Amplification of the c-myc gene has been reported in non-small cell lung cancer (NSCLC). We performed dual color fluorescence in situ hybridization (FISH) to detect amplifications of the c-myc gene on chromosome 8 to evaluate the relationship between these possible abnormalities and pathological stage. Tumor tissue samples were obtained from 29 patients of NSCLC in Stage I (n=15) and III (n=14) who underwent lobectomy at Saitama Cancer Center. Samples were analyzed for chromosome 8 centromere and c-myc gene by dual color FISH. The numerical aberration rate of chromosome 8 was 36.8±20.3% in Stage I and 40.6±24.8% in Stage III. The amplification rate of c-myc gene was 48.3±15.2% in Stage I and 57.4±17.0% in Stage III. There was a significant difference in the numerical aberration rate of chromosome 8 between patients who survived for 5 years or more (28.8±17.5%) and those who survived less than 5 years (44.7±23.1%). The amplification rate of c-myc gene was not different between patients who survived more and less than 5 years survival, and who survived more and less than 3 years. The 5 year-survival rate in patients who showed 40% or more of chromosome 8 aberrations (n=13) was 15.4%, which revealed significantly less than that of patients who showed less than 40% of aberrations (n=16) (56.3%). There was no difference between the 5 year-survival rate in patients whose amplification rates of c-myc gene were equal or more than 50% (n=16) and less than 50% (n=13) (25.0% and 53.9%). The rate of chromosome 8 aberrations and the c-myc gene amplification rate were not correlated with pathological stage. However, the rate of chromosome 8 aberration showed correlation in terms of longevity of survival rate, therefore we considered the rate of chromosome 8 aberration to be an additional prognostic factor of patient with NSCLC. (J Nippon Med Sch 1999 ; 66 : 107-112)

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The effects of catecholamines (CAs) other than their transmitter action were investigated using clonal neuronal cells, ML-DmBG 2-c2, derived from Drosophila in the larval central nervous system (CNS). All catecholamines tested, adrenaline (AD), dopamine (DA), noradrenaline (NA) and isoproterenol (ISO), prevented any increase in the number of cells during 2-to 7-day culture. α-, β-adrenergic and dopaminergic antagonists did not block the effects of CAs on the number of cells. Adrenochrome, a product of the oxidative degradation of AD, also prevented any increase in the number of cells, as AD did. The effect of AD was partially blocked by an antioxdant, dithiothreitol (DTT). These results suggest that the inhibition of the increase in cell numbers by CA might be mediated by CAs themselves and/or oxidative products in the CA metabolic process. It is concluded that CAs inhibit cell proliferation but do not induce cell death in the Drosophila clonal cells. (J Nippon Med Sch 1999 ; 66 : 113-118)

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Background : Syncope of patients with bradyarrhythmia is perceived as severe sign of low cardiac output caused by bradycardia and as a major criteria for pacemaker implantation (PMI). However, it has been reported that PMI can not always prevent syncope ; it has been suggested that not bradycardia but an abnormality of the autonomic nervous system blays a part in syncope. Purpose : To investigate the relation between autonomic nervous dysfunction and syncope in cases of sinus bradycardia (SB). Subjects : Thirty-nine patients with SB were divided into two groups according to the presence (group S, n=16, 46.9±20.0 years) or absence (group N, n=23, 40.4±17.6 years) of syncope or presyncope. Methods : Corrected sinus node recovery time (CSNRT) was measured by electrophysiologic study. Pharmacologic autonomic nervous tests were performed as follows in a quiet room. Increased HR by application of 0.04 mg/kg atropine (para-tone), and by 0.004 μg/kg/min isoproterenol divided by 0.004 (β-sens) were evaluated. β-tone was obtained by subtracting HR after application of propranolol (0.2 mg/kg) from that of atropine. Basal β-sympathetic activity was evaluated by β-sec that was obtained by β-tone/β-sens. Increased SBP by application of 0.4 μg/kg/min phenylephrine divided by 0.4 (α-sens) was evaluated. α-tone was obtained by subtracting minimum SBP after 0.2 mg/kg phentolamine from SBP after application of propranolol. Basal α-sympathetic activity was evaluated by α-sec, that was obtained by α-tone/α-sens. Result : There were no significant differences in basal clinical characteristics (age, sex, cardiac function) between the groups. The parameters of the functions of parasympathetic and β-sympathetic receptors (para-tone, β-sens, β-tone, β-sec) showed no significant differences between the groups. α-sens was attenuated (P<0.01) and α-sec was augmented (P<0.0001) significantly in group S. Conclusion : It was suggested that syncope or presyncope in SB patients could be attributed to failure of vasoconstriction mediated by α-sympathetic receptor but to severity of sinus node dysfunction. (J Nippon Med Sch 1999 ; 66 : 119-126)

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To determine whether the hepatocyte plasma membrane possesses a Ca²⁺ channel, we applied a patch clamp technique to isolated guinea-pig hepatocytes. In a cell-attached configuration, using an internal pipette solution of 110 mM BaCl₂ or CaCl₂, we observed sporadic inward single channel currents (Po=0.004±0.002, n=6) at various membrane potentials. The unit amplitude was 0.60±0.15 pA (n=6) at resting membrane potential. The single channel conductance was 20.4±4.6 pS (n=6) and this channel showed no rectification and no voltage dependence. Bay K 8644, a dihydropyridine Ca²⁺ channel activator, did not affect this channel activity. Although norepinephrine in the pipette solution did not activate this channel, its external application increased channel activity. These observations suggest that guinea-pig hepatocytes possess Ca²⁺ permeable channels that differ from the voltage-operated Ca²⁺ channels found in excitable cells and that such channels are responsible for the agonist-stimulated Ca²⁺ entry in hepatocytes. (J Nippon Med Sch 1999 ; 66 : 127-133)

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