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    Parámetros hematológicos y biomarcadores predictores de gravedad en Síndrome Inflamatorio Pediátrico Multisistémico asociado a SARS-CoV-2
    (2021)
    Patricia Verdugo
    ;
    Patricia Álvarez
    ;
    Patricia Aroca
    ;
    Vicente Enrique Montes-nogales
    ;
    <jats:p>El síndrome inflamatorio multisistémico pediátrico asociado a SARS-CoV-2 (MIS-C) se caracteriza por un estado hiperinflamatorio producto de una tormenta de citoquinas, evidenciado en alteraciones del laboratorio hematológico y proteínas de fase aguda.Objetivo: Describir las características clínicas y de laboratorio de pacientes hospitalizados por MIS-C e identificar marcadores predictores de gravedad.Pacientes y Método: Estudio retrospectivo de 32 pacientes. El grupo se dividió en crítico y no crítico según presentación clínica y tipo de terapia utilizada. En ellos se estudiaron aspectos clínicos y de laboratorio que incluyeron hemograma completo, pruebas de coagulación y biomarcadores. Resultados: 18/32 hombres, mediana de edad 6,8 años. Las manifestaciones más frecuentes fueron cardiovasculares (84,3%), digestivas (84%) y mucocutáneas (59%). El grupo de los críticos incluyó 15 pacientes, 12 hombres con mediana de edad de 8,9 años y los no críticos 17 pacientes; 6 hombres, con mediana de edad de 5,4 años. Los parámetros de laboratorio al ingreso en el grupo global mostraron aumento de la proteína C reactiva, dímero-D, leucocitos, neutrófilos, ferritina y fibrinógeno. La albúmina y la natremia en cambio se encontraban disminuidas. El grupo crítico se caracterizó por tener al ingreso: trombocitopenia, hipoalbuminemia, prolongación del tiempo de protrombina y elevación de la ferritina. Al deterioro hubo acentuación de la trombocitopenia, ascenso mayor de la proteína C reactiva junto a elevación de los neutrófilos.Conclusión: El hemograma, la proteína C reactiva y la albuminemia al ingreso resultaron ser de alto valor en la identificación de pacientes con riesgo de agravamiento clínico.</jats:p>
      20Scopus© Citations 10
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    Prognostic significance of early urinary catheterization after acute stroke: Secondary analyses of the international HeadPoST trial
    (2020)
    Menglu Ouyang
    ;
    Laurent Billot
    ;
    Lili Song
    ;
    Xia Wang
    ;
    Christine Roffe
    <jats:sec><jats:title>Background</jats:title><jats:p> An indwelling urinary catheter (IUC) is often inserted to manage bladder dysfunction, but its impact on prognosis is uncertain. We aimed to determine the association of IUC use on clinical outcomes after acute stroke in the international, multi-center, cluster crossover, Head Positioning in Acute Stroke Trial (HeadPoST). </jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p> Data were analyzed on HeadPoST participants (n = 11,093) randomly allocated to the lying-flat or sitting-up head position. Binomial, logistic regression, hierarchical mixed models were used to determine associations of early insertion of IUC within seven days post-randomization and outcomes of death or disability (defined as “poor outcome,” scores 3–6 on the modified Rankin scale) and any urinary tract infection at 90 days with adjustment of baseline and post-randomization management covariates. </jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p> Overall, 1167 (12%) patients had an IUC, but the frequency and duration of use varied widely across patients in different regions. IUC use was more frequent in older patients, and those with vascular comorbidity, greater initial neurological impairment (on the National Institutes of Health Stroke Scale), and intracerebral hemorrhage as the underlying stroke type. IUC use was independently associated with poor outcome (adjusted odds ratio (aOR): 1.40, 95% confidence interval (CI): 1.13–1.74), but not with urinary tract infection after adjustment for antibiotic treatment and stroke severity at hospital separation (aOR: 1.13, 95% CI: 0.59–2.18). The number exposed to IUC for poor outcome was 13. </jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p> IUC use is associated with a poor outcome after acute stroke. Further studies are required to inform appropriate use of IUC. </jats:p></jats:sec>
    Scopus© Citations 4  3
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    Association between spontaneous internal carotid artery dissection and perivascular adipose tissue attenuation on computed tomography angiography
    (2023)
    Kevin Cheng
    ;
    Andrew Lin
    ;
    ;
    Tomas Bernstein
    ;
    Paulo Zuñiga
    <jats:sec><jats:title>Background:</jats:title><jats:p> Spontaneous cervical artery dissection (sCAD) is a leading cause of ischemic stroke in young patients. Studies using high-resolution magnetic resonance imaging and positron emission tomography have suggested vessel wall inflammation to be a pathogenic factor in sCAD. Computed tomography (CT) attenuation of perivascular adipose tissue (PVAT) is an established non-invasive imaging biomarker of inflammation in coronary arteries, with higher attenuation values reflecting a greater degree of vascular inflammation. </jats:p></jats:sec><jats:sec><jats:title>Objectives:</jats:title><jats:p> We evaluate the CT attenuation of PVAT surrounding the internal carotid artery (PVAT<jats:sub>carotid</jats:sub>) with and without spontaneous dissection. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> Single-center prospective observational study of 56 consecutive patients with CT-verified spontaneous dissection of the internal carotid artery (ICA). Of these patients, six underwent follow-up computed tomography angiography (CTA). Twenty-two patients who underwent CTA for acute neurological symptoms but did not have dissection formed the control group. Using semi-automated research software, PVAT<jats:sub>carotid</jats:sub> was measured as the mean Hounsfield unit (HU) attenuation of adipose tissue within a defined volume of interest surrounding the ICA. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> PVAT<jats:sub>carotid</jats:sub> was significantly higher around dissected ICA compared with non-dissected contralateral ICA in the same patients (−58.7 ± 10.2 vs −68.9 ± 8.1 HU, p &lt; 0.0001) and ICA of patients without dissection (−58.7 ± 10.2 vs −69.3 ± 9.3 HU, p &lt; 0.0001). After a median follow-up of 89 days, there was a significant reduction in PVAT<jats:sub>carotid</jats:sub> around dissected ICA (−57.5 ± 13.4 to −74.3 ± 10.5 HU, p &lt; 0.05), while no change was observed around non-dissected contralateral ICA (−71.0 ± 4.4 to −74.1 ± 4.1 HU, p = 0.19). ICA dissection was an independent predictor of PVAT<jats:sub>carotid</jats:sub> following multivariable adjustment for age and the presence of ICA occlusion. </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> PVAT<jats:sub>carotid</jats:sub> is elevated in the presence of sCAD and may decrease following the acute event. </jats:p></jats:sec>
      3  1Scopus© Citations 5
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    Skeletal Muscle Atrophy Induced by Diabetes Is Mediated by Non-Selective Channels and Prevented by Boldine
    (2023)
    Luis A. Cea
    ;
    Walter Vásquez
    ;
    Romina Hernández-Salinas
    ;
    Alejandra Z. Vielma
    ;
    Mario Castillo-Ruiz
    <jats:p>Individuals with diabetes mellitus present a skeletal muscle myopathy characterized by atrophy. However, the mechanism underlying this muscular alteration remains elusive, which makes it difficult to design a rational treatment that could avoid the negative consequences in muscles due to diabetes. In the present work, the atrophy of skeletal myofibers from streptozotocin-induced diabetic rats was prevented with boldine, suggesting that non-selective channels inhibited by this alkaloid are involved in this process, as has previously shown for other muscular pathologies. Accordingly, we found a relevant increase in sarcolemma permeability of skeletal myofibers of diabetic animals in vivo and in vitro due to de novo expression of functional connexin hemichannels (Cx HCs) containing connexins (Cxs) 39, 43, and 45. These cells also expressed P2X7 receptors, and their inhibition in vitro drastically reduced sarcolemma permeability, suggesting their participation in the activation of Cx HCs. Notably, sarcolemma permeability of skeletal myofibers was prevented by boldine treatment that blocks Cx43 and Cx45 HCs, and now we demonstrated that it also blocks P2X7 receptors. In addition, the skeletal muscle alterations described above were not observed in diabetic mice with myofibers deficient in Cx43/Cx45 expression. Moreover, murine myofibers cultured for 24 h in high glucose presented a drastic increase in sarcolemma permeability and levels of NLRP3, a molecular member of the inflammasome, a response that was also prevented by boldine, suggesting that, in addition to the systemic inflammatory response found in diabetes, high glucose can promote the expression of functional Cx HCs and activation of the inflammasome in skeletal myofibers. Therefore, Cx43 and Cx45 HCs play a critical role in myofiber degeneration, and boldine could be considered a potential therapeutic agent to treat muscular complications due to diabetes.</jats:p>
      5Scopus© Citations 18