SenNet recommendations for detecting senescent cells in different tissues.

Once considered a tissue culture-specific phenomenon, cellular senescence has now been linked to various biological processes with both beneficial and detrimental roles in humans, rodents and other species. Much of our understanding of senescent cell biology still originates from tissue culture studies, where each cell in the culture is driven to an irreversible cell cycle arrest. By contrast, in tissues, these cells are relatively rare and difficult to characterize, and it is now established that fully differentiated, postmitotic cells can also acquire a senescence phenotype. The SenNet Biomarkers Working Group was formed to provide recommendations for the use of cellular senescence markers to identify and characterize senescent cells in tissues. Here, we provide recommendations for detecting senescent cells in different tissues based on a comprehensive analysis of existing literature reporting senescence markers in 14 tissues in mice and humans. We discuss some of the recent advances in detecting and characterizing cellular senescence, including molecular senescence signatures and morphological features, and the use of circulating markers. We aim for this work to be a valuable resource for both seasoned investigators in senescence-related studies and newcomers to the field.

Transcriptional control of leukemogenesis by the chromatin reader SGF29.

ABSTRACT: Aberrant expression of stem cell-associated genes is a common feature in acute myeloid leukemia (AML) and is linked to leukemic self-renewal and therapy resistance. Using AF10-rearranged leukemia as a prototypical example of the recurrently activated "stemness" network in AML, we screened for chromatin regulators that sustain its expression. We deployed a CRISPR-Cas9 screen with a bespoke domain-focused library and identified several novel chromatin-modifying complexes as regulators of the TALE domain transcription factor MEIS1, a key leukemia stem cell (LSC)-associated gene. CRISPR droplet sequencing revealed that many of these MEIS1 regulators coordinately controlled the transcription of several AML oncogenes. In particular, we identified a novel role for the Tudor-domain-containing chromatin reader protein SGF29 in the transcription of AML oncogenes. Furthermore, SGF29 deletion impaired leukemogenesis in models representative of multiple AML subtypes in multiple AML subtype models. Our studies reveal a novel role for SGF29 as a nononcogenic dependency in AML and identify the SGF29 Tudor domain as an attractive target for drug discovery.

Discovery of novel furanylbenzamide inhibitors that target oncogenic tyrosine phosphatase SHP2 in leukemia cells.

Disturbance of the dynamic balance between tyrosine phosphorylation and dephosphorylation of signaling molecules, controlled by protein tyrosine kinases and protein tyrosine phosphatases (PTPs), is known to lead to the development of cancer. While most approved targeted cancer therapies are tyrosine kinase inhibitors, PTPs have long been stigmatized as undruggable and have only recently gained renewed attention in drug discovery. One PTP target is the Src-homology 2 domain-containing phosphatase 2 (SHP2). SHP2 is implicated in tumor initiation, progression, metastasis, and treatment resistance, primarily because of its role as a signaling nexus of the extracellular signal-regulated kinase pathway, acting upstream of the small GTPase Ras. Efforts to develop small molecules that target SHP2 are ongoing, and several SHP2 allosteric inhibitors are currently in clinical trials for the treatment of solid tumors. However, while the reported allosteric inhibitors are highly effective against cells expressing WT SHP2, none have significant activity against the most frequent oncogenic SHP2 variants that drive leukemogenesis in several juvenile and acute leukemias. Here, we report the discovery of novel furanylbenzamide molecules as inhibitors of both WT and oncogenic SHP2. Importantly, these inhibitors readily cross cell membranes, bind and inhibit SHP2 under physiological conditions, and effectively decrease the growth of cancer cells, including triple-negative breast cancer cells, acute myeloid leukemia cells expressing either WT or oncogenic SHP2, and patient-derived acute myeloid leukemia cells. These novel compounds are effective chemical probes of active SHP2 and may serve as starting points for therapeutics targeting WT or mutant SHP2 in cancer.

A JAK/STAT-mediated inflammatory signaling cascade drives oncogenesis in AF10-rearranged AML.

Leukemias bearing fusions of the AF10/MLLT10 gene are associated with poor prognosis, and therapies targeting these fusion proteins (FPs) are lacking. To understand mechanisms underlying AF10 fusion-mediated leukemogenesis, we generated inducible mouse models of acute myeloid leukemia (AML) driven by the most common AF10 FPs, PICALM/CALM-AF10 and KMT2A/MLL-AF10, and performed comprehensive characterization of the disease using transcriptomic, epigenomic, proteomic, and functional genomic approaches. Our studies provide a detailed map of gene networks and protein interactors associated with key AF10 fusions involved in leukemia. Specifically, we report that AF10 fusions activate a cascade of JAK/STAT-mediated inflammatory signaling through direct recruitment of JAK1 kinase. Inhibition of the JAK/STAT signaling by genetic Jak1 deletion or through pharmacological JAK/STAT inhibition elicited potent antioncogenic effects in mouse and human models of AF10 fusion AML. Collectively, our study identifies JAK1 as a tractable therapeutic target in AF10-rearranged leukemias.

HIV-1 Antisense Protein of Different Clades Induces Autophagy and Associates with the Autophagy Factor p62.

The existence of the antisense transcript-encoded HIV-1 antisense protein (ASP) was recently reinforced by in silico analyses providing evidence for recent appearance of this gene in the viral genome. Our previous studies led to the detection of ASP in various cell lines by Western blotting, flow cytometry, and confocal microscopy analyses and reported that it induced autophagy, potentially through multimer formation. Here, our goals were to assess autophagy induction by ASP from different clades and to identify the implicated autophagy factors. We first demonstrated that ASP formed multimers, partly through its amino-terminal region and cysteine residues. Removal of this region was further associated with lower induction of autophagy, as assessed by autophagosome formation. ASPs from different clades (A, B, C, D, and G) were tested next and were detected in monomeric and multimeric forms at various levels, and all induced autophagy (clade A ASP was less efficient), as determined by LC3-II and p62 (SQSTM1) levels. Furthermore, CRISPR-based knockout of ATG5, ATG7, and p62 genes led to increased ASP levels. Confocal microscopy analyses showed that ASP colocalized with p62 and LC3-II in autophagosome-like structures. Coimmunoprecipitation experiments further demonstrated that p62 associated with ASP through its PB1 domain. Interestingly, immunoprecipitation experiments supported the idea that ASP is ubiquitinated and that ubiquitination was modulating its stability. We are thus suggesting that ASP induces autophagy through p62 interaction and that its abundance is controlled by autophagy, in which ubiquitin plays an important role. Understanding the mechanisms underlying ASP degradation is essential to better assess its function.IMPORTANCE In the present study, we provide the first evidence that a new HIV-1 protein termed ASP derived from different clades acts similarly in inducing autophagy, an important cellular process implicated in the degradation of excess or defective cellular material. We have gained further knowledge on the mechanism mediating the activation of autophagy. Our studies have important ramifications in the understanding of viral replication and the pathogenesis associated with HIV-1 in infected individuals. Indeed, autophagy is implicated in antigen presentation during immune response and could thus be rendered inefficient in infected cells, such as dendritic cells. Furthermore, a possible link with HIV-1-associated neurological disorder (HAND) might also be a possible association with the capacity of ASP to induce autophagy. Our studies hence demonstrate the importance in conducting further studies on this protein as it could represent a new interesting target for antiretroviral therapies and vaccine design.

The role of TP53 in acute myeloid leukemia: Challenges and opportunities.

The tumor suppressor gene TP53 is one of the most frequently mutated genes in human cancer. The central role of the TP53 protein in several fundamental processes such as cancer, aging, senescence, and DNA repair has ensured enormous attention. However, the role of TP53 in acute myeloid leukemia (AML) is enigmatic. Unlike many other human cancers, a vast majority of AMLs display no genomic TP53 alterations. There is now growing appreciation of the fact that the unaltered TP53 status of tumor cells can be exploited therapeutically. As most AMLs have an intact TP53 gene, its physiological tumor-suppressive roles could be harnessed. Therefore, the use of pharmacological activators of the TP53 pathway may provide clinical benefit in AML. Conversely, even though the frequency of TP53 mutations in AML is substantially lower than in other human cancers, TP53 mutations are associated with chemoresistance and high risk of relapse. In patients with TP53 mutations, these alterations may lead to novel, selective vulnerabilities, creating opportunities for therapeutic targeting of TP53 mutant AML. The mutational status of TP53 therefore poses challenges and opportunities in terms of advancing effective treatment strategies in AML. An increasing armamentarium of small-molecule activators of the TP53 pathway, and a growing understanding of molecular pathways triggered by mutant TP53 have accelerated efforts aimed at targeting TP53 function in AML. In combination with standard AML chemotherapy or emerging targeted therapies, pharmacological targeting of the TP53 pathway may provide therapeutic benefit in AML.

Crystallization of low saturated lipid blends of palm and canola oils with sorbitan monostearate and fully hydrogenated palm oil.

Several scientific investigations have focused on providing new strategies for supporting the development of low saturated and zero trans lipid materials, as healthier fat alternatives for food application. This work evaluated the consistency, crystallization behavior, microstructure and polymorphism of six blends composed of palm and canola oils at different concentrations (100:0, 80:20, 60:40, 40:60, 20:80 and 0:100, in w/w%) added with 5.0% of fully hydrogenated palm oil (FHPO) or with a mixture of 2.5% of FHPO and 2.5% of sorbitan monostearate (SMS). The results were compared with the non-structured blends (standard samples). Through microstructure images, the formation of a more homogeneous and denser packed crystal network was observed for samples added with both crystallization modifiers (FHPO/SMS) compared to the corresponding standard samples, after stabilization at 25 °C during 3 h. In particular, enhanced crystallization modifications were observed for the 40:60 blend, in which the crystal form ß' emerged after the addition of FHPO/SMS. Moreover, the 40:60 blend structured with FHPO/SMS showed increased consistency (from 30 to 658 gF/cm2) and induced onset crystallization in a higher temperature (from 13.1 to 23.9 °C) compared with the non-structured one, due to the specific crystallization effects provided by both added structurants.

Cognitive effects of piracetam in adults with memory impairment: A systematic review and meta-analysis.

INTRODUCTION: Piracetam, a widely recognized nootropic drug, is hypothesized to enhance memory function through its influence on synaptic plasticity and neurotransmitter levels. However, despite its popularity, there remains a lack of conclusive evidence regarding its impact on memory. Therefore, the present study aims to explore the effects of piracetam on memory in individuals with impaired cognitive function, comparing it to a placebo control group. OBJECTIVES: This study will evaluate how piracetam affects memory function, compared to placebo in adults with impairment in this area. METHODS: We carried out bibliographical research and meta-analysis of scientific clinical trials comparing memory function in people taking piracetam with those in the placebo group. The PubMed, Dimensions, Embase, and Cochrane Library databases were used. Statistical analysis was performed in R Studio version 4.3.1. RESULTS: In our analysis, 199 articles were identified, of which we included eighteen studies, comprising a total of 886 patients, of which Piracetam was the treatment option in 442 (49.88 %) patients. Memory enhancement (SMD 0.75; 95 % CI [-0.19; 1.69]; p=0.12; I²=96 %) had no clinical difference between the intervention and the control group. CONCLUSION: Upon the conclusion of this study, it is apparent that we cannot definitively ascertain the impact of piracetam on memory function. Further research is warranted to provide a clearer understanding of the cognitive effects of piracetam in individuals with memory impairment. This investigation serves as a significant contribution to the ongoing quest to elucidate the potential benefits of piracetam in the field of cognitive neuroscience.

Therapeutic targeting of leukemia stem cells in acute myeloid leukemia.

One of the distinguishing properties of hematopoietic stem cells is their ability to self-renew. Since self-renewal is important for the continuous replenishment of the hematopoietic stem cell pool, this property is often hijacked in blood cancers. Acute myeloid leukemia (AML) is believed to be arranged in a hierarchy, with self-renewing leukemia stem cells (LSCs) giving rise to the bulk tumor. Some of the earliest characterizations of LSCs were made in seminal studies that assessed the ability of prospectively isolated candidate AML stem cells to repopulate the entire heterogeneity of the tumor in mice. Further studies indicated that LSCs may be responsible for chemotherapy resistance and therefore act as a reservoir for secondary disease and leukemia relapse. In recent years, a number of studies have helped illuminate the complexity of clonality in bone marrow pathologies, including leukemias. Many features distinguishing LSCs from normal hematopoietic stem cells have been identified, and these studies have opened up diverse avenues for targeting LSCs, with an impact on the clinical management of AML patients. This review will discuss the role of self-renewal in AML and its implications, distinguishing characteristics between normal and leukemia stem cells, and opportunities for therapeutic targeting of AML LSCs.

Experimental Study on Mechanical Properties of 3D-Printed Specimens of Iron Oxide, Quartz, and Bedded Composites Under Uniaxial Compression and Indirect Tensile Strength.

The heterogeneity of natural rocks produces increased variations in the results of geomechanical and metallurgical tests making the repeatability of experimental work questionable. Fabricated test specimens have, therefore, become more attractive for fundamental studies. In this study, quasi-identical 3D-printed (3DP) specimens with 10 and 16 mm diameters were fabricated and tested to study material strength and understand the breakage characteristics at a scale more suitable for comminution. Cylinder specimens composed of quartz (named Si) and iron oxide (named Fe), with sorted grains of ∼100-150 µm in the form of homogeneous specimens (3DP-Si and 3DP-Fe) and heterogeneous specimens (bedded) (3DP-SiFeSi, 3DP-SiFe, and 3DP-FeSiFe) were tested. This article presents the results for experimental Unconfined Compressive Strength (UCS) and Brazilian Tensile Strength (BTS) tests. The elastic property was obtained from the UCS tests, while tensile strength was obtained from BTS tests. The strength of 3DP specimens of similar diameter decreases following the types: 3DP-Si (most competent), 3DP-Si-Fe, 3DP-SiFeSi, 3DP-FeSiFe, and 3DP-Fe (less competent). The results show that heterogeneous 3DP specimens were influenced by bedding angle, thickness, and mineral group composition. It also seems that the sequence of mineral composition and the number of beds play a role, rather than the overall grain percentage area for each cylinder, in influencing the strength and variability of fragments. Finally, the brittleness indices for 3DP specimens were calculated as a function of UCS and BTS.

The Role of DOT1L in Normal and Malignant Hematopoiesis.

Disruptor of telomeric silencing 1 (DOT1) was first identified in yeast (DOT1p) and is the sole methyltransferase responsible for histone three lysine 79 (H3K79) mono-, di-, and tri-methylation. Mammalian DOT1 (DOT1-like protein or DOT1L) has been implicated in many cellular processes, such as cell cycle progression, DNA damage response, and development. A notable developmental process reliant on DOT1L function is normal hematopoiesis, as DOT1L knockout leads to impairment in blood lineage formation. Aberrant activity of DOT1L has been implicated in hematopoietic malignancies as well, especially those with high expression of the homeobox (HOX) genes, as genetic or pharmacological DOT1L inhibition causes defects in leukemic transformation and maintenance. Recent studies have uncovered methyltransferase-independent functions and a novel mechanism of DOT1L function. Here, we summarize the roles of DOT1L in normal and malignant hematopoiesis and the potential mechanism behind DOT1L function in hematopoiesis, in light of recent discoveries.

A systematic genome-wide mapping of oncogenic mutation selection during CRISPR-Cas9 genome editing.

Recent studies have reported that genome editing by CRISPR-Cas9 induces a DNA damage response mediated by p53 in primary cells hampering their growth. This could lead to a selection of cells with pre-existing p53 mutations. In this study, employing an integrated computational and experimental framework, we systematically investigated the possibility of selection of additional cancer driver mutations during CRISPR-Cas9 gene editing. We first confirm the previous findings of the selection for pre-existing p53 mutations by CRISPR-Cas9. We next demonstrate that similar to p53, wildtype KRAS may also hamper the growth of Cas9-edited cells, potentially conferring a selective advantage to pre-existing KRAS-mutant cells. These selective effects are widespread, extending across cell-types and methods of CRISPR-Cas9 delivery and the strength of selection depends on the sgRNA sequence and the gene being edited. The selection for pre-existing p53 or KRAS mutations may confound CRISPR-Cas9 screens in cancer cells and more importantly, calls for monitoring patients undergoing CRISPR-Cas9-based editing for clinical therapeutics for pre-existing p53 and KRAS mutations.

The role of the PZP domain of AF10 in acute leukemia driven by AF10 translocations.

Chromosomal translocations of the AF10 (or MLLT10) gene are frequently found in acute leukemias. Here, we show that the PZP domain of AF10 (AF10PZP), which is consistently impaired or deleted in leukemogenic AF10 translocations, plays a critical role in blocking malignant transformation. Incorporation of functional AF10PZP into the leukemogenic CALM-AF10 fusion prevents the transforming activity of the fusion in bone marrow-derived hematopoietic stem and progenitor cells in vitro and in vivo and abrogates CALM-AF10-mediated leukemogenesis in vivo. Crystallographic, biochemical and mutagenesis studies reveal that AF10PZP binds to the nucleosome core particle through multivalent contacts with the histone H3 tail and DNA and associates with chromatin in cells, colocalizing with active methylation marks and discriminating against the repressive H3K27me3 mark. AF10PZP promotes nuclear localization of CALM-AF10 and is required for association with chromatin. Our data indicate that the disruption of AF10PZP function in the CALM-AF10 fusion directly leads to transformation, whereas the inclusion of AF10PZP downregulates Hoxa genes and reverses cellular transformation. Our findings highlight the molecular mechanism by which AF10 targets chromatin and suggest a model for the AF10PZP-dependent CALM-AF10-mediated leukemogenesis.

Acute myeloid leukemia driven by the CALM-AF10 fusion gene is dependent on BMI1.

A subset of acute myeloid and lymphoid leukemia cases harbor a t(10;11)(p13;q14) translocation resulting in the CALM-AF10 fusion gene. Standard chemotherapeutic strategies are often ineffective in treating patients with CALM-AF10 fusions. Hence, there is an urgent need to identify molecular pathways dysregulated in CALM-AF10-positive leukemias which may lay the foundation for novel targeted therapies. Here we demonstrate that the Polycomb Repressive Complex 1 gene BMI1 is consistently overexpressed in adult and pediatric CALM-AF10-positive leukemias. We demonstrate that genetic Bmi1 depletion abrogates CALM-AF10-mediated transformation of murine hematopoietic stem and progenitor cells (HSPCs). Furthermore, CALM-AF10-positive murine and human AML cells are sensitive to the small-molecule BMI1 inhibitor PTC-209 as well as to PTC-596, a compound in clinical development that has been shown to result in downstream degradation of BMI1 protein. PTC-596 significantly prolongs survival of mice injected with a human CALM-AF10 cell line in a xenograft assay. In summary, these results validate BMI1 as a bona fide candidate for therapeutic targeting in AML with CALM-AF10 rearrangements.

A instável verdade nos testemunhos sobre estupros na seção 'Eu, leitora' da revista Marie Claire / The unstable truth in the testimonies about rapes in the 'Eu, leitora' section of Marie Claire magazine / La inestable verdad en los testimonios sobre violaciones en la sección de 'Eu, leitora' de la revista Marie Claire

Neste artigo, investigamos os modos como o jornalismo enquadra narrativas testemunhais de estupro publicadas na última década na seção 'Eu, leitora' da revista Marie Claire brasileira. A partir de uma análise textual narrativa, cotejada com estudos de trauma e testemunho e com estudos feministas, buscamos problematizar a maneira como o jornalismo lida com o testemunho. Dialogamos com o conceito de fait divers e sua presença no jornalismo dito feminino para compreender os modos como Marie Claire enquadra esses relatos. Concluímos que a revista opera ambiguamente em relação à verdade testemunhal das feridas traumáticas dessas mulheres, ao mesmo tempo se aproximando e se afastando delas, por meio de estratégias narrativas e editoriais.

In this article, we investigate how the journalism frames narratives of testimonies about rapes published in the last decade in the 'Eu, leitora' section of the Brazilian Marie Claire magazine. By means of a narrative textual analysis, compared with testimony and trauma studies as well as feminist studies, we seek to problematize the way journalism deals with testimony. We dialogue with the concept of fait divers and its presence in so-called female journalism to understand how Marie Claire frames these reports. We conclude that the magazine operates ambiguously with regard to the testimony truth of the traumatic wounds of these women, at the same time approaching and moving away from them, through narrative and editorial strategies.

En este artículo investigamos cómo el periodismo encuadra las narrativas testimoniales de violación publicadas en la última década en la sección de 'Eu, leitora' de la revista brasileña Marie Claire. A partir de un análisis textual narrativa, comparado con estudios del trauma y del testimonio y con estudios feministas, buscamos problematizar la forma cómo el periodismo aborda el testimonio. Dialogamos con el concepto de fait divers y su presencia en el llamado periodismo femenino para entender las formas cómo Marie Claire enmarca esas narraciones. Concluimos que la revista opera de manera ambigua con relación a la verdad testimonial de las heridas traumáticas de esas mujeres, al mismo tiempo acercándose y alejándose de ellas, a través de estrategias narrativas y editoriales.

TOXINA BOTULÍNICA NA ODONTOLOGIA / THE USE OF BOTULINUM TOXIN IN DENTISTRY

A Clostridium botulinum é uma bactéria anaeróbia que produz 8 tipos de toxinas. A Toxina Botulínica tipo A (BTX-A) é a variedade mais potente e a única utilizada em procedimentos clínicos e aprovada para uso cosmético e terapêutico. A empresa Allergan Inc. (USA) foi a primeira a produzir a BTX-A com o nome comercial de "BOTOX®". No Brasil sua aplicação terapêutica foi aprovada pela ANVISA em 2000, e nos Estados Unidos da América em 2002 pela Food and Drug Administration. O Conselho Federal de Odontologia reconhece pela Resolução 198/2019 sua utilização em procedimentos de harmonização orofacial bem como em procedimentos terapêuticos. Sua aplicação em casos como bruxismo, hipertrofia dos músculos da mastigação, disfunções temporomandibulares, sialorreia, assimetria de sorriso e exposição gengival acentuada, apresenta bons resultados, muito embora temporários. As contraindicações para o uso da BTX-A são expressas principalmente para a miastenia grave e a síndrome de Lambert-Eaton, consistentes em uma desordem caracterizada pela redução da liberação da acetilcolina nas sinapses. O presente trabalho teve como objetivo revisar a literatura sobre as aplicações da Toxina Botulínica no âmbito da Odontologia, abrangendo tanto a área da estética facial quanto a resolução de problemas ligados à área odontológica. Concluiu-se que seu uso é de baixo risco e com efeito positivo evidente nos casos específicos de aplicação terapêutica, além de melhorar a estética e, por consequência, a autoestima do paciente, proporcionando-lhe conforto e bem-estar.

Clostridium botulinum is an anaerobic bacter, which produces until eight types of toxins. The botulinum toxin A (BTX-A) is the most potent among then, largely used in clinical procedures and approved for several therapeutic instances. The Allergan Inc. company was the first to produce BTX-A commercially called as "Botox®". The therapeutic use of BOTOX® is approved by ANVISA in Brazil since 2000, followed by Food and Drug Administrartion in 2002. In Brazil, the Federal Council of Dentistry recognizes BOTOX® by 198/2019 law and its utilization in procedures such as facial reconcilement; or in therapeutics such as bruxism, hypertrophy of chew muscles, temporomandibular joint dysfunction, sialorrhea, asymmetry smile, and gingival profusion. Despite its temporal use, the results are very interesting. BTX-A side effects are considered for uses in miastenia gravis and Lambert-Eaton Syndrome, which has, in common, a reduced acetylcholine release in synapses. Thus, the aim of this work was to review the main BTX-A uses in dentistry area, once its use has growing largely in aesthetics and in dentistry disorders. Herein, we report the low risk in the use of BTX-A, with several interesting benefits on dentistry areas, improving the quality of life and the self- esteem.

Resposta à Triagem Auditiva em Neonatos do Projeto Canguru Usuários de Medicamentos Ototóxicos / Hearing Screening Response in Neonates of the Kangaroo Project Using Ototoxic Medicines

Avaliar a resposta à triagem auditiva em recémnascidosque participaram do projeto Mãe Canguru eutilizaram medicamentos ototóxico. Material e métodos:Estudo do tipo transversal observacional quantitativo, comamostra de 66 pacientes. Foram incluídos na pesquisa recémnascidosque utilizaram pelo menos um medicamentoototóxico (Gentamicina, Vancomicina, e Furosemida)participantes do Projeto Canguru da Maternidade CândidaVargas em João Pessoa - PB no período de Novembro de2012 a Março de 2013. As variáveis quantitativas foramexpressas em média e desvio-padrão, e as variáveisqualitativas foram expressas por frequências absolutas erelativas. O resultado do teste de EOA e de outras variáveisfoi feito utilizando-se o teste qui-quadrado e calculada pelosoftware SPSS versão 21.0. Adotou-se o nível designificância (p) de 5%. Resultados: Dos 66 pacientesincluídos na pesquisa, 45 pacientes (68,2%) utilizaramototóxicos, e 21 (31,8%) não. A Gentamicina foi usada por43 neonatos, a Furosemida por 8 e a Vancomicina por 6.Entre os pacientes que fizeram uso de medicamento ototóxico,95,2% tinham o teste da orelhinha normal e 2 apresentaramresposta ausente (4,8%) (p=0,4). Conclusão: Resultadospositivos e negativos na triagem auditiva foram encontradostanto em recém-nascidos que usaram como naqueles quenão usaram drogas ototóxicas. Não sendo significativo ouso isolado do medicamento nos neonatos que tiveramresposta ausente no teste de EOA...

To evaluate the hearing screening response innewborns who participated in Kangaroo Mother Project andused ototoxic drugs. Material and methods: This is a crosssectional,quantitative study including a sample of 66newborns who made use of at least one ototoxic drug(gentamicin, vancomycin, and furosemide) participating ofthe Kangaroo project at the Candida Vargas Hospital in JoãoPessoa, PB, Brazil, from November 2012 to March 2013.Quantitative variables were expressed as mean and standarddeviation, and qualitative variables were expressed asabsolute and relative frequencies. The correlation betweenthe results of the OAE test and other variables was performedusing the chi-square test and calculated by SPSS softwareversion 21.0, with a significance level (p) of 5%. Results: Ofthe 66 patients included in the study, 45 (68.2%) had usedototoxic drugs and 21 (31.8%) had not. Gentamicin wasused for 43 neonates, furosemide by 8 and vancomycin by6. Among the patients who made use of ototoxic medication,95.2% had normal OAE test and 2 had absent response(4.8%) (p = 0.4). Conclusion: Positive and negative resultsin the hearing screening were found both in newborns whoused or did not use ototoxic drugs. The isolated use of drugby newborns with absent response in the OAE test was notsignificant...

Efeitos da shantala na interação entre mãe e criança com síndrome de down / Effects of shantala massage therapy on interaction between mother and child with Down's syndrome

O objetivo é verificar os efeitos da Shantala na interação entre mãe e criança com síndrome de Down. Utilizou-se por 60 dias, uma vez por semana, a técnica de massagem Shantala em três crianças com síndrome de Down, da instituição APAE, localizada em Itaquaquecetuba, SP, Brasil. Para a obtenção dos resultados foram aplicados dois questionários, um ao início, para se obter maiores informações sobre as crianças e outro ao final, para se verificar os resultados da técnica utilizada. Foi possível concluir que a Shantala beneficiou as crianças com síndrome de Down, proporcionando uma qualidade de vida melhor. Para as mães, a técnica permitiu uma melhor aceitação da doença e houve melhora no relacionamento entre as mães e as crianças