Process of nursing care in a post-operative patient of complete correction of Tetralogy of Fallot. Case study and literature review.

Tetralogy of Fallot is a congenital heart disease cyanotic common in childhood, whose surgical treatment has a high rate of success in the short and long term. Complications of surgical treatment may and should be corrected promptly, being crucial the nursing intervention in the evolution of the patient: sign valuations of right ventricular dysfunction, implementation of interventions for minimize the effects of this dysfunction, collaboration in the treatment of the entity and the constant evaluation of the patient. A case of a patient of 1 year and 5 months, is presented where after a cardiac valuation and an electrocardiogram is diagnosed with Tetralogy of Fallot, and you are subsequently underwent surgery without reporting no complications during the surgery. They were handled several diagnoses nursing, with objectives to be followed and specific interventions carried out according to the presentation of the manifestations of the patient in the study.La Tetralogía de Fallot es una cardiopatía congénita cianógena frecuente en la infancia, cuyo tratamiento quirúrgico presenta alta tasa de éxito a corto y largo plazos. Las complicaciones del tratamiento quirúrgico pueden y deben ser corregidas oportunamente, siendo crucial la intervención de enfermería en la evolución del paciente: valoración de signos de disfunción ventricular derecha, ejecución de intervenciones para minimizar los efectos de dicha disfunción, colaboración en el tratamiento de la entidad y la evaluación constante del paciente. Se presenta un caso de un paciente de 1 año y 5 meses, donde después de una valoración cardiológica y un electrocardiograma se le diagnostica Tetralogía de Fallot, y posteriormente fue intervenido quirúrgicamente sin reportarse ninguna complicación durante la cirugía. Se manejaron diagnósticos de enfermería, con objetivos a seguir e intervenciones específicas que se realizaron de acuerdo con la presentación de las manifestaciones del paciente en estudio

Linkage studies with chromosome 17 DNA markers in 45 neurofibromatosis 1 families

A locus for von Recklinghausen neurofibromatosis (NF1) has recently been mapped near the chromosome 17 centromere. We have extended these linkage studies by genotyping 45 NF1 families with three DNA probes known to be linked to the chromosome 17 centromeric region. Of 34 families informative for NF1 and at least one of the three probes, 28 families show no recombinants with the disease gene. These data provide additional support for genetic homogeneity of NF1 and for a primary NF1 locus linked to the chromosome 17 centromere. Among the informative families were 7 families with apparent new NF1 mutations. Our data suggest that these mutations are probably at the chromosome 17 NF1 locus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26487/1/0000023.pd

Loss of Sialic Acid Binding Domain Redirects Protein σ1 to Enhance M Cell-Directed Vaccination

Ovalbumin (OVA) genetically fused to protein sigma 1 (pσ1) results in tolerance to both OVA and pσ1. Pσ1 binds in a multi-step fashion, involving both protein- and carbohydrate-based receptors. To assess the relative pσ1 components responsible for inducing tolerance and the importance of its sialic binding domain (SABD) for immunization, modified OVA-pσ1, termed OVA-pσ1(short), was deleted of its SABD, but with its M cell targeting moiety intact, and was found to be immunostimulatory and enhanced CD4+ and CD8+ T cell proliferation. When used to nasally immunize mice given with and without cholera toxin (CT) adjuvant, elevated SIgA and serum IgG responses were induced, and OVA-pσ1(s) was more efficient for immunization than native OVA+CT. The immune antibodies (Abs) were derived from elevated Ab-forming cells in the upper respiratory tissues and submaxillary glands and were supported by mixed Th cell responses. Thus, these studies show that pσ1(s) can be fused to vaccines to effectively elicit improved SIgA responses

Attenuated Coxiella burnetii Phase II Causes a Febrile Response in Gamma Interferon Knockout and Toll-Like Receptor 2 Knockout Mice and Protects against Reinfection▿

Coxiella burnetii is a highly infectious obligate intracellular bacterium. The phase I form is responsible for Q fever, a febrile illness with flu-like symptoms that often goes undiagnosed. The attenuated C. burnetii phase II (having a truncated “O” chain of its lipopolysaccharide) does not cause disease in immunocompetent animals; however, phase II organisms remain infectious, and we questioned whether disease could be produced in immunodeficient mice. To study C. burnetii phase II infections, febrile responses in gamma interferon knockout (IFN-γ−/−), BALB/c, Toll-like receptor 2 knockout (TLR2−/−), and C57BL/6 mice were measured using the Nine Mile phase II (NMII) strain of C. burnetii. Immunocompetent mice showed minimal febrile responses, unlike those obtained with IFN-γ−/− and TLR2−/− mice, which showed elevated rectal temperatures that were sustained for ∼15 days with transient increases in splenic weights. Reinfection of IFN-γ−/− and TLR2−/− mice with C. burnetii NMII 30 days after primary infection protected mice as evident by reduced febrile responses and a lack of splenic inflammation. Although minimal detection of Coxiella in TLR2−/− mouse spleens was observed, greater colonization was evident in the IFN-γ−/− mice. Cytokine analysis was performed on infected peritoneal macrophages isolated from these mice, and immunocompetent macrophages showed robust tumor necrosis factor alpha, IFN-γ, and granulocyte-macrophage colony-stimulating factor (GM-CSF) but no interleukin-12 (IL-12) responses. IFN-γ−/− macrophages produced elevated levels of IL-6, IL-10, and IL-12, while TLR2−/− macrophages produced GM-CSF, IL-12, and minimal IL-10. To distinguish immunity conferred by innate or adaptive systems, adoptive transfer studies were performed and showed that immune lymphocytes obtained from immunocompetent mice protected against a subsequent challenge with NMII, indicating that adaptive immunity mediates the observed protection. Thus, our data show that NMII is capable of eliciting disease in immunocompromised mice, which may help in evaluation of vaccine candidates as well as the study of host-pathogen interactions

OVA-pσ1(s) is 5 times more effective per molar basis than native OVA in stimulating immune Abs.

<p>Groups of C57BL/6 mice (9/group) were immunized nasally with 30 µg OVA-pσ1(s) alone, 30 µg OVA-pσ1(s) plus cholera toxin (CT), or 100 µg OVA plus CT using the vaccination schedule described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0036182#pone-0036182-g004" target="_blank">Fig. 4</a>. <b>A.–D.</b> Although mice immunized with OVA-pσ1(s) alone consistently produced less Ag-specific Abs, CT co-administration enhanced anti-OVA endpoint titers than the 100 µg OVA plus CT-immunized group: <b>A.</b> serum IgG, <b>B.</b> serum IgA, <b>C.</b> fecal IgA, and <b>D.</b> day 35 nasal wash IgA and IgG endpoint anti-OVA Ab titers. A kinetic analysis of the indicated time points is depicted from two experiments as mean ± SEM; *<i>P</i><0.001, **<i>P</i>≤0.012 versus OVA plus CT-immunized mice; and ^†<i>P</i><0.001 versus nasal wash titers from OVA-pσ1(s) plus CT-immunized mice.</p