一种新型气缸及其动态位移的监测

介绍了一种带有位移传感系统的新型气缸及其位移传感系统的结构特点；据此开发一个用于计算机控制系统的位移反馈信号的处理与计数系统，以达到对这种对新型气缸动态位移的监测，并给出了计数系统性能实验数据及应用此监测系统的气缸动态位移特性实验结果。     

Dual role of cAMP duringDictyostelium development

cAMP plays an essential role duringDictyostelium development both outside and inside the cell. Membrane-bound receptors and adenylyl cyclase are responsible for sensing and producing extracellular cAMP, whereas a phosphodiesterase is responsible for maintaining a low basal level. The molecular events underlying this type of hormone like signalling, which are now beginning to be deciphered, will be presented, in the light of cAMP analogue studies. The importance of intracellular cAMP for cell differentiation has been demonstrated by the central role of the cAMP dependent protein kinase. Mutants as well as strains obtained by reverse genetics will be reviewed which lead to our current understanding of the role of intracellular cAMP in the differentiation of both stalk and spore cells.     

Ni－海泡石催化剂的结构与催化活性

研制Ｎｉ海泡石催化剂，并采用微型催化反应器－色谱仪－微机联合装置对该催化剂用于苯加氢制环已烷的活性进行评价．在此研究中，用氢化学吸附、程度升温脱附、ｘ－射线衍射、电子显微镜和比表面测定仪对催化剂进行结构表征，并对酸洗条件、催化剂结构和催化活性进行关联．     

旅行商问题（TSP）的模拟退火求解

提出了循环排序中６种不同的随机抽样方式，对旅行商问题（ＴＳＰ）的模拟退火求解进行了进一步深入研究．理论分析证明，６种抽样方式均满足模拟退火算法的全局收敛性条件．实例计算表明，子排列反序并移位抽样方式的求解寻优效率最高，且明显优于目前公认最好的著名的Ｓ．Ｌｉｎ“２－交换”抽样方法．本研究和结论对循环排序类优化问题及其求解具有普遍意义．     

丁酸钠对M期同步及非同步的HeLa细胞早G_1期阻断的可逆性

本文采用早熟染色体凝集(PCC)和~3H-TdR显微自显影技术,观察丁酸钠对同步及非同步的HeLa细胞早G_1期阻断的可逆性及其可逆的进程。实验发现丁酸钠对HeLa细胞早G_1期阻断完全是可逆的,且这种可逆是在洗去丁酸钠后立即产生,丁酸钠对HeLa细胞早G_1期阻断的时间点发生在细胞进入S期前的9.5h;发现早G_1期阻断后的恢复必须再经过中、晚G_1期然后才能进入S期.     

仿人操作手动力学模拟

本文主要讨论了仿人操作手动力学正问题的模拟,即给定操作手末端执行器的运动和位姿,求解各关节的广义力。机器人动力学模拟涉及到机器人的轨迹规划、运动学反解,以及动力学建模和求解问题。对于球腕结构的六自由度仿人操作手来说,本文提出了用系统分解法进行运动学反解,用凯恩方程建立机器人动力学模型。本方法解算简便,经略微修改可适用于一般关节型机器人动力学模型。     

Alpha 1-adrenoceptor subtypes linked to different mechanisms for increasing intracellular Ca2+ in smooth muscle

Receptor-mediated increases in intracellular Ca2+ levels can be caused by release from intracellular organelles and/or influx from the extracellular fluid. Noradrenaline (NA) released from sympathetic nerves acts on alpha 1-adrenoceptors to increase cytosolic Ca2+ and promote smooth muscle contraction. In many cells activation of alpha 1-adrenoceptors causes formation of inositol 1,4,5-trisphosphate which promotes Ca2+ release from intracellular stores. The mechanism by which receptor activation opens cell surface Ca2+ channels is not known, although in some cases it may be secondary to formation of inositol phosphates or release of stored intracellular Ca2+ (ref. 3). However, alpha 1-adrenoceptors have recently been shown to have different pharmacological properties in different tissues, and it has been proposed that different alpha 1-adrenoceptor subtypes may control mobilization of intracellular Ca2+ and gating of extracellular Ca2+ influx. We here report evidence for two subtypes of alpha 1-adrenoceptors which cause contractile responses through different molecular mechanisms. One subtype stimulates inositol phosphate (InsP) formation and causes contractions which are independent of extracellular Ca2+, and the other does not stimulate inositol phosphate formation and causes contractions which require the influx of extracellular Ca2+ through dihydropyridine-sensitive channels. These results suggest that neurotransmitters and hormones may control Ca2+ release from intracellular stores and influx through voltage-gated membrane channels through distinct receptor subtypes.     

Suppression of in vitro haematopoiesis following human immunodeficiency virus infection

Viral infections are frequently associated with haematological disorders. Abnormalities including leukopenia, anaemia and thrombocytopenia are commonly observed in patients with the acquired immune deficiency syndrome (AIDS) or the AIDS-related complex (ARC). The underlying cause of these haematological abnormalities is poorly understood. We report here that bone marrow progenitors isolated from AIDS or ARC patients are responsive to recombinant human granulocyte-macrophage colony stimulating factor (rGM-CSF) and recombinant erythropoietin. Antibodies present in the serum of patients infected with the human immunodeficiency virus (HIV), however, could suppress the growth of these progenitors, but not the growth of progenitors from HIV seronegative controls. A component of this immune-mediated suppression appears to be antibodies directed towards the envelope glycoprotein (gp120) of HIV.     

Activation of a G protein promotes agonist responses to calcium channel ligands

The activation of a guanine nucleotide binding (G) protein is an essential step in coupling certain receptors to the inhibition of voltage-activated calcium channels. We have previously observed that analogues of GTP potentiate the effect of receptor agonists and inhibit calcium currents in cultured dorsal root ganglion (DRG) neurones. A residual sustained 'L-type' component of the calcium channel current is resistant to inhibition by internal guanosine 5'-O-3-thiotriphosphate (GTP-gamma-S). Because calcium channel antagonists such as D600, nifedipine and diltiazem inhibit L currents, we examined their effect on GTP-gamma-S-modified currents. These compounds all produced a rapid and very marked potentiation of calcium channel currents in the presence of internal GTP-gamma-S and this effect was prevented by pertussis toxin which ADP ribosylates the G proteins Gi/Go (for review see ref. 10). We suggest that this potentiation indicates that activated G protein can interact with the calcium channel, and that this enhances the action of calcium channel ligands at their agonist sites on the channel in its resting state. These results represent the first electrophysiological evidence that guanine nucleotides are able to influence cellular responses to calcium channel ligands.     

Assignment of multiple endocrine neoplasia type 2A to chromosome 10 by linkage

Multiple endocrine neoplasis type 2A (MEN2A) is one of several kinds of cancers that appear to be inherited in an autosomally dominant fashion. We have assigned the MEN2A locus to chromosome 10 by linkage with a new DNA marker (D10S5). The linkage led us to investigate other chromosome 10 markers and demonstrate linkage between the disease locus and the interstitial retinol-binding protein (IRBP) gene. The D10S5 locus was sublocalized to 10q21.1 by hybridization in situ and the IRBP gene to p11.2----q11.2 with a secondary site at q24----q25. The linkages were established using 292 members of five families, three different restriction fragment length polymorphisms (RFLPs) at D10S5 and two RFLPs recognized by the IRBP probe. The recombination frequencies from pairwise linkage analysis between the disease and two marker loci D10S5 and IRBP were 0.19 and 0.11, with maximum lod scores of 3.6 and 8.0 respectively. Ordering of the three loci by multipoint analysis placed the IRBP gene approximately midway between the disease and D10S5 loci.