Defective IL-10 production in severe phenotypes of Crohn’s disease

et al.Loss of tolerance toward commensal bacteria has been invoked as a mechanism for Crohn's disease. IL-10 is a key anti-inflammatory cytokine that plays a role in induction and maintenance of tolerance. The aim of this study is to determine IL-10 production in response to bacterial components in Crohn's disease patients, who were classified according to their phenotypes as stricturing, penetrating, or inflammatory. Peripheral blood was obtained from Crohn's disease patients and healthy controls. Cytokine production was measured in whole blood cultures, isolated CD4(+) cells, and monocyte-derived dendritic cells (MDDCs). Under unstimulated conditions, IL-10, but not IL-12, was down-regulated significantly in blood cultures of patients with severe phenotypes, compared with inflammatory, nonpenetrating, nonstricturing Crohn's disease patients. In response to LPS, IL-10 was up-regulated more significantly in patients with no fistulae or fibrosis. Study of IL-10 production by isolated cell subsets showed that DCs, but not CD4(+) T cells, from penetrating Crohn's disease produced significantly less IL-10 in response to LPS. Differences were not associated with the 1082A/G polymorphism in the IL-10 gene promoter. We show a defect in IL-10 production in whole blood cell cultures and MDDCs in patients with severe forms of Crohn's disease. This defect in IL-10 production by a group of Crohn's disease patients may represent a mechanism mediating more severe manifestations of the disease. We propose that treatment with IL-10 or IL-10-inducing therapies could be of particular benefit to these group of patientsThis work was supported by Grant SAF2005-03755 from the Ministerio de Educación y Ciencia, Spain.Peer reviewe

Lipoma intrauricular derecho. Reporte de un caso

We present the case of a 56-year-old male patient with a history of atrial flutter for six months; he was admitted to the hospital for presenting a mass of 8 cm in maximum diameter in the right atrium, which prolapsed through the tricuspid valve into the right ventricle. Emergency surgery was scheduled, performing exeresis of the tumor and tricuspid annuloplasty. The Pathological anatomy determined that the removed mass corresponded to a cardiac lipoma.Se presenta el caso de un paciente varón de 56 años, con antecedente de Flutter auricular desde hace 6 meses; ingresó al hospital por presentar una masa de 8 cm de diámetro máximo en la aurícula derecha, la cual prolapsaba a través de la válvula tricúspide hacia el ventrículo derecho. Se programó la cirugía de urgencia en la que se realizó la exéresis de la tumoración y la anuloplastia tricuspídea. La anatomía patológica determinó que la masa extraida correspondía a un lipoma cardiaco

Arabidopsis AtDjA3 null mutant shows increased sensitivity to abscisic acid, salt, and osmotic stress in germination and post-germination stages

"DnaJ proteins are essential co-chaperones involved in abiotic and biotic stress responses. Arabidopsis AtDjA3 gene encodes a molecular co-chaperone of 420 amino acids, which belongs to the J-protein family. In this study, we report the functional characterization of the AtDjA3 gene using the Arabidopsis knockout line designated j3 and the 35S::AtDjA3 overexpression lines. Loss of AtDjA3 function was associated with small seed production. In fact, j3 mutant seeds showed a reduction of 24% in seed weight compared to Col-0 seeds. Expression analysis showed that the AtDjA3 gene was modulated in response to NaCl, glucose, and abscisic acid (ABA). The j3 line had increased sensitivity to NaCl and glucose treatments in the germination and cotyledon development in comparison to parental Col-0. Furthermore, the j3 mutant line exhibited higher ABA sensitivity in comparison to parental Col-0 and 35S::AtDjA3 overexpression lines. In addition, we examined the expression of ABI3 gene, which is a central regulator in ABA signaling, in j3 mutant and 35S:rAtDjA3 overexpression lines. Under 5 RNA ABA treatment at 24 h, j3 mutant seedlings displayed higher ABI3 expression, whereas in 35S::AtDjA3 overexpression lines, ABI3 gene expression was repressed. Taken together, these results demonstrate that the AtDjA3 gene is involved in seed development and abiotic stress tolerance.

Proyecto de emprendimiento para la microempresa BOLDONIC dedicada a la producción, comercialización y distribución de té a base de la planta medicinal Boldo, ubicada en el municipio de Jinotepe, en el departamento de Carazo, durante el segundo semestre del año 2019

BOLDONIC es una microempresa dedicada a la producción, comercialización y distribución de té a base de la planta medicinal peumus boldus, conocida como boldo. La creación de la micro empresa se debe a que hoy en día la población ingiere muchos productos tanto alimenticios como medicinales que son dañinos para la salud y por ende producen problemas en nuestro organismo. La microempresa BOLDONIC surge debido a la necesidad de reducir la alta tasa de desempleo que existe en el país, ya que es una forma de subsistencia aprovechando los beneficios que la naturaleza nos ofrece. Se pretende conseguir una gran posición en el mercado haciendo conciencia en la población de la necesidad de ingerir productos medicinales naturales beneficiosos para la salud debido a que la planta tiene importantes propiedades, por ejemplo: entre los más de 20 alcaloides presentes, se encuentra la Boldina, esta se encarga de estimular el funcionamiento de la vesícula biliar, actuando de forma directa con propiedades beneficiosas para el hígado, el Cineol también presente en la planta tiene propiedades expectorantes, ideales para aliviar resfriados, y ayuda a evitar las digestiones pesadas. Se ha elaborado una investigación de mercado para lograr identificar de manera concreta los principales clientes de este producto y como resultado de ello se logró observar que tiene un grado de aceptación del 87.59%, siendo la perspectiva de esto que las infusiones tenga calidad y un precio accesible. Para llevar a cabo la planificación de este, se necesitó de la indagación general de cómo establecer un negocio en el país, todo ello esta descrito en el presente trabajo siendo BOLDONIC clasificada como micro empresa y requiere de una inversión inicial de C$ 113,902.19 córdobas la cual se espera recuperar a más tardar en un plazo de 1 año y 4 meses años de inicio de operaciones

SINDROME POST COVID 19

El síndrome de post COVID es una entidad poco conocida, la epidemiologia es casi en un tercio de los pacientes que presentaron COVID en cualquiera de sus modalidades y además se sabe que presenta y comparte muchos síntomas del COVID 19; lo característico es que se presenta en forma más severa que la misma enfermedad en la mayoría de los casos siendo desconocido el origen de estos. El diagnostico se basa principalmente en hallazgos laboratoriales, imágenes y la clínica de la enfermedad y el tratamiento es según a las manifestaciones que se presentan durante la enfermedad

RIPK1 Mediates TNF-Induced Intestinal Crypt Apoptosis During Chronic NF-κB Activation

Tumor necrosis factor (TNF) is a major pathogenic effector and a therapeutic target in inflammatory bowel disease (IBD), yet the basis for TNF-induced intestinal epithelial cell (IEC) death is unknown, because TNF does not kill normal IECs. Here, we investigated how chronic nuclear factor (NF)- κB activation, which occurs in human IBD, promotes TNF-dependent IEC death in mice. Human IBD specimens were stained for p65 and cleaved caspase-3. C57BL/6 mice with constitutively active IKKβ in IEC (Ikkβ(EE) IEC ), Ripk1 D138N/D138N knockin mice, and Ripk3 -/- mice were injected with TNF or lipopolysaccharide. Enteroids were also isolated from these mice and challenged with TNF with or without RIPK1 and RIPK3 inhibitors or butylated hydroxyanisole. Ripoptosome-mediated caspase-8 activation was assessed by immunoprecipitation. NF-κB activation in human IBD correlated with appearance of cleaved caspase-3. Congruently, unlike normal mouse IECs that are TNF-resistant, IECs in Ikkβ(EE) IEC mice and enteroids were susceptible to TNF-dependent apoptosis, which depended on the protein kinase function of RIPK1. Constitutively active IKKβ facilitated ripoptosome formation, a RIPK1 signaling complex that mediates caspase-8 activation by TNF. Butylated hydroxyanisole treatment and RIPK1 inhibitors attenuated TNF-induced and ripoptosome-mediated caspase-8 activation and IEC death in vitro and in vivo. Contrary to common expectations, chronic NF-κB activation induced intestinal crypt apoptosis after TNF stimulation, resulting in severe mucosal erosion. RIPK1 kinase inhibitors selectively inhibited TNF destructive properties while preserving its survival and proliferative properties, which do not require RIPK1 kinase activity. RIPK1 kinase inhibition could be a potential treatment for IBD