The origin of certain nutritive substances in the eggs of hemiptera

1.

1) The end chambers of the ovarial lobes in coreid Hemiptera contribute to the nutritive materials which are stored in the growing egg.     

Role of phospholamban in NO/EDRF-induced relaxation in rat aorta.

The role of endothelium-derived nitric oxide (NO) to cause smooth muscle phospholamban (PLB) phosphorylation was studied in the isolated perfused rat aorta precontracted with norepinephrine using a back-phosphorylation technique. NO-induced relaxation was associated with increased PLB-phosphorylation while norepinephrine as such was ineffective. Removal of endothelium significantly reduced PLB-phosphorylation in indomethacin treated vessels. Stimulation of NO-formation by ATP augmented PLB-phosphorylation in intact vessels but was ineffective in denuded aortas. The results indicate that PLB-phosphorylation of vascular smooth muscle plays an important role in mediating NO-dependent relaxation by enhancing Ca(++)-uptake into sarcoplasmic reticulum.     

Artificial protein sensors

Protein recognition by synthetic molecules is a challenging endeavour, since these materials must bind to a large relatively flat surface domain and recognize a unique distribution of amino acid residues of varying charge, size and shape. The most promising routes involve specific metal coordination, epitope-docking on miniature proteins, aptamer selection, nonnatural peptide isosteres, functionalized platforms, secondary structure mimetics, molecular imprinting and receptors embedded in lipid layers.     

Modulating zymogen granule formation in pancreatic AR42J cells

Zymogen granules (ZG) are specialized organelles in the exocrine pancreas which allow digestive enzyme storage and regulated secretion. To investigate ZG biogenesis, cargo sorting and packaging, suitable cellular model systems are required. Here, we demonstrate that granule formation in pancreatic AR42J cells, an acinar model system, can be modulated by altering the growth conditions in cell culture. We find that cultivation of AR42J cells in Panserin^? 401, a serum-free medium, enhances the induction of granule formation in the presence or absence of dexamethasone when compared to standard conditions including serum. Biochemical and morphological studies revealed an increase in ZG markers on the mRNA and protein level, as well as in granule size compared to standard conditions. Our data indicate that this effect is related to pronounced differentiation of AR42J cells. To address if enhanced expression of ZG proteins promotes granule formation, we expressed several zymogens and ZG membrane proteins in unstimulated AR42J cells and in constitutively secreting COS-7 cells. Neither single expression nor co-expression was sufficient to initiate granule formation in AR42J cells or the formation of granule-like structures in COS-7 cells as described for neuroendocrine cargo proteins. The importance of our findings for granule formation in exocrine cells is discussed.     

Sunburn of Apple Fruit: Historical Background,Recent Advances and Future Perspectives

Sunburn is a physiological disorder of apples and other fruit species caused by excess solar radiation. Damage occurs in practically all growing regions of the world, causing severe crop loss every year. Direct factors required for induction of the three currently-known types of sunburn (i.e., sunburn necrosis, sunburn browning, and photooxidative sunburn) include excess radiant heating and/or exposure to excess sunlight. Several other factors (e.g., relative humidity, wind velocity, acclimation of fruit, and cultural management practices), which alone cannot induce sunburn damage, indirectly influence the induction of sunburn by interacting with the direct factors to influence the appearance and severity of the symptoms. Sunburn affects apple fruit at many levels; it causes structural and morphological changes, alters pigment composition, influences adaptive mechanisms, impairs photosynthesis, and consequently decreases fruit quality. Fruits employ multiple physiological and biochemical mechanisms as complex defense systems to minimize damage. Photoprotective pigments, antioxidant enzymes and metabolites, heat-shock proteins, and the xanthophyll cycle help mitigate damage, but are often inadequate under field conditions to fully protect from sunburn. Quality loss significantly affects postharvest behavior, marketing and consumer acceptance of fruit. Internal fruit quality (e.g., firmness, soluble solids concentration, and titratable acidity) is affected by sunburn, and changes in these traits continue during cold storage. Sunburn-related disorders (e.g., sunburn scald in ‘Granny Smith’ and ‘Fuji’ stain) can appear in cold storage. There are several methods with various modes of action (e.g., climate ameliorating techniques, and sunburn suppressants) available to growers to decrease sunburn under field conditions. At the end of this review, the potential impact of a changing climate on sunburn incidence is considered, as both UV-B radiation and temperature are projected to change. Finally, several topics that need further research are discussed.     

Peroxisomes and oxidative stress

The discovery of the colocalization of catalase with H2O2-generating oxidases in peroxisomes was the first indication of their involvement in the metabolism of oxygen metabolites. In past decades it has been revealed that peroxisomes participate not only in the generation of reactive oxygen species (ROS) with grave consequences for cell fate such as malignant degeneration but also in cell rescue from the damaging effects of such radicals. In this review the role of peroxisomes in a variety of physiological and pathological processes involving ROS mainly in animal cells is presented. At the outset the enzymes generating and scavenging H2O2 and other oxygen metabolites are reviewed. The exposure of cultured cells to UV light and different oxidizing agents induces peroxisome proliferation with formation of tubular peroxisomes and apparent upregulation of PEX genes. Significant reduction of peroxisomal volume density and several of their enzymes is observed in inflammatory processes such as infections, ischemia-reperfusion injury and hepatic allograft rejection. The latter response is related to the suppressive effects of TNFalpha on peroxisomal function and on PPARalpha. Their massive proliferation induced by a variety of xenobiotics and the subsequent tumor formation in rodents is evidently due to an imbalance in the formation and scavenging of ROS, and is mediated by PPARalpha. In PEX5-/- mice with the absence of functional peroxisomes severe abnormalities of mitochondria in different organs are observed which resemble closely those in respiratory chain disorders associated with oxidative stress. Interestingly, no evidence of oxidative damage to proteins or lipids, nor of increased peroxide production has been found in that mouse model. In this respect the role of PPARalpha, which is highly activated in those mice, in prevention of oxidative stress deserves further investigation.     

Redistribution of connexin43 in regional acute ischemic myocardium: influence of ischemic preconditioning

Connexins are known to play an essential role in the ischemic preconditioning (IP) of the heart; their functional role in this process, however, has not been clearly defined. For this reason, anesthetized rats were subjected to regional myocardial ischemia, with or without IP or reperfusion. In frozen sections of hearts, fluorescence immunohistochemical staining for connexin43 (Cx43) was performed. In contrast to undisturbed zones, tissue that had been subjected to ischemia revealed Cx43 immunostaining not only in the gap junctions but also in a conspicuous pattern in the free cellular membranes of the myocytes. In myocardium that was exposed to IP only, the ratio of immunofluorescence intensity in the free cellular membrane to that in the interior of the cell was 1.22 +/- 0.04 (ratio in non-ischemia-exposed area = 1.04 +/- 0.01). When 15 or 45 min of permanent ischemia followed IP, the effect became more evident (ratio = 1.31 +/- 0.03 and 1.46 +/- 0.03, respectively) and proved to be significantly greater than in the corresponding non-IP groups (ratio = 1.16 +/- 0.03 and 1.30 +/- 0.03, respectively, P < 0.01). Reperfusion led to an overall weakening of fluorescence intensities and a disappearance of the observed IP-specific differences. We conclude that IP initiates a redistribution of Cx43 from its natural position in the gap junctions toward the free plasma membrane, thereby improving the cell's chance of survival during the subsequent phase of prolonged ischemia by an unknown, supposedly gap junction-independent, mechanism.