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1.
Pharmacopsychiatry ; 38(4): 183-4, 2005 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-16025424

RESUMEN

New onset diabetes mellitus (DM) and diabetic ketoacidosis (DKA) among patients using atypical antipsychotics is of clinical importance [1,2,5,7-10]. Recently, atypical antipsychotics have been more widely used in the treatment of behavioral and psychological symptoms with dementia (BPSD) than conventional neuroleptics because of a reduced tendency for movement disorders and psychomotor retardation. We report a case of reversible DKA and new-onset DM that developed in a demented patient who was treated with quetiapine for 14 days.


Asunto(s)
Antipsicóticos/efectos adversos , Demencia/tratamiento farmacológico , Cetoacidosis Diabética/inducido químicamente , Dibenzotiazepinas/efectos adversos , Anciano , Alcoholismo/complicaciones , Antipsicóticos/uso terapéutico , Demencia/complicaciones , Diabetes Mellitus Tipo 2/complicaciones , Dibenzotiazepinas/uso terapéutico , Humanos , Masculino , Fumarato de Quetiapina
2.
Dev Cell ; 1(1): 127-38, 2001 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-11703930

RESUMEN

The role of Lefty2 in left-right patterning was investigated by analysis of mutant mice that lack asymmetric expression of lefty2. These animals exhibited various situs defects including left isomerism. The asymmetric expression of nodal was prolonged and the expression of Pitx2 was upregulated in the mutant embryos. The absence of Lefty2 conferred on Nodal the ability to diffuse over a long distance. Thus, Nodal-responsive genes, including Pitx2, that are normally expressed on the left side were expressed bilaterally in the mutant embryos, even though nodal expression was confined to the left side. These results suggest that Nodal is a long-range signaling molecule but that its range of action is normally limited by the feedback inhibitor Lefty2.


Asunto(s)
Tipificación del Cuerpo/fisiología , Proteínas Nucleares , Factor de Crecimiento Transformador beta/genética , Factor de Crecimiento Transformador beta/metabolismo , Animales , Proteínas de Unión al ADN/metabolismo , Difusión , Retroalimentación Fisiológica/fisiología , Eliminación de Gen , Regulación del Desarrollo de la Expresión Génica , Proteínas de Homeodominio/genética , Factores de Determinación Derecha-Izquierda , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Proteína Nodal , Fosforilación , Transducción de Señal/fisiología , Proteína Smad2 , Transactivadores/metabolismo , Factores de Transcripción/genética , Proteína del Homeodomínio PITX2
3.
Biochem Biophys Res Commun ; 288(3): 711-7, 2001 Nov 02.
Artículo en Inglés | MEDLINE | ID: mdl-11676501

RESUMEN

Arg-Gly-Asp (RGD)-containing peptide is a ligand for integrin alpha(V)beta3 and acts as an angiogenic inhibitor. A novel cyclic RGD peptide, cyclo(-RGDf==V-) (f==V), was synthesized and its biological activities were characterized and compared with its analogs, cyclo(-RGDfV-) (fV) and cyclo(-RGDf-MeV-) (fMeV). It bound to integrin alpha(V)beta3 with almost the same affinity as the fV and fMeV analogs. All three compounds inhibited the adhesion and growth of HUVEC cells in a dose-dependent manner in vitro. Out of three, fMeV had the strongest effect, f==V was almost as strong as fMeV, and fV had the least effect. However, in vivo, f==V significantly decreased the intratumoral microvessel density (MVD) in the DLD-1 (human colon cancer cell) inoculated mice, while fMeV had little effect. These results suggest the potential usefulness of the cyclo(-RGDf==V-) as an antiangiogenic agent for clinical use in the future.


Asunto(s)
Endotelio Vascular/efectos de los fármacos , Neovascularización Patológica/patología , Oligopéptidos/farmacología , Péptidos Cíclicos/farmacología , Animales , Sitios de Unión , Células Cultivadas , Modelos Animales de Enfermedad , Endotelio Vascular/fisiología , Humanos , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Trasplante de Neoplasias , Neoplasias Experimentales/tratamiento farmacológico , Neovascularización Patológica/tratamiento farmacológico , Oligopéptidos/uso terapéutico , Péptidos Cíclicos/uso terapéutico
4.
J Org Chem ; 66(14): 4904-14, 2001 Jul 13.
Artículo en Inglés | MEDLINE | ID: mdl-11442424

RESUMEN

Whereas palladium-catalyzed reaction of N-arylsulfonyl-alpha-amino allenes with an aryl iodide (4 equiv) in the presence of potassium carbonate (4 equiv) in DMF at around 70 degrees C affords the corresponding 3-pyrroline derivatives, the reaction in refluxing 1,4-dioxane under otherwise identical conditions yields exclusively or most predominantly the corresponding 2-alkenylaziridines bearing an aryl group on the double bond. Similarly, N-arylsulfonyl-beta-amino allenes can be also cyclized into the corresponding alkenylazetidines bearing a 2,4-cis-configuration under palladium-catalyzed cyclization conditions in DMF.

5.
Nihon Yakurigaku Zasshi ; 117(4): 255-61, 2001 Apr.
Artículo en Japonés | MEDLINE | ID: mdl-11338374

RESUMEN

It is known that prostaglandins (PGs) modify the inflammatory reaction in concert with other biologically active mediators. However, characteristics of these interactions or modulating actions have not yet been clarified well. Recently, the production of mice with specific receptor deficiencies by using the gene targeting procedure for PG receptors has accelerated elucidation of the roles of PGs through correlation of their phenotypes and experimental features. Here I discuss roles of PGs in experimental paw edema, the writhing reaction of a pain model, and regulation of cytokine production, as determined using some PG-receptor-deficient mice. From the experiment of carrageenin-induced paw edema in IP receptor-deficient mice, with an indomethacin or bradykinin antagonist, we conclude that bradykinin initially induces paw swelling and then stimulates the release PGI2, which in turn enhances the swelling with bradykinin. By comparing the writhing responses in IP-deficient and wild-type mice, we found that PGI2 is a main mediator for this pain reaction. However, in the LPS-pretreated mice, not only PGI2 but also other PGs produced by COX-2 may be involved in pain induction. Production of TNF alpha and IL-10 was modified with PGI2 or PGE2; the production of TNF alpha was down-regulated by the stimulation via IP-, EP2- or EP4 receptor, but that of IL-10 was up-regulated by these receptors, resulting in an anti-inflammatory effect.


Asunto(s)
Hipersensibilidad/etiología , Mediadores de Inflamación/fisiología , Inflamación/etiología , Prostaglandinas/fisiología , Animales , Citocinas/metabolismo , Modelos Animales de Enfermedad , Edema/etiología , Humanos , Dolor/etiología , Receptores de Prostaglandina/fisiología
6.
Biochemistry ; 40(9): 2854-9, 2001 Mar 06.
Artículo en Inglés | MEDLINE | ID: mdl-11258896

RESUMEN

To understand the effect of visible light on the stability of photoactive yellow protein (PYP), urea denaturation experiments were performed with PYP in the dark and with PYP(M) under continuous illumination. The urea concentrations at the midpoint of denaturation were 5.26 +/- 0.29 and 3.77 +/- 0.19 M for PYP and PYP(M), respectively, in 100 mM acetate buffer, and 5.26 +/- 0.24 and 4.11 +/- 0.12 M for PYP and PYP(M), respectively, in 100 mM citrate buffer. The free energy change upon denaturation (DeltaG(D)(H2O)), obtained from the denaturation curve, was 11.0 +/- 0.4 and 7.6 +/- 0.2 kcal/mol for PYP and PYP(M), respectively, in acetate buffer, and 11.5 +/- 0.3 and 7.8 +/- 0.1 kcal/mol for PYP and PYP(M), respectively, in citrate buffer. Even though the DeltaG(D)(H2O) value for PYP(M) is almost identical in the two buffer systems, the urea concentration at the midpoint of denaturation is lower in acetate buffer than in citrate buffer. Although their CD spectra indicate that the protein conformations of the denatured states of PYP and PYP(M) are indistinguishable, the configurations of the chromophores in their denatured structures are not necessarily identical. Both denatured states are interconvertible through PYP and PYP(M). Therefore, the free energy difference between PYP and PYP(M) is 3.4-3.7 kcal/mol for the protein moiety, plus the additional contribution from the difference in configuration of the chromophore.


Asunto(s)
Proteínas Bacterianas/metabolismo , Proteínas Bacterianas/efectos de la radiación , Luz , Fotorreceptores Microbianos , Acetatos/química , Proteínas Bacterianas/química , Tampones (Química) , Dicroismo Circular , Concentración de Iones de Hidrógeno , Desnaturalización Proteica/efectos de la radiación , Pliegue de Proteína , Soluciones , Espectrofotometría Ultravioleta , Termodinámica , Urea
7.
Cardiovasc Intervent Radiol ; 24(4): 274-6, 2001.
Artículo en Inglés | MEDLINE | ID: mdl-11779019

RESUMEN

We successfully stabilized severe hemorrhagic shock following traumatic liver injury by percutaneous transcarotid supraceliac aortic occlusion with a 5 Fr balloon catheter. Then we were able to perform transfemoral embolization therapy of the hepatic arterial bleeding source. Transient aortic occlusion using a balloon catheter appears to be a useful adjunct in select cases where stabilization of the patient is necessary to allow successful selective embolization of the bleeding source.


Asunto(s)
Aorta , Oclusión con Balón , Embolización Terapéutica , Hemorragia/terapia , Arteria Hepática , Hígado/lesiones , Resucitación , Presión Sanguínea , Transfusión Sanguínea , Hemorragia/etiología , Arteria Hepática/diagnóstico por imagen , Humanos , Masculino , Persona de Mediana Edad , Radiografía Intervencional , Choque Hemorrágico/fisiopatología , Choque Hemorrágico/terapia
9.
Yakugaku Zasshi ; 120(5): 455-62, 2000 May.
Artículo en Japonés | MEDLINE | ID: mdl-10825809

RESUMEN

Inflammatory signs, such as heat, redness, swelling and pain, have been described from the Greek era. In these phenomena various endogenous active substances, i.e., inflammatory mediators, could cause and manifest vascular dilatation, a vascular permeability increase and sensitization of pain receptors, etc. In order to evaluate the roles of inflammatory mediators, we have studied the time courses of inflammatory reaction along with detection of various active substances directly or indirectly in the experimental animal model of pleurisy, such as rat carrageenin-induced, and zymosan-induced pleurisy. These pleurisies showed almost similar time courses of pleural exudate accumulation and neutrophil migration. However, mediators detected in the exudates of such pleurisies were different; in carrageenin-induced pleurisy bradykinin and prostacyclin (PGI2) caused exudate formation, while zymosan-induced pleurisy showed early degradation of mast cells and activation of complements, followed by an increase in platelet activating factor (PAF). In both pleurisies TNF alpha, IL-1, IL-6 and CINC (cytokine-induced neutrophil chemoattractant) appeared similarly in the exudates to cause chemoattractant for neutrophils. TNF alpha and IL-1 could stimulate to produce IL-6 and IL-8. While prostaglandins may regulate cytokine production via a cellular cAMP-dependent mechanism. Thus one should consider the time for application of anti-inflammatory drugs, such as cyclooxygenase inhibitor, indomethacin, since it causes increases in TNF alpha and IL-1 production by reducing PGI2 and prostaglandin E2 (PGE2) levels. In conclusion, inflammatory reaction has its own automatic regulation mechanism through complex cross talks between inflammatory mediators.


Asunto(s)
Mediadores de Inflamación/fisiología , Inflamación/fisiopatología , Animales , Proteínas del Sistema Complemento/fisiología , Citocinas/fisiología , Histamina/fisiología , Humanos , Inflamación/metabolismo , Mediadores de Inflamación/metabolismo , Sistema Calicreína-Quinina/fisiología , Factor de Activación Plaquetaria/fisiología , Ratas , Factores de Tiempo
10.
Mol Cell ; 5(1): 35-47, 2000 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-10678167

RESUMEN

The left-right (L-R) asymmetric expression of lefty2 and nodal is controlled by a left side-specific enhancer (ASE). The transcription factor FAST2, which can mediate signaling by TGF beta and activin, has now been identified as a protein that binds to a conserved sequence in ASE. These FAST2 binding sites were both essential and sufficient for L-R asymmetric gene expression. The Fast2 gene is bilaterally expressed when nodal and lefty2 are expressed on the left side. TGF beta and activin can activate the ASE activity in a FAST2-dependent manner, while Nodal can do so in the presence of an EGF-CFC protein. These results suggest that the asymmetric expression of lefty2 and nodal is induced by a left side-specific TGF beta-related factor, which is most likely Nodal itself.


Asunto(s)
Proteínas de Unión al ADN/metabolismo , Regulación de la Expresión Génica , Transcripción Genética , Factor de Crecimiento Transformador beta/genética , Animales , Secuencia de Bases , Clonación Molecular , Secuencia Conservada , Proteínas de Unión al ADN/genética , Embrión de Mamíferos , Embrión no Mamífero , Elementos de Facilitación Genéticos , Retroalimentación , Factores de Transcripción Forkhead , Factores de Determinación Derecha-Izquierda , Ratones , Ratones Transgénicos , Proteína Nodal , Proteínas Recombinantes de Fusión/biosíntesis , Proteínas Recombinantes/metabolismo , Transducción de Señal , Factores de Transcripción/metabolismo , Xenopus laevis
11.
Kurume Med J ; 47(4): 291-7, 2000.
Artículo en Inglés | MEDLINE | ID: mdl-11197151

RESUMEN

As society ages, the composition of the diseases that occur within it changes accordingly. With that in mind, we examined the characteristics and trends in the recent inpatients and compared these recent inpatients with those of a previous report to identify the changes that accompany the aging of society. Subjects were 1,534 cases (men 56.9%, female 43.1%, average age 47.1 years) who were hospitalized at Kurume University Hospital for treatment during the 5-year period from January 1st, 1994 through December 31st, 1998. The ratio of inpatients over 65 years old was about 1.8 times higher than in the previous study, showing a clear trend toward an increased overall age of inpatients. As for the types of disease observed, the most common malignancies were epithelial tumor, followed by other benign tumors, as well as 76 cases which included diseases resembling tumor (epulis and exostosis etc.). A majority of the patients (55.6%) were directed to the Hospital by their dentist, a finding similar to that of the previous report. As for geographical distribution, 93.3% of the inpatients lived within 40 km of the center of Kurume City where our oral surgery is located, an increase of about 10% from the last report. In other words, our results showed a reduction in the sphere of treatment distribution.


Asunto(s)
Pacientes Internos , Admisión del Paciente/estadística & datos numéricos , Enfermedad/clasificación , Femenino , Humanos , Japón , Masculino , Auditoría Médica , Persona de Mediana Edad
12.
Mol Cell ; 4(3): 287-98, 1999 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-10518210

RESUMEN

Mammalian lefty and zebrafish antivin form a subgroup of the TGF beta superfamily. We report that mouse mutants for lefty2 have an expanded primitive streak and form excess mesoderm, a phenotype opposite to that of mutants for the TGF beta gene nodal. Analogously, overexpression of Antivin or Lefty2 in zebrafish embryos blocks head and trunk mesoderm formation, a phenotype identical to that of mutants caused by loss of Nodal signaling. The lefty2 mutant phenotype is partially suppressed by heterozygosity for nodal. Similarly, the effects of Antivin and Lefty2 can be suppressed by overexpression of the nodal-related genes cyclops and squint or the extracellular domain of ActRIIB. Expression of antivin is dependent on Nodal signaling, revealing a feedback loop wherein Nodal signals induce their antagonists Lefty2 and Antivin to restrict Nodal signaling during gastrulation.


Asunto(s)
Tipificación del Cuerpo , Gástrula/fisiología , Ratones/embriología , Factor de Crecimiento Transformador beta/metabolismo , Proteínas de Pez Cebra , Pez Cebra/embriología , Receptores de Activinas Tipo II , Animales , Retroalimentación , Regulación del Desarrollo de la Expresión Génica , Genes Letales , Heterocigoto , Histocitoquímica , Hibridación in Situ , Factores de Determinación Derecha-Izquierda , Mesodermo , Ratones Mutantes , Mutagénesis , Proteína Nodal , Fenotipo , ARN Mensajero , Receptores de Factores de Crecimiento/metabolismo , Transducción de Señal , Factor de Crecimiento Transformador beta/antagonistas & inhibidores , Factor de Crecimiento Transformador beta/genética
13.
Neuron ; 23(4): 725-36, 1999 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-10482239

RESUMEN

GFR alpha3 is a component of the receptor for the neurotrophic factor artemin. The role of GFR alpha3 in nervous system development was examined by generating mice in which the Gfr alpha3 gene was disrupted. The Gfr alpha3-/- mice exhibited severe defects in the superior cervical ganglion (SCG), whereas other ganglia appeared normal. SCG precursor cells in the mutant embryos failed to migrate to the correct position, and they subsequently failed to innervate the target organs. In wild-type embryos, Gfr alpha3 was expressed in migrating SCG precursors, and artemin was expressed in and near the SCG. After birth, SCG neurons in the mutant mice underwent progressive cell death. These observations suggest that GFR alpha3-mediated signaling is required both for the rostral migration of SCG precursors and for the survival of mature SCG neurons.


Asunto(s)
Movimiento Celular/fisiología , Proteínas de Drosophila , Factores de Crecimiento Nervioso/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Neuronas/fisiología , Proteínas Proto-Oncogénicas/fisiología , Proteínas Tirosina Quinasas Receptoras/fisiología , Receptores de Factor de Crecimiento Nervioso/genética , Receptores de Factor de Crecimiento Nervioso/metabolismo , Ganglio Cervical Superior/embriología , Animales , Muerte Celular/fisiología , Movimiento Celular/genética , Supervivencia Celular/fisiología , Genotipo , Inmunohistoquímica , Hibridación in Situ , Ratones , Ratones Noqueados , Proteínas Proto-Oncogénicas/genética , Proteínas Proto-Oncogénicas c-ret , Proteínas Tirosina Quinasas Receptoras/genética , Ganglio Cervical Superior/citología
14.
J Med Genet ; 36(7): 518-23, 1999 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-10424811

RESUMEN

Beckwith-Wiedemann syndrome (BWS) is a human imprinting disorder with a variable phenotype. The major features are anterior abdominal wall defects including exomphalos (omphalocele), pre- and postnatal overgrowth, and macroglossia. Additional less frequent complications include specific developmental defects and a predisposition to embryonal tumours. BWS is genetically heterogeneous and epigenetic changes in the IGF2/H19 genes resulting in overexpression of IGF2 have been implicated in many cases. Recently germline mutations in the cyclin dependent kinase inhibitor gene CDKN1C (p57KIP2) have been reported in a variable minority of BWS patients. We have investigated a large series of familial and sporadic BWS patients for evidence of CDKN1C mutations by direct gene sequencing. A total of 70 patients with classical BWS were investigated; 54 were sporadic with no evidence of UPD and 16 were familial from seven kindreds. Novel germline CDKN1C mutations were identified in five probands, 3/7 (43%) familial cases and 2/54 (4%) sporadic cases. There was no association between germline CDKN1C mutations and IGF2 or H19 epigenotype abnormalities. The clinical phenotype of 13 BWS patients with germline CDKN1C mutations was compared to that of BWS patients with other defined types of molecular pathology. This showed a significantly higher frequency of exomphalos in the CDKN1C mutation cases (11/13) than in patients with an imprinting centre defect (associated with biallelic IGF2 expression and H19 silencing) (0/5, p<0.005) or patients with uniparental disomy (0/9, p<0.005). However, there was no association between germline CDKN1C mutations and risk of embryonal tumours. No CDKN1C mutations were identified in six non-BWS patients with overgrowth and Wilms tumour. These findings (1) show that germline CDKN1C mutations are a frequent cause of familial but not sporadic BWS, (2) suggest that CDKN1C mutations probably cause BWS independently of changes in IGF2/H19 imprinting, (3) provide evidence that aspects of the BWS phenotype may be correlated with the involvement of specific imprinted genes, and (4) link genotype-phenotype relationships in BWS and the results of murine experimental models of BWS.


Asunto(s)
Síndrome de Beckwith-Wiedemann/genética , Mutación de Línea Germinal , Proteínas Nucleares/genética , Inhibidor p57 de las Quinasas Dependientes de la Ciclina , Impresión Genómica , Genotipo , Humanos , Fenotipo , Análisis de Secuencia de ADN
15.
Genes Dev ; 13(12): 1589-600, 1999 Jun 15.
Artículo en Inglés | MEDLINE | ID: mdl-10385627

RESUMEN

The nodal gene is expressed on the left side of developing mouse embryos and is implicated in left/right (L-R) axis formation. The transcriptional regulatory regions of nodal have now been investigated by transgenic analysis. A node-specific enhancer was detected in the upstream region (-9.5 to -8.7 kb) of the gene. Intron 1 was also shown to contain a left side-specific enhancer (ASE) that was able to direct transgene expression in the lateral plate mesoderm and prospective floor plate on the left side. A 3. 5-kb region of nodal that contained ASE responded to mutations in iv, inv, and lefty-1, all genes that act upstream of nodal. The same 3. 5- kb region also directed expression in the epiblast and visceral endoderm at earlier stages of development. Characterization of deletion constructs delineated ASE to a 340-bp region that was both essential and sufficient for asymmetric expression of nodal. Several sequence motifs were found to be conserved between the nodal ASE and the lefty-2 ASE, some of which appeared to be essential for nodal ASE activity. These results suggest that similar transcriptional mechanisms underlie the asymmetric expression of nodal and of lefty-2 as well as the earlier expression of nodal in the epiblast and endoderm.


Asunto(s)
Elementos de Facilitación Genéticos , Regulación del Desarrollo de la Expresión Génica , Factores de Transcripción , Factor de Crecimiento Transformador beta/genética , Animales , Tipificación del Cuerpo , Desarrollo Embrionario y Fetal , Endodermo , Gástrula , Expresión Génica , Intrones , Factores de Determinación Derecha-Izquierda , Ratones , Mutagénesis , Proteína Nodal , Proteínas/genética , Transgenes
16.
Genes Dev ; 13(3): 259-69, 1999 Feb 01.
Artículo en Inglés | MEDLINE | ID: mdl-9990851

RESUMEN

Both lefty-1 and lefty-2 genes are expressed on the left side of developing mouse embryos and are implicated in left-right (L-R) axis formation. With the use of transgenic analysis, the transcriptional regulatory regions of these genes responsible for their L-R asymmetric expression have now been investigated. The 9.5-kb upstream region of lefty-1 and the 5.5-kb upstream region of lefty-2 reproduced the expression pattern of the corresponding gene. Examination of deletion constructs revealed the presence of a left side-specific enhancer (ASE) that is essential and sufficient for lefty-2 asymmetric expression. In contrast, the asymmetric expression of lefty-1 was shown to be determined by a combination of bilateral enhancers and a right side-specific silencer (RSS). The 9. 5-kb region of lefty-1 and the 5.5-kb region of lefty-2 responded to iv and inv, upstream genes of lefty-1 and lefty-2. The regulation of lefty-2 by iv and inv was mediated by ASE. These results suggest that, in spite of the similarities between lefty-1 and lefty-2, different regulatory mechanisms underlie their asymmetric expression.


Asunto(s)
Regulación de la Expresión Génica , Factores de Transcripción , Factor de Crecimiento Transformador beta/genética , Animales , Secuencia de Bases , Elementos de Facilitación Genéticos , Factores de Determinación Derecha-Izquierda , Ratones , Ratones Endogámicos C3H , Ratones Endogámicos C57BL , Ratones Transgénicos , Datos de Secuencia Molecular , Mutagénesis , Proteínas/genética , Transcripción Genética
18.
Res Commun Mol Pathol Pharmacol ; 101(2): 187-99, 1998 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-9821215

RESUMEN

The blood pressure of the rat is influenced by the dietary restriction of calcium. Since the vasomotor activities may be affected by calcium restriction, we measured vasoconstriction as well as endothelium-dependent and endothelium-independent relaxation responses in isolated aortic rings of the Wistar rat. Compared with the control rat fed a normal diet (1.04% calcium), the femur mineral density was significantly reduced in the rat fed the low-calcium (< 0.01%) diet for one month (LC1M) or for three months (LC3M). Although neither LC1M nor LC3M changed Cmax (the maximum constriction induced by phenylephrine) in aortic rings without endothelium, LC3M, but not LC1M, significantly increased CD50 (the dose of phenylephrine inducing 50% of Cmax). On the other hand, the low-calcium diet did not change Cmax and CD50 in rings with intact endothelium. Thel low-calcium diet showed no significant change in the vasorelaxation responses to acetylcholine (Ach) or sodium nitroprusside (SNP). Cyclic GMP production stimulated by Ach or SNP was not affected by calcium restriction. These results suggest that an insufficient calcium supply for three months, attenuates alpha-adrenoceptor-mediated vasoconstriction in the normotensive rat but vasorelaxation responses to Ach or SNP are not affected.


Asunto(s)
Calcio de la Dieta/farmacología , Músculo Liso Vascular/efectos de los fármacos , Vasodilatación/efectos de los fármacos , Acetilcolina/farmacología , Animales , Aorta Torácica , Densidad Ósea/efectos de los fármacos , Calcio/sangre , Calcio/deficiencia , Calcio/fisiología , Calcio de la Dieta/administración & dosificación , Interacciones Farmacológicas , Masculino , Músculo Liso Vascular/fisiología , Óxido Nítrico/fisiología , Nitroprusiato/farmacología , Fenilefrina/farmacología , Ratas , Ratas Wistar , Vasoconstricción/efectos de los fármacos , Vasoconstrictores/farmacología , Vasodilatadores/farmacología
19.
Cell ; 94(3): 287-97, 1998 Aug 07.
Artículo en Inglés | MEDLINE | ID: mdl-9708731

RESUMEN

lefty-1, lefty-2, and nodal are expressed on the left side of developing mouse embryos and are implicated in left-right (L-R) determination. The role of lefty-1 was examined by analyzing mutant mice lacking this gene. The lefty-1-deficient mice showed a variety of L-R positional defects in visceral organs. Unexpectedly, however, the most common feature of lefty-1-/- mice was thoracic left isomerism (rather than right isomerism). The lack of lefty-1 resulted in bilateral expression of nodal, lefty-2, and Pitx2 (a homeobox gene normally expressed on the left side). These observations suggest that the role of lefty-1 is to restrict the expression of lefty-2 and nodal to the left side, and that lefty-2 or nodal encodes a signal for "leftness."


Asunto(s)
Tipificación del Cuerpo/genética , Regulación del Desarrollo de la Expresión Génica , Proteínas Nucleares , Proteínas/genética , Proteínas/fisiología , Factor de Crecimiento Transformador beta/genética , Factor de Crecimiento Transformador beta/fisiología , Animales , Animales Recién Nacidos , Proteínas de Homeodominio/biosíntesis , Proteínas de Homeodominio/genética , Factores de Determinación Derecha-Izquierda , Pulmón/anomalías , Ratones , Ratones Endogámicos C3H , Ratones Endogámicos C57BL , Ratones Noqueados , Ratones Transgénicos , Mutación , Proteína Nodal , Factores de Transcripción Paired Box , Factores de Transcripción/biosíntesis , Factores de Transcripción/genética , Factor de Crecimiento Transformador beta/deficiencia , Proteína del Homeodomínio PITX2
20.
Pflugers Arch ; 435(6): 767-74, 1998 May.
Artículo en Inglés | MEDLINE | ID: mdl-9518504

RESUMEN

The aim of the current study was to elucidate the synergism of dietary calcium restriction and exhaustive exercise in the antioxidant enzyme system of rat soleus muscle, and to investigate the involvement of neutrophils in exercise-induced muscle damage. Forty-eight male Wistar rats were assigned to the following groups: control (C) or calcium-restricted [1 month (1 M) or 3 months (3 M)]. Each group was subdivided into acutely exercised or non-exercised groups. Soleus muscle from each rat was analysed to determine the levels of antioxidant enzymes [Mn-superoxide dismutase (SOD), Cu, Zn-SOD, glutathione peroxidase (GPX), and catalase (CAT)]. Dietary calcium restriction resulted in calcium deficiency and upregulated the antioxidant enzymes examined except GPX. Conversely, exhaustive exercise significantly decreased GPX and CAT, but not SODs activities in the calcium-restricted (1 M and/or 3 M) rats. Contents of immunoreactive Mn-SOD and Cu,Zn-SOD were only increased in the 3 M rats. During calcium restriction, the mRNA expression of both forms of SOD showed initial upregulation, followed by downregulation. Exhaustive exercise significantly increased the mRNA expressions only in the 3 M rats. Moreover, exhaustive exercise markedly increased myeloperoxidase activity in soleus muscles from the 1 M and 3 M rats compared with the C rats, and significantly enhanced the ability of neutrophils to generate superoxide in the 3 M rats. The results demonstrate that dietary calcium restriction upregulates certain antioxidant enzyme activities in rat soleus muscle, indicating an enhanced resistance to potential increases in intracellular reactive oxygen species. The results also suggest that exhaustive exercise may cause oxidative damage in soleus muscle of calcium-deficient rats through the activation of neutrophils.


Asunto(s)
Antioxidantes/metabolismo , Calcio/deficiencia , Músculo Esquelético/enzimología , Esfuerzo Físico/fisiología , Animales , Peso Corporal , Calcio/sangre , Calcio de la Dieta/administración & dosificación , Catalasa/metabolismo , Glutatión Peroxidasa/metabolismo , Masculino , Músculo Esquelético/anatomía & histología , Neutrófilos/metabolismo , Tamaño de los Órganos , Peroxidasa/metabolismo , Fósforo/sangre , Resistencia Física , ARN Mensajero/metabolismo , Ratas , Ratas Wistar , Superóxido Dismutasa/genética , Superóxido Dismutasa/metabolismo , Superóxidos/metabolismo
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