Selection and properties of a mouse L-cell transformant expressing human transferrin receptor

Transferrin receptors are expressed in large quantities on tissues with high requirements for iron such as maturing erythroid cells and placenta. In addition, they are found in abundance on proliferating cells from other normal tissues as well as on a variety of tumours. Recent genetic analysis has shown that structural genes for the transferrin receptor, probably transferrin itself and for p97, a melanoma-associated antigen that exhibits primary sequence homology with transferrin and that can bind ferric iron, each map in man to chromosome 3 (refs 9-12). On this basis it has been suggested that there may be a region on chromosome 3 containing genes involved in Fe transport and that rearrangements in this region of chromosome 3 may in some circumstances be associated with malignant transformation. Furthermore, it is unresolved whether all cell types express structurally identical transferrin receptors. To study these problems, and as an initial step towards cloning the transferrin receptor gene, we describe here the derivation of mouse L-cell transformants expressing the human transferrin receptor.     

Restoration of p53 function leads to tumour regression in vivo

Tumorigenesis is a multi-step process that requires activation of oncogenes and inactivation of tumour suppressor genes. Mouse models of human cancers have recently demonstrated that continuous expression of a dominantly acting oncogene (for example, Hras, Kras and Myc) is often required for tumour maintenance; this phenotype is referred to as oncogene addiction. This concept has received clinical validation by the development of active anticancer drugs that specifically inhibit the function of oncoproteins such as BCR-ABL, c-KIT and EGFR. Identifying additional gene mutations that are required for tumour maintenance may therefore yield clinically useful targets for new cancer therapies. Although loss of p53 function is a common feature of human cancers, it is not known whether sustained inactivation of this or other tumour suppressor pathways is required for tumour maintenance. To explore this issue, we developed a Cre-loxP-based strategy to temporally control tumour suppressor gene expression in vivo. Here we show that restoring endogenous p53 expression leads to regression of autochthonous lymphomas and sarcomas in mice without affecting normal tissues. The mechanism responsible for tumour regression is dependent on the tumour type, with the main consequence of p53 restoration being apoptosis in lymphomas and suppression of cell growth with features of cellular senescence in sarcomas. These results support efforts to treat human cancers by way of pharmacological reactivation of p53.     

高技术指标：2007年度33国(地区)技术竞争力报告

文中的高技术指标（High Tech Indicators,HTI）为佐治亚理工大学发布的沿用多年的指标。数据对
比的时间段分别为1993年、1996年、1999年、2002/3年和2007年。论文给出了33个国家（地区）当前的竞争
力指标——技术排名(Technological Standing, TS), 同时提供了四个表征未来竞争力前景的主要指标——国家
发展取向指标(National Orientation, NO)、社会经济基础指标(Socio-Economic Infrastructure, SE)、技术基础指
标(Technological Infrastructure, TI)与生产能力指标(Productive Capacity, PC)。论文无意在高技术指标的结果上
多加笔墨,但是也的确注意到,中国已经取代美国占据了技术排名的首位。这一结果反映了高技术指标的特
点,更重要的是,它反映了中国过去15年的惊人发展速度。     

Glial and neuronal control of brain blood flow

Blood flow in the brain is regulated by neurons and astrocytes. Knowledge of how these cells control blood flow is crucial for understanding how neural computation is powered, for interpreting functional imaging scans of brains, and for developing treatments for neurological disorders. It is now recognized that neurotransmitter-mediated signalling has a key role in regulating cerebral blood flow, that much of this control is mediated by astrocytes, that oxygen modulates blood flow regulation, and that blood flow may be controlled by capillaries as well as by arterioles. These conceptual shifts in our understanding of cerebral blood flow control have important implications for the development of new therapeutic approaches.     

Inability of dithiols to cause activation ofLimulus endotoxin sensitive procoagulase

Summary Using a chromogenic substrate it has been shown that the endotoxin sensitive procoagulase ofLimulus lysate is not activated by dithiols. Increased turbidimetric readings in the presence of dithiols would therefore appear to be nonspecific.