and the other 2 were in intron 5, 1 at the splice acceptor site and the other in the vicinity of the splice donor site. The latter 4 mutations have not, or only rarely, been observed in gliomas or in other tumors. However, their effect on the structural and functional alteration of the p53 protein was suggested by positive intranuclear p53 immunostaining in neoplastic cells in 3 mutations including the 1 at the splice acceptor site. In connection with glioma grading, the p53 gene mutation was shown to have occurred in both low- and high-grade gliomas, often in most of the neoplastic cells, as suggested by lack of distinct normal bands and ladders in SSCP and direct sequencing, respectively. The absence of recurrence and malignant transformation over a considerably long postoperative time in our low-grade glioma cases suggested that the p53 gene mutation might not be sufficient for the progression from low- to high-grade gliomas. The frequency of detection of mutation was 7/19(37%) by PCR-SSCP, 8/19(42%) by immunohistochemistry and 10/19(53%) by both methods. The results of PCR-SSCP and immunohistochemistry were consistent in 14 cases (73.7%), but not in 5 cases(26.3%).(ABSTRACT TRUNCATED AT 250 WORDS)
Intracranial chordomas are rare in childhood. Only 15 cases have been reported in children less than 6 years old. Bone destruction and calcification have been stated to be characteristics of this tumor. We present the case of a 5-year-old boy with clival chordoma without bone involvement.
This manuscript reports the results of the first cooperative study on primary central nervous system lymphoma (PCNSL) in Japan. Of 196 patients registered, 170 were judged as having PCNSL. No patients were immunocompromised. Of the 170 patients with PCNSL, 93 were males and 77 were females. The mean was 56.7 years. One hundred and nineteen tumors were confirmed histopathologically, and 51 were diagnosed by neuroimaging alone. All the tumors were non-Hodgkin's lymphoma. According to the Working Formulation for Clinical Usage (WF), 96 out of 119 tumors were classifiable: 53 were diffuse large cell type (55.2%), 17 immunoblastic type (17.7%), 9 diffuse small cleaved type (9.4%), 6 diffuse mixed type (6.3%), 5 polymorphous type (5.2%), 5 small lymphocytic type (5.2%) and 1 small non-cleaved type (1.0%). Of 21 tumors studied immunohistochemically, 18 were B-cell type and 3 were T-cell type. Irradiated patients (144) survived significantly longer than non-irradiated patients, (median survival time, MST: 19.2 and 2.7 months, respectively; p < 0.001). There was a remarkable difference in survival among patients of the intermediate lymphomas; MST (18 months) of patients with large cell lymphoma was significantly shorter than MST (over 96 months) of patients with other intermediate grade lymphomas (small cleaved and mixed) (p < 0.001) and had no significant difference from MST (9 months) of patients with high grade lymphomas. If patients were irradiated with more than 40 Gy, higher doses and different modes of irradiation brought no further survival advantage. Chemotherapy was performed in 87 of 144 irradiated patients (60.4%). No regimens were effective in prolonging survival. Of 144 irradiated patients, a complete or partial response to initial treatment was demonstrated in 91 (63.2%) and 43 patients (29.9%), respectively. Improvement in performance status was confirmed in 82 patients (57.0%). Despite a good response to initial treatments, 88 out of 144 evaluatble patients have died of PCNSL (MST: 19 months). Multivariate analysis based on the Cox hazard model revealed that histology of tumor, age at onset, performance status, and radiotherapy were prognostic factors. Neither chemotherapy nor mode of surgery was a beneficial factor.
Expression of the cytokine genes in human glioma cell lines and specimens was studied. Primers for 7 different human cytokine, IL-1 beta, IL-6, IL-8, GM-CSF, TGF-beta 1, TNF-alpha and IFN-gamma were used to analyze messenger RNA transcripts by polymerase chain reaction (PCR). Messenger RNA encoding for IL-1 beta, IL-6, IL-8, GM-CSF and TGF-beta 1 was found to be expressed in some of glioma cell lines. And those showed a proliferative response to IL-1 beta. IL-8 mRNA was found in 2 of 5 low grade gliomas, in 8 of 9 high grade gliomas. TGF-beta 1 mRNA was found in all gliomas, in 1 of 2 normal brains. IL-1 beta mRNA was only found in normal brains. TNF-alpha and IFN-gamma were not found in glioma cell lines and specimens. IL-8 mRNA was apt to be found more frequently among high grade glioma specimens.
We report two cases of congenital occipital dermal sinus in which elongation of the vein of Galen, elevation of the straight sinus, division of the superior sagittal sinus, elevation of the confluence of sinuses, elevation of transverse sinus and narrowing of the torcular angle were observed in the venous phase of cerebral angiography. Enhanced computed tomography (CT) revealed enlargement of the supracerebellar cistern, elevation of the straight sinus and of the confluence of sinuses, but no evidence of intracranial lesions. In order to study the relationship between anomalies in the dural venous sinuses and congenital occipital dermal sinus, we examined both cases from an embryological viewpoint.
The growth rate of 19 residual acoustic neurinomas was examined in a long-term follow-up study (median, 10 years; range, 5 to 17 years) following intracapsular removal. Of these, 10 (53%) had regrowth, three (16%) showed regression, and six (32%) were unchanged. The 10 acoustic neurinomas showing regrowth were divided into two categories, either solid or cystic, according to computed tomographic findings. Five acoustic neurinomas with cyst formation showed rapid regrowth, with the tumour doubling time ranging from 0.15 to 5.0 years (median, 4.5 years), and required re-operation. Five solid tumours showed slow regrowth, with the tumour doubling time ranging from 9 to 34 years (median, 15 years). Although cyst formation is a major factor in rapid regrowth, residual acoustic neurinomas without cyst formation have a slower growth potential. In this study, 74% of the residual acoustic neurinomas have never required re-operation. It is advisable to choose intracapsular removal if there is major risk of neurological deficits.
Cerebral haemodynamic changes in 17 patients with cerebral arteriovenous malformations (AVMs), who showed hypoperfusion on single-photon emission computed tomography (SPECT) before endovascular treatment, were studied after embolization. Nine of them had non-haemorrhagic clinical manifestations and the other eight had a history of intracranial haemorrhage. Obliteration of AVMs was nearly total in six patients and partial in eleven. New low density lesions on X-ray computed tomography (CT) developed in 3 of 6 patients after nearly total obliteration and one of 11 patients after partial obliteration. The first SPECT after embolization showed diminished hypoperfusion in 11 of 13 patients without new low density lesions and one of 4 patients with new low density lesions. Diminution of hypoperfusion was seen even in two patients who underwent SPECT study immediately after the embolization. Cerebral circulation was improved in five of eight patients with low density lesions before embolization and in nine of eleven patients after partial obliteration. Hypoperfused state in the haemorrhagic group tended to remain unchanged compared with that in the non-haemorrhagic group. The hypoperfused area was expanded after embolization in three patients with new cerebral infarction. It is important for improvement of cerebral circulation to reduce the shunt flow without causing new infarction due to the embolization itself. In one of two patients who had a hyperperfused area surrounding the AVM after embolization, an unexpected and abnormal degree of brain swelling and haemorrhage occurred at the end of the surgery 20 days after the embolization. In the other patient, total extirpation was successfully performed after confirming disappearance of hyperperfusion in the follow-up SPECT.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of the present study is to investigate the effects of feline carotid-jugular (CJ) fistula (Spetzler's model) on cerebral blood flow (CBF) in the acute period after creation of the fistula. Using laser-Doppler flowmetry, cortical CBF was measured on the fistula side of 11 cats. Temporary occlusion and opening of the fistula led to an immediate increase and decrease, respectively, in cortical CBF. However, CBF returned to baseline within 1 minute, on average. CO2 reactivity in the closed fistula was preserved. It is suggested that cerebral hemodynamic changes due to Spetzler's CJ fistula model are minimal in the acute period after fistulization.
The first case of full recovery from deafness after radical intracapsular removal of a large acoustic neurinoma, more than 4 cm in diameter, is reported. The patient, a 17-year-old woman, had multiple intracranial and intraspinal tumors in addition to bilateral acoustic neurinomas. Radical intracapsular removal is a useful technique to preserve nerves in patients with large acoustic neurinoma. When identifiable evoked potentials are preserved in brain stem auditory evoked potential, hearing preservation should be tried despite preoperative hearing level.
We recently experienced two cases of symptomatic interhemispheric arachnoid cyst (IHAC) in the elderly, both extending into the frontoparietal region. Both patients presented with more than an 8-year history of progressive hemiparesis and underwent capsule resection in combination with internal drainage to the pericallosal cistern via the interhemispheric approach. Postoperatively, the cyst cavities were greatly reduced in size, and neurologic signs and symptoms were markedly improved. A discussion of the diagnosis, mechanism of symptom onset, and management of symptomatic IHAC in the elderly is presented.
The expression of aromatase mRNA in cultured mouse brain cells was measured by a quantitative reverse transcription-PCR method using an internal standard. Aromatase mRNA was expressed in the cultured neurons prepared from diencephalon at 0.037 +/- 0.005 attomol/microgram total RNA. However, the mRNA was detected in neither the neurons from cerebral cortex nor astrocytes. These results demonstrate that expression of aromatase mRNA is regulated in cell type- and region-specific manners in cultured brain cells. The aromatase mRNA levels in neurons obtained from diencephalon were not affected by administration of testosterone, estradiol, dexamethasone, forskolin, or 12-O-tetradecanoyl 13-acetate. The results are in apparent disagreement with previous reports concerning regulation by androgens of brain aromatase activity in vivo and may suggest that aromatase expression in brain neurons is not directly induced by androgens. Androgen induction of brain aromatase may be mediated by several steps including cell-cell (neuron-neuron and/or neuron-glia) interaction.
Rats with puromycin aminonucleoside (PAN) nephrosis were given either angiotensin I converting enzyme inhibitor (ACEI), angiotensin II type 1 receptor antagonist (Ang IIRA), or no treatment for four weeks and were then monitored for an additional 12 weeks. In untreated PAN rats, proteinuria reached a maximum at two weeks (271 +/- 38 mg/day). Proteinuria in this early phase was markedly attenuated by ACEI (96 +/- 35 mg/day, P < 0.01), but unaffected by Ang IIRA (306 +/- 34 mg/day). Acute administration of a bradykinin antagonist substantially dampened the antiproteinuric effect of ACEI in PAN rats, resulting in an average increase in proteinuria of 41 +/- 14% in ACEI-treated rats (P < 0.05, ACEI vs. ACEI+bradykinin antagonist). Acute phase therapy for four weeks with ACEI or Ang IIRA did not attenuate subsequent glomerulosclerosis. Separate groups of PAN rats with similar degree of glomerulosclerosis, assessed at 16 weeks after PAN by renal biopsy, were then treated as follows: ACEI [50 mg/liter drinking water (DW), or 200 mg/liter DW], Ang IIRA (20 mg/liter DW, or 80 mg/liter DW) or no treatment, starting after renal biopsy. Whereas glomerulosclerosis increased from biopsy to autopsy at 28 weeks with emergence of low grade proteinuria in untreated PAN rats, proteinuria was absent and glomerulosclerosis was ameliorated or reversed in ACEI and Ang IIRA groups. The results indicate that the early phase proteinuria of PAN nephropathy is independent of Ang II, and that the antiproteinuric effect of ACEI is, at least in part, channeled through activation of bradykinin, whereas the subsequent progression of glomerulosclerosis is caused by a mechanism involving endogenous Ang II actions.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of alpha-sialosylcholesterol (alpha-SC) on formation of either microfilament or glia filament of rat astrocytes were investigated using a reconstitution system. Polymerization of the depolymerized microfilament preparation that had been extracted from a crude cytoskeletal fraction of rat astrocytes, in the presence of 100 mM KCl and 10 mM MgCl2, was suppressed in a dose-dependent manner by alpha-SC. alpha-SC inhibited polymerization of G-actin in a similar manner. The intensity of alpha-SC inhibition of G-actin polymerization was as great as that of microfilament polymerization, suggesting that the inhibition of microfilament polymerization by alpha-SC was due to the direct action of alpha-SC on actin, the main component of microfilament. alpha-SC depolymerized partly the polymerized microfilament preparation, which resembled F-actin (microfilament-like filaments). alpha-SC suppressed, in a dose-dependent manner, polymerization of a glia filament preparation that had been extracted from astrocyte cytoskeletons in the presence of phalloidin. An increase in the amount of added alpha-SC (up to 15 microM) decreased the amount of the larger glia filament-like filaments, which were 10 nm thick and centrifuged down at 16,000 g for 30 min, and increased that of smaller ones precipitated only after centrifugation at 100,000 g for 1 h. The lower the concentration of the depolymerized glia filament extract, the greater was the inhibition by alpha-SC of the polymerization. alpha-SC repressed polymerization of vimentin, the dominant component of glia filament. Vimentin polymerization was more strongly inhibited by alpha-SC than polymerization of glia filament was.(ABSTRACT TRUNCATED AT 250 WORDS)
The postsynaptic density (PSD) fraction prepared from rat forebrains frozen with liquid nitrogen immediately after dissection (within 30 s after decapitation) contained major postsynaptic density protein (mPSDp), alpha subunit of Ca2+/calmodulin-dependent protein kinase II (CaMKII) at a level of merely 2.7% of the total protein. The content of the protein in the fraction was increased to approximately 10% by placing the forebrains on ice for a few minutes. Accumulation, but to a lesser extent, of the protein after placement was also observed in the particulate, synaptosome, and synaptic plasma membrane fractions with its concomitant decrease in the cytosolic fraction. The distribution change may be translocation of the protein, because the amounts of the losses of the protein in the cytosolic fraction were balanced by the gains in the particulate fractions. By translocation, CaMKII became Triton X-100 insoluble and partially inactivated. The amount of CaMKII transferred from the cytosol to particulate fractions at 0 degrees C was about the same as that contained in the conventional PSD fraction. Furthermore, the thickness of the PSD was increased by the treatment of the forebrains at 37 degrees C, by which the content of CaMKII alpha in the PSD fraction was increased to twofold. These results suggest that most of the CaMKII alpha subunit associated with the PSD fraction (mPSDp) is translocated from cytosol after decapitation. We also showed similar translocation of CaMKII beta/beta'.