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Biomedical subjects

I Lopez

Publications and source records attributed to I Lopez.

At least 19 recordsLinked to original sources
PubMed1996

Pollen specific expression of maize genes encoding actin depolymerizing factor-like proteins.

In pollen development, a dramatic reorganization of the actin cytoskeleton takes place during the passage of the pollen grain into dormancy and on activation of pollen tube growth. A role for actin-binding proteins is implicated and we report here the identification of a small gene family in maize that encodes actin depolymerizing factor (ADF)-like proteins. The ADF group of proteins are believed to control actin polymerization and depolymerization in response to both intracellular and extracellular signals. Two of the maize genes ZmABP1 and ZmABP2 are expressed specifically in pollen and germinating pollen suggesting that the protein products may be involved in pollen actin reorganization. A third gene, ZmABP3, encodes a protein only 56% and 58% identical to ZmABP1 and ZmABP2, respectively, and its expression is suppressed in pollen and germinated pollen. The fundamental biochemical characteristics of the ZmABP proteins has been elucidated using bacterially expressed ZmABP3 protein. This has the ability to bind monomeric actin (G-actin) and filamentous actin (F-actin). Moreover, it decreases the viscosity of polymerized actin solutions consistent with an ability to depolymerize filaments. These biochemical characteristics, taken together with the sequence comparisons, support the inclusion of the ZmABP proteins in the ADF group.

Actin Depolymerizing Factors↗
PubMed1996

Characterization and localization of adrenal nicotinic acetylcholine receptors: evidence that mAb35-nicotinic receptors are the principal receptors mediating adrenal catecholamine secretion.

Adrenal chromaffin cells contain at least two subtypes of nicotinic acetylcholine receptors (nAChRs). These studies were designed to identify and characterize the subtype of nAChR mediating adrenal catecholamine release using the monoclonal antibody mAb35, which recognizes the alpha-subunit of muscle nAChRs and cross-reacts with some neuronal nAChRs. Immunocytochemical studies demonstrated that mAb35 interacts with specific sites on cultured chromaffin cells. Pretreatment with mAb35 reduced nAChR-stimulated catecholamine release (IC50 of approximately 10nM). mAb35 had no effects on release stimulated through non-nAChR mechanisms. Unlike agonist-induced nAChR desensitization, the mAb35-induced reduction in nAChR-mediated secretion developed slowly. Although not immediately reversible, nAChR-stimulated release recovered after mAB35 removal. However, unlike recovery from agonist pretreatment, recovery from mAb35 pretreatment was relatively slow and was par tially blocked by vinblastine. Hybridization of adrenal chromaffin RNA with a rat alpha3 cDNA revealed two strong bands and two fainter bands: two higher-molecular-weight bands, 6.9 and 8.5 kb; a strong band of 3.2 kb; and a lower amount of 2.3kb RNA. With recovery of nAChR function after agonist or mAb35 treatment, no significant effects on alpha 3 subunit mRNA levels were seen. In summary, these studies demonstrate the presence of mAb35-nAChRs on adrenal chromaffin cells and provide evidence that these receptors represent the major population that regulates secretory events in adrenal chromaffin cells.

Adrenal Glands↗
PubMed1996

Histopathology of idiopathic chronic recurrent vertigo.

Vestibular neuritis is a degenerative neuropathy of the peripheral vestibular system. The etiology of this condition is uncertain, although it is generally believed to be viral. A small percentage of patients with vestibular neuritis have chronic recurrent episodes of vertigo. Detailed cytologic descriptions of acute or chronic vestibular neuritis are lacking, and no previous studies have reported evidence of chronic inflammation in human temporal bone specimens. The authors of this study examined temporal bone specimens from three patients with a history of chronic recurrent vertigo of unknown cause. Varying degrees of inflammation and destruction were seen in the vestibular system, and mild involvement of the cochlear system was noted. These findings are consistent with postinfectious inflammatory changes of the cochlear-vestibular system analogous to a postinfectious syndrome involving the central nervous system.

Cochlear Nerve↗
PubMed1996

Antipsychotic medications in children and adolescents.

Antipsychotic medications are commonly prescribed to children and adolescents. These medications, however, are not only prescribed for young patients with psychosis, but are often prescribed for youths with a variety of psychiatric disorders. Despite the fact that psychiatric illness in the pre-adult era is not rare, few controlled clinical trials have examined the short-term safety and efficacy of these agents in youths with psychosis. There are even fewer data regarding the long-term safety and efficacy of these agents in psychotic children and adolescents. As new antipsychotics become available, the study of these agents in youngsters with a variety of psychiatric illnesses may become an exciting new avenue for research.

Adolescent↗
PubMed1996

Thrombocytemia and abnormal megakaryopoiesis associated with abnormality of chromosome 1p34 in myelodysplastic syndromes.

Myelodysplastic syndromes (MDS) are a heterogeneous group of diseases characterized by a cytopenia related to abnormal proliferation and differentiation of marrow precursor cells. Some subtypes of MDS are associated with thrombocytemia or abnormal megakaryopoiesis and certain specific karyotypic abnormalities. We report on four cases of MDS with normal or elevated blood platelet count and a recurring abnormality in chromosome 1p34. The gene involved appears to be different from c-mpl and TPO.

Aged↗
PubMed1995

RhoA and a cytosolic 50-kDa factor reconstitute GTP gamma S-dependent phospholipase D activity in human neutrophil subcellular fractions.

Receptor activation of phospholipase D has been implicated in signal transduction in a variety of cells. Reconstitution of cell-free guanosine 5'-O-(3-thiotriphosphate)(GTP gamma S)-dependent phospholipase D activity from human neutrophils requires protein factors in both the plasma membrane and the cytosol. We previously proposed that one of the factors is a Ras-family small molecular weight GTPase of the Rho subtype (Bowman, E. P., Uhlinger, D. J., and Lambeth, J. D. (1993) J. Biol. Chem. 268, 21509-21512). Herein, we have used RhoGDI (GDP dissociation inhibitor), an inhibitory Rho-binding protein, to selectively extract Rho-type GTPases from the plasma membrane, and have used immunoprecipitation as well as chromatographic methods to remove cytosolic Rho. Depletion of RhoA from either the plasma membrane or the cytosol resulted in a partial loss in GTP gamma S dependent activity, while removal of RhoA from both fractions resulted in a nearly complete loss in activity. Activity was nearly completely restored by adding purified recombinant RhoA, which showed an EC50 of 52 nM, while Rac1 showed little activity. Cytosol fractionated using DEAE-cellulose chromatography separated ADP-ribosylation factor and Rho from the major activating fraction. Gel exclusion chromatography of this fraction revealed an activating factor of 50 kDa apparent molecular mass. Using RhoA-depleted membranes, reconstitution of phospholipase D activity required both RhoA and the 50-kDa factor. Thus, RhoA along with a non-Rho, non-ADP-ribosylation factor 50-kDa cytosolic factor are both required to reconstitute GTP gamma S-dependent phospholipase D activity by neutrophil plasma membranes.

Adult↗
PubMed1995

Regulation of phospholipase D by protein kinase C in human neutrophils. Conventional isoforms of protein kinase C phosphorylate a phospholipase D-related component in the plasma membrane.

In a variety of intact cells, phorbol esters are known to activate phospholipase D. In a cell-free system consisting of plasma membrane and cytosol from human neutrophils, phorbol esters activated phospholipase D in an adenosine nucleotide triphosphate-dependent manner. ATP gamma S (adenosine 5'-O-(thiotriphosphate)) was 2-3-fold more effective than ATP, while ADP and AppNHp (adenyl-5'-yl imidodiphosphate) were ineffective, and activation was blocked by the kinase inhibitor staurosporine. In cytosol deplete of protein kinase C by chromatography on threnoine-Sepharose, phorbol ester-dependent activation was lost, but was restored upon addition of purified rat brain protein kinase C. The target for phosphorylation was shown to be the plasma membrane plasma membrane was phosphorylated using ATP gamma S/phorbol 12,13-dibutyrate and protein kinase C and was reisolated to remove activators. Upon adding nucleotide-depleted cytosol, activator-independent phospholipase D activity was seen. Using this prephosphorylation protocol, PKC-dependent activation of plasma membranes was found to require micromolar calcium, implicating a conventional protein kinase C. Using recombinant isoforms of protein kinase C, only the conventional isoforms showed significant activation, with the following rank order of potency: beta 1 > alpha > gamma; the beta 2, delta, epsilon, eta, and sigma isoforms showed little or no activity. Thus, conventional isoform(s) of protein kinase C activate neutrophil phospholipase D by phosphorylating a target protein located in the plasma membrane.

Adenosine Triphosphate↗
PubMed1995

ADP-ribosylation factor functions synergistically with a 50-kDa cytosolic factor in cell-free activation of human neutrophil phospholipase D.

Proteins in both the cytosol and plasma membrane are needed to reconstitute cell-free phospholipase D activity from phagocytes (Olson, S., Bowman, E. P., and Lambeth, J. D. (1991) J. Biol. Chem. 266, 17236-17242); membrane factors include a small GTP-binding protein in the Rho family (Bowman, E., Uhlinger, D. J., and Lambeth, J. D. (1993) J. Biol. Chem. 268, 21509-21512). ADP-ribosylation factor (ARF) was recently implicated as the cytosolic factor, as it activates phospholipase D in HL-60 membranes. Herein, we show that ion exchange chromatography separates ARF from the major phospholipase D-stimulating cytosolic factor. Both bovine brain ARF and recombinant human ARF-1 stimulated a small amount of phospholipase D activity in the absence of cytosol (about 10% of the response seen with cytosol). With a high concentration of ARF-depleted cytosol, ARF did not further activate. However, at low cytosol, ARF caused marked activation. Thus, ARF synergizes with the cytosolic factor in phospholipase D activation.

ADP-Ribosylation Factors↗
PubMed1995

Expression of alpha 4 and beta 2 nicotinic acetylcholine receptor subunit mRNA and localization of alpha-bungarotoxin binding proteins in the rat vestibular periphery.

In situ hybridization histochemistry was used to map the distribution of alpha 2, alpha 3, alpha 4, and beta 2 nAChR subunit mRNAs throughout the peripheral vestibular system of the rat. The alpha 4 and beta 2 nAChR subunit genes were co-expressed by populations of primary afferent neurons within Scarpa's ganglion, while there was no expression of the alpha 2, alpha 3, alpha 4, or beta 2 nAChR subunit genes by type I or type II vestibular hair cells. alpha-bungarotoxin binding to nAChRs in the vestibular end-organs was primarily limited to the afferent chalices surrounding type I hair cells and the basal aspect of type II hair cells. These data suggest that nAChRs composed of alpha 4 and beta 2 subunits are localized on afferent chalices innervating the type I vestibular hair cells and that the direct cholinergic efferent innervation of the type II vestibular hair cells utilizes nAChR composed of other subunits.

Afferent Pathways↗
PubMed1995

Histological evidence for hair cell regeneration after ototoxic cell destruction with local application of gentamicin in the chinchilla crista ampullaris.

Two experiments were conducted to study the ototoxic effects of local gentamicin (GM) administration and the subsequent hair cell (HC) regeneration process in the chinchilla cristae ampullares (CA). In the first experiment, 3 different doses of GM (0.1, 0.2 and 1.2 mg) were administered by surgical implantation of GM-soaked Gelfoam pledgets in the perilymphatic space in the otic capsule of the left superior semicircular canal. The CA was histologically processed for light-microscopic examination. In the second experiment, 6 groups of 2 chinchillas each were treated with 0.1 mg of GM. To document cell proliferation and HC regeneration, Alzet micro-osmotic pumps were implanted in each chinchilla to deliver bromodeoxyuridine (BrdU) at 125 micrograms/h for 1 week. Chinchillas were subsequently killed at 1 and 4 days and 1, 2, 4 and 8 weeks post-treatment (PT). The CA was processed for light microscopy and BrdU immunocytochemistry. In the first experiment the smallest dose produced damage restricted to HCs alone, while the medium and large doses produced severe damage in the sensory epithelium, including supporting cells and HCs. Results in the second experiment demonstrated that at 1 and 4 days PT the HCs showed extensive damage, including clumping of nuclear material. By 4 days PT the supporting cell nuclei lost their monolayer configuration. Calyceal terminals appeared empty, and vacuolized remnants of nerve calyces were evident in the basal portion. At 1 week PT complete disappearance of HCs from the sensory epithelium was evident, and there was cytoplasmic extrusion into the endolymphatic space. At 2 weeks PT there was complete HC loss, the supporting cell nuclei were scattered randomly in the crista, and the nerve fibers were retracted from the sensory epithelium. At 4 weeks PT there was evidence of sensory epithelium repair and HC regeneration. Short cells resembling type-II HCs were evident in the surface of the sensory epithelium. At 8 weeks PT the number of HCs increased in a uniform fashion on the surface of the sensory epithelium, and the supporting cell nuclei were realigned on the basal membrane. Nerve fibers with growth cones penetrated the basal membrane. Supporting cell proliferation was evident by the presence of mitotic figures and BrdU immunoreactivity in the chromatin material of dividing cells at 2 weeks PT. The labeling was more evident in newly formed cells at 4 and 8 weeks PT. These results demonstrate that in chinchillas the vestibular organs have the capacity of self-repair and the process includes HC regeneration after local administration of GM. The overall process involves changes in different cells in the sensory epithelium and neural elements, all of which show modifications with an orderly pattern.

Animals↗
PubMed1995

Distribution of efferent cholinergic terminals and alpha-bungarotoxin binding to putative nicotinic acetylcholine receptors in the human vestibular end-organs.

Although acetylcholine (ACh) has been identified as the primary neurotransmitter of the efferent vestibular system in most animals studied, no direct evidence exists that ACh is the efferent neurotransmitter of the human vestibular system. Choline acetyltransferase immunohistochemistry (ChATi), acetylcholinesterase (AChE) histochemistry, and alpha-bungarotoxin binding were used in human vestibular end-organs to address this question. ChATi and AChE activity was found in numerous bouton-type terminals contacting the basal area of type II vestibular hair cells and the afferent chalices surrounding type I hair cells; alpha-bungarotoxin binding suggested the presence of nicotinic acetylcholine receptors on type II vestibular hair cells and on the afferent chalices surrounding type I hair cells. This study provides evidence that the human efferent vestibular axons and terminals are cholinergic and that the receptors receiving this innervation may be nicotinic.

Acetylcholinesterase↗
PubMed1994

Choline acetyltransferase immunoreactivity in the human vestibular end-organs.

Acetylcholine (ACh) is believed to play a major role in the efferent vestibular system in several animal models, however no information regarding the role of ACh in the human efferent vestibular system has been published. Post-embedding immunohistochemistry in a hydrophilic resin was used to investigate the choline acetyltransferase immunoreactivity (ChATi) and acetylcholinesterase (AChE) histochemistry in human vestibular end-organs. ChATi and AChE activity was found in numerous bouton-type terminals at the basal area of the vestibular hair cells. These terminals were found to contact type II vestibular hair cells and the afferent chalices surrounding type I hair cells. This study provides the first evidence that the human efferent vestibular axons and terminals are cholinergic.

Acetylcholinesterase↗
PubMed1994

Subcellular innervation patterns of the calcitonin gene-related peptidergic efferent terminals in the chinchilla vestibular periphery.

We examined the ultrastructural distribution of calcitonin gene-related peptide immunoreactivity in the peripheral vestibular system of the chinchilla to study the innervation patterns of this efferent neuropeptide. Immunoelectron microscopic localization of calcitonin gene-related peptide immunoreactive terminals in the maculae and cristae revealed an extensive innervation pattern on the afferent vestibular pathway. Calcitonin gene-related peptide immuno-reactive terminals made synaptic contacts with the unmyelinated portions of the primary afferent vestibular dendrites innervating both type I and type II hair cells. Abundant synaptic contact between calcitonin gene-related peptide immunoreactive terminals and the chalices surrounding type I hair cells was observed. Direct contact between calcitonin gene-related peptide immunoreactive terminals and type II hair cells was observed. In addition, vesiculated efferent terminals without calcitonin gene-related peptide immunoreactivity were seen synapsing on the chalices of type II hair cells and on the surrounding type I hair cells. The primary afferent somata in the vestibular ganglion of Scarpa did not contain calcitonin gene-related peptide immunoreactivity. Unmyelinated calcitonin gene-related peptide immunoreactive axons passed among the primary afferent fibers in Scarpa's ganglion, and these fibers continued through the subepithelial regions of the vestibular end-organs. The calcitonin gene-related peptide immunoreactive axons ramified to produce numerous calcitonin gene-related peptide immunoreactive terminals throughout the neurosensory epithelium of the maculae and cristae. These data suggest that calcitonin gene-related peptide-mediated modulation of the afferent vestibular system is functionally important.

Animals↗
PubMed1994

[Treatment of mucositis with vitamin E during administration of neutropenic antineoplastic agents].

Mucositis represents one of the most frequent complications during chemotherapy or radiotherapy. Few studies have showed effective prevention against mucositis in this setting. In this randomized study, we tested the efficacy of vitamin E in the treatment of chemotherapy-induced mucositis. Twenty patients with malignant haemopathies were included; 19 patients were evaluable for the prevention of mucositis. Ten patients were treated with induction therapy for acute myelogenous leukaemia and 9 were treated with intensive therapy followed by autologous bone marrow transplantations. The severity of mucositis was evaluated according to World Health Organization classification. Our results showed that vitamin E may be of therapeutical value in the prevention of mucositis especially during induction therapy for acute myelogenous leukaemia.

Adolescent↗