Acoustic Analysis of Voice in Laryngopharyngeal Cancers Pre and Post Radiotherapy.

Laryngopharyngeal cancers are one of the most commonly diagnosed head and neck malignancies frequently presenting primarily with change in voice. Radiotherapy being the main modality of treatment for early cancers continues to affect voice. Hence, acoustic analysis of the voice offers quantifiable values of several parameters delineating the obvious effect of the therapy. A total number of 60 patients, diagnosed with laryngopharyngeal cancers undergoing radiotherapy underwent acoustic voice assessment using Dr. speech software pre-treatment and at 1 and 3 months post radiotherapy. Data analysis was done using Mann-Whitney test and Wilcoxon signed rank test and a significant p value was obtained. The results of the study showed fundamental frequency (F0) and noise to harmonic ratio (NHR) to be the most affected in comparison to Jitter and Shimmer. The F0 and NHR values across baseline evaluation, first month and third month follow up showed a steady deterioration which was significant. The deterioration noted from the first to third month was not statistically significant. Across genders both F0 and NHR deterioration is more in males than in females. Radiotherapy causes definitive alterations in some acoustic measures of voice, which make the voice disharmonic and hoarse with contribution of harshness and breathiness. The effect is more pronounced on vocal parameters that are structure and projection based as evidenced by deterioration in values noted in F0 and NHR. Persistent deteriorated acoustic parameters for a longer duration of time are more likely which emphasizes the need for early voice rehabilitation.

Prevention of adenosine A2A receptor activation diminishes beat-to-beat alternation in human atrial myocytes.

Atrial fibrillation (AF) has been associated with increased spontaneous calcium release from the sarcoplasmic reticulum and linked to increased adenosine A2A receptor (A2AR) expression and activation. Here we tested whether this may favor atrial arrhythmogenesis by promoting beat-to-beat alternation and irregularity. Patch-clamp and confocal calcium imaging was used to measure the beat-to-beat response of the calcium current and transient in human atrial myocytes. Responses were classified as uniform, alternating or irregular and stimulation of Gs-protein coupled receptors decreased the frequency where a uniform response could be maintained from 1.0 ± 0.1 to 0.6 ± 0.1 Hz; p < 0.01 for beta-adrenergic receptors and from 1.4 ± 0.1 to 0.5 ± 0.1 Hz; p < 0.05 for A2ARs. The latter was linked to increased spontaneous calcium release and after-depolarizations. Moreover, A2AR activation increased the fraction of non-uniformly responding cells in HL-1 myocyte cultures from 19 ± 3 to 51 ± 9 %; p < 0.02, and electrical mapping in perfused porcine atria revealed that adenosine induced electrical alternans at longer cycle lengths, doubled the fraction of electrodes showing alternation, and increased the amplitude of alternations. Importantly, protein kinase A inhibition increased the highest frequency where uniform responses could be maintained from 0.84 ± 0.12 to 1.86 ± 0.11 Hz; p < 0.001 and prevention of A2AR-activation with exogenous adenosine deaminase selectively increased the threshold from 0.8 ± 0.1 to 1.2 ± 0.1 Hz; p = 0.001 in myocytes from patients with AF. In conclusion, A2AR-activation promotes beat-to-beat irregularities in the calcium transient in human atrial myocytes, and prevention of A2AR activation may be a novel means to maintain uniform beat-to-beat responses at higher beating frequencies in patients with atrial fibrillation.

Dificuldades enfrentadas na perspectiva da gestante adolescente cadastrada na Estratégia Saúde da Família / Difficulties faced in the context of adolescent pregnant women registered at the Family Health Strategy / Las dificultades enfrentadas en el contexto de las adolescentes embarazadas inscritas en la Estrategia Salud de la Familia

Objetivo:descrever as dificuldades encontradas por gestantes adolescentes cadastradas em Estratégias Saúde da Família. Metodologia:estudo exploratório e descritivo, com abordagem qualitativa, com17 gestantes adolescentes cadastradas nas Estratégias Saúde da Família no município de Cajazeiras/PB. Utilizou-se uma entrevista, com gravador portátil e roteiro semiestruturado.Os dados foram sistematizados conforme Análise de Conteúdo por categorias temáticas de Bardin. O projeto de pesquisa foi aprovado pelo Comitê de Ética em Pesquisa, protocolo 795.786. Resultados:a partir da análise dos discursos das participantes surgiram três categorias temáticas com respectivas subcategorias: << Dificuldades individuais (financeiras, pouca idade da gestante e falta de maturidade diante da maternidade) >>; << Dificuldades familiares (baixa renda familiar, e não aceitação da gravidez pelos familiares)>> e << Dificuldades sociais (falta de apoio e preconceito da população) >>. Conclusão:é um problema da sociedade moderna, sendo um fenômeno complexo que apresenta manifestações específicas que devem ser minimizadas pelos profissionais de saúde, sobretudo a enfermagem.(AU)

Objective:describing the difficulties found by pregnant adolescents registered in Family Health Strategies. Methodology:an exploratory and descriptive study with a qualitative approach. It was performed with17 pregnant adolescents registered in the Family Health Strategy in the city of Cajazeiras/PB. There was conducted an interview with a portable recorder and a semi-structured guidance. The data were systematized as Content Analysis by thematic categories of Bardin. The research project was approved by the Research Ethics Committee, protocol 795.786. Results:from the analysis of the speeches of the participants emerged three thematic categories with the respective sub-categories: << Individual difficulties (financial, low age of the pregnant and lack of maturity on motherhood) >>; << Family difficulties (low family income, and non-acceptance of pregnancy by the family) >> and << Social difficulties (lack of support and prejudice of the population) >>. Conclusion:it is a problem of modern society, being a complex phenomenon that has specific manifestations that should be minimized by health professionals, especially nurses.(AU)

Objetivo:describir las dificultades encontradas por las adolescentes embarazadas inscritas en las Estrategias Salud de la Familia. Metodología:un estudio exploratorio y descriptivo con enfoque cualitativoconun total de 17 adolescentes embarazadas inscritas en las Estrategias de Salud de la familia del municipio de Cajazeiras/PB. Se utilizó una entrevista con grabadora portátil y guión semi-estructurado. Los datos fueron sistematizados como Análisis de Contenido por categorías temáticas de Bardin. El proyectode investigación fue aprobado por el Comité de Ética en la Investigación, el protocolo 795.786. Resultados:desde el análisis de los discursos de los participantes emergieron tres categorías temáticas con sub-categorías: << Dificultades individuales (financiera, poca edad de la mujer embarazada y la falta de madurez de la maternidad) >>; << Dificultades familiares (de bajos ingresos, y no aceptación del embarazo por la familia) >> y << Dificultades sociales (falta de apoyo y los prejuicios de la población)>>. Conclusión:es un problema de la sociedad moderna, al ser un fenómeno complejo que presenta manifestaciones específicas que deben ser minimizadas por los profesionales de la salud, sobre todo enfermeras.(AU)

Repercussão da acomodação familiar no tratamento do transtorno obsessivo-compulsivo / Family accommodation repercussion on the treatment for obsessive-compulsive disorder

O transtorno obsessivo-compulsivo (TOC) provoca repercussões importantes no funcionamento familiar. Comportamentos de acomodação, como modificações na rotina devido aos sintomas dos portadores do TOC, são comuns. Esse fenômeno vem recebendo atenção crescente na literatura nos últimos anos, pois está associado a uma pior resposta aos tratamentos de primeira escolha para o TOC, como terapia cognitivo-comportamental (TCC) e farmacoterapia. Este artigo revisa o tema da acomodação familiar, abrangendo suas implicações no tratamento com TCC. Estudos têm investigado sua relação com os sintomas obsessivo-compulsivos apresentados pelos pacientes e, não raro, por pessoas da família. Ao compreender como a acomodação familiar ocorre e quais os comportamentos dos familiares que estão contribuindo para a manutenção dos sintomas, os terapeutas podem adequar estratégias de intervenção e psicoeducação. Embora o crescente entendimento sobre essa questão tenha contribuído para melhorar o tratamento do TOC, são necessários mais estudos para estabelecer o papel das diferentes intervenções psicoterápicas sobre esses comportamentos e sua contribuição na resposta à TCC para o TOC(AU)

Obsessive-Compulsive Disorder (OCD) has considerable impact on family functioning. Accommodation behaviors, such as changes in routine due to the symptoms of OCD patients, are highly frequent. This phenomenon has been receiving growing attention in the literature during the recent years, since it is associated with worse response to first-line treatments, as Cognitive-Behavioral Therapy (CBT) and pharmacotherapy. The present article reviews the issue of family accommodation, including its implications on the treatment with CBT. Studies have investigated the relationship between the accommodation behaviors in the family and patients and family members symptoms. Once therapists have the understanding about how family accommodation occurs and what are the behaviors in the family that could be associated with the maintenance of symptoms, they could adequate intervention and psycho-education strategies towards OCD treatment. Although our understanding on family accommodation phenomenon has been contributed to the improvement of OCD treatment, further studies are needed to clarify the role of the different existing psychotherapeutic interventions on this kind of behavior besides its contribution to CBT response in OCD(AU)

Ageing is associated with deterioration of calcium homeostasis in isolated human right atrial myocytes.

AIMS: Ageing-related cardiac disorders such as heart failure and atrial fibrillation often present with intracellular calcium homeostasis dysfunction. However, knowledge of the intrinsic effects of ageing on cellular calcium handling in the human heart is sparse. Therefore, this study aimed to analyse how ageing affects key mechanisms that regulate intracellular calcium in human atrial myocytes. METHODS AND RESULTS: Whole membrane currents and intracellular calcium transients were measured in isolated human right atrial myocytes from 80 patients with normal left atrial dimensions and no history of atrial fibrillation. Patients were categorized as young (<55 years, n = 21), middle aged (55-74 years, n = 42), and old (≥75 years, n = 17). Protein levels were determined by western blot. Ageing was associated with the following electrophysiological changes: (i) a 3.2-fold decrease in the calcium transient (P < 0.01); (ii) reduction of the L-type calcium current (ICa) amplitude (2.4 ± 0.3 pA/pF vs. 1.4 ± 0.2 pA/pF, P < 0.01); (iii) lower levels of L-type calcium channel alpha-subunit (P < 0.05); (iv) lower rates of both fast (14.5 ± 0.9 ms vs. 20.9 ± 1.9, P < 0.01) and slow (73 ± 3 vs. 120 ± 12 ms, P < 0.001) ICa inactivation; and (v) a decrease in the sarcoplasmic reticulum calcium content (10.1 ± 0.8 vs. 6.4 ± 0.6 amol/pF, P < 0.005) associated with a significant decrease in both SERCA2 (P < 0.05) and calsequestrin-2 (P < 0.05) protein levels. In contrast, ageing did not affect spontaneous sarcoplasmic reticulum calcium release. CONCLUSION: Ageing is associated with depression of SR calcium content, L-type calcium current, and calcium transient amplitude that may favour a progressive decline in right atrial contractile function with age.

Sarcoplasmic reticulum and L-type Ca²âº channel activity regulate the beat-to-beat stability of calcium handling in human atrial myocytes.

Irregularities in intracellular calcium on a beat-to-beat basis can precede cardiac arrhythmia, but the mechanisms inducing such irregularities remain elusive. This study tested the hypothesis that sarcoplasmic reticulum (SR) and L-type calcium channel activity determine the beat-to-beat response and its rate dependency. For this purpose, patch-clamp technique and confocal calcium imaging was used to record L-type calcium current (ICa) and visualize calcium in human atrial myocytes subjected to increasing stimulation frequencies (from 0.2 to 2 Hz). The beat-to-beat response was heterogeneous among a population of 133 myocytes, with 30 myocytes responding uniformly at all frequencies, while alternating and irregular responses were induced in 78 and 25 myocytes, respectively. Myocytes with uniform responses had the lowest frequency of calcium wave-induced transient inward currents (ITI; 0.4 ± 0.2 min⁻¹), ICa density (1.8 ± 0.3 pA pF⁻¹) and caffeine-releasable calcium load (6.2 ± 0.5 amol pF⁻¹), while those with alternating responses had the highest ITI frequency (1.8 ± 0.3 min⁻¹,P =0.003) and ICa density (2.4 ± 0.2 pA pF⁻¹, P =0.04). In contrast, the calcium load was highest in myocytes with irregular responses (8.5 ± 0.7 amol pF⁻¹, P =0.01). Accordingly, partial ICa inhibition reduced the incidence (from 78 to 44%, P <0.05) and increased the threshold frequency for beat-to-beat alternation (from 1.3 ± 0.2 to 1.9 ± 0.2 Hz, P <0.05). Partial inhibition of SR calcium release reduced the ITI frequency, increased calcium loading and favoured induction of irregular responses, while complete inhibition abolished beat-to-beat alternation at all frequencies. In conclusion, the beat-to-beat response was heterogeneous among human atrial myocytes subjected to increasing stimulation frequencies, and the nature and stability of the response were determined by the SR and L-type calcium channel activities, suggesting that these mechanisms are key to controlling cardiac beat-to-beat stability.

Hypoxia exacerbates Ca(2+)-handling disturbances induced by very low density lipoproteins (VLDL) in neonatal rat cardiomyocytes.

It is known that myocardium suffers serious alterations under ischemic conditions such as lipid overloading and electrophysiological alterations. However, it is unknown whether intracellular lipid accumulation and calcium dysfunction share common pathophysiological mechanisms under ischemia. The aims of this study were 1) to analyze the effect of normal and high doses of very low density lipoproteins (VLDL) on lipid content and calcium handling; 2) to investigate whether hypoxia modulates the effect of high VLDL doses; and 3) to identify potentially underlying mechanisms in cardiomyocytes. For this purpose, neonatal rat ventricular myocytes cultures were prepared from hearts of 3-4-day-old rats. High doses of VLDL that induced cholesteryl ester (CE) and triglyceride (TG) accumulation strongly reduced sarco(endo)plasmic reticulum Ca ATPase-2 (SERCA-2) expression, calcium transient amplitude and sarcoplasmic reticulum (SR) calcium loading. Interestingly, hypoxia, by upregulating VLDL-receptor expression (4.5-fold at 16h) increased CE (1.5-fold) and TG (3-fold) cardiomyocyte content and exacerbated the negative effect of VLDL on SERCA-2 expression. Functionally, the hypoxic exacerbation of VLDL-mediated SERCA-2 downregulation was translated into a stronger decrease in calcium transient amplitude and SR calcium loading in myocytes exposed simultaneously to hypoxia and high VLDL. In conclusion, high VLDL doses alter calcium handling in cardiomyocytes and SERCA-2 play a pivotal role in the hypoxic exacerbation of VLDL-mediated effects on cardiac calcium handling. Potentiation of VLDL's effects under hypoxia is explained, at least in part, by hypoxic upregulation of the expression of VLDL-receptor.

Abnormal calcium handling in atrial fibrillation is linked to up-regulation of adenosine A2A receptors.

AIMS: Atrial fibrillation (AF) is associated with abnormal sarcoplasmic reticulum (SR) calcium release, which is promoted by adenosine A(2A) receptor (A(2A)R) activation. Here, we tested the hypothesis that abnormal calcium release in AF is linked to A(2A)R remodelling. METHODS AND RESULTS: Western blotting and quantitative real-time PCR were used to determine A(2A)R mRNA and protein levels in right atrial samples from patients with and without AF. Effects of A(2A)R activation on calcium handling were assessed with patch-clamp technique and confocal calcium imaging. A(2A)R mRNA levels and functional A(2A)Rs were moderately up-regulated in patients with atrial dilation and markedly up-regulated in those with AF. Accordingly, A(2A)R stimulation significantly increased ryanodine receptor phosphorylation in AF patients, and spontaneous calcium waves increased moderately in myocytes from patients with atrial dilation and strongly in patients with AF (2.2 ± 2.1 to 14.3 ± 8.8 min(-1), n = 6, P = 0.01). Moreover, the high baseline level of calcium waves in AF was reduced by A(2A)R antagonists (3.5 ± 2.0 to 1.3 ± 1.3 min(-1), n = 6, P = 0.007) or adenosine deaminase (1.7 ± 1.5 to 0.5 ± 0.6 min(-1), n = 10, P = 0.02) suggesting that A(2A)Rs are activated by endogenous adenosine. Indeed, intracellular perfusion with adenosine significantly increased the calcium wave frequency (1.1 ± 0.8 to 8.2 ± 3.3 min(-1), n = 8), whereas adenosine removal from the cytosol decreased it (2.1 ± 0.9 to 0.3 ± 0.3 min(-1), n = 8, P = 0.04). CONCLUSIONS: Atrial fibrillation patients show increased A(2A)R expression that may account for the high baseline level of spontaneous SR calcium release seen in myocytes from these patients, and the ability of A(2A)R antagonists to reduce this abnormal calcium release points to the A(2A)R as a novel molecular target in AF.

The progesterone receptor regulates the expression of TRPV4 channel.

The transient receptor potential cationic channel TRPV4 contributes to different aspects of cell physiology via the generation of a Ca2+ signal and/or depolarization of the membrane potential. TRPV4 channel integrates distinct physical and chemical stimuli, including osmotic and mechanical stress, heat, acidic pH, endogenous ligands, and synthetic agonists such as 4alpha-phorbol 12,13-didecanoate (4alphaPDD). Although several regulatory sites controlling TRPV4 channel activity have been identified, very little is known about the regulation of TRPV4 expression, a situation common to other TRP channels. Here we show that TRPV4 expression is under the control of progesterone in both human airways and mammary gland epithelial cells, as well as in vascular smooth muscle cells. Exposure of human airways epithelial CFT1-LCFSN and mammary gland epithelial T47D cells to progesterone decreased TRPV4 mRNA and protein expression. Consequently, 4alphaPDD-induced cationic currents and Ca2+ signals were also diminished in progesterone-treated cells. The effect of progesterone was reverted by the progesterone receptor (PR) antagonist RU-486 or following transfection with small interference RNA (siRNA) against both PRA and PRB isoforms. Interestingly, TRPV4 expression and activity were increased in T47D mammary gland epithelial cells when PR was silenced with siRNA. Transcriptional regulation of -1.3 kB TRPV4 promoter-luciferase plasmids was also evaluated in vascular smooth muscle cells. TRPV4 promoter activity was reduced by coexpression with PR and further reduced in the presence of PG. Together, our data report the regulation of TRPV4 expression by progesterone, a process that requires a functional PR.

Functional coupling of TRPV4 cationic channel and large conductance, calcium-dependent potassium channel in human bronchial epithelial cell lines.

Calcium-dependent potassium channels are implicated in electrolyte transport, cell volume regulation and mechanical responses in epithelia, although the pathways for calcium entry and their coupling to the activation of potassium channels are not fully understood. We now show molecular evidence for the presence of TRPV4, a calcium permeable channel sensitive to osmotic and mechanical stress, and its functional coupling to the large conductance calcium-dependent potassium channel (BK(Ca)) in a human bronchial epithelial cell line (HBE). Reverse transcriptase polymerase chain reaction, intracellular calcium imaging and whole-cell patch-clamp experiments using HBE cells demonstrated the presence of TRPV4 messenger and Ca(2+) entry, and outwardly rectifying cationic currents elicited by the TRPV4 specific activator 4alpha-phorbol 12,13-didecanoate (4alphaPDD). Cell-attached and whole-cell patch-clamp of HBE cells exposed to 4alphaPDD, and hypotonic and high-viscosity solutions (related to mechanical stress) revealed the activation of BK(Ca) channels subsequent to extracellular Ca(2+) influx via TRPV4, an effect lost upon antisense-mediated knock-down of TRPV4. Further analysis of BK(Ca) modulation after TRPV4 activation showed that the Ca(2+) signal can be generated away from the BK(Ca) location at the plasma membrane, and it is not mediated by intracellular Ca(2+) release via ryanodine receptors. Finally, we have shown that, unlike the reported disengagement of TRPV4 and BK(Ca) in response to hypotonic solutions, cystic fibrosis bronchial epithelial cells (CFBE) preserve the functional coupling of TRPV4 and BK(Ca) in response to high-viscous solutions.

IP3 sensitizes TRPV4 channel to the mechano- and osmotransducing messenger 5'-6'-epoxyeicosatrienoic acid.

Mechanical and osmotic sensitivity of the transient receptor potential vanilloid 4 (TRPV4) channel depends on phospholipase A(2) (PLA(2)) activation and the subsequent production of the arachidonic acid metabolites, epoxyeicosatrienoic acid (EET). We show that both high viscous loading and hypotonicity stimuli in native ciliated epithelial cells use PLA(2)-EET as the primary pathway to activate TRPV4. Under conditions of low PLA(2) activation, both also use extracellular ATP-mediated activation of phospholipase C (PLC)-inositol trisphosphate (IP(3)) signaling to support TRPV4 gating. IP(3), without being an agonist itself, sensitizes TRPV4 to EET in epithelial ciliated cells and cells heterologously expressing TRPV4, an effect inhibited by the IP(3) receptor antagonist xestospongin C. Coimmunoprecipitation assays indicated a physical interaction between TRPV4 and IP(3) receptor 3. Collectively, our study suggests a functional coupling between plasma membrane TRPV4 channels and intracellular store Ca(2+) channels required to initiate and maintain the oscillatory Ca(2+) signal triggered by high viscosity and hypotonic stimuli that do not reach a threshold level of PLA(2) activation.

IP3 sensitizes TRPV4 channel to the mechano- and osmotransducing messenger 5'-6'-epoxyeicosatrienoic acid.

Mechanical and osmotic sensitivity of the transient receptor potential vanilloid 4 (TRPV4) channel depends on phospholipase A2 (PLA2) activation and the subsequent production of the arachidonic acid metabolites, epoxyeicosatrienoic acid (EET). We show that both high viscous loading and hypotonicity stimuli in native ciliated epithelial cells use PLA2-EET as the primary pathway to activate TRPV4. Under conditions of low PLA2 activation, both also use extracellular ATP-mediated activation of phospholipase C (PLC)-inositol trisphosphate (IP3) signaling to support TRPV4 gating. IP3, without being an agonist itself, sensitizes TRPV4 to EET in epithelial ciliated cells and cells heterologously expressing TRPV4, an effect inhibited by the IP3 receptor antagonist xestospongin C. Coimmunoprecipitation assays indicated a physical interaction between TRPV4 and IP3 receptor 3. Collectively, our study suggests a functional coupling between plasma membrane TRPV4 channels and intracellular store Ca2+ channels required to initiate and maintain the oscillatory Ca2+ signal triggered by high viscosity and hypotonic stimuli that do not reach a threshold level of PLA2 activation.

[Mothers' conceptions about their premature children in ICU]. / Concepções das mães sobre os filhos prematuros em UTI.

In this study, our purpose was to direct ourselves to the mothers who had babies that were born prematurely and needed to be assisted in a Neonatal Intensive Care Unit, searching for the comprehension of the feelings provoked in these mothers due to such situation and, thus, project new possibilities of caring aimed at these beings. For that, we opted for a qualitative-descriptive study, based on the principles of the existential phenomenology. From the analysis, four categories emerged; the pain to see her child be born prematurely and then be taken away from her arms; undergoing the possibility of losing a part of hers; revival of feelings from the understanding of the situation of the child and; the importance of the hospital's staff during the process of her child's recovering. We inferred that listening and paying attention are vital instruments to aid the mother and her child in their singularities.

Modeling of single noninactivating Na+ channels: evidence for two open and several fast inactivated states.

Voltage-gated Na(+) channels play a fundamental role in the excitability of nerve and muscle cells. Defects in fast Na(+) channel inactivation can cause hereditary muscle diseases with hyper- or hypoexcitability of the sarcolemma. To explore the kinetics and gating mechanisms of noninactivating muscle Na(+) channels on a molecular level, we analyzed single channel currents from wild-type and five mutant Na(+) channels. The mutations were localized in different protein regions which have been previously shown to be important for fast inactivation (D3-D4-linker, D3/S4-S5, D4/S4-S5, D4/S6) and exhibited distinct grades of defective fast inactivation with varying levels of persistent Na(+) currents caused by late channel reopenings. Different gating schemes were fitted to the data using hidden Markov models with a correction for time interval omission and compared statistically. For all investigated channels including the wild-type, two open states were necessary to describe our data. Whereas one inactivated state was sufficient to fit the single channel behavior of wild-type channels, modeling the mutants with impaired fast inactivation revealed evidence for several inactivated states. We propose a single gating scheme with two open and three inactivated states to describe the behavior of all five examined mutants. This scheme provides a biological interpretation of the collected data, based on previous investigations in voltage-gated Na(+) and K(+) channels.

Concepções das mães sobre os filhos prematuros em UTI / Concepciones de las madres acerca de sus hijos prematuros en la UTI / Mothers' conceptions about their premature children in ICU

Neste estudo, nossa proposta foi dirigir-nos às mães que tiveram bebês nascidos prematuros e necessitaram ser assistidas em UTI neonatal, buscando compreender os sentimentos suscitados nessas mães por tal situação e, assim, projetar novas possibilidades de cuidado a esses seres. Para tanto, optamos por um estudo qualitativo-descritivo, embasado nos princípios da fenomenologia existencial. Da análise emergiram quatro categorias; A dor de ver seu filho nascer prematuro e ser tirado de seus braços; padecimento ante a possibilidade de perder parte de si; sentimentos avivados a partir da compreensão da situação do filho e, a importância da equipe de saúde no processo de recuperação do filho. Depreendemos que escutar e olhar atentamente são instrumentos imprescindíveis para assistir a mãe e seu filho em suas singularidades.

In this study, our purpose was to direct ourselves to the mothers who had babies that were born prematurely and needed to be assisted in a Neonatal Intensive Care Unit, searching for the comprehension of the feelings provoked in these mothers due to such situation and, thus, project new possibilities of caring aimed at these beings. For that, we opted for a qualitative-descriptive study, based on the principles of the existential phenomenology. From the analysis, four categories emerged; the pain to see her child be born prematurely and then be taken away from her arms; undergoing the possibility of losing a part of hers; revival of feelings from the understanding of the situation of the child and; the importance of the hospital's staff during the process of her child's recovering. We inferred that listening and paying attention are vital instruments to aid the mother and her child in their singularities.

En este estudio nuestra propuesta fue dirigirnos a las madres que tuvieron bebés nacidos prematuros y necesitaron ser acompañados en UCI Neonatal, buscando comprender los sentimientos provocados en esas madres por tal situación y, así, proyectar nuevas posibilidad de cuidados a esos seres. Para eso, optamos por un estudio cualitativo descriptivo, con base en los principios de la fenomenología existencial. Del análisis emergieron cuatro categorías; El dolor de ver a su hijo nacer prematuro y ser arrancado de sus brazos; padecimientos ante la posibilidad de perder parte de sí misma; sentimientos avivados a partir de la comprensión de la situación del hijo y, la importancia del equipe de salud en el proceso de recuperación del hijo. Percibimos que escuchar y mirar atentamente son instrumentos imprescindibles para ayudar ala madre y a su hijo en sus singularidad.

TRPV4 channel is involved in the coupling of fluid viscosity changes to epithelial ciliary activity.

Autoregulation of the ciliary beat frequency (CBF) has been proposed as the mechanism used by epithelial ciliated cells to maintain the CBF and prevent the collapse of mucociliary transport under conditions of varying mucus viscosity. Despite the relevance of this regulatory response to the pathophysiology of airways and reproductive tract, the underlying cellular and molecular aspects remain unknown. Hamster oviductal ciliated cells express the transient receptor potential vanilloid 4 (TRPV4) channel, which is activated by increased viscous load involving a phospholipase A(2)-dependent pathway. TRPV4-transfected HeLa cells also increased their cationic currents in response to high viscous load. This mechanical activation is prevented in native ciliated cells loaded with a TRPV4 antibody. Application of the TRPV4 synthetic ligand 4alpha-phorbol 12,13-didecanoate increased cationic currents, intracellular Ca(2+), and the CBF in the absence of a viscous load. Therefore, TRPV4 emerges as a candidate to participate in the coupling of fluid viscosity changes to the generation of the Ca(2+) signal required for the autoregulation of CBF.