Biomedical subjects
Publications and source records attributed to Y Katayama.
To assure the quality of cytologic diagnosis, the most important process is review of the previous cytologic and histologic examinations. Correlations of cytologic-histologic diagnosis should be reconfirmed. If diagnostic inconsistency is found, the cause must be explained. Now the computer system combining cytologic and histologic records is indispensable for quality control of cytologic diagnosis.
We have determined the conditions for quantitative phagocytosis assay in human polymorphonuclear leukocytes by flow cytometry using fluorescent bioparticles (Zymosan A, S. aureus, E. coli). The changes in the phagocytic index after an exogenous stimulation and after addition of monoclonal antibodies against receptor antigens on polymorphonuclear leukocytes were examined by using fluorescent microspheres (FM particles) and bioparticles. When bioparticles were used, the phagocytic index decreased after an exogenous stimulation with phorbol myristate acetate (PMA). The phagocytic index obtained with the FM particles increased by the addition of PMA and the supernatant of E. coli, but decreased by the addition of the supernatant of S. aureus. After the addition of the monoclonal antibodies the phagocytosis for the S. aureus and E. coli particles was blocked by anti-CR3, that for the Zymosan A particles was blocked by anti-CR3 and IgGFcR2, and that for the PM particles was blocked by anti-CR1, CR3, and LFA-1 beta, partially. These findings implied the involvement of a complement receptor. However, the degree of its involvement varied with the target particle.
We observed recently three cases of ureteral polyps including a case of multiple polyps. The first patient was a 33-year-old man with multiple polyps at the left upper ureter. The second patient was a 51-year-old man and the third 49-year-old man, and both cases were complicated with ureteral stones. We divided 88 ureteral polyps reported in Japan from 1970 to 1990 into polyps in children and those in adults. We further divided the individual polyps into single and multiple polyps and examined them clinically. Characteristic findings were obtained in polyps in children; namely, multiple polyps were dominant, almost all of them occurred at the left upper ureter and no cases were complicated with ureteral stones. Furthermore, many of the multiple polyps in adults occurred at the left upper ureter and few were complicated with stones as in the children. In conclusion, the ureteral polyps in children and multiple ureteral polyps in adults were similar in character and we presumed that some congenital factors might be involved in their occurrence.
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We developed a kinetic assay for calcium in serum and urine, based on the activation of porcine pancreatic alpha-amylase (EC 3.2.1.1) with 2-chloro-4-nitrophenyl-alpha-maltotrioside as substrate. The kinetic generation of 2-chloro-4-nitrophenol, monitored at 405 nm, was proportional to the concentration of calcium in serum and urine. The assay was developed and evaluated with the Cobas Bio centrifugal analyzer. The average within-run and between-day imprecision (CV) was 0.96/1.26% and 1.07/1.63%, respectively, for serum calcium and 1.50/2.54% and 1.70/2.64%, respectively, for urine calcium. Results of the proposed method (y) correlated well with those determined by atomic absorption spectrophotometry (x): y(serum) = 1.005x + 0.028 mmol/L (Sy/x = 0.058, r = 0.974, n = 50), and y(urine) = 1.017x-0.115 mmol/L Sy/x = 0.30, r = 0.981, n = 25). We also present data showing that the method is highly sensitive, rapid, relatively free of interference, and amenable to automation.
Coronary artery bypass grafting in a 78-year-old female with severely calcified ascending aorta was performed successfully. Bilateral internal thoracic arteries and saphenous vein were anastomosed under ventricular fibrillation and hypothermia without aortic cross-clamping. Proxymal anastomosis of saphenous vein graft was performed directly under circulatory arrest in a normal part of ascending aorta which was confirmed by intraoperative ultrasonography. Weaning from ECC was easy and no neurological complication was observed after operation. Bypass grafts were patent on postoperative coronary angiogram and postoperative course was uneventful. We think the technique of circulatory arrest and intraoperative ultrasonography were useful in a patient with severely calcified ascending aorta.
A 44-year-old female with left to right shunt and persistent left superior vena cava (PLSVC) suspected of unroofed coronary sinus defect with patent right SVC and innominate vein was treated surgically. PLSVC was ligated and coronary sinus ostium was closed with a EPTFE patch. Roof defect of coronary sinus was left open and allowed the coronary venous blood to drain into the left atrium. Patient recovered well and post-operative cardiac catheterization revealed no significant right to left shunt nor desaturation of arterial blood. In the correction of unroofed coronary sinus defect and PLSVC and no other intra-cardiac defect, ligation of PLSVC and closure of coronary sinus ostium was simple and effective, although it was not anatomically corrected.
A Ca2+ imaging method has been used to demonstrate simultaneously the magnitude and time course of the increase in the intracellular Ca2+ concentration ([Ca2+]i) in 10-30 individual human peripheral T cells following stimulation by anti-CD4 or anti-CD8 monoclonal antibody (MAb) as well as anti-CD3 MAb. The rise in [Ca2+]i began within 10 s of the introduction of the MAb and reached a peak of 240 nM (mean of 73 cells) in 20-40 s. The peak was followed by a slow decrease persisting for 6-8 min. Comparing Ca2+ responses in the presence and absence of external Ca2+, the rise in [Ca2+]i was found to be caused by both transient intracellular Ca2+ release and a long-lasting Ca2+ influx from outside the cell. Cross-linking of CD4 or CD8 using anti-IgG antibody augmented the response in individual cells, as seen in the higher peak (365-390 nM) and the longer duration (over 10 min). Simultaneous stimulation of CD3 and CD4 did not cause a summation of Ca2+ responses but caused a suppression in the CD3-mediated Ca2+ response. The results support the view that CD4 and CD8 play a role in signal transduction for T cell activation and that the CD4-derived signal interferes with the CD3-derived signal at some stage in the signalling pathway causing the Ca2+ response.
Single neuron activities responding to peripheral stimuli with short latencies were recorded within the thalamic nucleus ventralis posterolateralis (VPL) after transection of the spinothalamic tract (STT) in the cat under alpha-chloralose anesthesia. The VPL neurons showed spontaneous and evoked hyperactivity after STT transection, which was revealed at 1-2 weeks. The spontaneous hyperactivity further progressed until 3-4 weeks. These hyperactivities were observed in core-area neurons as well as neurons found in the shell area, suggesting that some, if not many, of the N-methyl-D-aspartate (NMDA) receptor antagonist (MK-801, 4-16 mg; i.v.) attenuated both the spontaneous and evoked hyperactivity observed after STT transection. No such effects were demonstrated in sham-operated animals. These findings suggest that VPL neurons become hyperactive after STT transection through recruitment of NMDA receptors. The hyperactivity of VPL neurons may represent an important background process in the production of deafferentation pain induced by lesions involving the STT.
Cleavage of beta-aryl ether linkages is essential in lignin degradation. We identified another beta-etherase gene (ligF), which contains an open reading frame of 771 bp and lies between genes coding C alpha-dehydrogenase (ligD) and beta-etherase (ligE). The beta-etherase activity of LigF expressed in Escherichia coli was more than 80 times as high as that of LigE. ligF and ligE are homologous to glutathione-S-transferase, and upon addition of glutathione a remarkable acceleration of beta-etherase activity was found in E. coli carrying ligF. It is concluded that LigF plays a central role in beta-aryl ether cleavage and that glutathione is the hydrogen donor in this reaction.
The present study examined the functional changes in the hippocampal CA1 pyramidal cell system in vivo occurring after 12-min forebrain ischemia in the rat. A population excitatory postsynaptic potential and orthodromic population spike of CA1 pyramidal cells to stimulation of the Schaffer collaterals were potentiated at 6-8 h post-ischemia. These changes were not associated with an increase in excitability of the CA1 pyramidal cells as evaluated from the antidromic population spike induced by alveus stimulation, suggesting the presence of an increased synaptic efficacy. The post-ischemic potentiation was prevented by pretreatment with the N-methyl D-aspartate (NMDA) receptor antagonist, MK801, in a dose-dependent manner. These findings suggest that 12-min forebrain ischemia in the rat activates NMDA receptors, which results in an increase in synaptic efficacy to the CA1 pyramidal cells at 6-8 h post-ischemia.
A case of meningioma with extensive xanthomatous metaplasia occurring in the left frontal convexity of a 37-year-old woman is reported. The tumour was demonstrated as a hypodense mass with minimal enhancement on CT. Our findings suggest that magnetic resonance imaging may provide a clue to the diagnosis of meningiomas with extensive xanthomatous metaplasia when CT is less specific.
31P nuclear magnetic resonance (NMR) spectroscopy of the in situ rat kidney was performed by a surface coil method, and the effects of ischemia and furosemide infusion were assessed. 31P NMR spectra of the kidney subjected to 30 min of ischemia returned completely to the pre-ischemic level after 60 min of reperfusion. But the 31P NMR spectra after 60 min of ischemia did not recover, even after 120 min of reperfusion. Levels of beta-ATP and inorganic phosphate (Pi) decreased and the chemical shift of Pi increased after intravenous infusion of furosemide. This increase in chemical shift might signal an alkalotic change in intracellular pH. Furosemide infusion prior to ischemia is thought to protect the kidney from injury induced by 60 min of warm ischemia. The chemical shift of Pi returned to the pre-ischemic level earlier than beta-ATP and Pi. In conclusion, according to the findings of 31P NMR spectroscopy, furosemide infusion prior to ischemia may be effective in protecting the kidney against ischemic injury. But the change in Pi peak and the causes of the dissociation of Pi and beta-ATP should be examined further.
We examined the effect of nicardipine and hyperventilatin on pulmonary arterial pressure (PAP) in four patients with pulmonary hypertension in congenital heart defect especially in the early postoperative period. There was a significant positive correlation between the values of arterial carbon dioxide tension (PaCO2) and the ratio of mean PAP to mean systemic arterial pressure (Pp/Ps) in two patients whose Heath Edwards classification was Grade II; one of them also had 20% reduction of mean PAP by nicardipine without changing mean arterial pressure. In the remaining two patients showing no correlation between the values of PaCO2 and Pp/Ps, nicardipine did not reduce PAP. Although nicardipine reduced PAP without changing systemic arterial pressure in only one out of four patients, these results suggest that nicardipine may be a drug for control of PAP during weaning phase from the ventilator especially in patients whose PAP decreases under hyperventilation.
The effects of indeloxazine on the ischemia-induced death of hippocampal CA1 pyramidal cells following transient cerebral ischemia were examined in the mongolian gerbil. Increased survival of CA1 pyramidal cells was demonstrated in animals pre- and post-treated with indeloxazine. Increased survival of CA1 pyramidal cells was, however, not demonstrated in animals post-treated but not pre-treated with indeloxazine. A previous study has demonstrated that indeloxazine increases the glucose and adenosine triphosphate (ATP) contents in the brain probably through an enhanced capability of oxidative phosphorylation. It has been reported that increases in the glucose and ATP contents in the brain before ischemia delay the onset of massive ionic fluxes during ischemia. The delay in onset of this ionic event may help to protect these cells from death. The present data suggest that energy state before ischemia may play an important role in the protective effect of indeloxazine.
The morphology of the arteries in the uterine wall was studied in three multiparous aged mares that had suffered repeated pregnancy failure. The uterine wall arteries exhibited elastosis of the intima or adventitia, or both, resembling "physiological pregnancy sclerosis". In areas affected by elastosis, degeneration of the pre-existing elastic fibres and increased glycosaminoglycans were frequently observed. Newly formed elastic fibres were not evident. Delayed resorption due to disordered metabolic turnover of the elastin was thought to be an important factor in the pathogenesis of the arterial elastosis in the uterine wall.
The present study examined the changes in the long-term potentiation (LTP) of the hippocampal Schaffer collateral/CA1 pyramidal cell system in vivo occurring after 12-min forebrain ischaemia in the rat. A population spike (PS) of CA1 pyramidal cells were recorded in 18 rats at 7 h post-ischaemia. While the threshold and amplitude of pretetanic PS were not depressed, the induction of LTP was significantly impaired following ischaemic insult (155 +/- 28% of baseline PS, mean +/- SD, n = 6, p < 0.001), as compared to sham-controls (337 +/- 84%, n = 5), without reduction of single pulse responses. Pretreatment with 4(o-benzylphenoxy)-N-methylbutylamine hydrochloride (Bifemelane; 50 mg kg-1 i.p.) slightly but significantly attenuated the impairment in LTP induction (196 +/- 23%, n = 6; p < 0.02). The findings in the present study indicate that CA1 pyramidal cells are dysfunctional in synaptic plasticity long before their death. Bifemelane has been demonstrated to inhibit acetylcholine release strongly during cerebral ischaemia but not interfere with normal cholinergic synaptic transmission. The effect of bifemelane suggests that Ach release during ischaemia is partially involved in the post-ischaemic impairment of LTP induction.
The changes in cytochrome oxidase (CYO) activity in the primary somatosensory cortex (SI) induced by unilateral lesions restricted to the posterior ventrobasal region of the thalamus were investigated by histochemical techniques and photometric semi-quantitation in the rat. The CYO activity decreased rapidly and dramatically in layer IV of the lesioned side, reaching its lowest level within 2 weeks, and remained depressed at 8 weeks post-lesion. Segmentations normally seen in layer IV corresponding to barrels remained absent. While less marked decreases were also noted in other layers, obvious recovery was subsequently observed, attaining levels comparable to those on the intact size at 6 or 8 weeks post-lesion. The persistent decrease in layer IV appears to reflect a reduced thalamocortical activation of the dendritic profiles and neuronal perikarya. The recovery in other layers may represent an increase in the resting level of the initially depressed neuronal activity near to the original levels. The persistent reduction of function in the inhibitory surround, which is normally activated by thalamocortical input, may contribute to the increase in CYO activity.