Phorophyte size and soil profiles differentially correlate with community structure among hemiepiphytes and nomadic vines

Tropical non-self-supporting plants such as hemiepiphytes and nomadic vines are model organisms for disentangling biotic and environmental correlates which influence their occupancy patterns. We inventoried >4000 individuals from >3000 trees ranging from 1 to 200 cm diameter at breast height (DBH) in a northeastern Amazonian upland forest to address how tree (phorophyte) size, edaphic factors and recruitment strategy influence occupancy, diversity, and compositional patterns of two vascular non-self-supporting plant functional groups. Hemiepiphytes germinate on phorophytes prior to establishing soil connections, whereas nomadic vines initiate their life cycle on the forest floor and subsequently climb phorophytes for crown access, abandoning roots replaced by adventitious connections which may reach the ground. Our results show that larger phorophytes (≥30 cm DBH) supported more species for both hemiepiphytes and nomadic vines. However, nomadic vines' occupancy probabilities saturated faster at smaller stem sizes than that of hemiepiphytes indicating differential preferences for stem sizes among the two functional groups. For smaller phorophytes (<30 cm DBH), soil correlations were stronger with nomadic vines than hemiepiphytes, whereas no significant differences were detected among functional groups in relation to edaphic factors for larger (≥ 30 cm DBH) ones. Finally, a small core group of species showed disproportionately greater abundances among large phorophytes suggesting that autogenic processes differentially promote survivability. Such interactions among phorophyte size and edaphic factors may result from the contrasting ecological requirements of hemiepiphytes and nomadic vines at the recruitment stage, demonstrating the necessity for elaborate demographic-based studies to better understand these complex plant–plant interactions. Abstract in Spanish is available with online material     

Regulation of glucose 6-phosphate dehydrogenase expression in CHO-human fibroblast somatic cell hybrids

Human--hamster somatic cell hybrids have been obtained by fusion of a CHO line (NA31) doubly deficient in hypoxanthine guanine phosphoribosyltransferase and glucose 6-phosphate dehydrogenase (G6PD) with normal G6PD(+) human fibroblasts. Analysis of NA31 extracts has revealed that, although G6PD activity is nearly absent, significant activity can be detected with 2-deoxyglucose 6-phosphate as substrate, so that the mutant and normal forms of the enzyme can both be easily detected. The cell hybrids obtained express human G6PD. The human G6PD subunits are distributed in homodimeric molecules as well as in human--hamster heterodimeric molecules. However, whereas the amount of hamster G6PD subunits present in the hybrid is similar to that in the hamster parental cells, the amount of human G6PD subunits is decreased by 3- to 10-fold when compared to the human parental cell. These results indicate that either the expression of the G6PD gene or the stability of the gene product is altered in the hybrid. By mutagenesis and selection in diamide (a substance that oxidizes intracellular glutathione), we have isolated a clone with a 3- to 5-fold increase in human G6PD activity. This derivative may have an increased rate of expression of the human G6PD structural gene.     

Short malonyl dehydro peptides as potential scaffolds for peptidomimetics by an efficient Knoevenagel reaction

Non-symmetric disubstituted malonamides rAA-mGly-AA′, obtained from Meldrum’s acid, were considered as methylene active compounds and a Knoevenagel condensation methodology was developed involving piperidine and activated 4 Å molecular sieves as catalysts. The reaction is efficient, broad in scope, and easy to perform and allows access to E/Z mixtures of short malonyl dehydro peptides (MDHPs) rAA-mΔ²AA″-AA′, partially modified retro peptides characterized by an interesting combination of retro and dehydro modifications in the same structure.     

Antinociceptive and hypothermic effects of trimethyltin

Trimethyltin (TMT) induced a dose-dependent antinociceptive and hypothermic effect in mice. Antinociception was not attenuated by naloxone but was reversed by atropine. TMT, however, was ineffective in displacing (³H)-QNB binding $\text{in vitro}$ and did not affect (³H)-QNB binding or acetylcholinesterase activity after $\text{in vivo}$ administration. The ethyl ester of nipecotic acid, a specific inhibitor of synaptosomal GABA uptake, exerted a similar antinociceptive effect that could be blocked by atropine. The GABA receptor antagonist bicuculline attenuated antinociception induced by TMT and nipecotic acid ethyl ester but not by morphine or oxotremorine. γ-Vinyl GABA, an irreversible inhibitor of GABA metabolism, prolonged TMT but not morphine-induced antinociception. In contrast, neither the dose-response nor the time course of TMT-induced hypothermia were affected by any of the drugs tested. The findings suggest that the GABAergic system may be involved in TMT induced antinociception; however, the mechanism responsible for the hypothermic effect of TMT is not apparent.     

Ultrastructure and X-Ray Microanalysis of Blood Cells of Ascidia malaca

Ultrastructural studies of Ascidia malaca blood reveal particular cell types, which are characterized by a polymorphism in the organization of the electron dense cytoplasmic material. A new pathway of morula cell differentiation is suggested. X-ray microanalysis shows that vanadium is localized in vacuolated, granular and morular cells. Iron, which is accumulated by this species to a lesser degree than vanadium, is found in vacuolated amebocytes and, together with vanadium, in granular cells. Our results are discussed in the light of the relations between selective metal absorption in blood cells and their specialization and differentiation.     

Nuclear inositide signaling: An appraisal of phospholipase C β1 behavior in myelodysplastic and leukemia cells

Location impinges on function of some of the main players of nuclear inositol lipid cycle. Here we have discussed the behavior of PI-PLCβ1 in myelodysplastic and cultured leukemia cells.The presence of a cryptic deletion of PI-PLCβ1 gene in high-risk MDS patients is accompanied by altered expression of its mRNA in that the overall decrease of mRNA is characterized by a dramatic decrease of the splicing variant 1a, which is cytosolic and partially nuclear, whilst the splicing variant 1b is still highly represented. This suggests that altered expression of nuclear PI-PLCβ1 could be involved in a disregulation of the cell cycle and have also important effects on cell apoptotic pathways.Moreover, in cultured leukemia cells (Felc) it has been reported by means of a proteomic approach that the splicing factor SRp20 interacts with nuclear PI-PLCβ1 and its expression is modulated by this signaling molecule.All in all, it appears more and more evident that nuclear signaling elicited by PI-PLCβ1 is a key event in the control of cell cycle progression.     

Apoptosis and cell proliferation in proximal tubular cells exposed to apoptotic bodies. Novel pathophysiological implications in cisplatin-induced renal injury

The therapeutic efficacy of the antineoplastic drug cisplatin is limited by its nephrotoxicity, which affects particularly to proximal tubular cells (PTC). Cisplatin-induced cytotoxicity appears to be multifactorial and involves inflammation, oxidative stress as well as apoptosis. We have recently shown that the cyclo-oxygenase-2 (COX-2)/intracellular prostaglandin E₂ (iPGE₂)/EP receptor pathway mediates the apoptotic effect of cisplatin on human proximal tubular HK-2 cells. Here, we studied the effects on HK-2 cells of apoptotic bodies (ABs) generated after treatment of HK-2 cells with cisplatin. We found that ABs inhibited cell growth, induced apoptosis and increased COX-2 expression and iPGE₂ in ABs-recipient HK-2 cells. Inhibition of the COX-2/iPGE₂/EP receptor pathway in these cells prevented the effects of ABs without interfering with their internalization. Interestingly, 2nd generation ABs (i.e. ABs released by cells undergoing apoptosis upon treatment with ABs) did not trigger apoptosis in naïve HK-2 cells, and stimulated cell proliferation through the COX-2/iPGE₂/EP receptor pathway. These results suggest that ABs, through iPGE₂-dependent mechanisms, might have a relevant role in the natural history of cisplatin-induced acute kidney failure because they contribute first to the propagation of the noxious effects of cisplatin to non-injured PTC and then to the promotion of the proliferative tubular response required for proximal tubule repair. Since iPGE₂ also mediates both cisplatin-induced HK-2 cell apoptosis, intervention in the COX-2/iPGE₂/EP receptor pathway might provide us with new therapeutic avenues in patients with cisplatin-induced acute kidney injury.