Enrichment of hepatic glycogen and plasma glucose from H218 O informs gluconeogenic and indirect pathway fluxes in naturally feeding mice.

Deuterated water (2 H2 O) is a widely used tracer of carbohydrate biosynthesis in both preclinical and clinical settings, but the significant kinetic isotope effects (KIE) of 2 H can distort metabolic information and mediate toxicity. 18 O-water (H2 18 O) has no significant KIE and is incorporated into specific carbohydrate oxygens via well-defined mechanisms, but to date it has not been evaluated in any animal model. Mice were given H2 18 O during overnight feeding and 18 O-enrichments of liver glycogen, triglyceride glycerol (TG), and blood glucose were quantified by 13 C NMR and mass spectrometry (MS). Enrichment of oxygens 5 and 6 relative to body water informed indirect pathway contributions from the Krebs cycle and triose phosphate sources. Compared with mice fed normal chow (NC), mice whose NC was supplemented with a fructose/glucose mix (i.e., a high sugar [HS] diet) had significantly higher indirect pathway contributions from triose phosphate sources, consistent with fructose glycogenesis. Blood glucose and liver TG 18 O-enrichments were quantified by MS. Blood glucose 18 O-enrichment was significantly higher for HS versus NC mice and was consistent with gluconeogenic fructose metabolism. TG 18 O-enrichment was extensive for both NC and HS mice, indicating a high turnover of liver triglyceride, independent of diet. Thus H2 18 O informs hepatic carbohydrate biosynthesis in similar detail to 2 H2 O but without KIE-associated risks.

p-Aminobenzoic acid as an alternative chemical biopsy agent for human hepatic UDP-glucose.

p-Aminobenzoic acid (PABA) was evaluated for noninvasive sampling of UDP-glucose in the liver. Six healthy subjects ingested 550 mg PABA during a breakfast meal. Urine was collected 0-2 and 2-4 h after PABA ingestion. N-acetyl PABA glucuronide (NAPG) was identified with 522 ± 212 µmol recovered in the 2-4 h urines. One of the subjects ingested 2 g of 98% [U-2H7]glucose alongside PABA and the NAPG was analyzed for positional 2H-enrichment by 2H NMR following derivatization to 5-O-acetyl monoacetone glucuronolactone. In conclusion, PABA is an effective agent for the chemical biopsy of hepatic UDP-glucose in humans.

The role of microtubules and their dynamics in cell migration.

Although microtubules have long been implicated in cell locomotion, the mechanism of their involvement remains controversial. Most studies have concluded that microtubules play a positive role by regulating actin polymerization, transporting membrane vesicles to the leading edge, and/or facilitating the turnover of adhesion plaques. Here we used wild-type and mutant CHO cell lines with alterations in tubulin to demonstrate that microtubules can also act to restrain cell motility. Tubulin mutations or low concentrations of drugs that suppress microtubule dynamics without affecting the amount of microtubule polymer inhibited the rate of migration by preventing microtubule reorganization in the trailing portion of the cells where the more dynamic microtubules are normally found. Under these conditions, cells along the edge of a wound still extended lamellipodia and elongated toward the wound but were inhibited in their ability to retract their tails, thus retarding forward progress. The idea that microtubules normally act to restrain cell locomotion was confirmed by treating cells with high concentrations of nocodazole to depolymerize the microtubule network. In the absence of microtubules, wild-type CHO and HeLa cells could still move at near normal speeds, but the movement became more random. We conclude that microtubules act both to restrain cell movement and to establish directionality.

Mitotic centromere-associated kinesin (MCAK) mediates paclitaxel resistance.

Paclitaxel has powerful anticancer activity, but some tumors are inherently resistant to the drug, whereas others are initially sensitive but acquire resistance during treatment. To deal with this problem, it will be necessary to understand the mechanisms of drug action and resistance. Recent studies indicate that paclitaxel blocks cell division by inhibiting the detachment of microtubules from centrosomes. Here, we demonstrate that mitotic centromere-associated kinesin (MCAK), a kinesin-related protein that destabilizes microtubules, plays an important role in microtubule detachment. Depletion of MCAK altered mitotic spindle morphology, increased the frequency of lagging chromosomes, and inhibited the proliferation of WT CHO cells, confirming that it is an essential protein for cell division. In contrast, MCAK depletion rescued the proliferation of mutant paclitaxel-dependent cell lines that are unable to divide because of defective spindle function resulting from altered α-tubulin or class III ß-tubulin overexpression. In concert with the correction of mitotic defects, loss of MCAK reversed an aberrantly high frequency of microtubule detachment in the mutant cells and increased their sensitivity to paclitaxel. The results indicate that MCAK affects cell sensitivity to mitotic inhibitors by modulating the frequency of microtubule detachment, and they demonstrate that changes in a microtubule-interacting protein can reverse the effects of mutant tubulin expression.

New insights into mechanisms of resistance to microtubule inhibitors.

Mechanisms to explain tumor cell resistance to drugs that target the microtubule cytoskeleton have relied on the assumption that the drugs act either to suppress microtubule dynamics or to perturb the balance between assembled and nonassembled tubulin. Recently, however, it was found that these drugs also alter the stability of microtubule attachment to centrosomes, and do so at the same concentrations that are needed to inhibit cell division. Based on this new information, a new model is presented that explains resistance resulting from a variety of molecular changes that have been reported in the literature. The improved understanding of drug action and resistance has important implications for chemotherapy with these agents.

Random mutagenesis of ß-tubulin defines a set of dispersed mutations that confer paclitaxel resistance.

PURPOSE: Previous research showed that mutations in ß1-tubulin are frequently involved in paclitaxel resistance but the question of whether the mutations are restricted by cell-type specific differences remains obscure. METHODS: To circumvent cellular constraints, we randomly mutagenized ß-tubulin cDNA, transfected it into CHO cells, and selected for paclitaxel resistance. RESULTS: A total of 26 ß1-tubulin mutations scattered throughout the sequence were identified and a randomly chosen subset were confirmed to confer paclitaxel resistance using site-directed mutagenesis of ß-tubulin cDNA and transfection into wild-type cells. Immunofluorescence microscopy and biochemical fractionation studies indicated that cells expressing mutant tubulin had decreased microtubule polymer and frequently suffered mitotic defects that led to the formation of large multinucleated cells, suggesting a resistance mechanism that involves destabilization of the microtubule network. Consistent with this conclusion, the mutations were predominantly located in regions that are likely to be involved in lateral or longitudinal subunit interactions. Notably, fourteen of the new mutations overlapped previously reported mutations in drug resistant cells or in patients with developmental brain abnormalities. CONCLUSIONS: A random mutagenesis approach allowed isolation of a wider array of drug resistance mutations and demonstrated that similar mutations can cause paclitaxel resistance and human neuronal abnormalities.

Inhibition of cell migration and cell division correlates with distinct effects of microtubule inhibiting drugs.

Drugs that target microtubules are thought to inhibit cell division and cell migration by suppressing dynamic instability, a "search and capture" behavior that allows microtubules to probe their environment. Here, we report that subtoxic drug concentrations are sufficient to inhibit plus-end microtubule dynamic instability and cell migration without affecting cell division or microtubule assembly. The higher drug concentrations needed to inhibit cell division act through a novel mechanism that generates microtubule fragments by stimulating microtubule minus-end detachment from their organizing centers. The frequency of microtubule detachment in untreated cells increases at prophase suggesting that it is a regulated cellular process important for spindle assembly and function. We conclude that drugs produce differential dose-dependent effects at microtubule plus and minus-ends to inhibit different microtubule-mediated functions.

Caferana seeds (Bunchosia glandulifera) as a new source of nutrients: Evaluation of the proximal composition, solvent extraction, bioactive compounds, and δ-lactam isolation.

The proximal composition, amino acid, carbohydrate, and volatile profiles of caferana (Bunchosia glandulifera) seeds flour were here assessed. Seeds were also subjected to the following extraction processes: one with pressurized ethanol (PLE) and two with ethanol + supercritical CO2 mixture at different temperatures and pressures (SC1 and SC2). Extracts were characterized in terms of caffeine, total phenolic, and δ-lactam. The characterization of caferana seed and its extracts is unprecedented in terms of carbohydrate and volatiles profiles, besides the δ-lactam identification/isolation. SC2 extract exhibited a higher caffeine (9.3 mg/g) and δ-lactam (29.4 mg/g) content, whereas the PLE extract contained a higher total phenolic amount (3.0 mgGAE/g). Caferana is regionally associated to protective effects on mental health. Its byproduct (seed) revealed to be a promising source of bioactive compounds, and a potential raw material of nutritive extracts and flours that can be incorporated into pharmaceutical, nutraceutical, cosmetic, and food products.

Femoral torsion evaluation by computed tomography in a young Brazilian population with hip pain and femoroacetabular impingement.

INTRODUCTION: The aim of the study was to evaluate femoral torsion (FT) by computed tomography (CT) in young patients with hip pain and femoroacetabular impingement (FAI) in a Brazilian population. After the diagnosis of impingement, the complete analysis from the hip biomechanics and morphology has become essential. METHODS: Forty-one patients from 18 to 45 years presenting hip pain without arthrosis (Tönnis<2) were evaluated by CT scan from February 2017 to February 2018. All patients presented hip pain for at least 3 months and FAI. They have followed the same radiographic protocol and modified Harris Hip Score (mHHS) evaluation. Statistical analyses by software R version 3.4.4. with significance p < 0,05. RESULTS: After exclusion criterias, twenty-six patients (9 bilateral) were included, mostly man (73%). The average age was 35 years for both genders. BMI was 19 kg/m2 for women and 24 kg/m2 for men and the mean modified Harris Hip Score was 67 points. We have found femoral torsion changes in 11 hips with pain (31%) and high variability (60%). The mean FT was 14,5°, ranging from 0 to 39°. Patients with hip pain, CAM impingement and altered FT had no correlation when compared to controls (without pain) (p = 0.234), neither Mixed impingement (p = 0.314). Patients with Pincer impingement and painful hips had higher FT (16,63°) than controls (11,77°) (p = 0.045). Conclusion: The presence of torsional alterations in almost 1/3 of the patients with FAI and the high variability reveal the importance of measuring FT at this disease.

A minor beta-tubulin essential for mammalian cell proliferation.

Mammals use tubulin from multiple genes to construct microtubules. Some genes are expressed in a tissue specific manner, while others are expressed in almost all cell types. beta5-Tubulin is a minor, ubiquitous isoform whose overexpression was recently shown to disrupt microtubules. Using inhibitory RNA, we now report that suppression of beta5 production in both human and hamster cells blocks cell proliferation. Cells depleted of beta5 either trigger the mitotic checkpoint and undergo apoptosis; or they experience a transient mitotic block, a high incidence of lagging chromosomes, and progression into G1 without cytokinesis to become large, flat cells with elevated DNA content. Microtubules appear to be normally organized in cells depleted of beta5, but they are rich in acetylated alpha-tubulin indicating that they may be more stable than normal. The results provide the first evidence that a specific isoform of beta-tubulin is required for mitosis.

Amino acid substitutions at proline 220 of beta-tubulin confer resistance to paclitaxel and colcemid.

Chinese hamster ovary cells selected for resistance to paclitaxel have a high incidence of mutations affecting L215, L217, and L228 in the H6/H7 loop region of beta1-tubulin. To determine whether other mutations in this loop are also capable of conferring resistance to drugs that affect microtubule assembly, saturation mutagenesis of the highly conserved P220 codon in beta1-tubulin cDNA was carried out. Transfection of a mixed pool of plasmids encoding all possible amino acid substitutions at P220 followed by selection in paclitaxel produced cell lines containing P220L and P220V substitutions. Similar selections in colcemid, on the other hand, yielded cell lines with P220C, P220S, and P220T substitutions. Site-directed mutagenesis and retransfection confirmed that these mutations were responsible for drug resistance. Expression of tubulin containing the P220L and P220V mutations reduced microtubule assembly, conferred resistance to paclitaxel and epothilone A, but increased sensitivity to colcemid and vinblastine. In contrast, tubulin with the P220C, P220S, and P220T mutations increased microtubule assembly, conferred resistance to colcemid and vinblastine, but increased sensitivity to paclitaxel and epothilone A. The results are consistent with molecular modeling studies and support a drug resistance mechanism based on changes in microtubule assembly that counteract the effects of drug treatment. These studies show for the first time that different substitutions at the same amino acid residue in beta1-tubulin can confer cellular resistance to either microtubule-stabilizing or microtubule-destabilizing drugs.

A ubiquitous beta-tubulin disrupts microtubule assembly and inhibits cell proliferation.

Vertebrate tubulin is encoded by a multigene family that produces distinct gene products, or isotypes, of both the alpha- and beta-tubulin subunits. The isotype sequences are conserved across species supporting the hypothesis that different isotypes subserve different functions. To date, however, most studies have demonstrated that tubulin isotypes are freely interchangeable and coassemble into all classes of microtubules. We now report that, in contrast to other isotypes, overexpression of a mouse class V beta-tubulin cDNA in mammalian cells produces a strong, dose-dependent disruption of microtubule organization, increased microtubule fragmentation, and a concomitant reduction in cellular microtubule polymer levels. These changes also disrupt mitotic spindle assembly and block cell proliferation. Consistent with diminished microtubule assembly, there is an increased tolerance for the microtubule stabilizing drug, paclitaxel, which is able to reverse many of the effects of class V beta-tubulin overexpression. Moreover, transfected cells selected in paclitaxel exhibit increased expression of class V beta-tubulin, indicating that this isotype is responsible for the drug resistance. The results show that class V beta-tubulin is functionally distinct from other tubulin isotypes and imparts unique properties on the microtubules into which it incorporates.

Paclitaxel resistance in cells with reduced beta-tubulin.

We previously described the isolation of colcemid resistant Chinese hamster ovary cell lines containing alpha- and beta-tubulin mutations that increase microtubule assembly and stability. By analyzing colcemid sensitive revertants from one of the beta-tubulin mutants, we now find that loss or inactivation of the mutant allele represents the most common mechanism of reversion. Consistent with this loss, the revertants have 35% less tubulin at steady state, no evidence for the presence of a mutant polypeptide, and a normal extent of tubulin polymerization. In addition to the loss of colcemid resistance, the revertant cells exhibit increased resistance to paclitaxel relative to wild-type cells. This paclitaxel resistance can be suppressed by transfecting the revertant cells with a cDNA for wild-type beta-tubulin, indicating that the reduction in tubulin in the revertant cells is responsible for the resistance phenotype. We propose that reducing tubulin levels may represent a novel mechanism of paclitaxel resistance.

Varicella zoster in Guinea-Bissau: intensity of exposure and severity of infection.

OBJECTIVE: To describe the epidemiology of and risk factors for severe chickenpox in Guinea- Bissau. METHODS: A prospective household study in a semiurban area of the capital. Severity was assessed by number of pox, fever response and presence of pneumonia. Severity was compared for the first case in a house, that is, the index case, and the secondary cases infected at home. RESULT: We identified 1539 cases of chickenpox. The median age was lower for boys and secondary cases (both P < 0.03); 44.6% of children were 1-4 years of age. The likely minimum interval between index and secondary cases was 10 days; most secondary cases occurred 14-17 days after the index case. The length of the incubation period was related to the intensity of exposure (P < 0.01). The number of pox was higher for secondary cases (P < 0.01) and was related to intensity of exposure (P < 0.01). Secondary cases had higher fever and more frequently pneumonia (relative risk, 2.17; 95% confidence interval, 1.54-3.08). Children with pneumonia were younger and had more pox. Nutritional status was not related to severity. CONCLUSIONS: Age and intensity of exposure are important determinants for severity of chickenpox infection. The length of the incubation period depends on intensity of exposure, suggesting that the dose of infection might be important.

Mutations in alpha- and beta-tubulin that stabilize microtubules and confer resistance to colcemid and vinblastine.

Single-step selections were used to obtain Chinese hamster ovary cell lines resistant to Colcemid and vinblastine. Verapamil was included in the selections to circumvent the isolation of cells with P-glycoprotein-mediated multidrug resistance and thereby enrich for cells with tubulin alterations. The isolated cell lines were 2-fold resistant to the selecting drug, exhibited cross-resistance to other drugs that inhibit microtubule assembly, and had enhanced sensitivity to the microtubule-stabilizing drug paclitaxel. The concomitant resistance to microtubule-destabilizing drugs and enhanced sensitivity to paclitaxel suggested that these cell lines have changes in microtubule assembly. Consistent with this interpretation, drug-resistant cell lines exhibited altered alpha- or beta-tubulin mobility on two-dimensional gels and higher levels (47-54%) of assembled tubulin compared with wild-type (39%) or paclitaxel-resistant cells (25%). Some drug-resistant cells also had bundled microtubules as judged by immunofluorescence. Genomic sequencing of 11 drug-resistant cell lines predicted five different alterations (D45Y, C211F, D224N, S234N, and K350N) in beta-tubulin and four different alterations (H283Y, E55K, A383V, and R390C) in alpha-tubulin. The amino acid substitutions are dispersed on the primary and tertiary structures of tubulin and, together with the other mutant properties, argue against a mechanism involving changes in drug binding. Rather, we propose that the alterations in alpha- and beta-tubulin increase microtubule stability by promoting longitudinal interdimer and intradimer interactions and/or lateral interactions between protofilaments. This enhanced stability of microtubules increases their resistance to drugs that inhibit assembly.

Peloruside A is a microtubule-stabilizing agent with exceptional anti-migratory properties in human endothelial cells.

Peloruside A is a novel antimitotic drug originally isolated from the marine sponge Mycale hentschieli. Previous studies showed that peloruside A stabilizes microtubules by binding to a site on tubulin distinct from paclitaxel, another microtubule stabilizing drug. Peloruside A blocks mitosis, but little is known about the effects on other cellular activities. Here we report that peloruside A is the most potent microtubule inhibitor yet tested for its ability to block endothelial cell migration. Quantitative analysis indicated that it inhibits microtubule dynamics and endothelial cell migration at 1/200(th) of the concentration needed to inhibit cell division (the cytotoxic concentration), indicating that it could potentially have a large margin of safety when used to specifically target angiogenesis. By comparison, paclitaxel, a well-known cancer therapeutic drug, suppresses cell migration at 1/13(th) of its cytotoxic concentration; and vinblastine suppresses cell migration at just slightly below its cytotoxic antimitotic concentration. Thus, different microtubule targeted drugs have varying relative potencies for inhibition of cell migration versus cell division. The results suggest that peloruside A may be an especially useful agent for anti-angiogenesis therapy and point to the likelihood that other antimitotic drugs might be found with an even larger potential margin of safety.

Enfermagem e a educação em saúde / Nursing and health education

Introdução: A educação em saúde promove uma estratégia que potencializa o cuidado de enfermagem ao envolver atividades educativas na assistência ao paciente. Objetivo: Refletir sobre as ações de educação em saúde realizadas pela enfermagem e, a construção do vínculo para transferência de conhecimento científico voltado para a área. Método: O texto é uma revisão narrativa realizada com base em periódicos nacionais e internacionais. As bases consultadas foram: Literatura Latino-Americana e do Caribe em Ciências da Saúde (LILACS), Biblioteca Regional de Medicina (BIREME) e Biblioteca Virtual de Saúde (BVS) utilizando os descritores: "Educação em Saúde"; "Enfermagem" e "Paciente", em idiomas português e inglês. Resultados: Foram agrupados em duas categorias temáticas: "Ações de educação em saúde e enfermagem" e "Educação em saúde e a transformação do conhecimento pelos usuários", de modo a permitir uma compreensão dos dados encontrados. Considerações Finais: O processo pedagógico na realização de uma atividade educativa em enfermagem pode apresentar melhor resultado, quando aplicado com a confiança de um bom atendimento para um fácil aprendizado

Introduction: Health education promotes a strategy that enhances nursing care by involving educational activities in patient care. Objective: Reflect on the health education actions carried out by nursing and the construction of the link for the transfer of scientific knowledge aimed at the area. Method: The text is a narrative review based on national and international journals. The bases consulted were: Latin American and Caribbean Literature in Health Sciences (LILACS), Regional Library of Medicine (BIREME) and Virtual Health Library (VHL) using the descriptors: "Health Education"; "Nursing" and "Patient", in Portuguese and English. Results: They were grouped into two thematic categories: "Health and nursing education actions" and "Health education and the transformation of knowledge by users", in order to allow an understanding of the data found. Final considerations: The pedagogical process in carrying out an educational activity in nursing can present a better result, when applied with the confidence of good service for easy learning

Malnourished children and supplementary feeding during the war emergency in Guinea-Bissau in 1998-1999.

BACKGROUND: Supplementary feeding programs (SFPs) are intended to mitigate the deterioration of nutritional status and the increase in mortality among malnourished children. OBJECTIVE: We investigated the effect of an SFP on malnourished children in Guinea-Bissau who were returning to their homes after having been displaced within the country because of war in 1998-1999. DESIGN: The effect of the war on the nutritional status of children aged 6-59 mo who were present in Bissau sometime from September 1998 to June 1999 was evaluated by comparing the mortality and the prevalence of malnutrition with the values expected had the war not occurred and by comparing the severity of malnutrition in malnourished children before and during the war. The quality of the SFP was also evaluated. Children with midupper arm circumference < 130 mm were provided weekly medical consultations and supplementary feeding until recovery. RESULTS: The degree of malnutrition did not increase during the war. The prevalence of malnutrition increased with the start of the war but then decreased. The mortality of malnourished children did not increase during the war. Seventy-four percent of the referred children received treatment; of those, 1% died, 67% recovered, and 32% abandoned treatment. Compliance was 89%. The recovery rate was 13.1. 1000(-1). d(-1), and the median time to recovery was 48 d. Better compliance was associated with shorter time to recovery. CONCLUSIONS: Our findings may be biased by changes in the cultural and socioeconomic background of the malnourished children. However, 3 different analyses indicated a beneficial effect of the SFP. Thus, the home-based SFP probably prevented nutritional deterioration during the war in Guinea-Bissau.

Resistance to peloruside A and laulimalide: functional significance of acquired ßI-tubulin mutations at sites important for drug-tubulin binding.

Cancer cell lines selected for resistance to microtubule targeting agents (MTA) often have acquired mutations in the ß-tubulin binding sites for these agents. Despite strong correlational evidence, the functional and quantitative significance of such mutations in the resistance to MTA remains unknown. We recently showed that peloruside A (PLA) and laulimalide (LAU)-resistant cancer cell lines, 1A9-R1 (R1) and 1A9-L4 (L4), generated through multi-step selection of human 1A9 ovarian cancer cells with high concentrations of either PLA (for R1) or LAU (for L4) have single distinct mutations in their ßI-tubulin gene. The R1 cells have a mutation at amino acid position 296 (A296T), and the L4 cells have a mutation at position 306 (R306H/C), both of which lie at the putative binding sites of PLA and LAU. To gain insights on the functional role of these mutations in the resistance phenotype, R1 and L4 cells were transfected with wild type ßI-tubulin. MTT cell proliferation assays revealed that restoration of wild type ßI-tubulin expression partially sensitized the R1 and L4 cells to PLA and LAU. Cell cycle analysis and intracellular tubulin polymerization assays demonstrated that the increased sensitivity was correlated with an increased ability of PLA and LAU to induce G2-M arrest and tubulin polymerization in the cells. Unlike paclitaxel-selected clones of 1A9 cells, both R1 and L4 cells exhibited a functional p53 gene, and the abundance of the mismatch repair gene hMSH2 (human mutS homolog 2) was comparable to the parental 1A9 cells. This study provides the first direct evidence that A296 and R306 of ßI-tubulin are important determinants of the PLA and LAU response in cancer cells.

Reflexão sobre a classificação de risco como tendência para o pronto-socorro infantil / Reflection on risk classification as a trend for the infant emergency room / La reflexión sobre la calificación de riesgo como una tendencia para la emergencia del niño

Objetivo: explanar acerca da classificação de risco como uma tendência para o serviço de pronto-socorro infantil. Método: trata-se de um ensaio teórico-reflexivo, realizado no período de maio de 2017 a outubro de 2018, fundamentando na literatura encontrada nas bases de dados: PubMed, CINAHL e LILACS. Os descritores utilizados foram: "Medição de Risco", "Serviços Médicos de Emergência", "Serviço Hospitalar de Emergência", "Pediatria", "Identificação da Emergência"; "Triagem" e "Superlotação". Foram utilizados como critérios de inclusão: publicações em português, inglês e espanhol, no período de 2000 a 2016, com textos completos disponíveis gratuitamente. Excluídas as publicações que não se relacionavam à temática do estudo e que apresentassem duplicidade. Resultados: a classificação de risco mostra-se como tendência, com possibilidade de avançar, uma vez que a solução de muitos dos fatores que contribuem para a superlotação dos prontossocorros acarretaria maiores custos financeiros do que a implantação da classificação de risco infantil. Considerações Finais: a classificação de risco pode contribuir para a organização dos atendimentos ao cliente pediátrico que, procura por atendimento em prontos-socorros sem critérios clínicos.(AU)

Objective: to explain about the classification of risk as a tendency for the emergency room service for children. Method: it is a theoretical-reflective essay, carried out from May 2017 to October 2018, based on the literature found in the databases: PubMed, CINAHL and LILACS. The descriptors used were: "Risk Measurement", "Emergency Medical Services", "Emergency Hospital Service", "Pediatrics", "Emergency Identification", "Screening" and "Overcrowding". Inclusion criteria were: publications in Portuguese, English and Spanish, from 2000 to 2016, with full texts available free of charge. Publications that were not related to the subject of the study and which presented duplicity were excluded. Results: the risk classification is a trend with the possibility of advancing, since the solution of many of the factors that contribute to the overcrowding of the emergency rooms would entail higher financial costs than the implantation of the classification of child risk. Final Considerations: risk classification may contribute to the organization of pediatric care to the patient that seeks care in emergency rooms without clinical criteria.(AU)

Objetivo: explicar acerca de la clasificación de riesgo como una tendencia al servicio de socorro infantil. Método: se trata de un ensayo teórico-reflexivo, realizado en el período de mayo de 2017 a octubre de 2018, fundamentando en la literatura encontrada en las bases de datos: PubMed, CINAHL y LILACS. Los descriptores utilizados fueron: "Medición de Riesgo", "Servicios Médicos de Emergencia", "Servicio Hospitalario de Emergencia", "Pediatría", "Identificación de la Emergencia"; "Triage" y "Superlotación". Fueron utilizados como criterios de inclusión: publicaciones en portugués, Inglés y Español, de 2000 a 2016, con el texto completo de libre acceso. Excluidas las publicaciones que no se relacionaban a la temática del estudio y que presentasen duplicidad. Resultados: la clasificación de riesgo se muestra como tendencia, con posibilidad de avanzar, ya que la solución de muchos de los factores que contribuyen a la superpoblación de los prontos de socorro acarrearía mayores costos financieros que la implantación de la clasificación de riesgo infantil. Consideraciones finales: la clasificación de riesgo puede contribuir a la organización de las atenciones al cliente pediátrico que, busca por atención en prontos de socorro sin criterios clínicos.(AU)