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Biomedical subjects

A Isaac

Publications and source records attributed to A Isaac.

At least 19 recordsLinked to original sources
PubMed2003

Endoparasite infracommunities of Hemisorubim platyrhynchos (Valenciennes, 1840) (Pisces: Pimelodidae) of the Baía River, Upper Parana River floodplain, Brazil: specific composition and ecological aspects.

Parasites of 136 specimens of Hemisorubim platyrhynchos, popularly called jurupoca, were analyzed. Fourteen parasite species were recorded: four digeneans (Crocodilicola pseudostoma, one Gorgoderidae species, Sanguinicola platyrhynchi, and Sphincterodiplostomum sp.); three cestodes (Goezeella paranaensis, Spatulifer maringaensis, and Mariauxiella piscatorum); five nematodes (Contracaecum Type 1 larvae of Moravec, Kohn, & Fernandes, 1993; Contracaecum Type 2 larvae of Moravec, Kohn, & Fernandes, 1993; Cucullanus (Cucullanus) zungaro; Eustrongylides ignotus; and Goezia sp.); one acanthocephalan (Quadrigyrus machadoi), and one pentastomid (Sebekia sp.). Most of the helminth specimens were found in larval stages, confirming that H. platyrhynchos is a significant source of their transmission. No dominance was reported. With the exception of Contracaecum Type 2 (featuring random dispersion), the species had a clumped pattern of dispersion in the host sample. Evidence of competition among parasite species was not reported. Several species of parasites were correlated with host size and sex. This fact may be explained by increase in food content and possible behavioral modifications of male and female hosts. Infracommunity diversity was not related to host size or sex.

Animals↗
PubMed2003

Sanguinicola platyrhynchi n. sp. (Digenea: Sanguinicolidae) parasite of visceral cavity of Hemisorubim platyrhynchos (Valenciennes, 1840) (Pisces: Pimelodidae) from the floodplain of the upper Paraná River, Brazil.

A new species is of the genus Sanguinicola Plehn, 1905 described, Sanguinicola platyrhynchi n. sp., digenetic parasite of visceral cavity of Hemisorubim platyrhynchos (Valenciennes, 1840) from the floodplain of the upper Paraná River, Brazil. The species has been thus included because of the presence of separate dorsal genital pores, while differing from other species of the same genus mainly in digestive apparatus features, genital pore position, and infection site. Emendation of generic diagnosis is included.

Animals↗
PubMed2000

Induction of apoptosis in rat cardiocytes by A3 adenosine receptor activation and its suppression by isoproterenol.

The purpose of the present study was to investigate the mechanisms involved in the induction of apoptosis in newborn cultured cardiomyocytes by activation of adenosine (ADO) A3 receptors and to examine the protective effects of beta-adrenoceptors. The selective agonist for A3 ADO receptors Cl-IB-MECA (2-chloro-N6-iodobenzyl-5-N-methylcarboxamidoadenosine) and the antagonist MRS1523 (5-propyl-2-ethyl-4-propyl-3-(ethylsulfanylcarbonyl)-6-phenylpy rid ine-5-carboxylate) were used. High concentrations of the Cl-IB-MECA (> or = 10 microM) agonist induced morphological modifications of myogenic cells, such as rounding and retraction of cell body and dissolution of contractile filaments, followed by apoptotic death. In addition, Cl-IB-MECA caused a sustained and reversible increase in [Ca2+]i, which was prevented by the selective antagonist MRS1523. Furthermore, MRS1523 protected the cardiocytes if briefly exposed to Cl-IB-MECA and partially protected from prolonged (48 h) agonist exposure. Apoptosis induced by Cl-IB-MECA was not redox-dependent, since the mitochondrial membrane potential remained constant until the terminal stage of cell death. Cl-IB-MECA activated caspase-3 protease in a concentration-dependent manner after 7 h of treatment and more effectively after 18 h of exposure. Bcl-2 protein was readily detected in control cells, and its expression was significantly decreased after 24 and 48 h of treatment with Cl-IB-MECA. Beta-adrenergic stimulation antagonized the pro-apoptotic effects of Cl-IB-MECA, probably through a cAMP/protein kinase A-independent mechanism, since addition of dibutyryl-cAMP did not abolish the apoptosis induced by Cl-IB-MECA. Incubation of cultured myocytes with isoproterenol (5 microM) for 3 or 24 h almost completely abolished the increase in [Ca2+]i. Prolonged incubation of cardiomyocytes with isoproterenol and Cl-IB-MECA did not induce apoptosis. Our data suggest that the apoptosis-inducing signal from activation of adenosine A3 receptors (or counteracting beta-adrenergic signal) leads to the activation of the G-protein-coupled enzymes and downstream pathways to a self-amplifying cascade. Expression of different genes within this cascade is responsible for orchestrating either cardiomyocyte apoptosis or its protection.

Adenosine↗
PubMed2000

FGF and genes encoding transcription factors in early limb specification.

SnR, twist and Fgf10 are expressed in presumptive limb territories of early chick embryos. When FGF-2/FGF-8 beads are implanted in chick flank, an ectopic limb develops and SnR is irreversibly activated as early as 1 h. Ectopic Fgf10 and twist expression are activated much later at 17 and 20 h, respectively. FGF-10 can also induce SnR, but much later, and in this case activation occurs simultaneously with that of twist and Fgf10 via the Fgf8- expressing ridge. Tbx-4 and Tbx-5 are expressed in leg and wing forming regions, respectively, in a similar pattern to SnR and twist. FGF-2 leads to ectopic expression of Tbx-4 and Tbx-5 as rapidly as ectopic expression of SnR, but the patterns of ectopic transcripts suggest that induction of SnR and Tbx gene expression occur via different pathways.

Animals↗
PubMed2000

Gene interference using antisense oligodeoxynucleotides on whole chick embryos. Optimal ring and roller-bottle culture technique.

Details are given of an advanced version of the ring method of chick embryo culture. This ensures good development from early blastoderm stages even when the culturing procedure is interrupted by the extended periods required for collecting matched embryo samples and for preparing antisense treatment. Antisense oligodeoxynucleotide treatment, in short-term incubation before return of blastoderms to their ring cultures, is then described. An alternative, roller-bottle, culture method for continued development after treatment is also described. Criteria for the validity and success of this gene interference method are given. While the text is meant to be of detailed practical help to those inexperienced in embryo culture, a preliminary reading, and familiarity with its sectional (Subheading) structure, is recommended before work is undertaken.

Animals↗
PubMed1999

Flik, a chick follistatin-related gene, functions in gastrular dorsalisation/neural induction and in subsequent maintenance of midline Sonic hedgehog signalling.

We have targetted the chick gene Flik with antisense oligodeoxynucleotide treatment at gastrular stages, when it is expressed in organiser-derived structures of the midline (K. Patel et al., 1996, Dev. Biol. 178, 327-342). A specific syndrome of deficient axial patterning and holoprosencephaly is produced. Most aspects of this syndrome can be understood as due to attenuation of dorsalising and neural-inducing signals during gastrulation, followed by failure to maintain the later signals from chordamesoderm/neural midline that pattern the mesodermal and neural cross sections during subsequent stages. Anatomical effects are first apparent at early neurula stages and correspond with what might be expected from a reduced counteraction of the ventralising Bone morphogenetic protein (BMP) pathway at the earlier stages, coupled with inadequate Sonic hedgehog (Shh) signalling subsequently. Delay in the clearing of BMP-4 RNA expression from the presumptive neural region at gastrulation is indeed seen, though chordin RNA expression within organiser derivatives remains normal. Subsequently, specific attenuation of chordamesoderm and neural midline Shh expression is observed. Brief preincubation of stage 4 chick blastoderms in supernatant from Xenopus oocytes that have been injected with Flik RNA prolongs and enhances the competence of their peripheral epiblast to respond to neural inductive signals from grafted Hensen's nodes. This effect specifically mimics that recently observed using microg/ml solutions of recombinant Follistatin (D. J. Connolly et al., 1999, Int. J. Dev. Biol., in press), further suggesting that Flik protein might act in vivo by somehow modulating activity of signalling pathways through BMP or other TGFbeta-related ligands. We discuss the significance of the observations in relation to recent ideas about neural induction, about possible redundancy in gene action, and about subsequent patterning of the axial cross section, suggesting that a Flik function in autocrine/paracrine maintenance of later midline Shh signalling represents a role of the gene separate from that in primary dorsalisation/neural induction.

Amino Acid Sequence↗
PubMed1999

Nodal signalling and the roles of the transcription factors SnR and Pitx2 in vertebrate left-right asymmetry.

Left-specific mesodermal expression of the homeobox gene Pitx2 links a gastrula-stage intercellular signalling cascade to the later development of vertebrate left-right organ asymmetry through the Nodal signalling pathway [1] [2][3] [4][5] [6]. SnR (Drosophila snail-related), a gene conserved in vertebrates and encoding a zinc-finger protein, appears to function in a similar manner to Pitx2, but through right-specific mesodermal expression [7] [8]. Here, we present direct evidence for an earlier proposal [7] that Nodal signalling specifically represses expression of SnR in left lateral mesoderm, and thus ensures its normal confinement to the right, while activating Pitx2 on the left. We addressed the relationship between Pitx2 and SnR using antisense disruption of SnR. Relatively severe antisense-SnR treatment led to massive ectopic expression of Pitx2 on the right, accompanied by randomisation of situs with embryos showing aspects of left-cardiac isomerism. This indicates a gene cascade relationship in the propagation of left-right information, whereby nodal activates Pitx2 on the left through a double-negative mechanism involving the repression of SnR's repressor role on Pitx2. Milder antisense-SnR treatment reversed heart-loop direction and embryo torsion at significant incidence, although Pitx2 expression remained normally left-confined throughout. This reversed morphology following SnR disruption alone appeared different from that in which additional ectopic right-hand Pitx2 expression was seen. Therefore, in addition to their regulatory gene cascade relationship, these two transcription factors appear to have further, parallel but non-redundant, roles in directly controlling normally right- and left-specific morphogenetic processes.

Animals↗
PubMed1999

Expression of Drosophila trithorax-group homologues in chick embryos.

Mll, Brg1 and Brm are vertebrate homologues of Drosophila trithorax group (trxG) genes. We isolated chicken Mll cDNA clones, and examined patterns of Mll, Brg1 and Brm expression in chick embryos. All three genes were expressed from embryonic stage 2 onwards. Mll transcripts were just detectable in all tissues by in situ hybridization, with highest level in dorsal neural tube and notochord. Brg1 transcripts were readily detectable in all tissues, with highest levels in dorsal neural tube, dorsal trunk epithelium and limb bud epithelium and mesenchyme. Brm transcripts were more restricted, being found in dermomyotome, notochord, dorsal limb bud epithelium, eye and the roof and floor plates of the neural tube.

Animals↗
PubMed1998

A cascade of gene action controlling heart asymmetry and torsion in embryonic development.

Lateralized looping of the heart tube, with associated torsion of the embryo axis, is the first structural sign of the consistent left-right asymmetrical organization that characterizes all vertebrate embryos. Rare failures or reversals of this asymmetry in humans lead to clinically important syndromes of malformation in heart and great blood vessels. Recently, elements of the genetic control sequence underlying this left-right aspect of development have been uncovered. The normal sequence of transmission for asymmetry information can now be traced to a point close to the actual execution of right-hand looping in the heart tube, with the hope that the further sequence of gene activity, within the heart itself and directing these events, may soon be uncovered.

Journal Article↗
PubMed1998

Tbx genes and limb identity in chick embryo development.

Tbx-2, Tbx-3, Tbx-4 and Tbx-5 chick genes have been isolated and, like the mouse homologues, are expressed in the limb regions. Tbx-2 and Tbx-3 are expressed in anterior and posterior domains in wings and legs, as well as throughout the flank. Of particular interest, however, are Tbx-5, which is expressed in wing and flank but not leg, and Tbx-4, which is expressed very strongly in leg but not wing. Grafts of leg tissue to wing and wing tissue to leg give rise to toe-like or wing-like digits in wing and leg respectively. Expression of Tbx-4 is stable when leg tissue is grafted to wing, and Tbx-5 expression is stable when wing tissue is grafted to leg. Induction of either extra wings or legs from the flank by applying FGF-2 in different positions alters the expression of Tbx-4 and Tbx-5 in such a way that suggests that the amount of Tbx-4 that is expressed in the limb determines the type that will form. The ectopic limb always displays a limb-like Tbx-3 expression. Thus Tbx-4 and Tbx-5 are strong candidates for encoding 'wingness' and 'legness'.

Amino Acid Sequence↗
PubMed1997

Control of vertebrate left-right asymmetry by a snail-related zinc finger gene.

A gene encoding a zinc finger protein of the Snail family, cSnR, is expressed in the right-hand lateral mesoderm during normal chick development. Antisense disruption of cSnR function during the hours immediately preceding heart formation randomized the normally reliable direction of heart looping and subsequent embryo torsion. Implanted ectopic sources of intercellular signal proteins that are involved in establishing normal left-right information randomized the handedness of heart development and also altered the asymmetry of cSnR expression. cSnR thus appears to act downstream of these signals, or perhaps in parallel with the latest expressed of them, the Nodal protein, in controlling the anatomical asymmetry.

Activin Receptors↗
PubMed1994

Acute ethanol consumption synergizes with trauma to increase monocyte tumor necrosis factor alpha production late postinjury.

The hypothesis that acute ethanol uptake plus trauma can synergize to increase immunosuppression was tested. We found that, unlike non-alcohol-exposed patients, patients with acute alcohol use prior to trauma have a transient decrease in monocyte tumor necrosis factor alpha (TNF alpha) production during the very early postinjury (0-3 days) period. However, TNF alpha production by these alcohol-exposed patients' monocytes (M0) became hyperelevated late postinjury (> 9 days). Consequently, these massively elevated M0 TNF alpha levels can contribute to posttrauma immunosuppression after acute alcohol use. We also demonstrate that normal monocyte activation with the superantigen, Staphylococcus enterotoxin B (SEB), results in a preferential induction of cell-associated M0 TNF alpha production, described as characteristic of immunosuppressed trauma patients. Acute in vitro ethanol treatment down-regulated the elevated TNF alpha production by trauma patients' M0 after either SEB, muramyl-dipeptide (MDP), interferon-gamma plus MDP, or lipopolysaccharide (LPS) stimulation. Both SEB- and LPS-induced TNF alpha mRNA induction was inhibited by acute alcohol treatment in normal M0, indicating that ethanol can regulate cytokine gene expression. An additional immunosuppressive effect of acute ethanol's stimulation was suggested by its induction of elevated transforming growth factor beta production in trauma patients' activated M0.

Adult↗