PERCEPÇÃO DE SUPORTE FAMILIAR E QUALIDADE DE VIDA: UM ESTUDO COM ADOLESCENTES E SEUS PAIS

A família é o primeiro grupo social ao qual o individuo pertence e exerce importante função no desenvolvimento dos seres humanos. Levando-se em consideração o fato da adolescência ser considerada um período do desenvolvimento, marcada por diversas transformações, tanto do individuo quanto do meio familiar, assim como a importância que a família exerce na constituição desses adolescentes, faz-se necessário pensar na qualidade das relações que são estabelecidas. Diante disso, a presente pesquisa teve como objetivo identificar possíveis relações entre a percepção de suporte familiar e qualidade de vida relacionada à saúde de adolescentes e seus responsáveis. Para tanto, buscou-se identificar a percepção dos adolescentes sobre sua qualidade de vida e suporte familiar, bem como a percepção de seus responsáveis sobre os mesmos. Trata-se de um estudo descritivo, quantitativo e de delineamento transversal. Participaram desse estudo 348 sujeitos, sendo 174 adolescentes e 174 responsáveis, escolhidos por conveniência. Dentre os resultados pode-se salientar que os adolescentes possuem percepção de melhor qualidade de vida relacionada à saúde do que seus responsáveis, porém ambos revelam que possuem visão positiva acerca da adolescência. No que se refere à percepção de suporte familiar os dados revelaram que os homens (independente de serem responsáveis ou adolescentes) apresentam melhor percepção acerca da expressão afetiva entre os membros da família e os responsáveis possuem melhor percepção acerca do fator autonomia do que os adolescentes. Conclui se que os objetivos do presente estudo foram atingidos na medida em que foram identificadas inúmeras correlações entre os fatores de percepção de suporte familiar e as dimensões de qualidade de vida relacionada à saúde. Os resultados obtidos sugerem a necessidade de ações que favoreçam o dialogo entre responsáveis e adolescentes favorecendo a aproximação e, consequentemente favorecendo a promoção da saúde.

A novel requirement for C. elegans Alix/ALX-1 in RME-1-mediated membrane transport

BACKGROUND: Alix/Bro1p family proteins have recently been identified as important components of multivesicular endosomes (MVEs) and are involved in the sorting of endocytosed integral membrane proteins, interacting with components of the ESCRT complex, the unconventional phospholipid LBPA, and other known endocytosis regulators. During infection, Alix can be co-opted by enveloped retroviruses, including HIV, providing an important function during virus budding from the plasma membrane. In addition, Alix is associated with the actin cytoskeleton and might regulate cytoskeletal dynamics. RESULTS: Here we demonstrate a novel physical interaction between the only apparent Alix/Bro1p family protein in C. elegans, ALX-1, and a key regulator of receptor recycling from endosomes to the plasma membrane, called RME-1. The analysis of alx-1 mutants indicates that ALX-1 is required for the endocytic recycling of specific basolateral cargo in the C. elegans intestine, a pathway previously defined by the analysis of rme-1 mutants. The expression of truncated human Alix in HeLa cells disrupts the recycling of major histocompatibility complex class I, a known Ehd1/RME-1-dependent transport step, suggesting the phylogenetic conservation of this function. We show that the interaction of ALX-1 with RME-1 in C. elegans, mediated by RME-1/YPSL and ALX-1/NPF motifs, is required for this recycling process. In the C. elegans intestine, ALX-1 localizes to both recycling endosomes and MVEs, but the ALX-1/RME-1 interaction appears to be dispensable for ALX-1 function in MVEs and/or late endosomes. CONCLUSIONS: This work provides the first demonstration of a requirement for an Alix/Bro1p family member in the endocytic recycling pathway in association with the recycling regulator RME-1.

Apoptotic cell‐associated ICAM‐3 in the phagocytic removal of apoptotic cells

Apoptosis is a highly controlled cell death programme that culminates in the exposure of molecular ‘flags’ at the dying cell surface that permit recognition and removal by viable phagocytes. Failure to efficiently remove dying cells can lead to devastating inflammatory and autoimmune disorders. The molecular mechanisms underlying apoptotic cell surface changes are poorly understood. Our previous work has shown an apoptosis-associated functional change in ICAM-3 (a heavily glycosylated, leukocyte-restricted Immunoglobulin Super-Family member) resulting in a molecular ‘flag’ to mediate corpse removal. Here we detail apoptosis-associated changes in ICAM-3 and define their role in ICAM-3’s novel function in apoptotic cell clearance. We show ICAM-3 functions to tether apoptotic leukocytes to macrophages via an undefined receptor. Though CD14 has been suggested as a possible receptor for apoptotic cell-associated ICAM-3, we demonstrate ICAM-3 functions for apoptotic cell clearance in the absence of CD14. Furthermore, we demonstrate leukocytes display early changes in cell surface glycosylation and a marked reduction in ICAM-3, a change that correlates reduced cell volume throughout apoptosis. This loss of ICAM-3 occurs via shedding of ICAM-3 in microparticles (‘apoptotic bodies’). Such microparticles are potent chemoattractants for macrophages. Notably, microparticles from ICAM-3-deficient leukocytes are significantly less chemoattractive than microparticles from their ICAM-3-replete counterparts. These data support the hypothesis that ICAM-3 acts as an apoptotic cell-associated ligand to tether dying cells to phagocytes in a CD14-independent manner. Furthermore our data suggest that released ICAM-3 may promote the recruitment of phagocytes to sites of apoptosis.

Apoptotic cell-derived ICAM-3 promotes both macrophage chemoattraction to and tethering of apoptotic cells

Damaged, aged or unwanted cells are removed from the body by an active process known as apoptosis. This highly orchestrated programme results in cell disassembly and the exposure of ‘flags’ at the dying cell surface that permit recognition and removal by viable cells (phagocytes). Efficient phagocytic removal of dying cells is essential to prevent inflammatory and autoimmune disorders. Relatively little is known of the molecular mechanisms underlying changes at the apoptotic cell surface. We have previously shown that ICAM-3 (a heavily glycosylated, leukocyte-restricted Immunoglobulin Super-Family member) undergoes a change of function as cells die so that it acts as a molecular ‘flag’ to mediate corpse removal. Our work seeks to characterise apoptosis-associated changes in ICAM-3 and define their role in ICAM-3’s novel function in apoptotic cell clearance. Here we extend earlier studies to show that apoptotic cell-associated ICAM-3 functions, at least minimally, to tether apoptotic leukocytes to macrophages via an undefined receptor. Whilst CD14 has been suggested as a possible innate immune receptor for apoptotic cell-associated ICAM-3, we demonstrate ICAM-3 functions for apoptotic cell clearance in the absence of CD14. Our data additionally indicate, that during apoptosis, leukocytes display early changes in cell surface glycosylation and a marked reduction in ICAM-3, a change that correlates with a reduction in cell volume. This reduction in ICAM-3 is explained by cell surface shedding of microparticles (‘apoptotic bodies’) that contain ICAM-3. Such microparticles, released from apoptotic leukocytes, are strongly chemoattractive for macrophages. In addition, microparticles from ICAM-3-deficient leukocytes are significantly less chemoattractive than microparticles from their ICAM-3-replete counterparts. Taken together these data support the hypothesis that ICAM-3 acts as an apoptotic cell-associated ligand to tether dying cells to phagocytes in a CD14-independent manner. Furthermore our data suggest that released ICAM-3 may promote the recruitment of phagocytes to sites of leukocyte apoptosis.

Apoptotic cell-derived ICAM-3 promotes both macrophage chemoattraction to and tethering of apoptotic cells

Damaged, aged or unwanted cells are removed from the body by an active process known as apoptosis. This highly orchestrated programme results in cell disassembly and the exposure of ‘flags’ at the dying cell surface that permit recognition and removal by viable cells (phagocytes). Efficient phagocytic removal of dying cells is essential to prevent inflammatory and autoimmune disorders. Relatively little is known of the molecular mechanisms underlying changes at the apoptotic cell surface. We have previously shown that ICAM-3 (a heavily glycosylated, leukocyte-restricted Immunoglobulin Super-Family member) undergoes a change of function as cells die so that it acts as a molecular ‘flag’ to mediate corpse removal. Our work seeks to characterise apoptosis-associated changes in ICAM-3 and define their role in ICAM-3’s novel function in apoptotic cell clearance. Here we extend earlier studies to show that apoptotic cell-associated ICAM-3 functions, at least minimally, to tether apoptotic leukocytes to macrophages via an undefined receptor. Whilst CD14 has been suggested as a possible innate immune receptor for apoptotic cell-associated ICAM-3, we demonstrate ICAM-3 functions for apoptotic cell clearance in the absence of CD14. Our data additionally indicate, that during apoptosis, leukocytes display early changes in cell surface glycosylation and a marked reduction in ICAM-3, a change that correlates with a reduction in cell volume. This reduction in ICAM-3 is explained by cell surface shedding of microparticles (‘apoptotic bodies’) that contain ICAM-3. Such microparticles, released from apoptotic leukocytes, are strongly chemoattractive for macrophages. In addition, microparticles from ICAM-3-deficient leukocytes are significantly less chemoattractive than microparticles from their ICAM-3-replete counterparts. Taken together these data support the hypothesis that ICAM-3 acts as an apoptotic cell-associated ligand to tether dying cells to phagocytes in a CD14-independent manner. Furthermore our data suggest that released ICAM-3 may promote the recruitment of phagocytes to sites of leukocyte apoptosis.

DNA chip designed antisense oligodeoxynucleotides targeting EGFR MRNA for brain tumour therapy

Glioblastoma multiforme (GBM) is a malignant brain tumour for which there is currently no effective treatment regime. It is thought to develop due to the overexpression of a number of genes, including the epidermal growth factor receptor (EGFR), which is found in over 40% of GBM. Novel forms of treatment such as antisense therapy may allow for the specific inhibition of aberrant genes and thus they are optimistic therapies for future treatment of GBM. Oligodeoxynucleotides (ODNs) are small pieces of DNA that are often modified to increase their stability to nucleases and can be targeted to the aberrant gene in order to inhibit it and thus prevent its transcription into protein. By specifically binding to mRNA in an antisense manner, they can bring about its degradation by a variety of mechanisms including the activation of RNase H and thus have great potential as therapeutic agents. One of the main drawbacks to the utilisation of this therapy so far is the lack of techniques that can successfully predict accessible regions on the target mRNA that the ODNs can bind to. DNA chip technology has been utilised here to predict target sequences on the EGFR mRNA and these ODNs (AS 1 and AS2) have been tested in vitro for their stability, uptake into cells and their efficacy on cellular growth, EGFR protein and mRNA. Studies showed that phosphorothioate and 2'O-methyl ODNs were significantly more stable than phosphodiester ODNs both in serum and serum-free conditions and that the mechanism of uptake into A431 cells was temperature dependent and more efficient with the use of optimised lipofectin. Efficacy results show that AS 1 and AS2 phosphorothioate antisense ODNs were capable of inhibiting cell proliferation by 69% ±4% and 65% ±4.5% respectively at 500nM in conjunction with a non-toxic dose of lipofectinTM used to enhance cellular delivery. Furthermore, control ODN sequences, 2' O-methyl derivatives and a third ODN sequence, that was found not to be capable of binding efficiently to the EGFR mRNA by DNA chip technology, showed no significant effect on cell proliferation. AS 1 almost completely inhibited EGFR protein levels within 48 hours with two doses of 500nM AS 1 with no effect on other EGFR family member proteins or by control sequences. RNA analysis showed a decrease in mRNA levels of 32.4% ±0.8% but techniques require further optimisation to confirm this. As there are variations found between human glioblastoma in situ and those developed as xenografts, analysis of effect of AS 1 and AS2 was performed on primary tumour cell lines derived from glioma patients. ODN treatment showed a specific knockdown of cell growth compared to any of the controls used. Furthermore, combination therapies were tested on A431 cell growth to determine the advantage of combining different antisense approaches and that of conventional drugs. Results varied between the combination treatments but indicated that with optimisation of treatment regimes and delivery techniques that combination therapies utilising antisense therapies would be plausible.

Hypercapnia induces cleavage and nuclear localization of RelB protein, giving insight into CO2 sensing and signaling

Carbon dioxide (CO(2)) is increasingly being appreciated as an intracellular signaling molecule that affects inflammatory and immune responses. Elevated arterial CO(2) (hypercapnia) is encountered in a range of clinical conditions, including chronic obstructive pulmonary disease, and as a consequence of therapeutic ventilation in acute respiratory distress syndrome. In patients suffering from this syndrome, therapeutic hypoventilation strategy designed to reduce mechanical damage to the lungs is accompanied by systemic hypercapnia and associated acidosis, which are associated with improved patient outcome. However, the molecular mechanisms underlying the beneficial effects of hypercapnia and the relative contribution of elevated CO(2) or associated acidosis to this response remain poorly understood. Recently, a role for the non-canonical NF-?B pathway has been postulated to be important in signaling the cellular transcriptional response to CO(2). In this study, we demonstrate that in cells exposed to elevated CO(2), the NF-?B family member RelB was cleaved to a lower molecular weight form and translocated to the nucleus in both mouse embryonic fibroblasts and human pulmonary epithelial cells (A549). Furthermore, elevated nuclear RelB was observed in vivo and correlated with hypercapnia-induced protection against LPS-induced lung injury. Hypercapnia-induced RelB processing was sensitive to proteasomal inhibition by MG-132 but was independent of the activity of glycogen synthase kinase 3ß or MALT-1, both of which have been previously shown to mediate RelB processing. Taken together, these data demonstrate that RelB is a CO(2)-sensitive NF-?B family member that may contribute to the beneficial effects of hypercapnia in inflammatory diseases of the lung.

Production, purification and characterization of recombinant, full-length human claudin-1

The transmembrane domain proteins of the claudin superfamily are the major structural components of cellular tight junctions. One family member, claudin-1, also associates with tetraspanin CD81 as part of a receptor complex that is essential for hepatitis C virus (HCV) infection of the liver. To understand the molecular basis of claudin-1/CD81 association we previously produced and purified milligram quantities of functional, full-length CD81, which binds a soluble form of HCV E2 glycoprotein (sE2). Here we report the production, purification and characterization of claudin-1. Both yeast membrane-bound and detergent-extracted, purified claudin-1 were antigenic and recognized by specific antibodies. Analytical ultracentrifugation demonstrated that extraction with n-octyl-ß-d-glucopyranoside yielded monodispersed, dimeric pools of claudin-1 while extraction with profoldin-8 or n-decylphosphocholine yielded a dynamic mixture of claudin-1 oligomers. Neither form bound sE2 in line with literature expectations, while further functional analysis was hampered by the finding that incorporation of claudin-1 into proteoliposomes rendered them intractable to study. Dynamic light scattering demonstrated that claudin-1 oligomers associate with CD81 in vitro in a defined molar ratio of 1:2 and that complex formation was enhanced by the presence of cholesteryl hemisuccinate. Attempts to assay the complex biologically were limited by our finding that claudin-1 affects the properties of proteoliposomes. We conclude that recombinant, correctly-folded, full-length claudin-1 can be produced in yeast membranes, that it can be extracted in different oligomeric forms that do not bind sE2 and that a dynamic preparation can form a specific complex with CD81 in vitro in the absence of any other cellular components. These findings pave the way for the structural characterization of claudin-1 alone and in complex with CD81.

Occupational therapists' attitudes toward homosexuality

Two hundred and eighty-five occupational therapists were surveyed to determine their general attitudes toward homosexuality, and whether certain demographic variables and means of exposure affected these attitudes. Attitudes ranged from neutral to positive. Those demographic variables that did affect respondents' attitudes were: sexual orientation, gender, and educational level. Those respondents who identified themselves as homosexual or bisexual had more positive attitudes than those who were heterosexual. Female respondents had more positive attitudes than male respondents and those respondents who held a Master's degree had more positive attitudes than those who held a Bachelor's degree. It was determined that respondents who had a family member or friend who was gay had more positive attitudes than those who did not. An unexpected finding was that respondents who had received adequate information about homosexuality in their occupational therapy curriculum had more negative attitudes than those who did not receive adequate information. It was therefore concluded that those occupational therapists who had not been provided with adequate information on homosexuality in their occupational therapy curriculum but had more positive attitudes toward homosexuality, were older and had more years of experience in occupational therapy. ^

Estratégias de cuidados por familiares de portadores de transtornos mentais severos residentes na zona rural do alto sertão paraibano

In the current configuration of the Brazilian Psychiatric Reform, family plays a key role in mental health care: shared responsibility and active participation in the process of rehabilitation of people with severe mental disorders. It´s considered that the family member who cares can help users in their daily tasks and articulating trajectories, networks and ways to potentiate social connections. This research was motivaded by interest in the subject and by the lack of research and studies about this reality in rural areas. This study aimed to identify ways of mental health care by relatives of severe mental disorder patients living in rural zone located at sertão of Paraiba. Methodologically was made a work with qualitative research structured in two moments. In the first one, was held a Documentary Research in CAPS II in order to identify: a) users living in rural that had a history of at least one psychiatric hospitalization, b) users who no longer use the reference service (CAPS II) for at least one year. The second stage consisted by home visits and semi-structured interviews with eleven families in rural areas. Results pointed out a profile composed by 56 users: 56 women and 26 men aged between 50 and 64 years, unmarried, without study, farmers and housewives, living six miles from CAPS II and carriers with severe mental disorders. Strategies and resources used by the families for mental health care were: religion, work, medication and help from relatives, neighbors and community. Factors related to non-use of substitute services were lack of internment in CAPS II and lack of money and transportation. The hospital, the house arrest, the police aid and religion were strategies used by family members as support to psychiatric crises. The data pointed to non-solving of care offered by psychosocial support network and the importance of redirecting practices aligned to the asylum model in favor of psychosocial strategies that aimed at rehabilitation and community participation in mental health care

Internação involuntária e o abuso de substâncias psicoativas - o pathos familiar

The use and abuse of Psychoactive Substances (PAS) in contemporaneity corresponds to a social issue and a public health issue. Few social phenomena entail more costs with justice and health, family difficulties, and appearances in the media than the PAS abuse comsumption. The government power has been facing this situation allocating investments and developing public policies. Despite the current Mental Health Policy, based on the principles of Psychiatric Reform that prioritizes outpatient services, the number of investments from various government spheres and families requests for admissions continue increasing. This study aimed to understand the pathos experienced by an individual toward the involuntary internment of a family member who is an abusive user of PAS. The research also aimed to investigate what led that individual to choose this type of treatment. The Psychoanalysis was the theoretical basis of this work, and the exercise of the psychoanalytic method, from the collection of bibliographic references up to the interpretation of the semi-structured interview, conducted in depth, was intended. The findings of this research gave us the oportunity of thinking about how the social callings to the family were made, especially in regard of atention and care with their family members who are user of PAS and how it affects this family individual. It also allowed to discuss how the public policies that preconize involuntary internment, affectivity, prohibitionist and mono-disciplinarity – that cross the State in the attention given to this issue – are formulated and implemented. The interview analysis showed us how happen the agencying of pathos, the libidinal aspects of joy and guilt, the desire to punish and atonement, working in family relations and in caring relations, especially in the decision for involuntary internment. The survey also made possible to understand how a mother, facing the chaotic scene of public health, helpless, finds in the involuntary internment a way to reverberate her affections.

Characterization of ALDH1A1 as a novel tumorigenic target mediating TAZ-induced lung tumorigenesis and stem cell phenotypes

Recent studies suggest that lung cancer stem cells (CSCs) may play major roles in lung cancer development, metastasis and drug resistance. Therefore, identification of lung CSC drivers may provide promising targets for lung cancer. TAZ (transcriptional co-activator with PDZ-binding motif) is a transcriptional co-activator and key downstream effector of the Hippo pathway, which plays critical roles in various biological processes. TAZ has been shown to be overexpressed in non-small cell lung cancer (NSCLC) and involved in tumorigenicity of lung epithelial cells. However, whether TAZ is a driver for lung CSCs and tumor formation in vivo is unknown. In addition, the molecular mechanism underlying TAZ-induced lung tumorigenesis remains to be determined. In this study, we provided evidence that constitutively active TAZ (TAZ-S89A) is a driver for lung tumorigenesis in vivo in mice and formation of lung CSC. Oncogenes upregulated in TAZ-overexpressing cells were identified with further validation. The most dramatically activated gene, Aldh1a1 (Aldehyde dehydrogenase 1 family member a1), a well-established CSC marker, showed that TAZ induces Aldh1a1 transcription by activating its promoter activity through interaction with the transcription factor TEA domain (TEAD) family member. Most significantly, inhibition of ALDH1A1 with its inhibitor A37 or CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) gene knockout in lung cancer cells suppressed lung tumorigenic and CSC phenotypes in vitro, and tumor formation in mice in vivo. In conclusion, this study identified TAZ as a novel inducer of lung CSCs and the first transcriptional activator of the stem cell marker ALDH1A1. Most significantly, we identified ALDH1A1 as a critical meditator of TAZ-induced tumorigenic and CSC phenotypes in lung cancer. Our studies provided preclinical data for targeting of TAZ-TEAD-ALDH1A1 signaling to inhibit CSC-induced lung tumorigenesis and drug resistance in the future.

Transitions in Contentious Behaviour in Infancy and Later Aggressive Conduct Problems

Background. Individual trajectories toward aggression originate in early infancy, before there is intent to harm. We focused on infants who were contentious, i.e., prone to engage in anger and use of physical force with other people, and examined change in levels of contentiousness between 6 and 12 months of age with reference to later aggressive conduct problems.
Sample. The CCDS is a nationally representative sample of 321 firstborn children whose families were recruited from antenatal clinics in two National Health Service Trusts.
Method. Mothers, fathers, and a third family member or friend who knew infants well completed the Cardiff Infant Contentiousness Scale (CICS) at 6 months, which was stable form 6 to 12 months, and validated by direct observation of infants’ use of force against peers. Primary caregivers again completed the CICS at 12 months, and up to three informants completed the Child Behaviour Check List at mean ages of 36 and 84 months. We used Latent Transition Analysis to identify different groups of infants in respect to their patterns of contentiousness from 6 to 12 months.
Results
Three ordered classes of contentiousness from low to high were found at 6 and 12 months. Infants exposed to greater family adversity were more likely to move into the high-contentious class from 6 to 12 months. Higher contentiousness in infancy predicted more aggressive conduct problems at 33 months and thereafter.
Conclusions
Infants exposed to family adversity are already at disadvantage by 6 months and likely to escalate in their anger and aggressiveness over time.

Attitudes and Knowledge Concerning Corneal Donation in a Population-Based Sample of Urban Chinese Adults.

PURPOSE: To better understand knowledge and attitudes concerning corneal donation among Chinese adults.
METHODS: Randomly selected residents in predetermined age strata 20 to 60+ years completed home-based questionnaires in each of 12 randomly chosen communities in Guangzhou, southern China.
RESULTS: Among 1217 selected persons, 430 (35.3%) completed the questionnaires (mean age 40.4 yrs, 57.9% female). Refusers were older (44.8 yrs, P < 0.001), but sex did not differ (52.2% female, P = 0.07). Among participants, 175 (40.7%) were willing to donate their corneas (WTD). Differences between WTD and not WTD included donation knowledge score (range, 1-12) [WTD (SD) 6.91 ± 2.21, not WTD 5.62 ± 2.43, P < 0.001]; having discussed donation (WTD 26.3%, not WTD 8.63%, P < 0.001); viewing donation as unpopular (WTD 88.0%, not WTD 96.5%, P = 0.001); and feeling donation "damages the body" (WTD 15.4%, not WTD 25.7%, P = 0.013). Associated significantly with WTD in multiple regression models were higher knowledge score [odds ratio (OR) = 1.18, 95% confidence interval (CI), 1.04-1.32, P = 0.008]; not feeling donation "damages the body" (OR = 1.91, 95% CI, 1.07-3.43, P = 0.030); and willingness to discuss donation (OR = 10.6, 95% CI, 3.35-33.9, P < 0.001). WTD did not differ by age (>60 yrs: 22/51, 43.1%; ≤60 yrs: 153/379, 40.4%, P = 0.706). Assuming all those refusing the survey would not donate, 14.4% (175/1217) were WTD for themselves, though only 7.1% (86/1217) would do so on behalf of a family member if they did not know the deceased's preference.
CONCLUSIONS: Interventions to increase knowledge and promote discussions about donation, and policies allowing widespread expression of donation preference, are needed in this setting.

Fenômeno vivido por familiares de pacientes internados em unidade de terapia intensiva

COMASSETTO, Isabel, ENDERS, Bertha Cruz. Fenômeno vivido por familiares de pacientes internados em Unidade de Terapia Intensiva. Revista Gaúcha de Enfermagem., Porto Alegre(RS), v.30,n., p.46-53. Mar. 2009. Disponivel em: < http://www.seer.ufrgs.br/index.php/RevistaGauchadeEnfermagem/search/results>.