BIOPHYSICAL MECHANISMS IN LEUKOCYTES AND MELANOCYTES

计划研究的吞噬和非吞噬功能， 白细胞，它与炎症反应有关。的 研究计划特别针对具体的 但白细胞活动的重叠区域：粘附，运动，靶向 识别、趋化性、内皮细胞单层的渗透、摄取， 通常伴随吞噬作用的代谢活动增加 或其它细胞触发反应，溶酶体结构的脱粒， 和细胞内杀伤。 这些活动的方式可以 相互分离可以区分专性相互作用和单纯相互作用。 共存，并可能揭示细胞功能的特定途径 被改变了 实验方法是通过各种代理人和情况， 其中一项或多项活动似乎发生了变化，包括1） 以各种方式处理的白细胞，以产生缺乏颗粒的无核细胞 碎片（细胞质），保留运动和/或呼吸功能， 亲本细胞，2）用试剂处理的细胞质或白细胞，所述试剂 影响其对微生物的杀灭能力，3）细胞质或 用分子和颗粒处理的白细胞， 通量，蛋白激酶C或腺苷酸环化酶的活化，蛋白质 磷酸化，微管和微丝的聚合，和 特定细胞表面受体的重排或改变的表达， 4)用受控的短暂加热处理白细胞，以改变它们的 呼吸爆发氧化酶活性，5）白细胞从患者 儿童慢性肉芽肿性疾病或其他白细胞疾病 结构和功能，以及6）用 在纤维元件中产生超微结构改变的物质， 如中期阻滞剂、秋水仙碱、长春碱和 灰黄霉素（影响微管）和细胞松弛素（影响 微丝）。

Studies are planned of phagocytic and non-phagocytic functions of leukocytes, that bear on aspects of the inflammatory response. The research plan is particularly aimed at the relationships among specific but overlapping areas of leukocyte activity: adherence, locomotion, target recognition, chemotaxis, penetration of endothelial monolayers, ingestion, the increased metabolic activity that ordinarily accompanies phagocytosis or other cell-triggering reactions, degranulation of lysosomal structures, and intracellular killing. The ways in which these activities can be separated from one another may distinguish obligate interactions from mere concomitance, and may reveal the specific pathways by which cell function is altered. The experimental approach is through various agents and situations in which one or more of these activities appear to be altered, including 1) leukocytes treated in a variety of ways to produce granule-poor anucleate fragments (cytoplasts) that retain motile and/or respiratory functions of the parent cell, 2) cytoplasts or leukocytes treated with agents that affect their killing capacity for microorganisms, 3) cytoplasts or leukocytes treated with molecules and particles that initiate calcium fluxes, activation of protein kinase C or of adenylate cyclase, protein phosphorylation, polymerization of microtubules and microfilaments, and rearrangements or altered expression of specific cell-surface receptors, 4) leukocytes treated with controlled brief heat to alter their respiratory burst oxidase activity, 5) leukocytes from patients with chronic granulomatous disease of childhood or other disorders of leukocyte structure and function, and 6) cytoplasts or leukocytes treated with substances that produce ultrastructural alterations in fibrillar elements, such as the metaphase-arresting agents, colchicine, vinblastine and griseofulvin (affecting microtubules), and cytochalasins (affecting microfilaments).