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Las alteraciones en la motilidad esofágica y el reflujo gastroesofágico (RGE) son comunes en pacientes con enfermedad pulmonar avanzada, aun en ausencia de síntomas de RGE.

An electronic nose sensor array can classify and quantify different types of gases; however, the sensor can alter its measurement capability over time. The main problem presented during the measurements of the sensors is related to the variation of the data acquired for long periods due to changes in the chemosensory response, thus affecting the correct functioning of the implemented measuring system. This research presents an approach to improve gas quantification through the implementation of machine learning regression techniques in an array of nose-type electronic sensors. The implemented methodology uses a domain adaptation approach with the Kullback–Leibler importance estimation procedure (KLIEP) to improve the performance of the gas quantification electronic nose array. This approach is validated using a three-year dataset measured by a 16-electronic-nose-sensor array. The R2 regression error obtained for each of the gases fits the resulting dataset’s measured values with good precision.

Chronic Myeloid Leukemia (CML) originates in a leukemic stem cell that resides in the bone marrow microenvironment, where they coexist with cellular and non-cellular elements. The vascular microenvironment has been identified as an important element in CML development since an increase in the vascularization has been suggested to be related with poor prognosis; also, using murine models, it has been reported that bone marrow endothelium can regulate the quiescence and proliferation of leukemic stem and progenitor cells. This observation, however, has not been evaluated in primary human cells. In this report, we used a co-culture of primitive (progenitor and stem) CML cells with endothelial colony forming cells (ECFC) as an in vitro model to evaluate the effects of the vascular microenvironment in the leukemic hematopoiesis. Our results show that this interaction allows the in vitro maintenance of primitive CML cells through an inflammatory microenvironment able to regulate the proliferation of progenitor cells and the permanence in a quiescent state of leukemic stem cells.

Resumen: Introducción: Dolor torácico no cardíaco (DTNC) se define como un síndrome clínico caracterizado por dolor retroesternal semejante a la angina de pecho, pero de origen no cardiaco y generado por enfermedades esofágicas, osteomusculares, pulmonares o psiquiátricas. Objetivo: Presentar una revisión consensuada basada en evidencias sobre definición, epidemiología, fisiopatología, diagnóstico y opciones terapéuticas para pacientes con DTNC. Métodos: Tres coordinadores generales realizaron una revisión bibliográfica de todas las publicaciones en inglés y español sobre el tema y elaboraron 38 enunciados iniciales divididos en tres categorías principales: 1) definiciones, epidemiología y fisiopatología; 2) diagnóstico, y 3) tratamiento. Los enunciados fueron votados (3 rondas) utilizando el sistema Delphi, y los que alcanzaron un acuerdo > 75% fueron considerados y calificados de acuerdo con el sistema GRADE. Resultados y conclusiones: El consenso final incluyó 29 enunciados Todo paciente que debuta con dolor torácico debe ser inicialmente evaluado por un cardiólogo. La causa más común de DTNC es la enfermedad por reflujo gastroesofágico (ERGE). Como abordaje inicial, si no existen síntomas de alarma, se puede dar una prueba terapéutica con inhibidor de bomba de protones (IBP) por 2-4 semanas. Si hay disfagia o síntomas de alarma, se recomienda hacer una endoscopia. La manometría de alta resolución es el mejor método para descartar trastornos motores espásticos y acalasia. La pHmetría ayuda a demostrar exposición esofágica anormal al ácido. El tratamiento debe ser dirigido al mecanismo fisiopatológico, y puede incluir IBP, neuromoduladores y/o relajantes de músculo liso, intervención psicológica y/o terapia cognitiva, y ocasionalmente cirugía o terapia endoscópica. Abstract: Introduction: Non-cardiac chest pain is defined as a clinical syndrome characterized by retrosternal pain similar to that of angina pectoris, but of non-cardiac origin and produced by esophageal, musculoskeletal, pulmonary, or psychiatric diseases. Aim: To present a consensus review based on evidence regarding the definition, epidemiology, pathophysiology, and diagnosis of non-cardiac chest pain, as well as the therapeutic options for those patients. Methods: Three general coordinators carried out a literature review of all articles published in English and Spanish on the theme and formulated 38 initial statements, dividing them into 3 main categories: (i) definitions, epidemiology, and pathophysiology; (ii) diagnosis, and (iii) treatment. The statements underwent 3 rounds of voting, utilizing the Delphi system. The final statements were those that reached > 75% agreement, and they were rated utilizing the GRADE system. Results and conclusions: The final consensus included 29 statements. All patients presenting with chest pain should initially be evaluated by a cardiologist. The most common cause of non-cardiac chest pain is gastroesophageal reflux disease. If there are no alarm symptoms, the initial approach should be a therapeutic trial with a proton pump inhibitor for 2-4 weeks. If dysphagia or alarm symptoms are present, endoscopy is recommended. High-resolution manometry is the best method for ruling out spastic motor disorders and achalasia and pH monitoring aids in demonstrating abnormal esophageal acid exposure. Treatment should be directed at the pathophysiologic mechanism. It can include proton pump inhibitors, neuromodulators and/or smooth muscle relaxants, psychologic intervention and/or cognitive therapy, and occasionally surgery or endoscopic therapy. Palabras clave: Dolor, Torácico, No cardíaco, ERGE, Trastornos motores esofágicos, México, Keywords: Pain, Chest, Non-cardiac, GERD, Esophageal motor disorders, Mexico

Introduction: Non-cardiac chest pain is defined as a clinical syndrome characterized by retrosternal pain similar to that of angina pectoris, but of non-cardiac origin and produced by esophageal, musculoskeletal, pulmonary, or psychiatric diseases. Aim: To present a consensus review based on evidence regarding the definition, epidemiology, pathophysiology, and diagnosis of non-cardiac chest pain, as well as the therapeutic options for those patients. Methods: Three general coordinators carried out a literature review of all articles published in English and Spanish on the theme and formulated 38 initial statements, dividing them into 3 main categories: (i) definitions, epidemiology, and pathophysiology; (ii) diagnosis, and (iii) treatment. The statements underwent 3 rounds of voting, utilizing the Delphi system. The final statements were those that reached > 75% agreement, and they were rated utilizing the GRADE system. Results and conclusions: The final consensus included 29 statements. All patients presenting with chest pain should initially be evaluated by a cardiologist. The most common cause of non-cardiac chest pain is gastroesophageal reflux disease. If there are no alarm symptoms, the initial approach should be a therapeutic trial with a proton pump inhibitor for 2-4 weeks. If dysphagia or alarm symptoms are present, endoscopy is recommended. High-resolution manometry is the best method for ruling out spastic motor disorders and achalasia and pH monitoring aids in demonstrating abnormal esophageal acid exposure. Treatment should be directed at the pathophysiologic mechanism. It can include proton pump inhibitors, neuromodulators and/or smooth muscle relaxants, psychologic intervention and/or cognitive therapy, and occasionally surgery or endoscopic therapy. Resumen: Introducción: Dolor torácico no cardíaco (DTNC) se define como un síndrome clínico caracterizado por dolor retroesternal semejante a la angina de pecho, pero de origen no cardiaco y generado por enfermedades esofágicas, osteomusculares, pulmonares o psiquiátricas. Objetivo: Presentar una revisión consensuada basada en evidencias sobre definición, epidemiología, fisiopatología, diagnóstico y opciones terapéuticas para pacientes con DTNC. Métodos: Tres coordinadores generales realizaron una revisión bibliográfica de todas las publicaciones en inglés y español sobre el tema y elaboraron 38 enunciados iniciales divididos en tres categorías principales: 1) definiciones, epidemiología y fisiopatología; 2) diagnóstico, y 3) tratamiento. Los enunciados fueron votados (3 rondas) utilizando el sistema Delphi, y los que alcanzaron un acuerdo > 75% fueron considerados y calificados de acuerdo con el sistema GRADE. Resultados y conclusiones: El consenso final incluyó 29 enunciados Todo paciente que debuta con dolor torácico debe ser inicialmente evaluado por un cardiólogo. La causa más común de DTNC es la enfermedad por reflujo gastroesofágico (ERGE). Como abordaje inicial, si no existen síntomas de alarma, se puede dar una prueba terapéutica con inhibidor de bomba de protones (IBP) por 2-4 semanas. Si hay disfagia o síntomas de alarma, se recomienda hacer una endoscopia. La manometría de alta resolución es el mejor método para descartar trastornos motores espásticos y acalasia. La pHmetría ayuda a demostrar exposición esofágica anormal al ácido. El tratamiento debe ser dirigido al mecanismo fisiopatológico, y puede incluir IBP, neuromoduladores y/o relajantes de músculo liso, intervención psicológica y/o terapia cognitiva, y ocasionalmente cirugía o terapia endoscópica. Keywords: Pain, Chest, Non-cardiac, GERD, Esophageal motor disorders, Mexico, Palabras clave: Dolor, Torácico, No cardíaco, ERGE, Trastornos motores esofágicos, México

This paper presents a descriptive study aimed at identifying the main active ingredients, frequency of use, and the processes employed in the application of the agrochemicals most used around the Lake of Tota, which is considered the most important freshwater ecosystem in Colombia. A key source for this study is a survey to farmers, which sampling frame was established from a Geographical Institute Agustin Codazzi (IGAC) digital map, considering only the plots with some agricultural activity and runoff into the lake. This information was supplemented with geographic data obtained from Google Maps®. As control mechanism, two additional sources were used: i) a manual count of packaging of agrochemicals in a certified collection center, and ii) a census of stores that supply such products in the study area. The results allow knowing the set of agrochemicals most used around the lake, their active ingredients, and the most common farming practices, some of which could entail some risk to farmers, consumers and the environment.

En este artículo se estimaron los desperdicios totales procedentes de la producción de trucha arcoíris, Oncorhynchus mykiss Walbaum (Salmoniformes: Salmonidae), en el lago de Tota, ecosistema de agua dulce ubicado en el departamento de Boyacá (Colombia), y su potencial impacto sobre este. La producción de trucha se desarrolla de manera intensiva en dicho lago desde 2005, utilizando jaulas inmersas. Con datos obtenidos de la Autoridad Nacional de Acuicultura y Pesca (Aunap), la Corporación Autónoma Regional de Boyacá (Corpoboyacá) y la Cámara de Comercio de Sogamoso, se identificaron los piscicultores, su ubicación geográfica en el lago y la producción autorizada de las fincas. Con esta información se calculó la cantidad de desperdicios producidos y las cantidades de nitrógeno y fósforo generados en este proceso. Según los resultados obtenidos, se evidencia la contaminación del lago por la producción intensiva de trucha y se recomienda mejorar o modificar los métodos de producción para minimizar la contaminación del agua.

Venous thromboembolic disease (VTD) is a public health problem. We recently reported that endothelial colony-forming cells (ECFCs) derived from endothelial cells (EC) (ECFC-ECs) from patients with VTD have a dysfunctional state. For this study, we proposed that a dysfunctional status of these cells generates a reduction of its proliferative ability, which is also associated with senescence and reactive oxygen species (ROS).Human mononuclear cells (MNCs) were obtained from peripheral blood from 40 healthy human volunteers (controls) and 50 patients with VTD matched by age (20-50 years) and sex to obtain ECFCs. We assayed their proliferative ability with plasma of patients and controls and supernatants of cultures from ECFC-ECs, senescence-associated β-galactosidase (SA-β-gal), ROS, and expression of ephrin-B2/Eph-B4 receptor. Compared with cells from controls, cells from VTD patients showed an 8-fold increase of ECFCs that emerged 1 week earlier, reduced proliferation at long term (39%) and, in passages 4 and 10, a highly senescent rate (30±1.05% vs. 91.3±15.07%, respectively) with an increase of ROS and impaired expression of ephrin-B2/Eph-4 genes. Proliferation potential of cells from VTD patients was reduced in endothelial medium [1.4±0.22 doubling population (DP)], control plasma (1.18±0.31 DP), or plasma from VTD patients (1.65±0.27 DP).As compared with controls, ECFC-ECs from individuals with VTD have higher oxidative stress, proliferation stress, cellular senescence, and low proliferative potential. These findings suggest that patients with a history of VTD are ECFC-ECs dysfunctional that could be associated to permanent risk for new thrombotic events.

Background: Endothelial colony-forming cells (ECFCs) contribute to postnatal vasculogenesis. In venous thromboembolic disease (VTD), they are functionally abnormal and produce high concentrations of TNF-α., Objective: To analyze the TNF-α signaling pathway and its relationship with the expression of cell-cycle regulators., Methods: Mononuclear cells (MNCs) were collected from the peripheral blood of 20 healthy human volunteers (controls) and 30 patients with VTD matched by age (20-50 years) and sex to obtain ECFCs. We analyzed the relative quantification of the gene transcripts of TNF, NFkB1, PLAU, HMOX1, GSS, eNOS, CDKN1A, and CDKN1B through quantitative RT-PCR (qRT-PCR assays). Identification of NF-κB and activated targets of each pathway: NF-κB (Ser536); IκBα (Ser32/Ser36); p38 (Thr180/Tyr182) JNK (Thr183/Tyr185), p53 and cell-cycle regulators: p16, p18, p21, p27, p57, Cyclin D, Cyclin E, Cyclin A, Cyclin B, CDK2, CDK4; cell-cycle status was determined by KI-67 and 7-AAD. Cells were analyzed with flow cytometry and the FlowJo vX software., Results: In ECFCs from VTD patients, TNF-α receptor and NFkB were overexpressed and hyper-phosphorylated; eNOS and HMOX1 were down-regulated; cell-cycle regulators (p53, p18, p21) were elevated. In addition, the cell cycle was locked in the G2 phase., Conclusions: Our results strongly suggest that these molecular alterations in the pathway of TNF-α and cell cycle regulation induce endothelial dysfunction, reduced proliferation potential and vascular regeneration, and consequently, the occurrence of new thrombotic events., Competing Interests: Conflict of Interest The authors have no conflicts of interest., (Copyright © 2022. Published by Elsevier Inc.)

Chronic Myeloid Leukemia (CML) originates in a leukemic stem cell that resides in the bone marrow microenvironment, where they coexist with cellular and non-cellular elements. The vascular microenvironment has been identified as an important element in CML development since an increase in the vascularization has been suggested to be related with poor prognosis; also, using murine models, it has been reported that bone marrow endothelium can regulate the quiescence and proliferation of leukemic stem and progenitor cells. This observation, however, has not been evaluated in primary human cells. In this report, we used a co-culture of primitive (progenitor and stem) CML cells with endothelial colony forming cells (ECFC) as an in vitro model to evaluate the effects of the vascular microenvironment in the leukemic hematopoiesis. Our results show that this interaction allows the in vitro maintenance of primitive CML cells through an inflammatory microenvironment able to regulate the proliferation of progenitor cells and the permanence in a quiescent state of leukemic stem cells., Competing Interests: The authors confirm that there are no conflicts of interest.

Chronic myeloid leukemia (CML) is a myeloproliferative disease that results from the BCR-ABL gene-induced transformation of a primitive hematopoietic cell. This disease has been extensively studied, and, as a result, a very effective therapy has been developed: the tyrosine kinase inhibitors. Although, there is a significant knowledge about the intrinsic biology of CML cells, alterations in their bone marrow microenvironment are not yet completely understood. In this concise review, we summarized recent findings on the composition and function of the bone marrow microenvironment in CML, and their importance in the progression of the disease and treatment resistance., Competing Interests: Conflict of Interest The authors declare no conflict of interest, (Copyright © 2021 Elsevier Masson SAS. All rights reserved.)

From the knowledge that hematopoiesis does not occur randomly in the bone marrow but is regulated by the different components of the microenvironment, the use of in vitro coculture systems has been used as a powerful tool in the analysis of different processes that are involved in the maintenance of blood cells. In this chapter, we describe a methodological strategy to perform a coculture between primitive hematopoietic cells and endothelial cells to evaluate cell cycle, an aspect of relevant importance in the permanence of primitive leukemic cells.

Background: Venous thromboembolic disease (VTD) is a public health problem. We recently reported that endothelial colony-forming cells (ECFCs) derived from endothelial cells (EC) (ECFC-ECs) from patients with VTD have a dysfunctional state. For this study, we proposed that a dysfunctional status of these cells generates a reduction of its proliferative ability, which is also associated with senescence and reactive oxygen species (ROS)., Methods and Results: Human mononuclear cells (MNCs) were obtained from peripheral blood from 40 healthy human volunteers (controls) and 50 patients with VTD matched by age (20-50 years) and sex to obtain ECFCs. We assayed their proliferative ability with plasma of patients and controls and supernatants of cultures from ECFC-ECs, senescence-associated β-galactosidase (SA-β-gal), ROS, and expression of ephrin-B2/Eph-B4 receptor. Compared with cells from controls, cells from VTD patients showed an 8-fold increase of ECFCs that emerged 1 week earlier, reduced proliferation at long term (39%) and, in passages 4 and 10, a highly senescent rate (30±1.05% vs. 91.3±15.07%, respectively) with an increase of ROS and impaired expression of ephrin-B2/Eph-4 genes. Proliferation potential of cells from VTD patients was reduced in endothelial medium [1.4±0.22 doubling population (DP)], control plasma (1.18±0.31 DP), or plasma from VTD patients (1.65±0.27 DP)., Conclusions: As compared with controls, ECFC-ECs from individuals with VTD have higher oxidative stress, proliferation stress, cellular senescence, and low proliferative potential. These findings suggest that patients with a history of VTD are ECFC-ECs dysfunctional that could be associated to permanent risk for new thrombotic events.