Deltoid tendon reflexes are mainly innervated by the C5 reflex arc, and show hyperactivity in spinal cord lesions of the occipito-cervical region. The author has been using Deltoid tendon reflex in the diagnosis of the level of injury in cervical myelopathy. However the evaluation of tendon reflexes is subject to examiner bias. Therefor the author has focused attention on qualitative analysis of the tendon reflex utilizing T-wave as a method of objective evaluation. T-waves of Deltoid tendon reflex (DRT) and biceps tendon reflex (BRT) were first recorded in a contrast group of 40 healthy adults. The mean onset latency for DRT was 10.48±1.02 msec. The contrast group was divided as follows. Normal activity group : within mean onset latency ±2S.D. Hypoactivity group : over mean onset latency +2S.D. Hyperactivity group : under mean onset latency -2S.D. Then T-waves were recorded likewise in 30 upper extremities of 15 patients with cervical disorders. Electrophysiological diagnosis of the level of injury was possible in 12 of the 15 patients. In seven of these, the electrophysiological diagnosis was in concordance with the clinical diagnosis of the level of injury. Because this method can be performed at the outpatient department, is noninvasive, is relatively easy to perform, and is not subject to examiner bias, I believe that it is very useful for evaluating the pathology of high cervical lesions.

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The mechanism by which Helicobacter pylori (H. pylori) and nonsteroidal anti-inflammatory drugs (NSAIDs) injure gastric mucosal cells was investigated by assessing their effects in inducing apoptosis of gastric epithelial cells and analyzing synergism of their effects. Normal gastric mucosal cells collected from rabbits were cultured with viable H. pylori or an NSAID for 24 hours to create an in vitro model of gastric epithelial cell injury. Fluorescent antibody was conjugated to Fas antigen (one of the molecules known to induce and disseminate apoptosis). The Fas antigen expression rate, i.e., percentage of positively stained cells among 1×10^6 cells was measured using a FACScan as an indicator of the degree of injury of gastric mucosal cells. The Fas antigen expression rate was significantly higher in the H. pylori infection group (Group D; me an±SE=43.9±4.4%) than in the untreated control group (Group A; 29.5±0.3%) (P<0.01). Group E, in which H. pylori inoculation was followed by treatment with an NSAID, had a significantly higher Fas antigen expression rate (64.0±3.4%) than Group B (treated with an NSAID alone; 32.3±0.3%) and Group D (P<0.001, E vs. B; P<0.001, E vs. D). Group C, in which an NSAID treatment was followed by with H. pylori inoculation, had a significantly higher Fas antigen expression rate (51.5±2.3%) than Group B (treated with an NSAID alone; 32.3±0.3%) (P<0.01). Fas antigen expression rate did not differ significantly between Groups A and B. These results indicate that H. pylori and NSAID induce cell injury in a synergistic manner, and that this effect is particularly strong when NSAID treatment follows H. pylori infection. This indicates the necessity of eradicating H. pylori before using NSAIDs in H. pylori positive patients, in order to prevent gastric mucosal injury induced by the combination of H. pylori and NSAIDs.

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QT dispersion (QTd) is affected by inhomogenous ventricular repolarization, and increased QTd is associated with a higher risk of ventricular tachycardia. Recent studies have shown an increase in QTd in patients with myocardial infarction (MI). However, the importance of changes in QTd with exercise has not been carefully investigated in MI patients. The aims of this study were to identify factors associated with changes in QTd induced by exercise in MI patients and to elucidate their clinical significance. QTd immediately after exercise was studied in 41 control patients and 128 MI patients, 1 month after the onset of MI, using treadmill exercise electrocardiography. The MI patients were divided into two groups based on the results: those with a QTd >50 msec immediately after exercise (the long QTd group), and those with a QTd ≦50 msec immediately after exercise (the short QTd group). The clinical findings for the two groups were then compared. Maximum ST-segment depression in the noninfarct-related leads (p<0.01), the defect score and incidence of redistribution at the infarct site on exercise thallium-201 scintigraphy (p<0.05), the prevalence of multivessel disease (p<0.01), and the incidence of detectable late potentials (p<0.05) were significantly higher, and the left ventricular ejection fraction (p<0.01) and heart rate immediately after exercise (p<0.01) were significantly lower in the long QTd group than in the short QTd group. The cumulative survival rate was significantly higher (p<0.001) in the short QTd group than in the long QTd group. In conclusion, increased QTd with exercise in MI patients is associated with transient myocardial ischemia, a large infarct size, and depressed left ventricular function. Measurements of QTd with exercise may be useful for determining the long-term prognosis of MI patients.

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Although several diagnostic criteria focusing on variations in the ST-T segment during exercise and in the recovery phase have been proposed to obviate this shortcoming, no satisfactory method has yet been devised. The aim of the present study was to investigate the degree of coronary artery disease reflected by ST-T changes seen in the recovery phase of treadmill exercise electrocardiography (ECG). The subjects were 215 men (mean age±standard deviation : 56±10 years) with chest pain syndrome who underwent both treadmill exercise ECG and coronary angiography. The ST-T changes seen at various time intervals after exercise stress were classified into four groups : unchanged (group A ; 91 patients) ; improved during the recovery phase (group B; 40 patients) ; worsened during the recovery phase (group C ; 54 patients) ; and appeared only during the recovery phase (group D; 30 patients). The ECG results were then compared with the angiography findings. Multivariate analysis identified the Gensini score as an independent factor associated with worsening of ST-T changes in the post-exercise recovery period, and positive acetylcholine injection test findings as an independent factor associated with the appearance of ST-T changes only in the recovery phase. Multi-vessel disease was diagnosed with a sensitivity of 58% and a specificity of 84% in patients whose ST-T changes worsened during the recovery phase. Coronary spasm was diagnosed with a sensitivity of 59% and a specificity of 96% when the appearance of ST-T changes only during the recovery phase was used. These results indicate that worsening of ST-T changes during the recovery phase suggests the presence of severe coronary artery disease, whereas the appearance of ST-T changes only during the recovery phase suggests the presence of coronary spasm.

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Severe stenosis of a non-infarct-related artery may cause regional remote ventricular asynergy during the acute phase of myocardial infarction (MI). Such lesions may contribute to left ventricular dysfunction and poor prognosis following MI. We performed two-dimensional echocardiography in 140 patients with their first acute anterior MI on admission and 1 month after MI. Using the modified centerline method, the left ventricular short axis image was used to determine % wall thickening (%WT) of the left anterior descending artery (LAD) area, the right coronary artery (RCA) area, and the left circumflex artery (LCX) area. The study compared the accuracy of %WT and visual assessment of wall motion for the diagnosis of remote coronary stenosis. Of the 140 patients, 100 had single-vessel disease occurring in the LAD (group S) and 40 had multivessel disease (group M). In group M, remote asynergy in the non-infarcted area was identified in 33 patients (83%) by abnormal %WT and in 16 (40%) by abmormal wall motion (p<0.001). The %WT of the RCA area was lower in group M than in group S (p<0.0001). The %WT of the LCX area was also lower in group M than in group S (p<0.0001). The %WT in the non-infarcted area improved 1 month after the onset of MI (p<0.0001). %WT determined by two-dimensional echocardiography and the modified centerline method is more sensitive than visual assessment of wall motion for the identification of multivessel disease in patients with acute anterior wall MI.

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Seventy-three women with uterine leiomyoma, who did not want to undergo surgery, received four months of administration of gonadotropin-releasing hormone agonist (GnRHa) which was repeated at intervals of 4-6 months. Forty-two women resumed their menstruation after discontinuation of GnRHa (non-menopause group), whereas 31 women reached menopause after GnRHa, avoiding surgery for leiomyomas (menopause group) successfully. In non-menopause group, the serum concentrations of LH, FSH, estradiol (E_2) and uterine volume decreased significantly during GnRHa therapy and returned to pretreatment values 4 months after cessation of therapy. In menopause group, these parameters decreased during GnRHa therapy similarly to non-menopause group. After cessation of therapy, however, the serum concentrations of LH and FSH increased up to significantly higher values than pretreatment ones, the serum concentrations of E_2 remained in the castrate range, and their uteri maintained reduced volumes. The pretreatment values of LH and FSH in serum were significantly higher in menopause group than in non-menopause group. Long-term follow-up after GnRHa therapy revealed that it took 16.3 ±9.7 months to reach menopause following occasional metrorrhagia and that a transient decrease in serum LH and FSH levels with a transient increase in serum E_2 levels caused an increase in uterine volume and metrorrhagia. Bone mineral density (BMD) decreased during GnRHa therapy and returned to pretreatment levels 6 to 10 months after cessation of therapy. Long-term follow-up after menopause showed a similar decrease in BMD with increasing age to that in normal women.

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Caffeine is known to act as an adensine receptor antagonist (in vitro study), however the exact mechanisms of its actions in the CNS remain unclear. Therefore the present study has been designed to examine the effects of caffeine on behavioral action, and whether its effecs mediate adenosine A_2 receptor using behavioral and pharmacological method. As measurement of behavioral activity, locomotor activity (total distance and time) and frequency of standing on hind limbs (rearing) were evaluated with the open-field apparatus. The results was as follow : Administration of caffeine and selective adenosine A_2 receptor antagonist (DMPX) dose-dependently increased in locomotor activity in rats. Behavioral stimulant effects of caffeine (10mg and 30mg/kg, I.P.) and 3,7-dimethyl-1-propargylxanthine (DMPX ; 1.3mg/kg, I.P.) were dose-dependently attenuated by selective adenosine A_2 receptor agonist, 5'-(N-cyclopropyl)-carboxamidoadenosine (CPCA, I.P.), respectively. It was suggested that caffeine-induced stimulating effects on behavioral action in the CNS were direct consequences of adenoceptor blockade.

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The expression level of genes related to the cell cycle regulation system were determined by a quantitative RT-PCR (QPCR) method in liver of the tumor-bearing mice transplanted with methylcholanthrene-induced fibrosarcoma. Effect of bleomycin administration was also studied in these genes in both animal groups. Results indicate that the expression level in all of the p53, p21, p16, p35, and cdk5 genes 2-5 times increased in tumor-bearing mouse liver than those found in normal liver. But K-ras level showed no difference between the two groups. Bleomycin induced, in normal mouse liver, a 3 to 4 fold increase in p53 and p21 expression level, but it decreased p16 level to one half of the initial level. While the level for p35 twice increased but, one for cdk5 did not show any change after the administration. The level of K-ras gradually increased 96h after the administration. On the other hand, tumor-bearing mouse liver showed slight increase (1.6 fold) in p53 expression, but no obvious changes in p21 and p16 expression by the stimulation of bleomycin. The agent induced a slight decrease (20%) in p35, no change in cdk5, and gradual increase in K-ras gene expression. These results suggest that the expression level in the genes related to the cell cycle regulation is altered in tumor-bearing animal leading the enhanced ytanscription rate in a certain enzyme system.

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The purpose of this study was to evaluate the significance of ST segment re-elevation within 24 hours after the onset of myocardial infarction. The study included 77 patients with their first anteroseptal (n=43) or inferior (n=34) MI who had 12-lead electrocardiograms recorded every 5 minutes using an automatic intermittent recording electrocardiograph. Thirty-five (45.5%) patients had ST segment re-elevation within 24 hours after the onset of myocardial infarction. The incidence of congestive heart failure and cardiogenic shock was significantly higher in patients with ST segment re-elevation than in patients without ST segment re-elevation (37.1% vs. 14.3%, p=0.04026 and 57.1% vs. 19.0%, p=0.00054, respectively). The peak serum creatine kinase activity was significantly higher in patients with ST segment re-elevation than in patients without ST segment re-elevation (5341±4281IU/L vs. 2908±2405IU/L, p=0.00276). The left ventricular ejection fraction was significantly lower in patients with ST segment re-elevation than in patients without ST segment re-elevation (48.2±10.1 vs. 56.9±11.8, p=0.00111). However, there were no significant differences between the two groups with respect to coronary angiographic findings (infarction related artery, presence of collateral arteries, presence of multivessel disease, or reocclusion after 1 month) or type of therapy employed (conservative or reperfusion therapy). These data suggest that ST segment re-elevation within 24 hours after the onset of myocardial infarction is a predictor of large infarct size, decreased cardiac function, and a high incidence of complications of myocardial infarction.

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A practical method was developed for the histological observation of the gene expression level in retina using an in situ RT-PCR technique. Eye balls were dissected out from a BALB/c mouse, which had been perfused via the left ventricle with 4% paraformaldehyde solution, post-fixed for 20hr in the same fixative, embedded in paraffin and sectioned at 5μm thickness. The sections were then digested with pepsin and DNase. The period required for the optimal protease digestion, which is the most important for the successful detection of PCR-amplified cDNA, varied among retinal layers. The digested section was followed by the one step in situ RT-PCR using rTth polymerase and primers labeled with dinitrophenyls for K-ras and p53 genes. In normal mouse retina, the two genes was expressed in the all layer in retina except for outer segment. The most remarkable signal was seen in inner segment for both genes. The signal pattern of the gene expression were obviously different between the both genes in inner plexiform layer (IPL), in outer plexiform layer (OPL) and in outer nuclear layer (ONL). Bleomycin administration induced an increase in K-ras expression level in ONL 10hr and in IPL 20hr after the injection. While no change was observed in p53 expression in IPL but the level increased obviously in ONL 20hr after the injection. This method proved to be a useful tool for the histological observation of the gene expression level in tissue.

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We investigated the mechanism of cardiac lipofuscin accumulation induced by a short-term intake of fish oil supplemented diet. Rats were fed with the ordinary diet (control group) for 8 weeks, the ordinary diet for 4 weeks followed by a 5 % sardine oil-supplemented diet for 4 weeks (fish oil group), or the 5% fish oil-supplemented diet for 4 weeks followed by the ordinary diet for 4 weeks (wash-out group). Ultramicroscopic examination of ventricular myocytes in the fish oil group revealed a marked accumulation of lipofuscin (p<0.01 vs. control group). However, this accumulation was barely detectable in both of the control group and the wash-out group. The organic solvent-soluble fluorescence compounds were analyzed by the reversed-phase HPLC in the myocardial tissue in the fish oil group. The content of those compounds was significantly higher in the fish oil group than those found in the control group and the wash-out group (p<0.01). Myocardial content of vitamin E was significantly reduced in rats fed with the fish oil diet (p<0.01). It can be concluded that the short term intake of fish oil supplemented diet induces cardiac lipofuscinosis through the lipid peroxidation metabolism and the lipofuscin accumulated in the myocardium can be eliminated by the termination of the oil supplemented diet.

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The purpose of the study is to obtain ECG findings in the acute stage of infarctions that reflect short-term prognosis of inferior infarctions. The subjects were 222 patients with first acute inferior infarctions without conduction disturbances such as bundle branch block. In ECGs on admission, the Q wave amplitude at the II, III and aVF leads, the amplitudes of the R and S waves at leads VI and V2, the ST segment deviation at all leads except aVR were measured and the results were compared between living and deceased cases. Thirty-six patients (16.6%) died of cardiac disease during hospitalization. Among the ECG parameters on admission, the highest sensitivity for differentiation of living and deceased cases was ST deviation in lead I (STI)&le;-1mm(72.2%), followed by STII-STIII&le;-1mm (66.7%), and ST deviation at V6 (STV6)&le;-1.5 or &ge;1mm (63.9%). The specificity was highest for STV6 &ge;1mm (73.7%). The diagnostic accuracy was highest for STV6 &ge;1mm (77.7%). In a logistic analysis, STI&le;-1mm and SST (V4 to V6)&le;-3.5mm were extracted as independent factors in in-hospital deaths.

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