Total systems intervention and human inquiry: The search for a common ground

Total Systems Intervention (TSI) is an approach to intervening in problem situations which has much to offer where complex interacting issues need to be addressed by the complementary use of intervention methodologies. That such an approach has much in common with Action Research (AR) has been recognized, with much recent effort being devoted to the relationship between AR and Critical Systems Thinking (CST), the theoretical endeavor underpinning TSI. This paper further develops this line of debate and relates AR or Human Inquiry (HI) more directly to TSI, using an information systems intervention to enhance the study. The outcome is a demonstration of how TSI implicitly uses techniques informed from the field of Action Research, and how a more thorough synthesis of HI with TSI might serve to improve the overall intervention process.     

Induction of hemopoietic chimerism in the caprine fetus by intraperitoneal injection of fetal liver cells

Summary Intraperitoneal injection of allogeneic liver cells from 43-day-old male fetuses into normal 60-day female goat fetuses resulted in persistent hemopoietic chimerism in surviving recipients without clinical evidence of graft-versus-host disease. Transplantation of normal fetal liver cells into preimmunocompetent goat fetuses affected with -D-mannosidosis may provide an alternative strategy for evaluating hemopoietic stem cell transplantation in the treatment of human lysosomal storage diseases.     

吸附制冷系统中吸附床的传热传质分析及结构设计

对化学吸附制冷系统中吸附剂颗粒之间以及整个吸附床的传热传质特性进行了分析，并总结了目前国内外强化吸附床传热传质性能的主要措施和方法．分析比较了两种用于化学吸附制冷的典型吸附床结构，在此基础上设计了一种新型的吸附床．     

肌肉自发振动过程中结合几率与化学反应速率的变化

定量分析肌球蛋白与肌动蛋白丝的结合几率及相关化学反应的速率常数,对于准确掌握肌肉收缩的内在机制具有非常重要的意义.以肌肉自发振动的实验结果为依据,从振动过程所满足的动力学方程出发,推导出结合几率与肌丝滑行速度及肌节长度之间的定量关系,并求得化学反应速率随肌肉收缩的速度变化而改变的数学规律.结果显示,结合几率的基准值由溶液中主要化学成分的浓度决定;结合几率的变化值与肌肉收缩的速度成正比,与肌节长度成反比;而化学反应速率随收缩速度按指数规律变化.上述结果与实验值基本一致.     

Prion propagation and toxicity in vivo occur in two distinct mechanistic phases

Mammalian prions cause fatal neurodegenerative conditions including Creutzfeldt-Jakob disease in humans and scrapie and bovine spongiform encephalopathy in animals. Prion infections are typically associated with remarkably prolonged but highly consistent incubation periods followed by a rapid clinical phase. The relationship between prion propagation, generation of neurotoxic species and clinical onset has remained obscure. Prion incubation periods in experimental animals are known to vary inversely with expression level of cellular prion protein. Here we demonstrate that prion propagation in brain proceeds via two distinct phases: a clinically silent exponential phase not rate-limited by prion protein concentration which rapidly reaches a maximal prion titre, followed by a distinct switch to a plateau phase. The latter determines time to clinical onset in a manner inversely proportional to prion protein concentration. These findings demonstrate an uncoupling of infectivity and toxicity. We suggest that prions themselves are not neurotoxic but catalyse the formation of such species from PrP(C). Production of neurotoxic species is triggered when prion propagation saturates, leading to a switch from autocatalytic production of infectivity (phase 1) to a toxic (phase 2) pathway.     

The DNA sequence and analysis of human chromosome 13

Chromosome 13 is the largest acrocentric human chromosome. It carries genes involved in cancer including the breast cancer type 2 (BRCA2) and retinoblastoma (RB1) genes, is frequently rearranged in B-cell chronic lymphocytic leukaemia, and contains the DAOA locus associated with bipolar disorder and schizophrenia. We describe completion and analysis of 95.5 megabases (Mb) of sequence from chromosome 13, which contains 633 genes and 296 pseudogenes. We estimate that more than 95.4% of the protein-coding genes of this chromosome have been identified, on the basis of comparison with other vertebrate genome sequences. Additionally, 105 putative non-coding RNA genes were found. Chromosome 13 has one of the lowest gene densities (6.5 genes per Mb) among human chromosomes, and contains a central region of 38 Mb where the gene density drops to only 3.1 genes per Mb.