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Biomedical subjects

Guillermo Romero

Publications and source records attributed to Guillermo Romero.

16 recordsLinked to original sources
PubMed2006

[Digital acrometastasis].

Cutaneous metastases are infrequent and in some cases represent the first manifestation of an unknown neoplasm. Acrally located metastases are particularly rare, and the prognosis is very poor, with a survival time of only a few months. Although the clinical presentation varies, they are generally confused with an infectious or inflammatory process, which delays diagnosis. When they are located on the fingers, the most frequent cause is lung carcinoma, while those located on the toes are usually due to tumors in the genitourinary tract. The histology of the metastasis is similar to that of the primary tumor, although less differentiated. In most acrometastases, first the bone and then the skin are affected. Treatment is palliative. We present the case of a patient with a metastasis on the big toe as an initial sign of a previously unknown lung tumor.

Aged, 80 and over↗
PubMed2005

[Panniculitic T-cell lymphoma].

Panniculitic T-cell lymphoma is a rare, aggressive variant of cutaneous T-cell lymphoma, with fewer than 100 cases described. The main problem is its diagnosis, as both the clinical and the histological features may simulate benign panniculitis. We present the case of a 34-year-old male patient, who had presented with an indurated plaque, sclerodermiform in appearance, on the front of the right thigh for 4 months, later accompanied by fever and constitutional symptoms. The initial diagnosis was cellulitis, but no clinical improvement was seen despite systemic antibiotic therapy. After two skin biopsies, the patient was diagnosed with panniculitic cutaneous T-cell lymphoma. The patient was treated with 8 cycles of CHOP chemotherapy, with resolution of the symptoms.

Adult↗
PubMed2005

[Normolipemic plane xanthomas and mycosis fungoides].

Diffuse normolipemic plane xanthomas are characterized by the presence of yellowish plaques on the eyelids, neck, upper trunk, buttocks and flexures. Histology shows foamy histiocytes in the dermis. Approximately half of all cases are associated with hematological disorders. On rare occasions, they have been described in the context of cutaneous T-cell lymphomas. We present the case of a female patient with tumor-stage mycosis fungoides who developed normolipemic plane xanthomas coinciding with the appearance of new lymphoma lesions. We review English-language literature regarding the rare association of xanthomas and cutaneous T-cell lymphomas.

Aged↗
PubMed2005

[Superficial angiomyxoma].

Superficial angiomyxomas are clinically variable, infrequent, benign skin lesions. They are usually located on the trunk, but can also appear on the lower limbs, head and neck. They are diagnosed histologically, and are characterized by the fact that they are poorly delimited, multinodular tumors, and by the presence of interstitial myxoid material with scanty cellularity. Treatment is through surgery, and local recurrence is possible. An associated Carney's complex must always be ruled out with superficial angiomyxoma. We present the case of a woman with a solitary, fast-growing superficial angiomyxoma.

Adult↗
PubMed2005

Swi/SNF-GCN5-dependent chromatin remodelling determines induced expression of GDH3, one of the paralogous genes responsible for ammonium assimilation and glutamate biosynthesis in Saccharomyces cerevisiae.

It is accepted that Saccharomyces cerevisiae genome arose from complete duplication of eight ancestral chromosomes; functionally normal ploidy was recovered because of the massive loss of 90% of duplicated genes. There is evidence that indicates that part of this selective conservation of gene pairs is compelling to yeast facultative metabolism. As an example, the duplicated NADP-glutamate dehydrogenase pathway has been maintained because of the differential expression of the paralogous GDH1 and GDH3 genes, and the biochemical specialization of the enzymes they encode. The present work has been aimed to the understanding of the regulatory mechanisms that modulate GDH3 transcriptional activation. Our results show that GDH3 expression is repressed in glucose-grown cultures, as opposed to what has been observed for GDH1, and induced under respiratory conditions, or under stationary phase. Although GDH3 pertains to the nitrogen metabolic network, and its expression is Gln3p-regulated, complete derepression is ultimately determined by the carbon source through the action of the SAGA and SWI/SNF chromatin remodelling complexes. GDH3 carbon-mediated regulation is over-imposed to that exerted by the nitrogen source, highlighting the fact that operation of facultative metabolism requires strict control of enzymes, like Gdh3p, involved in biosynthetic pathways that use tricarboxylic acid cycle intermediates.

Adenosine Triphosphatases↗
PubMed2005

Characterization of endocytic vesicles using magnetic microbeads coated with signalling ligands.

Iron microbeads coated with the protein ligands insulin and EGF (Fe-INS and Fe-EGF) were prepared. Examination of the traffic of these ligand-coated microbeads demonstrated their internalization via clathrin-coated vesicles. Using magnetic methods, we have purified vesicles derived from the endocytic pathway. Vesicles prepared by this method are essentially free of contamination with other endomembrane compartments. Examination of the vesicles derived from cells treated with Fe-INS beads demonstrated the presence of the components of the Ras/Erk cascade on their surface. We conclude that the coupling of the Erk-signalling cascade induced by insulin takes place on the surface of endocytic vesicles derived from the internalization of the insulin receptor.

Animals↗
PubMed2004

A novel in situ assay for the identification and characterization of soluble nuclear mobility factors.

The development of green fluorescent protein (GFP) technology combined with live cell microscopy techniques have revealed the dynamic properties of GFP-tagged proteins in the nucleus. The mobility of a GFP-tagged protein can be assessed using a quantitative photobleaching technique, fluorescence recovery after photobleaching (FRAP) analysis. FRAP experiments demonstrate that many nuclear proteins are highly mobile within the nucleus. However, the factors within the nucleus that regulate this mobility are not known. This is partly due to an absence of protocols that can be used to identify such nuclear mobility factors. We developed a novel in situ assay that combines a biochemical permeabilization and extraction procedure with a quantitative FRAP technique, a method we used to uncover a new functional role for molecular chaperones in the nuclear mobility of steroid receptors. This assay can readily be adapted to identify and characterize other nuclear mobility factors.

Active Transport, Cell Nucleus↗
PubMed2004

Molecular chaperones function as steroid receptor nuclear mobility factors.

Live cell imaging has revealed the rapid mobility of steroid hormone receptors within nuclei and their dynamic exchange at transcriptionally active target sites. Although a number of other proteins have been shown to be highly mobile within nuclei, the identity of soluble factors responsible for orchestrating nuclear trafficking remains unknown. We have developed a previously undescribed in situ subnuclear trafficking assay that generates transcriptionally active nuclei, which are depleted of soluble factors required for the nuclear mobility of glucocorticoid (GR) and progesterone receptors (PR). Using this system and a fluorescence recovery after photobleaching technique, we demonstrate that nuclear mobility of GR recovered on incubation with reticulocyte lysate was inhibited by geldanamycin, a drug that blocks the chaperone activity of heat-shock protein 90. Direct proof of molecular chaperone involvement in steroid receptor subnuclear trafficking was provided by the ATP-dependent recovery of nuclear mobility of GR and PR on incubation with various combinations of purified chaperone and/or cochaperone proteins. Additionally, for both receptors, the inclusion of hormone during the recovery period leads to a retardation of nuclear mobility. Thus, our results provide a description of soluble nuclear mobility factors and furthermore demonstrate a previously unrecognized role for molecular chaperones in the regulation of steroid receptor function within the nucleus.

Active Transport, Cell Nucleus↗
PubMed2003

The guanine nucleotide exchange factor ARNO mediates the activation of ARF and phospholipase D by insulin.

BACKGROUND: Phospholipase D (PLD) is involved in many signaling pathways. In most systems, the activity of PLD is primarily regulated by the members of the ADP-Ribosylation Factor (ARF) family of GTPases, but the mechanism of activation of PLD and ARF by extracellular signals has not been fully established. Here we tested the hypothesis that ARF-guanine nucleotide exchange factors (ARF-GEFs) of the cytohesin/ARNO family mediate the activation of ARF and PLD by insulin. RESULTS: Wild type ARNO transiently transfected in HIRcB cells was translocated to the plasma membrane in an insulin-dependent manner and promoted the translocation of ARF to the membranes. ARNO mutants: DeltaCC-ARNO and CC-ARNO were partially translocated to the membranes while DeltaPH-ARNO and PH-ARNO could not be translocated to the membranes. Sec7 domain mutants of ARNO did not facilitate the ARF translocation. Overexpression of wild type ARNO significantly increased insulin-stimulated PLD activity, and mutations in the Sec7 and PH domains, or deletion of the PH or CC domains inhibited the effects of insulin. CONCLUSIONS: Small ARF-GEFs of the cytohesin/ARNO family mediate the activation of ARF and PLD by the insulin receptor.

ADP-Ribosylation Factors↗
PubMed2003

Activation of phospholipase D by the small GTPase Sar1p is required to support COPII assembly and ER export.

The small GTPase Sar1p controls the assembly of the cytosolic COPII coat that mediates export from the endoplasmic reticulum (ER). Here we demonstrate that phospholipase D (PLD) activation is required to support COPII-mediated ER export. PLD activity by itself does not lead to the recruitment of COPII to the membranes or ER export. However, PLD activity is required to support Sar1p-dependent membrane tubulation, the subsequent Sar1p-dependent recruitment of Sec23/24 and Sec13/31 COPII complexes to ER export sites and ER export. Sar1p recruitment to the membrane is PLD independent, yet activation of Sar1p is required to stimulate PLD activity on ER membranes, thus PLD is temporally regulated to support ER export. Regulated modification of membrane lipid composition is required to support the cooperative interactions that enable selective transport, as we demonstrate here for the mammalian COPII coat.

1-Butanol↗
PubMed2003

Deletional mutation of the external domain of the human granulocyte colony-stimulating factor receptor in a patient with severe chronic neutropenia refractory to granulocyte colony-stimulating factor.

Severe chronic neutropenia (SCN) is characterized by a profound neutropenia, which mostly presents during the neonatal period. The precise genetic basis of SCN remains elusive. Acquired somatic mutations involving the carboxy-terminus of the G-CSF receptor (G-CSFR) have been found, often in association with myelodysplastic syndrome. The authors describe a girl with SCN who did not respond to pharmacologic doses of filgrastim. Genetic analysis of bone marrow and germline cells revealed a 182-bp deletion in the extracellular domain of the G-CSFR. Co-precipitation studies showed an association between the wild-type and mutant G-CSFR, confirmed by their co-localization by confocal microscopy. Coexpression of the mutant receptor inhibited the wild-type response in Ba/F3 cells. These findings establish a novel constitutional defect in the G-CSFR that supports a partial dominant negative mechanism for receptor dysfunction in SCN.

Amino Acid Sequence↗
PubMed2002

The role of phosphatidic acid in the regulation of the Ras/MEK/Erk signaling cascade.

Phosphatidic acid (PA) is an important second messenger produced by the activation of numerous cell surface receptors. Recent data have suggested that PA regulates multiple cellular processes. This review addresses primarily the role of PA in the regulation of the Erk1/2 cascade pathway. A model for the regulation of Erk1/2 phosphorylation by cell surface receptors is presented. According to this model, agonists stimulate the binding of GTP to Ras and the activation of phospholipase D to generate phosphatidic acid. PA promotes the binding of cRaf-1 kinase to the membrane, where it interacts with Ras.GTP and other regulatory components of the pathway. Ras-Raf complexes remain bound to the surface of endosomes, where scaffolding complexes involving Ras, cRaf-1, MEK and Erk are formed. Complete activation and coupling of the cascade requires endocytosis, a process that is also modulated by PA.

Amino Acid Sequence↗
PubMed2002

Anticonvulsant drug hypersensitivity.

BACKGROUND: Cutaneous adverse reactions are frequently described with anticonvulsant drugs, especially with aromatic drugs such as carbamazepine, phenytoin, and phenobarbital. Patch tests could be useful for diagnosing this clinical picture. Hypersensitivity to several anticonvulsant drugs is common but unpredictable. MATERIAL AND METHODS: 15 patients from our allergy section, suffering from anticonvulsant skin allergy, were included. We describe their analitic alterations, responsible drugs, and anticonvulsants tolerated, the results of patch tests with anticonvulsant drugs (5% pet. and aq.), and skin biopsies wherever carried out. RESULTS: 23 adverse skin reactions with different anticonvulsant drugs occurred in the 15 patients: 13 resulted in fever and generalized cutaneous rash, 7 patients suffered only from cutaneous rash. There was one case of palpable purpura, one of erythema multiforme (target lesions), and another one suffered only cutaneous pruritus. Eosinophilia was found in 5 cases. Liver enzymes were elevated in 9 (7 of whom suffered fever and cutaneous rash). The responsible drugs were carbamazepine (8 adverse reactions), phenytoin (5), lamotrigine (4), phenobarbital (4), sodium valproate (1), and felbamate (1). The drugs tolerated were sodium valproate (6 patients), topiramate (4), vigabatrin (2), lamotrigine (1), clonazepam (1), and gabapentin (1). We found 12 positive patch tests: 6 with carbamazepine, 3 with phenytoin and, 1 each with lamotrigine, sodium valproate and phenobarbital. Skin biopsies were carried out in 5 patients, 4 of whom showed some characteristic findings of erythema multiforme (lymphocytic exocytosis, dyskeratotic cells, vacuolation of basal cells and pigmentary incontinence) and the other one showed a typical leucocytoclastic angitis. CONCLUSIONS: The cutaneous adverse reactions more frequently seen in our allergy section because of anticonvulsant drugs are rashes with fever. Eosinophilia and elevated levels of liver enzymes are frequently associated. This clinical picture is called "anticonvulsant hypersensitivity syndrome." The drugs implicated most frequently are carbamazepine and phenytoin. Hypersensitivity to more than one drug was variable and unpredictable. The best-tolerated drug was sodium valproate, but it was not tolerated by a patient with phenytoin and carbamazepine hypersensitivity. Patch tests are useful for diagnosing anticonvulsant hypersensitivity. The most frequently findings in the skin biopsies were typical of erythema multiforme.

Adolescent↗
PubMedDate not supplied

[Cutaneous epithelioid hemangioendothelioma].

Epithelioid hemangioendothelioma is a rare vascular tumor of intermediate aggressiveness, which usually appears in adults. It generally affects soft tissues and, less frequently, the lungs and liver. Diagnosis is by histological evaluation, and the epithelioid appearance of the neoplastic endothelial cells is typical, as is the tendency to form vascular channels. Treatment is surgical excision, with broad margins. This tumor may in exceptional cases affect the skin, with few cases having been described in literature. We describe the case of a male patient with plantar epithelioid hemangioendothelioma, and we review the literature.

Adult↗
PubMedDate not supplied

Pharmacological importance of phospholipase D and phosphatidic acid in the regulation of the mitogen-activated protein kinase cascade.

The stimulation of cells with many extracellular agonists leads to the activation of phospholipase (PL)D. PLD metabolizes phosphatidylcholine to generate phosphatidic acid (PA). Neither the mechanism through which cell surface receptors regulate PLD activation nor the functional consequences of PLD activity in mitogenic signaling are completely understood. PLD is activated by protein kinase C, phospholipids, and small GTPases of the ADP-ribosylation factor and Rho families, but the mechanisms linking cell surface receptors to the activation of PLD still require detailed analysis. Furthermore, the latest data on the functional consequences of the generation of cellular PA suggest an important role for this lipid in the regulation of membrane traffic and on the activation of the mitogen-activated protein kinase cascade. This review addresses these issues, examining some novel models for the physiological role of PLD and PA and discussing their potential usefulness as specific targets for the development of new therapies.

Animals↗