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[Olfactory origin of luteinizing hormone-releasing hormone (LHRH) neurons]. [黄体生成素释放激素(LHRH)神经元的嗅觉来源]。
Pub Date : 1999-04-01 DOI: 10.1272/jnms.66.94
S Daikoku
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引用次数: 2
[Possible contribution of alpha-adrenergic abnormalities to cerebral ischemia in the patients with sinus bradycardia. Analysis by pharmacologic autonomic nervous test]. 肾上腺素能异常对窦性心动过缓患者脑缺血的可能贡献。自主神经药理试验分析[j]。
Pub Date : 1999-04-01 DOI: 10.1272/jnms.66.119
A Nomura, H Saitoh, H Atarashi, H Hayakawa

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 plays 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 microgram/kg/min isoproterenol divided by 0.004 (beta-sens) were evaluated, beta-tone was obtained by subtracting HR after application of propranolol (0.2 mg/kg) from that of atropine. Basal beta-sympathetic activity was evaluated by beta-sec that was obtained by beta-tone/beta-sens. Increased SBP by application of 0.4 microgram/kg/min phenylephrine divided by 0.4 (alpha-sens) was evaluated. alpha-tone was obtained by subtracting minimum SBP after 0.2 mg/kg phentolamine from SBP after application of propranolol. Basal alpha-sympathetic activity was evaluated by alpha-sec, that was obtained by alpha-tone/alpha-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 beta-sympathetic receptors (para-tone, beta-sens, beta-tone, beta-sec) showed no significant differences between the groups, alpha-sens was attenuated (P < 0.01) and alpha-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 alpha-sympathetic receptor but to severity of sinus node dysfunction.

背景:缓性心律失常患者晕厥被认为是由心动过缓引起的低心输出量的严重症状,也是起搏器植入(PMI)的主要标准。然而,有报道称PMI并不能总是预防晕厥;有人认为,不是心动过缓,而是自主神经系统的异常在晕厥中起作用。目的:探讨窦性心动过缓(SB)患者自主神经功能障碍与晕厥的关系。研究对象:39例SB患者根据有无晕厥或晕厥前期(S组,n = 16, 46.9 +/- 20.0年)或有无晕厥(n组,n = 23, 40.4 +/- 17.6年)分为两组。方法:采用电生理法测定窦房结恢复时间(CSNRT)。自主神经药理学试验在安静的房间进行。分别评价0.04 mg/kg阿托品(副酮)和0.004微克/kg/min异丙肾上腺素/ 0.004 (β -sens)对HR的增加,用0.2 mg/kg心得安与阿托品的HR相减,得到β -tone。基底-交感神经活动由-tone/ -sens获得的-sec来评估。应用0.4微克/千克/分钟苯肾上腺素/ 0.4 (α -sens)评估收缩压升高。用普萘洛尔后的收缩压减去0.2 mg/kg酚妥拉明后的最小收缩压得到α -tone。通过α -tone/ α -sens获得的α -sec来评估基础α -交感神经活动。结果:两组患者的基本临床特征(年龄、性别、心功能)无显著差异。副交感神经和-交感神经功能参数(para-tone, β -sens, β -tone, β -sec)在两组间无显著差异,s组α -sens明显减弱(P < 0.01), α -sec明显增强(P < 0.0001)。结论:SB患者晕厥或晕厥前期可能与α -交感神经受体介导的血管收缩功能衰竭有关,而与窦结功能障碍的严重程度有关。
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引用次数: 0
Chromosome 8 copy numbers and the c-myc gene amplification in non-small cell lung cancer. Analysis by interphase cytogenetics. 非小细胞肺癌的8号染色体拷贝数与c-myc基因扩增。间期细胞遗传学分析。
Pub Date : 1999-04-01 DOI: 10.1272/jnms.66.107
H Kubokura, K Koizumi, M Yamamoto, S Tanaka

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 significnat 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.

c-myc基因扩增在非小细胞肺癌(NSCLC)中有报道。我们采用双色荧光原位杂交(FISH)检测8号染色体上c-myc基因的扩增,以评估这些可能的异常与病理分期之间的关系。肿瘤组织样本来自29例在埼玉癌症中心接受肺叶切除术的I期(n = 15)和III期(n = 14) NSCLC患者。用双色FISH分析8号染色体着丝粒和c-myc基因。8号染色体数值畸变率I期为36.8 +/- 20.3%,III期为40.6 +/- 24.8%。I期c-myc基因扩增率为48.3 +/- 15.2%,III期为57.4 +/- 17.0%。存活5年及以上患者8号染色体数值畸变率(28.8 +/- 17.5%)与存活5年以下患者(44.7 +/- 23.1%)差异有统计学意义。c-myc基因扩增率在生存期大于5年与小于5年、生存期大于3年与小于3年的患者间无显著差异。8号染色体畸变40%及以上患者(n = 13)的5年生存率为15.4%,明显低于畸变40%以下患者(n = 16)的56.3%。c-myc基因扩增率等于或大于50% (n = 16)和小于50% (n = 13)患者的5年生存率(25.0%和53.9%)无差异。8号染色体畸变率和c-myc基因扩增率与病理分期无关。然而,8号染色体畸变率与生存率存在相关性,因此我们认为8号染色体畸变率是影响非小细胞肺癌患者预后的另一个因素。
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引用次数: 10
[Examination of non-transmitter effects of catecholamines on clonal cells derived from Drosophila CNS]. [儿茶酚胺对果蝇中枢神经系统克隆细胞非递质作用的研究]。
Pub Date : 1999-04-01 DOI: 10.1272/jnms.66.113
T Zhang

The effects of catecholamines (CAs) other than their transmitter action were investigated using clonal neuronal cells, ML-DmBG2-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. alpha-, beta-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 antioxidant, 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.

利用来源于果蝇的克隆神经细胞ML-DmBG2-c2,研究了儿茶酚胺(catecholamines, CAs)在幼虫中枢神经系统(CNS)中的作用。所有测试的儿茶酚胺,肾上腺素(AD),多巴胺(DA),去甲肾上腺素(NA)和异丙肾上腺素(ISO),在2至7天的培养中阻止细胞数量的增加。α -、β -肾上腺素能和多巴胺能拮抗剂不能阻断CAs对细胞数量的影响。肾上腺素色素,AD氧化降解的产物,也能阻止细胞数量的增加,就像AD一样。抗氧化剂二硫苏糖醇(DTT)可部分阻断AD的作用。这些结果表明,CA对细胞数量增加的抑制可能是由CA本身和/或CA代谢过程中的氧化产物介导的。结果表明,在果蝇克隆细胞中,CAs对细胞增殖有抑制作用,但不诱导细胞死亡。
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引用次数: 0
Evidence for norepinephrine-activated Ca2+ permeable channels in guinea-pig hepatocytes using a patch clamp technique. 使用膜片钳技术在豚鼠肝细胞中发现去甲肾上腺素激活的Ca2+可渗透通道的证据。
Pub Date : 1999-04-01 DOI: 10.1272/jnms.66.127
T Nagano, R Sato, H Matsuda, T Aramaki
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.
确定肝细胞质膜是否具有Ca2+通道。我们将膜片钳技术应用于分离的豚鼠肝细胞。在细胞连接配置中,使用110 mM BaCl2或CaCl2的内部移液管溶液,我们观察到在不同的膜电位下零星的向内单通道电流(Po = 0.004 +/- 0.002, n = 6)。静息膜电位的单位振幅为0.60±0.15 pA (n = 6)。单通道电导为20.4 +/- 4.6 pS (n = 6),该通道无整流,无电压依赖性。双氢吡啶类Ca2+通道激活剂Bay K 8644对Ca2+通道活性没有影响。虽然移液管溶液中的去甲肾上腺素没有激活该通道,但其外用增加了通道活性。这些观察结果表明,豚鼠肝细胞具有Ca2+渗透性通道,不同于在可兴奋细胞中发现的电压操作的Ca2+通道,这些通道负责激动剂刺激的Ca2+进入肝细胞。
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引用次数: 2
[Analysis of ovarian tumors treated at Nippon Medical School Hospital in a 5-year period. Problems in a frozen section diagnosis]. 日本医科大学附属医院5年卵巢肿瘤治疗分析冷冻切片诊断中的问题[j]。
Pub Date : 1999-04-01 DOI: 10.1272/jnms.66.134
K Morishima, K Tamura, R Narato, S Tanaka, N Sakai, K Asakawa, M Matsubara, Y Watarai, Y Sugisaki
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引用次数: 0
[Diabetes in the elderly: diagnosis and therapy]. 老年糖尿病:诊断与治疗。
Pub Date : 1999-04-01 DOI: 10.1272/jnms.66.139
K Oba, H Nakano, T Watanabe
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引用次数: 0
[Case record from Nippon Medical School. Seatbelt injury]. [日本医学院的病例记录]安全带受伤)。
Pub Date : 1999-04-01 DOI: 10.1272/jnms.66.143
E Naitoh, Y Moriyama
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引用次数: 0
[In vitro fertilization and embryo transfer. Present and future]. 体外受精和胚胎移植。现在和将来]。
Pub Date : 1999-02-01 DOI: 10.1272/jnms.66.45
S Akira, T Takeshita, T Araki
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引用次数: 0
The development and clinical feasibility of percutaneous transluminal coronary angioscopy. 经皮冠状动脉腔内检查的发展及临床可行性。
Pub Date : 1999-02-01 DOI: 10.1272/jnms.66.7
K Mizuno, S Sakai, S Ohkuni, Z Jing, H Hayakawa
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引用次数: 1
期刊
Nihon Ika Daigaku zasshi
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