胸导管引流对慢性哮喘病人外周血淋巴细胞内环核苷酸代谢的影响

观察7例慢性哮喘病人胸导管引流治疗前后外周血淋巴细胞内 cAMp/cGMP 值的变化。结果发现,慢性哮喘病人外周血淋巴细胞内 cAMP/cGMP 的值较正常人低(P<0.001);胸导管引流治疗后,哮喘病人外周血淋巴细胞内 cAMP/cGMP 值较治疗前升高(P<0.01)。提示,慢性哮喘病人外周血淋巴细胞功能异常、活性增强,这可能是哮喘发病的重要原因之一。胸导管引流引起的免疫抑制作用,一个重要的机理就是影响淋巴细胞内环核苷酸的代谢,而使淋巴细胞的活性降低,这可能也是胸导管引流治疗慢性哮喘的机理之一。     

Mercaptopurine in childhood leukaemia: the effects of dose escalation on thioguanine nucleotide metabolites

The current U.K. trial protocol (UKALL XI) for childhood lymphoblastic leukaemia demands mercaptopurine (MP) dose escalation in children who tolerate daily 75  mg/m² MP (100% dose) without cytopenias. The previous trial (UKALL X) did not. MP metabolism was studied in a group of UKALL XI children ( n =21) who tolerated 100% dosages and who were matched in this respect with a similar group of UKALL X children. Red blood cell MP derived thioguanine nucleotide (TGN) concentrations were measured in both groups under comparable conditions; at 75  mg/m² MP there was no significant difference. MP dose escalation in the UKALL XI children produced higher TGN concentrations (TGNs at 100% vs 125% dosages, median difference 90  pmol/8×10⁸ RBCs, 95% CI 25 to 165  pmol, P <0.02). Assayed at the time of cytopenia induced dose reduction, the UKALL XI children had accumulated significantly higher TGN concentrations than the UKALL X children (median difference 78  pmol/8×10⁸ RBCs, 95% CI 20 to 144, P <0.02). These findings indicate that dose escalation in children tolerant of 100% MP dosages produces higher peak TGN concentrations.     

自动平衡记录仪与HPLC匹配定量测定腺苷酸

本文以腺苷酸为测定物,探讨了以国产自动平衡记录仪为高效液相色谱记录并定量分析结果的方法。结果表明,从自动平衡记录上得到峰形、计算结果均与原机所带积分仪的一致。其稳定性、灵敏度和线性响应均能达到高效液相色谱检测器的要求,是一种可以代替积分仪分析结果的经济、可靠的方法。     

18氟-胸腺嘧啶核苷正电子发射体层-CT显像在胸部肿瘤上的初步研究

目的：评价^18氟-胸腺嘧啶核苷（^18F-FLT）正电子发射体层（PET）-CT显像对胸部肿瘤定性诊断的价值。方法：对17例做了^18氟-脱氧葡萄糖（^18F-FDG）PET-CT检查，但定性诊断困难的患者，在第2～3天进行了^18F-FLITPET-CT显像。分析病变在两种不同显像剂PET-CT上的表现，分别测量二者的最大标准摄取值（maxSUV）。结果：8例恶性病变（5例肺癌、1例纵隔淋巴瘤、1例胸椎恶性肿瘤、1例胸椎转移瘤），其中7例见FLT异常摄取，5例肺癌平均maxSUV为4．2（鳞癌2例、腺癌2例、肺泡癌1例）；9例良性病变（5例肺结核、1例肺炎、3例纵隔淋巴结结核）无或轻度摄取FLT，其中6例肺内良性病变平均maxSUV为1．6；9例良性病变中8例见FDG异常浓聚，其中6例肺内良性病灶平均maxSUV为3．9，3例纵隔淋巴结结核也见FDG明显摄取，平均maxSUV为11．0。11例肺内病灶FDG和FLT显像的敏感性、特异性、准确性分别为100．0％（5／5）、16．7％（1／6）、54．5％（6／11）和80．0％（4／5）、66．7％（4／6）、72．7％（8／11）。结论：胸部肿瘤^18F-FLT显像的特异性较高，在^18F-FDG显像阳性，难以确定病变性质时，FLIT可以作为FDG的有益补充，二者联合显像有助于提高胸部肿瘤诊断的准确性。     

Two novel gastric cancer-associated genes identified by differential display

AIM To clone novel gastric cancer-associated genes and investigate their roles in gastric cancer occurrence.METHODS A method called differential display was used which allows the identification of differentially expressed genes by using PAGE to display PCR-amplified cDNA fragments between gastric cancer cells and normal gastric mucosa cells. These fragments were cloned into plasmid vector pUC18. Homology analysis was made after sequencing these fragments.RESULTS Two novel genes were identified compared with sequences from GenBank. One was registered with the AD number AF 051783. In situ hybridization showed that these two novel genes expressed specifically in gastric cancer tissues.CONCLUSION The two novel genes obtained by differential display were confirmed to be gastric cancer-associated genes using in situ hybridization.     

Neurotransmitter release evoked by α-latrotoxin in the smooth muscle of the female pig urethra

Neuronal regulation of smooth muscle tone in the female pig urethra has mainly been studied in vitro using electrical field stimulation (EFS) of nerves. Excitatory control is considered to be exerted by released noradrenaline, whereas inhibitory control is non-adrenergic non-cholinergic (NANC), and mediated by nitric oxide (NO), and an as yet unidentified agent. We investigated the functional and morphological effects of α-latrotoxin (αLTX), a spider neurotoxin believed to cause massive release of vesicle-stored neurotransmitters, on spontaneously developed urethral smooth muscle tone. The effects were compared to those of EFS and high potassium. In the presence of the NO-synthesis inhibitor N^ω-nitro-L-arginine (L-NOARG: 0.3 mM) both αLTX and EFS evoked contractions. After treatment with scopolamine and phentolamine, no contraction was observed, and under these conditions αLTX and EFS induced relaxation. At low frequencies (<12 Hz), the EFS-induced relaxations were rapid, whereas at higher frequencies (>12 Hz), they were biphasic, consisting of a rapid first phase followed by a more long-lasting second phase. L-NOARG abolished the relaxations at low frequencies, as well as the first phase of the biphasic relaxation. The second phase was not affected by treatment with L-NOARG, but 0.1 μM ω-conotoxin GVIA, blocker of N-type voltage-operated calcium- channels (VOCCs), markedly reduced or abolished the response. In the presence of L-NOARG or ω-conotoxin GVIA, the αLTX-induced relaxation was significantly decreased, and the combination of L-NOARG and ω-conotoxin GVIA further reduced or abolished the relaxation. In preparationstreated with tetrodotoxin or scorpion venom, believed to inactivate nerves by acting on sodium channels, αLTX and EFS had no effects. αLTX-induced relaxation was not associated with changes in cyclic GMP or cyclic AMP content. High (80 mM) potassium solution induced a triphasic response of the preparation. A transient relaxation was followed by a restoration of tone, and then by a persistent relaxation. The persistent relaxation was slightly reduced by scorpion venom or L-NOARG, but reduced by 50% by a combination of L-NOARG and ω-conotoxin GVIA. Ultrastructural analysis of the urethral circular smooth muscle layer revealed a moderate amount of nerve profiles supplying the smooth muscle. In control preparations, the nerve profiles contained both small synaptic vesicles and large dense core vesicles. αLTX caused a major loss of both types of vesicle. The present data suggest that αLTX has the ability to release not only adrenergic and cholinergic transmitters, but also NANC mediators of relaxation, including NO, from nerve terminals in the urethra. Received: 13 January 1997 / Accepted: 17 April 1997     

Abnormal nucleotide pattern in the eosinophils of a patient with acute lymphoblastic leukemia associated with eosinophilia

In this article we present a patient with acute lymphoblastic leukemia (ALL) associated with eosinophilia, in which the eosinophilia preceded a meningeal and bone-marrow relapse of ALL. We analysed the purine and pyrimidine nucleotide content of the eosinophils (92% pure) and compared the nucleotide pattern with that of eosinophils from healthy donors and from patients with eosinophilia not associated with leukemia. The ratios of purine : pyrimidine and of uracil :cytosine nucleotides were decreased compared with those in eosinophils from healthy donors and from patients with eosinophilia with other aetiologies. The total nucleotide concentration was increased, especially the concentration of UDP-sugars and pyrimidine nucleotides.

The decrease in these ratios and the increase in concentration of the nucleotides and the UDPsugars were also detected in leukemic cells of patients with ALL (de Korte et al., Leukemia Res. 10, 389–396 (1986)) compared to normal lymphocytes. We suggest a malignant character of the eosinophils in our patient with ALL associated with eosinophilia, in contrast with the nonmalignant state suggested previously for these cells.     

Adenosine and adenine nucleotides are independently released from both the nerve terminals and the muscle fibres upon electrical stimulation of the innervated skeletal muscle of the frog

The independent release of adenosine and adenine nucleotides upon electrical stimulation was studied in the innervated sartorius muscle of the frog after blockade of the extracellular catabolism of adenosine monophosphate (AMP) through exo-AMP deaminase and ecto-5-nucleotidase. Nerve stimulation (30 min, 0.2Hz) induced the release of both adenosine (19±3 pmol) and adenine nucleotides (101±7 pmol). Experiments performed in the presence of tubocurarine (5 M) to prevent purine release due to nerve-evoked muscle twitching, or under direct stimulation of the muscle in low calcium solutions to prevent pre-synaptic release of purines, showed that there was an evoked release of adenosine and adenine nucleotides both from the nerve endings and from the twitching muscle fibres. Removal of ecto-5-nucleotidase inhibition shows that the catabolism of adenine nucleotides released during stimulation contributes in about 50% to the amount of endogenous extracellular adenosine. When only one of the enzymes catabolizing AMP (ecto-5-nucleotidase or exo-AMP deaminase) was inhibited, the evoked release of adenine nucleotides was undetectable, suggesting that each enzyme is able to catabolize all the AMP formed from adenine nucleotides released upon stimulation. It is concluded that the concentration of endogenous extracellular adenosine is under the control of the relative activities of exo-AMP deaminase and ecto-5-nucleotidase.Brief accounts of some of the results in this study have been published previously (refs. [6, 7]).     

Changes in tissue energy metabolism in animals exposed to continuous and interrupted low-frequency vibration

The action of continuous low-frequency vibration on rats for 1 month caused no changes in the total adenine nucleotides of the brain but led to a marked decrease in the ATP content and total adenine nucleotides in the limb muscles. After exposure to vibration for 3 months considerable exhaustion of the total adenine nucleotides of both muscles and brain was found. In the case of interrupted exposure to vibration the state of the adenine-nucleotide system depended on the duration of the pauses between periods of continuous exposure to vibration. During vibration with the shortest pauses (4 min) between successive periods of 30 min of vibration no changes were observed in the energy metabolism of the muscles and brain. Vibration with pauses of 8 and 15 min was found to be unfavorable for the adenine nucleotides of the muscles and vibration with a pause of 8 min for the brain.Kiev Institute of Work Hygiene and Occupational Diseases, (Presented by Academician of the Academy of Medical Sciences of the USSR L. I. Medved'.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 7, pp. 35–38, July, 1978.