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1.
Front Immunol ; 14: 1299639, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-38116010

RESUMO

Introduction: The D antigen variants are classified as weak, partial, and extremely weak (DEL) and can be differentiated using molecular tests. In Chile, the laboratories of local blood centers do not identify variants of the D antigen, referring them for study to the Reference Laboratory of the Public Health Institute of Chile. So, our aim was to talk about the results of the molecular analysis of variants of the D antigen in samples that had different results in the serological classification. Methods: In the D antigen classification of the Rh system, 479 samples with serological discrepant results were sent for molecular analysis. The Rh phenotype was performed with monoclonal anti-C, anti-c, anti-E, and anti-e antisera by direct agglutination. To find the D antigen, researchers used direct agglutination with monoclonal antisera and indirect antiglobulin testing with the column (gel) agglutination method. Molecular analysis was performed with a polymerase chain reaction with sequence-specific primers (SSP-PCR) and sequencing. Results and discussion: The presence of D antigen variants was confirmed in 332 samples (69.3%), with an initial discrepancy in serological classification. In this group of discrepant samples, the frequency of weak RhD variants was 66% (219/332), that of extremely weak RhD was 28% (93/332), and that of partial RhD was 6% (20/332). The weak variants type 2 (27.4%), type 3 (8.4%), type 48 (8.4%), and type 1 (8.1%) were the next most prevalent variants after RHD*DEL43 (28%). The ccEe (R2r) phenotype was the most frequently detected (38.4%) and is present in 87% of the RHD*DEL43 samples. The E antigen is associated with the presence of this variant. Our analyses give the first description of D antigen variants in Chile. The most common variants are DEL type (RHD*DEL43) and weak (weak type 2), which are linked to the ccDEe (R2r) phenotype. These findings allow us to characterize the variants of the D antigen in Chile and, according to the obtained data, to design strategies for the management of donors, patients, and pregnant women.


Assuntos
Sistema do Grupo Sanguíneo Rh-Hr , Feminino , Humanos , Gravidez , Chile , Genótipo , Soros Imunes , Fenótipo , Reação em Cadeia da Polimerase , Sistema do Grupo Sanguíneo Rh-Hr/genética
2.
BMC Med Educ ; 20(1): 401, 2020 Nov 02.
Artigo em Inglês | MEDLINE | ID: mdl-33138817

RESUMO

BACKGROUND: Physiology is a subject that is considered difficult; it is associated with academic failure and causes high levels of stress and anxiety in students. METHODS: This study compared the effectiveness of a traditional lecture-based methodology with that of a flipped classroom scheme focusing on cooperative ludic learning among gastrointestinal and renal physiology students. Two groups were subjected to these two different methods to teach gastrointestinal and renal physiology content divided into 14 topics. Additionally, two subgroups were identified in each group: entrants and repeaters. There were no differences in age or gender between the subgroups. RESULTS: Levels of self-perceived stress (measured by the SISCO scale), biological stress (measured by awakening salivary cortisol levels), and anxiety (measured by the Zung scale) were high in all of the students; the cortisol levels increased in the entrants and some of the scores in SISCO scale increased in the repeaters, throughout the study. The self-reported study time was longer in the students subjected to the flipped classroom-based method. The final exam results were better only in the new students facing the flipped methodology, but not in the repeaters, who scored lower on the final evaluation. The quantitative and qualitative assessments completed by the participants regarding the different aspects of the flipped-classroom-based methodology were favorable; however, the participants believed that traditional lectures should be maintained for specific topics. CONCLUSIONS: A methodology based on flipped teaching was an effective strategy to improve academic performance ingastrointestinal and renal physiology, but only in new students.


Assuntos
Aprendizagem , Estudantes , Currículo , Humanos , Aprendizagem Baseada em Problemas
3.
Front Plant Sci ; 11: 469, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32373149

RESUMO

Flowering is a rigorously timed and morphologically complex shift in plant development. This change depends on endogenous as well as environmental factors. FLOWERING LOCUS T (FT) integrates several cues from different pathways acting as a flowering promoter. Contrary to the role of FT, its paralog TERMINAL FLOWER 1 (TFL1) delays floral transition. Although FT/TFL1 homologs have been studied in model eudicots and monocots, scarce studies are available in non-model monocots like the Orchidaceae. Orchids are very diverse and their floral complexity is translated into a unique aesthetic display, which appeals the ornamental plant market. Nonetheless, orchid trade faces huge limitations due to their long vegetative phase and intractable indoor flowering seasons. Little is known about the genetic basis that control reproductive transition in orchids and, consequently, manipulating their flowering time remains a challenge. In order to contribute to the understanding of the genetic bases that control flowering in orchids we present here the first broad-scale analysis of FT/TFL1-like genes in monocots with an expanded sampling in Orchidaceae. We also compare expression patterns in three selected species and propose hypotheses on the putative role of these genes in their reproductive transition. Our findings show that FT-like genes are by far more diversified than TFL1-like genes in monocots with six subclades in the former and only one in the latter. Within MonFT1, the comparative protein sequences of MonFT1A and MonFT1B suggest that they could have recruited functional roles in delaying flowering, a role typically assigned to TFL1-like proteins. On the other hand, MonFT2 proteins have retained their canonical motifs and roles in promoting flowering transition. This is also shown by their increased expression levels from the shoot apical meristem (SAM) and leaves to inflorescence meristems (IM) and floral buds (FBs). Finally, TFL1-like genes are retained as single copy and often times are lost. Their loss could be linked to the parallel recruitment of MonFT1A and MonFT1B homologs in delaying flowering and maintaining indeterminacy of the inflorescence meristem. These hypotheses lay the foundation for future functional validation in emerging model orchid species and comparative analyses in orchids with high horticultural potential in the market.

4.
Materials (Basel) ; 11(11)2018 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-30355959

RESUMO

Interactive multi-beam laser machining simulation is crucial in the context of tool path planning and optimization of laser machining parameters. Current simulation approaches for heat transfer analysis (1) rely on numerical Finite Element methods (or any of its variants), non-suitable for interactive applications; and (2) require the multiple laser beams to be completely synchronized in trajectories, parameters and time frames. To overcome this limitation, this manuscript presents an algorithm for interactive simulation of the transient temperature field on the sheet metal. Contrary to standard numerical methods, our algorithm is based on an analytic solution in the frequency domain, allowing arbitrary time/space discretizations without loss of precision and non-monotonic retrieval of the temperature history. In addition, the method allows complete asynchronous laser beams with independent trajectories, parameters and time frames. Our implementation in a GPU device allows simulations at interactive rates even for a large amount of simultaneous laser beams. The presented method is already integrated into an interactive simulation environment for sheet cutting. Ongoing work addresses thermal stress coupling and laser ablation.

5.
Med. interna (Caracas) ; 32(3): 245-251, 2016. tab
Artigo em Espanhol | LIVECS, LILACS | ID: biblio-1009380

RESUMO

Se trata de un estudio observacional, analítico y prospectivo cuyo objetivo es analizar la concentración de enzimas cardíacas en pacientes con enfermedad renal crónica en hemodiálisis sin evidencia clínica de cardiopatía isquémica aguda, hospitalizados en el Servicio de Medicina Interna del Hospital Universitario de Caracas, Venezuela durante el período 2014-2015. Métodos: Se tomó muestra de suero a 48 pacientes con enfermedad renal crónica en hemodiálisis sin evidencia de cardiopatía isquémica aguda, y se midieron las concentraciones de creatin quinasa (CK), creatin quinasa fracción MB (CK-MB) y Troponina I (Tn-I) antes y después de la diálisis. Resultados: la mediana de los valores obtenidos de CK fue 42 prediálisis y 38 postdiálisis (p = 0,434), CK-MB: 10 pre y postdiálisis (p = 0,629), con respecto a troponina I, la mediana fue 0,00 pre y postdiálisis (p = 0,586). Se obtuvo valores dentro de límites normales de CK en 91,1% pre y 93,3% postdiálisis, CKMB 93,3% prediálisis y postdiálisis y Troponina I en 97,67% pre y 95,35% postdiálisis. Conclusiones: no se evidenciaron cambios significativos en las concentraciones de CK, CK-MB y Troponina I tanto pre como postdiálisis, encontrándose dentro de la normalidad en más de 90% de los casos. No se encontró relación entre concentración Troponina I, CK y CK-MB según edad, sexo, factores de riesgo cardiovasculares (diabetes mellitus e hipertensión arterial) y tiempo de hemodiálisis. Cualquiera de las enzimas puede tener utilidad clínica, siendo de preferencia las más cardioespecíficas, individualizando cada caso según su clínica y sus valores basales de enzimas cardíacas(AU)


This is an observational, analytical prospective study aimed to analyze cardiac enzymes concentrations in chronic kidney disease patients in hemodialysis without evidence of acute coronary disease at Internal Medicine Service of Hospital Universitario de Caracas, Venezuela during 2014-2015. Methods: serum samples were taken in 46 patients' with chronic kidney disease in hemodialysis without evidence of acute coronary disease and creatin kinase (CK), creatin kinase fraction MB (CK-MB) and Troponin I (Tn-I) were measured before and after hemodialysis. Results: was 42 predialysis and 38 postdialysis (p = 0.434), CK-MB 10 predialysis and post-dialysis (p = 0.629) the median value of troponin I, was 0.00 before and after dialysis (p = 0.586). It was obtained values within normal range of CK in 91.1% and 93.3% pre and post-dialysis, CK-MB in 93.3% predialysis and postdialysis and Troponin I in 97.67% pre and 95.35 % postdialysis. Conclusions: No significant changes were found in concentrations of CK, CK-MB and Troponin I bothpre and post-dialysis, with normal values in over 90% of cases. No relationship between concentration of Troponin I, CK and CK-MB and age, sex, cardiovascular risk factors (diabetes and hypertension) or time in hemodialysis were found. Any of the enzymes may have clinical utility, being the cardiospecific ones preferably, individualizing each case based on clinical and baseline cardiac enzymes(AU)


Assuntos
Humanos , Masculino , Feminino , Troponina I , Doença das Coronárias/fisiopatologia , Enzimas , Insuficiência Renal Crônica/fisiopatologia , Diálise Renal , Medicina Interna
6.
Investig. andin ; 17(31)dic. 2015.
Artigo em Espanhol | LILACS-Express | LILACS | ID: biblio-1550307

RESUMO

El Síndrome Metabólico (SM) es una entidad de alta prevalencia mundial y regional, que frecuentemente se acompaña de complicaciones tanto a nivel cardiovascular como metabólico; razón por la cual se ha convertido en un gran riesgo para la salud de nuestra población. A pesar de la controversia existente alrededor de los criterios para hacer el diagnóstico y su fisiopatología, muchos de estos mecanismos ya han sido suficientemente estudiados. Con esta revisión se pretende desarrollar algunos de los mecanismos fisiopatológicos propuestos en la aparición del SM, partiendo de la resistencia a la insulina como el eje principal.


Metabolic syndrome (MetS) is a disease of high global and regional prevalence, which is often associated with complications at both cardiovascular and metabolic level, becoming into a major health risk for our population. Despite controversy about the diagnosis criteria and pathophysiology, many of these mechanisms have been sufficiently studied. The aim of this review is to summarize the proposed pathophysiological mechanisms to develop MetS, including insulin resistance as the main axis.


A Síndrome Metabólica (SM) é uma entidade da mais alta relevância mundial e regional, frequentemente acompanhada de complicações tanto em nível cardiovascular como metabólico; por esta razão se tem convertido num grande risco para a saúde da nossa população. Apesar da controvérsia existente sobre critérios para efetuar o diagnóstico e sua fisiopatologia, muitos desses mecanismos já tem sido suficientemente estudados. Com esta revisão se pretendem desenvolver alguns dos mecanismos fisiopatológicos propostos na aparição do SM, partindo da resistência à insulina, como eixo principal.

7.
Cartilage ; 6(1): 45-54, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26069708

RESUMO

OBJECTIVE: To evaluate the effects of adipokines and insulin on intracellular calcium concentration ([Ca(2+)]i) and pH (pHi) in human articular chondrocytes from healthy (CHC) and osteoarthritic cartilage (COC). DESIGN: pHi and [Ca(2+)]i were measured using BCECF and Fura-2 fluorometric probes in CHC and COC under control conditions and following a hypotonic shock. The effects of interleukin-1ß (IL1ß), tumor necrosis factor-α (TNFα), insulin, leptin, resistin, and adiponectin were assessed. RESULTS: pHi was lower in COC than in CHC. Only IL1ß ß decreased pHi in both cell types; all the agents enhanced pHi recovery following an ammonium prepulse in CHC, effect that was attenuated by Na(+)-H(+) exchanger inhibitors, but they had no effect in COC. Hypotonic shock (HTS) caused a pHi increase, which was significantly smaller in COC. All the hormones attenuated this response and the effect of IL1ß was greater. The basal [Ca(2+)]i was similar in COC and CHC; IL1ß, TNFα, and insulin increased the [Ca(2+)]i, but leptin, resistin, and adiponectin did not. These effects were greater in COC. This [Ca(2+)]i increase was dependent on extracellular Ca(2+) and attenuated by Na(+)-Ca(2+) exchanger inhibitors. HTS caused a [Ca(2+)]i increase, which was inhibited by transient receptor potential vanilloid blockers and attenuated by all the hormones tested with the exception of adiponectin. CONCLUSIONS: These findings may help explain the association between obesity and osteoarthritis, in which these hormones are altered. The responses of CHC and COC are different, which suggests that a modification of pH and Ca(2+) homeostasis is part of the osteoarthritis pathophysiology.

8.
Investig. andin. (En línea) ; 17(31): 1328-1342, 2015. tab
Artigo em Espanhol | LILACS, COLNAL | ID: biblio-1561824

RESUMO

El Síndrome Metabólico (SM) es una entidad de alta prevalencia mundial y regional, que frecuentemente se acompaña de complicaciones tanto a nivel cardiovascular como metabólico; razón por la cual se ha convertido en un gran riesgo para la salud de nuestra población. A pesar de la controversia existente alrededor de los criterios para hacer el diagnóstico y su fisiopatología, muchos de estos mecanismos ya han sido suficientemente estudiados. Con esta revisión se pretende desarrollar algunos de los mecanismos fisiopatológicos propuestos en la aparición del SM, partiendo de la resistencia a la insulina como el eje principal.


The Metabolic Syndrome (MS) is an entity of high global and regional prevalence, often accompanied by complications at both cardiovascular and metabolic level; reason why it has become a great risk to the health of our population. Despite the controversy surrounding the criteria for diagnosis and its pathophysiology, many of these mechanisms have already been sufficiently studied. This review aims to develop some of the pathophysiological mechanisms proposed in the appearance of MS, starting from insulin resistance as the main axis.


A Síndrome Metabólica (SM) é uma entidade de alta prevalência mundial e regional, frequentemente acompanhada de complicações tanto a nível cardiovascular como metabólico; razão pela qual se tornou um grande risco para a saúde de nossa população. Apesar da controvérsia em torno dos critérios de diagnóstico e fisiopatologia, muitos destes mecanismos já foram suficientemente estudados. Com esta revisão pretende-se desenvolver alguns dos mecanismos fisiopatológicos propostos no aparecimento do SM, partindo da resistência à insulina como o eixo principal.

9.
Gen Physiol Biophys ; 30(1): 20-7, 2011 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-21460408

RESUMO

Chondrocytes, the only cell in cartilage, are subjected to hyperosmotic challenges continuously since extracellular osmolarity in articular cartilage increases in response to mechanical loads during joint movement. Hyperosmolarity can affect membrane transport, and it is possible that load modulates matrix synthesis through alterations in intracellular composition. In the present study, the effects of hyperosmotic challenges were evaluated using the whole-cell patch clamp technique, whole cell mode on freshly isolated human and bovine articular chondrocytes. In human chondrocytes, hypertonicity induced the activation of outward Ca(2+)-sensitive K(+) currents, which were inhibited by iberiotoxin and TEA-Cl. The current induced by hypertonic switching (osmolarity from 300 to 400 mOsm/l) caused cell hyperpolarization (from -39 mV to -70 mV) with a reversal potential of -96 ± 7 mV. These results suggest a role for Ca(2+)-activated K(+) channels in human articular chondrocytes, leading to hyperpolarization as a consequence of K(+) efflux through these channels. These channels could have a role in the articular chondrocyte's response to a hyperosmotic challenge and matrix metabolism regulation by load.


Assuntos
Cartilagem Articular/citologia , Condrócitos/metabolismo , Canais de Potássio Cálcio-Ativados/química , Canais de Potássio Cálcio-Ativados/metabolismo , Animais , Bovinos , Eletrofisiologia , Humanos , Líquido Intracelular/fisiologia , Potenciais da Membrana/efeitos dos fármacos , Concentração Osmolar , Técnicas de Patch-Clamp/métodos , Peptídeos/antagonistas & inibidores , Peptídeos/farmacologia
10.
Cell Mol Neurobiol ; 31(4): 619-27, 2011 May.
Artigo em Inglês | MEDLINE | ID: mdl-21311966

RESUMO

The Na(+)/Ca(2+) exchanger (NCX) is an important bidirectional transporter of calcium in neurons and has been shown to be involved in neuroprotection. Calcium can activate a number of cascades that can result in apoptosis and cell death, and NCX is a key factor in regulating the cytoplasmic concentration of this ion. 17-ß-estradiol and insulin-like growth factor 1 (IGF-1) are known neuroprotective hormones with interacting mechanisms and effects on intracellular calcium; however, their relationship with the NCX has not been explored. In this article, the effects of these two hormones on neuronal NCX were tested using the whole-cell patch clamp technique on rat primary culture neurons. Both 17-ß-estradiol and IGF-1 produced an increase in the NCX-mediated inward current and a decrease in the NCX-mediated outward current. However, the IGF-1 effect was lower than that of 17-ß-estradiol, and the effect of both agents together was greater than the sum of each agent alone. Neither of the agents affected the pattern of regulation by extracellular or intrapipette calcium. Inhibitors of the IGF-1 and 17-ß-estradiol receptors and inhibitors of the main signaling pathways failed to change the observed effects, indicating that these actions were not mediated by the classical receptors of these hormones. These effects on the NCX could be a mechanism explaining the neuroprotective actions of 17-ß-estradiol and IGF-1, and these findings could help researchers to understand the role of the NCX in neuroprotection.


Assuntos
Córtex Cerebral/citologia , Estradiol/farmacologia , Fator de Crescimento Insulin-Like I/farmacologia , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Trocador de Sódio e Cálcio/metabolismo , Animais , Cálcio/metabolismo , Células Cultivadas , Feminino , Ativação do Canal Iônico/efeitos dos fármacos , Ratos , Ratos Wistar , Trocador de Sódio e Cálcio/antagonistas & inibidores
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