um cuidado especializado do enfermeiro obstetra

Observa-se, hoje em dia, que algumas práticas na maternidade tendem a ignorar as preferências das mulheres em trabalho de parto, uniformizando os cuidados com prejuízo para o bem-estar e a qualidade de vida das famílias. As práticas em Obstetrícia têm vindo a tornar-se cada vez mais repletas de intervenção, focando-se apenas nos resultados físicos (mortalidade e morbilidade) e descurando as vivências das parturientes e família, assim como as consequências psicossociais de um parto traumático. O presente Relatório de Estágio pretende refletir os cuidados em maternidade na perspetiva EEESMOG, que se visa holística, centrada no cliente e baseada na evidência. Da mesma forma, espelha as aprendizagens efetuadas em contexto do Estágio com Relatório inserido no 6º CMESMO da ESEL. Foram escolhidos como referenciais teóricos norteadores os modelos de Nola Pender – Modelo de Promoção da Saúde, e a Teoria de Empowerment em Saúde de Nelma Shearer. Foi também realizada uma Revisão Sistemática da Literatura que visou responder à seguinte questão de investigação: “Quais os cuidados do EEESMOG promotores do empowerment das mulheres direcionado para uma tomada de decisão informada relativa ao trabalho de parto?”. Adicionalmente, foi efetuado um registo da interação durante a prestação de cuidados no decorrer do estágio, sobre os quais foi efetuada uma reflexão e confrontação com os resultados da RSL. Concluiu-se que os cuidados que o EEESMOG presta que são promotores de uma tomada de decisão informada para o trabalho de parto se inserem dentro de três grandes temas, nomeadamente Competências da esfera relacional, Competências da esfera da prática clínica e Competências da esfera científica, com especial referência para os cuidados que se relacionam com o Estabelecimento de Relação Terapêutica, a Educação para a Saúde, o Cuidado da Mulher em trabalho de parto, a Promoção do exercício do Consentimento Informado e a Prática baseada na Evidência

Cell phone-generated radio frequency electromagnetic field effects on the locomotor behaviors of the fishes <i>Poecilia reticulata</i> and <i>Danio rerio</i>

<div><p><i>Purpose</i>: The locomotor behavior of small fish was characterized under a cell phone-generated radio frequency electromagnetic field (RF EMF).</p><p><i>Materials and methods</i>: The trajectory of movement of 10 pairs of guppy (<i>Poecilia reticulate</i>) and 15 pairs of Zebrafish (<i>Danio rerio</i>) in a fish tank was recorded and tracked under the presence of a cell phone-generated RF EMF. The measures were based on spatial and temporal distributions. A time-series trajectory was utilized to emphasize the dynamic nature of locomotor behavior. Fish movement was recorded in real-time. Their spatial, velocity, turning angle and sinuosity distribution were analyzed in terms of <i>F</i>(<i>v,x</i>), <i>P</i>[<i>n</i>(<i>x,t</i>)], <i>P</i>(<i>v</i>), <i>F</i> (θ) and <i>F</i>(<i>s</i>), respectively. In addition, potential temperature elevation caused by a cellular phone was also examined.</p><p><i>Results</i>: We demonstrated that a cellular phone-induced temperature elevation was not relevant, and that our measurements reflected RF EMF-induced effects on the locomotor behavior of <i>Poecilia reticulata</i> and <i>Danio rerio</i>. Fish locomotion was observed under normal conditions, in the visual presence of a cell phone, after feeding, and under starvation. Fish locomotor behavior was random both in normal conditions and in the presence of an off-signaled cell phone. However, there were significant changes in the locomotion of the fish after feeding under the RF EMF.</p><p><i>Conclusions</i>: The locomotion of the fed fish was affected in terms of changes in population and velocity distributions under the presence of the RF EMF emitted by the cell phone. There was, however, no significant difference in angular distribution.</p></div

Id Proteins Regulate Capillary Repair and Perivascular Cell Proliferation following Ischemia-Reperfusion Injury - Table 1

<p>Id Proteins Regulate Capillary Repair and Perivascular Cell Proliferation following Ischemia-Reperfusion Injury - Table 1 </p

Doxycycline induced β-galactosidase expression is localized in interstitial cells in areas of collagen deposition in TRE Id1/Tie2-rtTA/TRE lacz mice but not in Tie2-rtTA/TRE lacz mice 7 days following IRI.

<p>Mice (n = 5/group) were fed doxycycline for indicated time prior to IRI. Mice were fed chow diets and sacrificed 7 days following IRI. X-gal (blue) followed by Picro Sirius Red staining for collagen of kidney cryosections for genotypes/doxycycline treatment: A) Control TRE Id1/Tie2-rtTA/TRE lacz mouse/doxycycline × 1 week, arrowhead: glomerular arteriole, B) IR day 7 TRE Id1/Tie2-rtTA/TRE lacz mouse, doxycycline × 1 week, arrows: capillary endothelial cells, C) IR day 7 TRE Id1/Tie2-rtTA/TRE lacz mouse, doxycycline × 2 weeks, arrows: capillary endothelial cells, D) IR day 7 TRE Id1/Tie2-rtTA/TRE lacz mouse, doxycycline × 4 weeks, arrowheads: area of medullary collagen deposition, E) High power magnification of area outlined in (D), F) IR day 7 Tie2-rtTA/TRE lacz mouse, doxycycline ×4 weeks, arrows: capillary endothelial cells. Original magnification: 400X (A–C, E–F), 100X (D).</p

Medullary collagen deposition in TRE Id1/Tie2-rtTA mice is increased at 42 days following IRI compared with WT mice.

<p>A) Western blot of Id1 expression and corresponding densitometry in WT control (lanes 1–2), WT day 42 post IRI (lanes 3–6), Id1/Id3 KO day 42 post IRI (lanes 7–9) and TRE Id1 day 42 post IR (lanes 10–14) with β-tubulin as loading control *p<.05, *p<.001 B) Representative Sirius Red stained sections of WT, Id1/Id3 KO and TRE Id1/Tie2-rtTA mice at 42 days following IRI and comparison of areas of collagen deposits shown as mean +/− SEM for 5–7 mice/genotype group. *p = .05 compared with TRE Id1 control. C) Ki67 positive peritubular interstitial cells (nuclei/low power field: 40X) at indicated time points following IRI. *p = .003, **p = .01 compared with WT control. D) Kidney weight (mg) normalized to total body weight (grams) at 42 days following IRI compared with contralateral kidney weights at nephrectomy/ischemia surgery. *p<.01, **p<.0001. E) Plasma creatinine (means +/− SEM) levels for control mice and 42 days following IRI *p = .05 for Id1/Id3 KO vs. TRE Id1 mice (unpaired two-tailed t-test). F) Urine albumin/creatinine ratios for spot urine samples at 42 days following IRI.</p

Transgenic mice have doxycycline inducible endothelial Id1 expression in normal kidneys and following IRI.

<p>A) Western blot of Id1 expression in control kidneys from mice with indicated genotype: Id1−/−, Id3RFP/+ = Id1/Id3 knockout (KO), wild-type littermate = WT, TRE Id1 = TRE Id1, Tie2 rtTA mice. Mice were fed doxycycline (+ doxy) for 1 week before isolation of kidney tissue or ischemia-perfusion injury. Control chow fed TRE Id1 mice (− doxy, lane 2) did not demonstrate ‘leaky’ Id1 expression compared with WT mice (lane 3). B) Densitometry of kidney Id1 levels from control (con) and day 7 following IRI (IRD7) TRE Id1 mice (n = 3/group) compared with WT control littermates. *p = .01, **p<.001 (unpaired two-tailed t-test).</p

Id1 and 3 are co-localized in kidney endothelial cells and expression levels are transiently increased following ischemia-reperfusion injury (IRI).

<p>Immunofluorescence images for indicated antigens of normal (A–E) and 3 days post ischemia-reperfusion injury (F) kidneys from Id1+/+, Id3RFP/+ (C–F) and wild-type (WT) (A–B) mice. Red fluorescent protein (RFP) signal corresponds with Id3 expression. A) Green: Id1, red: CD31, arrows: Id1 negative, CD31 positive cells, arrowheads: Id1 low, CD 31 positive cells, B) Green: Id1, red: PDGFRβ, arrows: Id1 negative, PDGFRβ positive cells, C) Green: CD31, red: Id3RFP, arrows: double positive cells, D) Green: PDGFRβ, red: Id3RFP, arrows: single PDGFRβ positive cells, arrowheads: double positive mesangial cells, E) Green: Id1, red: Id3RFP, yellow: double positive cells in glomeruli (arrow) and interstitium (arrowhead), F) Green: Id1, red: Id3RFP, yellow: double positive cells in interstitium (arrows) 3 days following IRI, Original magnification: 400X. Representative Western blots of Id1 (G) and Id3 (H) expression following ischemia-reperfusion at indicated time points with corresponding densitometry from 5 mice for each time point. *p<.05 (unpaired two-tailed t-test).</p

Id1/Id3 knockout mice have increased tubular damage following IRI compared with WT and Id1 transgenic mice.

<p>Hematoxylin and eosin staining of kidney sections from WT (A), Id1/Id3 KO (B) and TRE Id1 (C) mice at day 3 following IRI with corresponding assessment of tubular damage expressed as tubular injury index (1–5) (D) from 5 mice (mean +/− SEM) in each genotype *p<.01. Ki67 staining of from WT (E), Id1/Id3 KO (F) and TRE Id1 (G) mice at day 3 following IRI with corresponding cell counts (H) from 5 mice (Ki67 positive cells/HPF from 10 fields/kidney, mean +/− SEM) in each genotype *p<.001 (unpaired two-tailed t-test). Original magnification = 400X.</p

Id1/Id3 knockout mice have decreased baseline capillary density and Id1 transgenic mice have decreased capillary rarefaction 7 days following IRI followed by increased rarefaction at 42 days following IRI compared with WT mice.

<p>A) Immunofluorescence labeling of CD31 on outer medullary peritubular capillaries in normal kidneys (con) and at day 7 following IRI (IRD7) of indicated genotypes. B) Capillary rarefaction index (% area with no CD31 staining using 100 square grid) following IRI at indicated time points. *p<.001, **p = .04 compared with WT control kidneys (one way ANOVA with Tukey HSD test).</p

Angiopoietin 1 levels are increased in TRE Id1 mice and Angiopoietin 2 levels are decreased following IRI in knockout and transgenic mice.

<p>A) Comparative PCR expressed as levels relative to WT control kidneys for Ang1 levels in control and day 7 post IRI kidneys of WT, Id1/Id3 KO, and TRE Id1 mice. *p<.05, **p<.01. B) Western blot of Ang2 levels in control and day 7 post IRI kidneys of WT, Id1/Id3 KO, and TRE Id1 mice. Results expressed as levels relative to WT control kidneys. *p<.001, **p<.05. (one way ANOVA with Tukey HSD test).</p