Search PubMed⌕ Search

Biomedical subjects

F Casares

Publications and source records attributed to F Casares.

27 records · Page 2Linked to original sources

Functional similarity in appendage specification by the Ultrabithorax and abdominal-A Drosophila HOX genes.

In Drosophila, the Ultrabithorax, abdominal-A and Abdominal-B HOX genes of the bithorax complex determine the identity of part of the thorax and the whole abdomen. Either the absence of these genes or their ectopic expression transform segments into the identity of different ones along the antero-posterior axis. Here we show that misexpression of Ultrabithorax, abdominal-A and, to some extent, Abdominal-B genes cause similar transformations in some of the fruitfly appendages: antennal tissue into leg tissue and wing tissue into haltere tissue. abdominal-A can fully, and Abdominal-B partially, substitute for Ultrabithorax in haltere development. By contrast, when ectopically expressed, the three genes specify different segments in regions of the main body axis like notum or abdomen. Insects may have originally used the HOX genes primarily to specify this main body axis. By contrast, the homeotic requirement to form appendages is, in some cases, non-specific.

Animals↗

Hyperstimulation of leukocytes by plasma from cardiopulmonary bypass patients is diminished by alpha-MSH pretreatment.

Cardiopulmonary bypass (CPB) results in a diffuse inflammatory response characterized in part by hyperstimulation of leukocytes. We have previously shown that this hyperstimulation appears to be due, in part, to an increase in the release of biological response modifiers (BRMs) such as cytokines. In the present study, we evaluated the ability of a naturally occurring immunocyte inhibitory substance, alpha-melanocyte-stimulating hormone (alpha-MSH), to prevent the hyperstimulation caused by CPB. Monocytes and granulocytes were pretreated with alpha-MSH (10(-6) M) before exposing the cells to plasma obtained from patients who had undergone CPB, as CPB plasma would stimulate native monocytes and granulocytes in a manner similar to that observed in CPB patients. Pretreatment of these cells with alpha-MSH significantly diminished the hyperstimulation induced by CPB plasma in a concentration-dependent manner. In contrast, when the cells were first or simultaneously exposed to CPB plasma and then to alpha-MSH, alpha-MSH had no effect. Furthermore, use of the specific neutral endopeptidase inhibitor, phosphoramidon, significantly increased the efficacy of alpha-MSH in inhibiting CPB-induced immunocyte activation. The data demonstrate that pretreatment of monocyte/macrophages and granulocytes with alpha-MSH effectively inhibits the immune hyperstimulation induced by CPB-plasma exposure. In addition, the data strongly suggest that preexposure to other naturally occurring immune inhibitory substances may diminish the hyperstimulation associated with CPB. The study also further confirms that this hyperstimulation may, in part, be due to BRMs released from immunocytes.

Cardiopulmonary Bypass↗

Presence of the mu3 opiate receptor in endothelial cells. Coupling to nitric oxide production and vasodilation.

Initial confinement of opiate receptors to the nervous system has recently been broadened to several other cell types. Based on the well established hypotensive effect of morphine, we hypothesized that endothelial cells may represent a target for this opiate substance. Endothelial cells (human arterial and rat microvascular) contain a high affinity, saturable opiate binding site presumed to mediate the morphine effects that is stereoselectively and characteristically antagonized by naloxone. This opiate alkaloid-specific binding site is insensitive to opioid peptides. It is, therefore, considered to be the same subtype of opiate receptor (designated mu3) used in the mediation of morphine in other cell types exhibiting the same binding profile. Experiments with endothelial cultures and the aortic ring of rats cultured in vitro demonstrate that morphine exerts direct modulatory control over the activities of endothelial cells, which leads to vasodilation. It induces the production of nitric oxide, a process that is sensitive to naloxone antagonism and nitric oxide synthase inhibition. In contrast with that of opiates, the administration of opioid peptides does not induce nitric oxide production by endothelial cells. In conclusion, the data presented above reveal a novel site of morphine action, endothelial cells, where a mu3 receptor is coupled to nitric oxide release and vasodilation.

Animals↗

Changes in the blood-thymus barrier of adult rats after estradiol-treatment.

The accessibility of the thymus parenchyma for relatively large Mw (+/- 150 Kd) proteins has been studied by the intravenous injection of monoclonal antibodies (mAbs) specific either for all T cells (His-17) or MHC class II molecules (His-19) in control and estradiol benzoate (EB)-treated adult Wistar rats. In controls, the transcapsular route rather than cortical capillaries seems to be involved in the entry of molecules into the thymus. By contrast, a specific staining for either T cells (His-17) or MHC class II molecules (His-19 positive cells) disappears almost completely from the thymic cortex of EB-treated rats except in the immediate subcapsular epithelial cell layer. In these rats, T cells and epithelial cells intimately associated to blood vessels from both inner cortex and corticomedullary border showed additional staining with the respective mAbs confirmed by electron microscopy. The disappearance of the transcapsular route together with the increased vascular permeability of cortical blood vessels would be related to the reinforcement of the subcapsular epithelial cell layer and to direct effects of EB on vascular endothelia, respectively. These results are discussed in relationship to the cell migration into and out of adult thymus, as suggested by the changes in intrathymic T cell subsets evaluated by flow cytometry.

Animals↗

Regulation of the infraabdominal regions of the bithorax complex of Drosophila by gap genes.

The expression of the abdominal-A and Abdominal-B genes of the bithorax complex of Drosophila is controlled by cis-regulatory infraabdominal regions. The activation of these regions along the anteroposterior axis of the embryo determines where abdominal-A and Abdominal-B are transcribed. There is spatially restricted transcription of the infraabdominal regions (infraabdominal transcripts) that may reflect this specific activation. We show that the gap genes hunchback, Krüppel, tailless and knirps control abdominal-A and Abdominal-B expression early in development. The restriction of abdominal-A and Abdominal-B transcription is preceded by (and requires) the spatially localized activation of regulatory regions, which can be detected by the distribution of infraabdominal transcripts. The activation of these regions (except the infraabdominal-8 one) could require no specific gap gene. Instead, a general mechanism of activation, combined with repression by gap genes in the anteroposterior axis, seems to be responsible for delimiting infraabdominal active domains. The gradients of the hunchback and Krüppel products seem to be key elements in this restricted activation.

Animals↗

Naltrindole sensitive delta 2 opioid receptor mediates invertebrate immunocyte activation.

Previous studies demonstrated the presence of a delta 2 opioid receptor on human and invertebrate immunocytes. The present study demonstrates that this new binding site regulates invertebrate immunocyte activation. In the present study we note that the select delta antagonist, naltrindole, at a low concentration (10(-11) M), can significantly inhibit DAMA induced activation. Interestingly, the general opioid and opiate antagonist, naloxone, is not effective at this low concentration, further suggesting that the delta 2 opioid receptor mediates opioid immunocyte activation. This conclusion is further supported by the fact that DPDPE and DADLE, known to influence delta 1 activity did not affect immunocyte activation at low concentrations.

Animals↗

In vitro antigen trapping by gill cells of the rainbow trout: an immunohistochemical study.

An in vitro assay was used to study the involvement of gill cells in the trapping and processing of particulate antigens. Gills were routinely processed for light microscopy after being placed in medium containing either Yersinia ruckeri O-antigen-labelled fluorescent beads, unlabelled fluorescent beads, Y, ruckeri O-antigen or formalin-killed Y. ruckeri, for 0, 30 s, 1, 5 and 30 min. Y. ruckeri formalin-killed cells, Y. ruckeri O-antigen and fluorescent beads labelled with Y. ruckeri O-antigen were taken in by gill epithelial cells as soon as 30 s after administration. In contrast, unlabelled fluorescent beads adhered to the epithelial cell membranes, but did not occur inside the gill cells. These results are discussed principally in relationship with the specificity of antigen trapping.

Animals↗

Dynamics and function of intron sequences of the wingless gene during the evolution of the Drosophila genus.

To understand the function and evolution of genes with complex patterns of expression, such as the Drosophila wingless gene, it is essential to know how their transcription is regulated. However, extracting the relevant regulatory information from a genome is still a complex task. We used a combination of comparative genomics and functional approaches to identify putative regulatory sequences in two introns (1 and 3) of the wingless gene and to infer their evolution. Comparison of the sequences obtained from several Drosophila species revealed colinear and well-conserved sequence blocks in both introns. Drosophila willistoni showed a rate of evolution, in both introns, faster than expected from its phylogenetic position. Intron 3 appeared to be composed of two separate modules, one of them lost in the willistoni group. We tested whether sequence conservation in noncoding regions is a reliable indicator of regulatory function and, if this function is conserved, by analyzing D. melanogaster transgenic reporter lines harboring intron 3 sequences from D. melanogaster (Sophophora subgenus) and the species from the Drosophila subgenus presenting the most divergent sequence, D. americana. The analysis indicated that intron 3 contains pupal enhancers conserved during the evolution of the genus, despite the fact that only 30% of the D. melanogaster intron 3 sequences lie in conserved blocks. Additional analysis of D. melanogaster transgenic reporter lines harboring intron 3 sequences from D. willistoni revealed the absence of an abdomen-specific expression pattern, probably due to the above-mentioned loss of a regulatory module in this species.

Animals↗

[Endocranial hypertension].

INTRODUCTION AND OBJECTIVE: The endocranial hypertension syndrome is one of the commonest and most feared neurological complications in clinical practice. This encourages its continued study, and is the subject of this review. DEVELOPMENT: Endocranial hypertension is the common pathway for the presentation of many neurological and non neurological disorders. An increase in the volume of one or more intracranial structures causes secondary lesions of the brain and even the death of the patient, although this may frequently be avoided by prompt recognition and suitable action by the doctor involved. General, non specific therapeutic measures should be instituted to achieve a normal endocranial pressure. The clinical presentation and complementary investigations should be correctly interpreted to determine the aetiology of the condition so that specific treatment may be given. Continuous monitoring of the intracranial pressure and other neuromonitorization techniques are essential for correct decisions as to treatment. CONCLUSIONS: Understanding the physiopathology, diagnosis and treatment of the syndrome of endocranial hypertension are still essential in modern medicine. In recent years there have been advances in the use of well known treatments and new drugs have been introduced. Use of the different neuromonitoring techniques permits optimum use of the treatment available.

Brain Edema↗