The passage of macromolecules through biological membranes is an essential process for all multicellular organisms. Insects have developed a mechanism different from that known for all other eukaryotes investigated so far. This review discusses the function and evolution of this mechanism. Insect pupae do not feed during metamorphosis. Therefore they depend on material that has been accumulated during the larval life. At the end of this period, shortly before pupariation, a rise in titer of ecdysteroid hormones induces the incorporation of a large fraction of storage proteins (hexamerins) from the body fluid into the fat body cells. The transport of hexamerins across the cell-membrane is mediated by a specific ecdysteroid-controlled receptor. It is synthesized as a precursor protein that is subsequently processed into the active receptor. This receptor protein is very unusual because it is closely related to its own hexamerin ligand. Sequence comparison shows that the hexamerins and hexamerin receptors diverged early in insect evolution and derive from a common hemocyanin ancestor.

SUMMARYCXC chemokines modulate host immunity, neovascularization, growth and invasive behaviour of tumours. Despite their relevance in tumour biology, chemokine expression in intestinal-and diffusetype gastric carcinoma, which exhibit a completely different growth pattern, has not been investigated in detail. In this study, expression of the CXC chemokines CXCL8 [interleukin (IL)-8], CXCL1 [growth-related oncogene alpha (Gro a )], CXCL9 [monokine induced by interferon (IFN)-g ] and CXCL10 [IFN-g -inducible protein-10 (IP-10)] and the corresponding chemokine receptors CXCR1-3 was investigated by immunohistochemistry in intestinal-and diffuse-type gastric carcinoma. Tumour cells of all patients expressed CXCL8. CXCL8 expression was significantly stronger in tumour cells of diffuse-rather than intestinal-type gastric carcinoma ( P < 0·01) as determined by a semiquantitative score. CXCL1 was expressed almost exclusively by diffuse-but not intestinal-type carcinoma cells. The corresponding chemokine receptors, CXCR1 and CXCR2, were found on carcinoma cells. Furthermore, CXCL8 expression correlated with number of tumour vessels ( P < 0·01), suggesting an angiogenetic function in gastric carcinoma not only in vitro but also in vivo . CXCL10 and CXCL9, attractants for T cells, were expressed by peritumorous macrophages in close proximity to IFN-g -producing CXCR3-positive T cells in both tumour types. These chemokines may attract gastric carcinomainfiltrating T cells via an IFN-g -mediated pathway and enhance host immunity against the tumour. In gastric carcinoma a complex interplay between CXC-chemokine signals derived from both tumour cells and tumour-infiltrating immune cells may exhibit pleiotropic effects in tumour biology that go far beyond their originally described functions as leucocyte chemoattractants. Because CXCL8 and CXCL1, which are known to increase growth and invasive behaviour of malignant tumours, are significantly stronger expressed in diffuse-than intestinal-type gastric carcinoma, one may speculate that these chemokines influence the different growth pattern of gastric carcinoma types.

SUMMARYInfection with Helicobacter pylori causes chronic active gastritis, which is characterized by neutrophils infiltrating the gastric epithelial layer and the underlying lamina propria as well as by T, B lymphocytes and macrophages accumulating in the lamina propria. In this study, the chemokine profile responsible for the recruitment of these inflammatory cells is investigated. Using both RNA/RNA in situ hybridization and immunohistochemistry, the expression of the neutrophil and/or lymphocyte-attractant CXC chemokines growth-related oncogene alpha (Groa ), IL-8, interferon-gamma (IFN-g)-inducible protein-10 (IP-10), monokine induced by IFN-g (MIG) and the CC chemokines macrophage inflammatory protein-1a (MIP-1a ), -1b , regulated on activation normal T cell expressed and secreted (RANTES) and monocyte chemoattractant protein-1 (MCP-1) is studied and microanatomically localized in the gastric mucosa. Macrophages in the lamina propria at sites with neutrophil infiltration and gastric epithelium infiltrated by neutrophils highly expressed the neutrophil-attractant chemokines Groa and IL-8. Additionally, Groa and IL-8 were expressed by neutrophils themselves localized within gastric epithelium, in the foveolar lumen and in the cellular debris overlying mucosal erosion. IP-10 and to a lower extent MIG, both selectively chemotactic for inflammatory T cells, were expressed by endothelial cells of gastric mucosal vessels and by mononuclear cells at sites with T cell infiltration. Expression of all other CC chemokines tested was significantly lower. These in vivo data indicate that a set of predominantly CXC chemokines modulates the inflammation in H. pylori gastritis. Groa and IL-8 may play an important role in neutrophil trafficking from the mucosal vessel into the gastric epithelium, whereas IP-10 and MIG contribute to the recruitment of inflammatory T cells into the mucosa.

The energy production of a cell is tuned to its needs. Most of the energy requirements are met by oxidative phosphorylation taking place in the respiratory chain of the mitochondria and approximately 90 % of the oxygen is consumed there. Depending on the challenge, the oxidative capacity can slightly increase or can vary over an order of magnitude, the mitochondria reacting accordingly with either subtle changes in the activity of OXPHOS, with an increased biosynthesis of some of the OXPHOS subunits, or with an increase in the number and size of the organelles (mitogenesis) (Enriquez et al. 1999b, Weber et al. 2002. Therefore, mitochondria are prime targets for regulatory agents affecting ATP yield, and such major regulators of mitochondrial energy metabolism are the steroid and thyroid hormones.This review deals with the role and mechanisms of action of steroid hormones on mitochondria in connection with energy production and their biogenesis. Most of the actions of steroids in this respect affect transcription of OXPHOS genes, the intensity of which parallels the enzymatic activity of the OXPHOS. The OXPHOS represent enzyme proteins composed of several subunits, some of which are encoded in the nuclear and some in the mitochondrial genome. Steroid effects have been documented on mitochondrial gene transcription, without or with parallel involvement of nuclear OXPHOS gene transcription, in a coordinate or not manner, implying the need to consider mechanisms of steroid hormone action on these two distinct organelles and to elaborate on modes of coordination of the nuclear and the mitochondrial transcriptional processes (Scheller et al. 2002).1. Physiological action of steroid hormones on energy metabolism Steroid hormones regulate a wide variety of physiological processes -developmental, growth and metabolic -which require increased energy expenditure. Among the steroid hormones, glucocorticoids play a major role in survival during traumatic stress and injury which require energy (Frayn, 1986;De Feo, 1996). The energy demands depend on the levels of the circulating glucocorticoid, increased concentrations of hormones leading to increased resting energy expenditure (REE) and metabolic rate (Brillon et al. 1995) and to a parallel decrease of the respiratory quotient, suggesting that energy expenditure is fuelled by fatty acid

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