Cuidado humanizado del profesional de enfermería en la atención del paciente oncológico hospitalizado / Humanized care of the nursing professional in the care of hospitalized cander patients

Introducción: El cuidado a pacientes oncológicos consiste, más allá de satisfacer necesidades físicas, en una atención holística, pues el cuidado humanizado favorece una interrelación esencial entre ciencia y valores para establecer una asistencia de calidad, que dé solución a las demandas humanas del usuario. Objetivo: Identificar el nivel de cuidado humanizado que proporciona el profesional enfermero a pacientes hospitalizados en un centro de oncología. Material y métodos: Estudio descriptivo, observacional-transversal. Muestreo no probabilístico de oportunidad y secuencial con cuota de 35 pacientes. Medición realizada con el instrumento "Percepción del cuidado humanizado en pacientes hospitalizados". Análisis de resultados mediante estadística descriptiva. Resultados: El cuidado proporcionado a pacientes oncológicos hospitalizados es humanizado, pues afirman recibir trato amable con efecto positivo en ellos derivado de la actitud de la enfermera en su labor, en la que impera el conocimiento y la experiencia para proveer cuidados individualizados y empáticos a partir de comunicación, expresión de sentimientos y escucha, atendiendo no sólo necesidades físicas, sino también sociales, culturales y espirituales. Discusión: Los pacientes oncológicos mencionan que el profesional de enfermería actúa comprendiendo al usuario integralmente, lo que les permite enfrentar positivamente su proceso de enfermedad. Conclusiones: El cuidado humanizado de calidad es una relación entre el profesional de enfermería y el paciente a cuidar, en la que impera la comunicación, el debido uso de la palabra y la escucha para generar confianza, lo cual se suma a la base científica y las habilidades técnicas, a fin de intervenir de forma humana, eficiente y segura.

Introduction: Caring for cancer patients is an interaction that goes beyond satisfying physical needs, it is caring for the person in a holistic way, where the humanization of care favors the essential link of the profession, it is an interaction between science and values to establish quality care. quality, giving solution to the human responses of the patient. Objective: To identify the level of humanized care provided by the nursing professional to patients hospitalized in an oncology center. Material and methods: Descriptive, observational cross-sectional study. Non-probabilistic opportunity and sequential sampling with a quota of 35 patients. Measurement carried out with the: "Instrument Perception of Humanized Care in Hospitalized Patients". Analysis of results through descriptive statistics. Results: The level of care provided to hospitalized cancer patients is very humanized, patients report receiving friendly treatment with a positive effect on them, derived from the attitude of the nurse in her being and doing care, they perceive a relationship of trust where knowledge and Experience in favor of your health since the nursing professional provides individualized and empathetic care, favoring communication, expression of feelings and emotions; listening to them beyond their illness satisfying their physical, social, cultural and spiritual needs. Discussion: People with oncological disease perceive receiving humanized care when mentioning that the nursing professional acts understanding the patient from knowing, knowing how to do and knowing how to be, which allows them to positively face their disease process. Conclusions: The level of quality humanized care is a relationship that occurs between the nursing professional and the person they care for, in this human quality of care, communication prevails, the power that the word and hearing have in the field of attention, transcendental to generate confidence; coupled with the scientific foundation, empathetic attitude, technical and professional skills given by experience, allowing intervention in a humane, effective, efficient and safe way.

Seguridad del cuidado profesional enfermero en atención al paciente oncológico en contexto de contingencia COVID-19 / Safety in professional nursing care for oncology patients in the context of the COVID-19 pandemic

Introducción: La pandemia por COVID-19 requirió que los profesionales de enfermería enfocaran su atención en salvaguardar la integridad, seguridad y salud tanto del paciente como la propia. Objetivo: Analizar la percepción de la seguridad del cuidado profesional enfermero al paciente oncológico durante la contingencia por COVID-19. Material y métodos: Estudio descriptivo, observacional-transversal. Muestra de 50 profesionales de enfermería. Medición realizada con el instrumento Hospital Survey on Patient Safety adaptado al contexto de contingencia por COVID-19. Análisis de resultados mediante estadística descriptiva. Resultados: El grado de seguridad del cuidado profesional enfermero al paciente oncológico en contingencia por COVID-19 es aceptable en 11 de 16 dimensiones, según los rangos de medición: muy pobre, pobre, aceptable, muy bueno y excelente. Se identificaron las siguientes áreas de oportunidad para mejorar la seguridad del cuidado profesional enfermero: se pone en riesgo la seguridad de paciente con mayor presión de trabajo, la dotación del personal de enfermería es insuficiente para afrontar la carga de trabajo por pandemia, pues no se puede proporcionar la mejor atención si la jornada laboral es agotadora. Conclusiones: Los profesionales de enfermería ofrecen un cuidado aceptable a los pacientes oncológicos durante a la pandemia, pues afirman que tienen un protocolo de actuación adecuado y funcional que les brinda seguridad; sin embargo, existen factores como vulnerabilidad, equipo de protección y falta de personal que influyen en dicho grado de seguridad.

Introduction: The COVID-19 pandemic required nursing professionals to focus their attention on safeguarding the integrity, safety and health of cancer patients as well as their own. Objective: To analyze safety perception of professional nursing care for cancer patients during the COVID-19 contingency. Material and methods: Descriptive, cross-sectional observational study. Sample of 50 nursing professionals. Measurement was made according to the Hospital Survey on Patient Safety instrument adapted to the COVID-19 contingency context. The results were analyzed through descriptive statistics. Results: The safety level of professional nursing care for cancer patients during COVID-19 contingency was acceptable in 11 of 16 dimensions, according to the following scale: very poor, poor, acceptable, very good and excellent. Opportunity areas to improve safety of professional nursing care were identified: patient safety is put at risk when work pressure increases, staffing is not sufficient enough to deal with workload due to the pandemic, optimal patient care cannot be provided because of exhausting work schedules. Conclusions: Nursing professionals provide acceptable care for cancer patients during the pandemic, since they declare they have an adequate and functional action protocol that makes them feel secure; however, there are factors such as vulnerability, protective equipment and lack of personnel that influence this degree of safety.

Antitumor effects of a monoclonal antibody to human CCR9 in leukemia cell xenografts.

Tumor expression of certain chemokine receptors is associated with resistance to apoptosis, migration, invasiveness and metastasis. Because CCR9 chemokine receptor expression is very restricted in healthy tissue, whereas it is present in tumors of distinct origins including leukemias, melanomas, prostate and ovary carcinomas, it can be considered a suitable candidate for target-directed therapy. Here, we report the generation and characterization of 91R, a mouse anti-human CCR9 IgG2b monoclonal antibody that recognizes an epitope within the CCR9 N-terminal domain. This antibody inhibits the growth of subcutaneous xenografts from human acute T lymphoblastic leukemia MOLT-4 cells in immunodeficient Rag2(-/-) mice. Tumor size in 91R-treated mice was reduced by 85% compared with isotype-matched antibody-treated controls. Tumor reduction in 91R-treated mice was concomitant with an increase in the apoptotic cell fraction and tumor necrotic areas, as well as a decrease in the fraction of proliferating cells and in tumor vascularization. In the presence of complement or murine natural killer cells, 91R promoted in vitro lysis of MOLT-4 leukemia cells, indicating that this antibody might eliminate tumor cells via complement- and cell-dependent cytotoxicity. The results show the potential of the 91R monoclonal antibody as a therapeutic agent for treatment of CCR9-expressing tumors.

Maximal T cell-mediated antitumor responses rely upon CCR5 expression in both CD4(+) and CD8(+) T cells.

Immune responses against cancer rely upon leukocyte trafficking patterns that are coordinated by chemokines. CCR5, the receptor for chemotactic chemokines MIP1alpha, MIP1beta, and RANTES (CCL3, CCL4, CCL5), exerts major regulatory effects on CD4(+)- and CD8(+) T cell-mediated immunity. Although CCR5 and its ligands participate in the response to various pathogens, its relevance to tumoral immune control has been debated. Here, we report that CCR5 has a specific, ligand-dependent role in optimizing antitumor responses. In adoptive transfer studies, efficient tumor rejection required CCR5 expression by both CD4(+) and CD8(+) T cells. CCR5 activation in CD4(+) cells resulted in CD40L upregulation, leading to full maturation of antigen-presenting cells and enhanced CD8(+) T-cell crosspriming and tumor infiltration. CCR5 reduced chemical-induced fibrosarcoma incidence and growth, but did not affect the onset or progression of spontaneous breast cancers in tolerogenic Tg(MMTV-neu) mice. However, CCR5 was required for TLR9-mediated reactivation of antineu responses in these mice. Our results indicate that CCR5 boosts T-cell responses to tumors by modulating helper-dependent CD8(+) T-cell activation.

Chemokine receptor 2 blockade prevents asthma in a cynomolgus monkey model.

The pathophysiology of asthma is characterized by accumulation and activation of several cell types in the lung, which correlates with coordinated production of specific cytokines and chemokines. To study the effect of selective CCR2 chemokine receptor blockade on leukocyte recruitment to the lung and on bronchial function, we used a nonhuman primate model of allergic airway disease that closely resembles human asthma. Allergic cynomolgus monkeys were treated with the antagonist anti-CCR2 (CCR2-05) monoclonal antibody and then challenged with Ascaris suum antigen; the effect of antibody treatment on macrophage and eosinophil infiltration was determined. Pulmonary function was calculated by measurement of lung resistance and dynamic compliance. Local inflammatory responses were analyzed after intradermal challenge with A. suum antigen. CCL2 up-regulation in bronchoalveolar lavage (BAL) was analyzed by enzyme-linked immunosorbent assay, and in vitro CCR2-05 antagonistic activity was tested in monkey peripheral blood mononuclear cells using chemotaxis and calcium mobilization assays. The results show that neutralization of CCR2 reduces antigen-induced bronchial hyper-responsiveness and attenuates macrophage and eosinophil accumulation in the BAL of asthmatic monkeys. The results confirm that selective blockade of a single chemokine receptor involved in early stages of asthma can condition later disease stages and suggest the utility of anti-CCR2-neutralizing monoclonal antibodies in the treatment of asthma in man.

SOCS up-regulation mobilizes autologous stem cells through CXCR4 blockade.

The chemokine CXCL12 influences self-renewal and differentiation of hematopoietic stem cell precursors in bone marrow by directing them toward specific stromalcell components. CXCL12 up-regulates members of the SOCS family through JAK/STAT activation, a mechanism that attenuates chemokine responses. SOCS expression may thus modulate retention of hematopoietic precursors (Sca-1(+) c-Kit(+)Lin(-) cells) in bone marrow. We show that in bovine growth hormone transgenic mice and in growth hormone-treated mice, SOCS up-regulation correlated with a large number of Sca-1(+) c-Kit(+)Lin(-) cells in blood. Retroviral transduction of SOCSs blocked in vitro migration of Sca-1(+)c-Kit(+)Lin(-) cells, as well as their capacity to reconstitute lethally irradiated mice. Furthermore, in lethally irradiated mice reconstituted with bone marrow infected by a tetracycline-regulated, SOCS-expressing lentiviral vector, doxycycline treatment promoted rapid, extensive precursor mobilization to the periphery. The results indicate that by blocking CXCR4-mediated functions, SOCSs modulate hematopoietic precursor cell retention in bone marrow, and suggest the therapeutic interest of SOCS manipulation in several pathologic situations.

ZAP-70 upregulation in transformed B cells after early pre-BI cell transplant into NOD/SCID mice.

Understanding of the signal transduction pathways that lead to B cell development is of extreme interest to learn how alterations in these pathways might initiate malignant transformation. Long-term cultured early pre-BI cells can differentiate into IgM+ B cells after transplant into NOD/SCID mice, offering the possibility to explore checkpoints in B cell development. Using DNA microarray and Western blot analysis of IgM+ B cells vs parental early pre-BI cells, we demonstrated that zeta-associated protein 70 (ZAP-70) is upregulated in our B cell differentiation model. Unlike parental ZAP-70- early pre-BI cells, ZAP-70+ IgM+ B cells exhibited a transformed phenotype, as indicated by BCL-6 expression, a high Ki-67 proliferation index, resistance to IL-7 deprivation-induced apoptosis, and an increased repopulation rate in NOD/SCID mice. These data show the characterization and generation of a novel murine leukemia model with many similarities to human ZAP-70+ B cell chronic lymphocytic leukemia.

CCR6 regulates CD4+ T-cell-mediated acute graft-versus-host disease responses.

We studied the role of chemokine receptor CCR6 in acute graft-versus-host disease (GvHD), a pathology in which activated, host antigen-specific donor T cells selectively damage tissues such as skin, liver, and gut. GvHD incidence was reduced in major histocompatibility complex (MHC) class II-mismatched recipients of CD4+ T cells from CCR6-deficient donors. In MHC-matched/minor histocompatibility antigen-mismatched recipients of CD4+CD45RB(high) T cells from CCR6-deficient donors, infiltration of CD45+ and CD4+ cells to skin and gut, as well as lesion onset, were significantly delayed, and pathologic symptoms were milder. Consistent with this, in skin and gut of recipients of naive T cells from CCR6-deficient donors we observed lower levels of interferon gamma (IFN-gamma), interleukin 10 (IL-10), and the chemokines that control activated T-cell homing. We suggest a role for CCR6 in recruiting alloreactive CD4+ T cells to target tissues and identify CCR6 as a potential therapeutic target for GvHD.

CXCR4-mediated suppressor of cytokine signaling up-regulation inactivates growth hormone function.

Coordinated action between cytokines and chemokines is required for effective endocrine and immune responses. Proteins of both families promote receptor oligomerization, activation of the Janus kinase (JAK)/STAT pathway, and transcription of many genes, including the suppressor of cytokine signaling (SOCS) family. In this study, we show that chemokine-mediated SOCS1 and SOCS3 up-regulation modulates the signaling and function associated to a cytokine receptor, both in vitro and in vivo. The effect is mediated by SOCS binding to JAK2 and to the cytokine receptor, which blocks subsequent signaling events. The data reinforce the premise of cytokine-chemokine cross-talk, which helps contribute to modulating individual responses and in defining the functional plasticity of the immune system.

Leukocyte attraction through the CCR5 receptor controls progress from insulitis to diabetes in non-obese diabetic mice.

Lymphocyte infiltration to pancreatic islets is associated to chemoattraction, as are other inflammatory autoimmune processes. We examined whether development of insulitis and diabetes depends on chemoattraction of lymphocytes via the CCR5 chemokine receptor. In non-obese diabetic (NOD) mice, a substantial fraction of peripheral T cells and virtually all B cells expressed high CCR5 levels. CCR5 expression characterized the effector T cell phenotype, suggesting their potential involvement in disease development. In view of these findings and the CCL5 (RANTES, the CCR5 ligand) expression by pancreatic islets, we treated NOD mice with a neutralizing anti-CCR5 antibody. This did not influence peri-insulitis advancement, but inhibited beta-cell destruction and diabetes. These data demonstrate a role of CCR5-dependent chemoattraction in insulitis progression to islet destruction, suggesting the potential value of therapeutic intervention by CCR5 targeting.

Identification of amino acid residues crucial for chemokine receptor dimerization.

Chemokines coordinate leukocyte trafficking by promoting oligomerization and signaling by G protein-coupled receptors; however, it is not known which amino acid residues of the receptors participate in this process. Bioinformatic analysis predicted that Ile52 in transmembrane region-1 (TM1) and Val150 in TM4 of the chemokine receptor CCR5 are key residues in the interaction surface between CCR5 molecules. Mutation of these residues generated nonfunctional receptors that could not dimerize or trigger signaling. In vitro and in vivo studies in human cell lines and primary T cells showed that synthetic peptides containing these residues blocked responses induced by the CCR5 ligand CCL5. Fluorescence resonance energy transfer showed the presence of preformed, ligand-stabilized chemokine receptor oligomers. This is the first description of the residues involved in chemokine receptor dimerization, and indicates a potential target for the modification of chemokine responses.

Inhibition of programmed cell death impairs in vitro vascular-like structure formation and reduces in vivo angiogenesis.

Tissue remodeling during embryonic development and in the adult organism relies on a subtle balance between cell growth and apoptosis. As angiogenesis involves restructuring of preexisting endothelium, we examined the role of apoptosis in new vessel formation. We show that apoptosis occurs before capillary formation but not after vessels have assembled. Using the human umbilical vein endothelial cell (HUVEC) in vitro Matrigel angiogenesis model, we show that vascular-like structure formation requires apoptotic cell death through activation of a caspase-dependent mechanism and mitochondrial cytochrome c release. Vascular-like structure formation was further blocked by caspase inhibitors such as z-VAD or Ac-DEVD-CHO, using HUVEC and human lung microvascular endothelial cells. Overexpression of anti-apoptotic human Bcl-2 or baculovirus p35 genes in HUVEC altered endothelial cell rearrangement during in vitro angiogenesis, causing impaired vessel-like structure formation. Caspase inhibitors blocked VEGF- or bFGF-induced HUVEC angiogenesis on 2- or 3-D collagen gels, respectively, confirming that apoptosis was not the result of nonspecific cell death after seeding on the matrix. In an in vivo angiogenesis assay, caspase inhibitors blocked VEGF-dependent vascular formation at the alignment step, as demonstrated histologically. This evidence indicates that endothelial cell apoptosis may be relevant for precise vascular tissue rearrangement in in vitro and in vivo angiogenesis.

STAG2 and Rad21 mammalian mitotic cohesins are implicated in meiosis.

STAG/SA proteins are specific cohesin complex subunits that maintain sister chromatid cohesion in mitosis and meiosis. Two members of this family, STAG1/SA1 and STAG2/SA2,double dagger are classified as mitotic cohesins, as they are found in human somatic cells and in Xenopus laevis as components of the cohesin(SA1) and cohesin(SA2) complexes, in which the shared subunits are Rad21/SCC1, SMC1 and SMC3 proteins. A recently reported third family member, STAG3, is germinal cell-specific and is a subunit of the meiotic cohesin complex. To date, the meiosis-specific cohesin complex has been considered to be responsible for sister chromatid cohesion during meiosis. We studied replacement of the mitotic by the meiotic cohesin complex during mouse germinal cell maturation, and we show that mammalian STAG2 and Rad21 are also involved in several meiosis stages. Immunofluorescence results suggest that a cohesin complex containing Rad21 and STAG2 cooperates with a STAG3-specific complex to maintain sister chromatid cohesion during the diplotene stage of meiosis.