935 resultados para playing by ear


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La Directiva 2003/10/CE del Parlamento Europeo y del Consejo, del 6 de febrero de 2003, específica con arreglo al apartado 1 del artículo 16 de la Directiva 89/391/CEE las disposiciones mínimas de seguridad y de salud relativas a la exposición de los trabajadores a los riesgos derivados de los agentes físicos (ruido). En la industria musical, y en concreto en los músicos de orquesta, una exposición de más de ocho horas al día a un nivel de presión sonora de 80dB(A) o más es algo muy común. Esta situación puede causar a los trabajadores daños auditivos como la hiperacusia, hipoacusia, tinitus o ruptura de la membrana basilar entre otros. Esto significa que deben tomarse medidas para implementar las regulaciones de la forma más razonable posible para que la interpretación del músico, la dinámica y el concepto musical que se quiere transmitir al público se vea lo menos afectada posible. Para reducir la carga auditiva de los músicos de orquesta frente a fuertes impactos sonoros provenientes de los instrumentos vecinos, se está investigando sobre el uso de unos paneles acústicos que colocados en puntos estratégicos de la orquesta pueden llegar a reducir el impacto sonoro sobre el oído hasta 20dB. Los instrumentos de viento metal y de percusión son los responsables de la mayor emisión de presión sonora. Para proteger el oído de los músicos frente a estos impactos, se colocan los paneles en forma de barrera entre dichos instrumentos y los músicos colocados frente a ellos. De esta forma se protege el oído de los músicos más afectados. Para ver el efecto práctico que producen estos paneles en un conjunto orquestal, se realizan varias grabaciones en los ensayos y conciertos de varias orquestas. Los micrófonos se sitúan a la altura del oído y a una distancia de no más de 10cm de la oreja de varios de los músicos más afectados y de los músicos responsables de la fuerte emisión sonora. De este modo se puede hacer una comparación de los niveles de presión sonora que percibe cada músico y evaluar las diferencias de nivel existentes entre ambos. Así mismo se utilizan configuraciones variables de los paneles para comparar las diferencias de presión sonora que existen entre las distintas posibilidades de colocarlos y decidir así sobre la mejor ubicación y configuración de los mismos. A continuación, una vez obtenidos las muestras de audio y los diferentes archivos de datos medidos con un analizador de audio en distintas posiciones de la orquesta, todo ello se calibra y analiza utilizando un programa desarrollado en Matlab, para evaluar el efecto de los paneles sobre la percepción auditiva de los músicos, haciendo especial hincapié en el análisis de las diferencias de nivel de presión sonora (SPL). Mediante el cálculo de la envolvente de las diferencias de nivel, se evalúa de un modo estadístico el efecto de atenuación de los paneles acústicos en los músicos de orquesta. El método está basado en la probabilidad estadística de varias muestras musicales ya que al tratarse de música tocada en directo, la dinámica y la sincronización entre los músicos varía según el momento en que se toque. Estos factores junto con el hecho de que la partitura de cada músico es diferente dificulta la comparación entre dos señales grabadas en diferentes puntos de la orquesta. Se necesita por lo tanto de varias muestras musicales para evaluar el efecto de atenuación de los paneles en las distintas configuraciones mencionadas anteriormente. El estudio completo del efecto de los paneles como entorno que influye en los músicos de orquesta cuando están sobre el escenario, tiene como objetivo la mejora de sus condiciones de trabajo. Abstract For several years, the European Union has been adopting many laws and regulations to protect and give more security to people who are exposed to some risk in their job. Being exposed to a loud sound pressure level during many hours in the job runs the risk of hearing damage. Particularly in the field of music, the ear is the most important working tool. Not taking care of the ear can cause some damage such as hearing loss, tinnitus, hyperacusis, diplacusis, etc. This could have an impact on the efficiency and satisfaction of the musicians when they are playing, which could also cause stress problems. Orchestra musicians, as many other workers in this sector, are usually exposed to a sound level of 80dB(A) or more during more than eight hours per day. It means that they must satisfy the law and their legal obligations to avoid health problems proceeding from their job. Putting into practice the new regulations is a challenge for orchestras. They must make sure that the repertoire, with its dynamic, balance and feeling, is not affected by the reduction of sound levels imposed by the law. This study tries to investigate the benefits and disadvantages of using shields as a hearing protector during rehearsals and orchestral concerts.

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The human and shark Na–K–Cl cotransporters (NKCC), although 74% identical in amino acid sequence, exhibit marked differences in ion transport and bumetanide binding. We have utilized shark–human chimeras of NKCC1 to search for regions that confer the kinetic differences. Two chimeras (hs3.1 and its reverse sh3.1) with a junction point located at the beginning of the third transmembrane domain were examined after stable transfection in HEK-293 cells. Each carried out bumetanide-sensitive 86Rb influx with cation affinities intermediate between shark and human cotransporters. In conjunction with the previous finding that the N and C termini are not responsible for differences in ion transport, the current observations identify the second transmembrane domain as playing an important role. Site-specific mutagenesis of two pairs of residues in this domain revealed that one pair is indeed involved in the difference in Na affinity, and a second pair is involved in the difference in Rb affinity. Substitution of the same residues with corresponding residues from NKCC2 or the Na-Cl cotransporter resulted in cation affinity changes, consistent with the hypothesis that alternative splicing of transmembrane domain 2 endows different versions of NKCC2 with unique kinetic behaviors. None of the changes in transmembrane domain 2 was found to substantially affect Km(Cl), demonstrating that the affinity difference for Cl is specified by the region beyond predicted transmembrane domain 3. Finally, unlike Cl, bumetanide binding was strongly affected by shark–human replacement of transmembrane domain 2, indicating that the bumetanide-binding site is not the same as the Cl-binding site.

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A systematic screen termed the allelic message display (AMD) was developed for the hunting of imprinted genes. In AMD, differential display PCR is adopted to image allelic expression status of multiple polymorphic transcripts in two parental mouse strains, reciprocal F1 hybrids and pooled backcross progenies. From the displayed patterns, paternally and maternally expressed transcripts can be unequivocally identified. The effectiveness of AMD screening was clearly demonstrated by the identification of a paternally expressed gene Impact on mouse chromosome 18, the predicted product of which belongs to the YCR59c/yigZ hypothetical protein family composed of yeast and bacterial proteins with currently unknown function. In contrast with previous screening methods necessitating positional cloning efforts or generation of parthenogenetic embryos, this approach requires nothing particular but appropriately crossed mice and can be readily applied to any tissues at various developmental stages. Hence, AMD would considerably accelerate the identification of imprinted genes playing pivotal roles in mammalian development and the pathogenesis of various diseases.

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Our recent studies have shown that deregulated expression of R2, the rate-limiting component of ribonucleotide reductase, enhances transformation and malignant potential by cooperating with activated oncogenes. We now demonstrate that the R1 component of ribonucleotide reductase has tumor-suppressing activity. Stable expression of a biologically active ectopic R1 in ras-transformed mouse fibroblast 10T½ cell lines, with or without R2 overexpression, led to significantly reduced colony-forming efficiency in soft agar. The decreased anchorage independence was accompanied by markedly suppressed malignant potential in vivo. In three ras-transformed cell lines, R1 overexpression resulted in abrogation or marked suppression of tumorigenicity. In addition, the ability to form lung metastases by cells overexpressing R1 was reduced by >85%. Metastasis suppressing activity also was observed in the highly malignant mouse 10T½ derived RMP-6 cell line, which was transformed by a combination of oncogenic ras, myc, and mutant p53. Furthermore, in support of the above observations with the R1 overexpressing cells, NIH 3T3 cells cotransfected with an R1 antisense sequence and oncogenic ras showed significantly increased anchorage independence as compared with control ras-transfected cells. Finally, characteristics of reduced malignant potential also were demonstrated with R1 overexpressing human colon carcinoma cells. Taken together, these results indicate that the two components of ribonucleotide reductase both are unique malignancy determinants playing opposing roles in its regulation, that there is a novel control point important in mechanisms of malignancy, which involves a balance in the levels of R1 and R2 expression, and that alterations in this balance can significantly modify transformation, tumorigenicity, and metastatic potential.

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Efforts to identify the specific components of the mammalian inner ear have been hampered by the small number of neuroepithelial cells and the variety of supporting cells. To circumvent these difficulties, we used a PCR-based subtractive method on cDNA from 2-day-old mouse cochlea. A cDNA encoding a predicted 2910-amino acid protein related to mucin has been isolated. Several lines of evidence indicate, however, that this protein does not undergo the O-glycosylation characteristic to mucins. As confirmed by immunocytochemistry and biochemical experiments, this protein is specific to the inner ear. Immunohistofluorescence labeling showed that this protein is a component of all the acellular membranes of the inner ear: i.e., the tectorial membrane of the cochlea, the otoconial and accessory membranes of the utricule and saccule, the cupula of the semicircular canals, and a previously undescribed acellular material covering the otoconia of the saccule. The protein has been named otogelin with reference to its localization. A variety of nonsensory cells located underneath these membranes could be identified as synthesizing otogelin. Finally, this study revealed a maturation process of the tectorial membrane, as evidenced by the progressive organization of otogelin labeling into thick and spaced radial fiber-like structures.

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The recessive mouse mutant Mpv17 is characterized by the development of early-onset glomerulosclerosis, concomitant hypertension, and structural alterations of the inner ear. The primary cause of the disease is the loss of function of the Mpv17 protein, a peroxisomal gene product involved in reactive oxygen metabolism. In our search of a common mediator exerting effects on several aspects of the phenotype, we discovered that the absence of the Mpv17 gene product causes a strong increase in matrix metalloproteinase 2 (MMP-2) expression. This was seen in the kidney and cochlea of Mpv17-negative mice as well as in tissue culture cells derived from these animals. When these cells were transfected with the human Mpv17 homolog, an inverse causal relationship between Mpv17 and MMP-2 expression was established. These results indicate that the Mpv17 protein plays a crucial role in the regulation of MMP-2 and suggest that enhanced MMP-2 expression might mediate the mechanisms leading to glomerulosclerosis, inner ear disease, and hypertension in this model.

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Amplification of auditory stimuli by hair cells augments the sensitivity of the vertebrate inner ear. Cell-body contractions of outer hair cells are thought to mediate amplification in the mammalian cochlea. In vertebrates that lack these cells, and perhaps in mammals as well, active movements of hair bundles may underlie amplification. We have evaluated a mathematical model in which amplification stems from the activity of mechanoelectrical-transduction channels. The intracellular binding of Ca2+ to channels is posited to promote their closure, which increases the tension in gating springs and exerts a negative force on the hair bundle. By enhancing bundle motion, this force partially compensates for viscous damping by cochlear fluids. Linear stability analysis of a six-state kinetic model reveals Hopf bifurcations for parameter values in the physiological range. These bifurcations signal conditions under which the system’s behavior changes from a damped oscillatory response to spontaneous limit-cycle oscillation. By varying the number of stereocilia in a bundle and the rate constant for Ca2+ binding, we calculate bifurcation frequencies spanning the observed range of auditory sensitivity for a representative receptor organ, the chicken’s cochlea. Simulations using prebifurcation parameter values demonstrate frequency-selective amplification with a striking compressive nonlinearity. Because transduction channels occur universally in hair cells, this active-channel model describes a mechanism of auditory amplification potentially applicable across species and hair-cell types.

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Within the mammalian inner ear there are six separate sensory regions that subserve the functions of hearing and balance, although how these sensory regions become specified remains unknown. Each sensory region is populated by two cell types, the mechanosensory hair cell and the supporting cell, which are arranged in a mosaic in which each hair cell is surrounded by supporting cells. The proposed mechanism for creating the sensory mosaic is lateral inhibition mediated by the Notch signaling pathway. However, one of the Notch ligands, Jagged1 (Jag1), does not show an expression pattern wholly consistent with a role in lateral inhibition, as it marks the sensory patches from very early in their development—presumably long before cells make their final fate decisions. It has been proposed that Jag1 has a role in specifying sensory versus nonsensory epithelium within the ear [Adam, J., Myat, A., Roux, I. L., Eddison, M., Henrique, D., Ish-Horowicz, D. & Lewis, J. (1998) Development (Cambridge, U.K.) 125, 4645–4654]. Here we provide experimental evidence that Notch signaling may be involved in specifying sensory regions by showing that a dominant mouse mutant headturner (Htu) contains a missense mutation in the Jag1 gene and displays missing posterior and sometimes anterior ampullae, structures that house the sensory cristae. Htu/+ mutants also demonstrate a significant reduction in the numbers of outer hair cells in the organ of Corti. Because lateral inhibition mediated by Notch predicts that disruptions in this pathway would lead to an increase in hair cells, we believe these data indicate an earlier role for Notch within the inner ear.

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Pendrin is an anion transporter encoded by the PDS/Pds gene. In humans, mutations in PDS cause the genetic disorder Pendred syndrome, which is associated with deafness and goiter. Previous studies have shown that this gene has a relatively restricted pattern of expression, with PDS/Pds mRNA detected only in the thyroid, inner ear, and kidney. The present study examined the distribution and function of pendrin in the mammalian kidney. Immunolocalization studies were performed using anti-pendrin polyclonal and monoclonal antibodies. Labeling was detected on the apical surface of a subpopulation of cells within the cortical collecting ducts (CCDs) that also express the H+-ATPase but not aquaporin-2, indicating that pendrin is present in intercalated cells of the CCD. Furthermore, pendrin was detected exclusively within the subpopulation of intercalated cells that express the H+-ATPase but not the anion exchanger 1 (AE1) and that are thought to mediate bicarbonate secretion. The same distribution of pendrin was observed in mouse, rat, and human kidney. However, pendrin was not detected in kidneys from a Pds-knockout mouse. Perfused CCD tubules isolated from alkali-loaded wild-type mice secreted bicarbonate, whereas tubules from alkali-loaded Pds-knockout mice failed to secrete bicarbonate. Together, these studies indicate that pendrin is an apical anion transporter in intercalated cells of CCDs and has an essential role in renal bicarbonate secretion.

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Recent theoretical advances have dramatically increased the relevance of game theory for predicting human behavior in interactive situations. By relaxing the classical assumptions of perfect rationality and perfect foresight, we obtain much improved explanations of initial decisions, dynamic patterns of learning and adjustment, and equilibrium steady-state distributions.

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The sensory patches in the ear of a vertebrate can be compared with the mechanosensory bristles of a fly. This comparison has led to the discovery that lateral inhibition mediated by the Notch cell–cell signaling pathway, first characterized in Drosophila and crucial for bristle development, also has a key role in controlling the pattern of sensory hair cells and supporting cells in the ear. We review the arguments for considering the sensory patches of the vertebrate ear and bristles of the insect to be homologous structures, evolved from a common ancestral mechanosensory organ, and we examine more closely the role of Notch signaling in each system. Using viral vectors to misexpress components of the Notch pathway in the chick ear, we show that a simple lateral-inhibition model based on feedback regulation of the Notch ligand Delta is inadequate for the ear just as it is for the fly bristle. The Notch ligand Serrate1, expressed in supporting cells in the ear, is regulated by lateral induction, not lateral inhibition; commitment to become a hair cell is not simply controlled by levels of expression of the Notch ligands Delta1, Serrate1, and Serrate2 in the neighbors of the nascent hair cell; and at least one factor, Numb, capable of blocking reception of lateral inhibition is concentrated in hair cells. These findings reinforce the parallels between the vertebrate ear and the fly bristle and show how study of the insect system can help us understand the vertebrate.

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The membranous labyrinth of the inner ear establishes a precise geometrical topology so that it may subserve the functions of hearing and balance. How this geometry arises from a simple ectodermal placode is under active investigation. The placode invaginates to form the otic cup, which deepens before pinching off to form the otic vesicle. By the vesicle stage many genes expressed in the developing ear have assumed broad, asymmetrical expression domains. We have been exploring the possibility that these domains may reflect developmental compartments that are instrumental in specifying the location and identity of different parts of the ear. The boundaries between compartments are proposed to be the site of inductive interactions required for this specification. Our work has shown that sensory organs and the endolymphatic duct each arise near the boundaries of broader gene expression domains, lending support to this idea. A further prediction of the model, that the compartment boundaries will also represent lineage-restriction compartments, is supported in part by fate mapping the otic cup. Our data suggest that two lineage-restriction boundaries intersect at the dorsal pole of the otocyst, a convergence that may be critical for the specification of endolymphatic duct outgrowth. We speculate that the patterning information necessary to establish these two orthogonal boundaries may emanate, in part, from the hindbrain. The compartment boundary model of ear development now needs to be tested through a variety of experimental perturbations, such as the removal of boundaries, the generation of ectopic boundaries, and/or changes in compartment identity.

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Nitric oxide (NO) is an important mediator of inflammatory responses in the lung and a key regulator of bronchomotor tone. An airway NO synthase (NOS; EC 1.14.13.39) has been proposed as a source of endogenous NO in the lung but has not been clearly defined. Through molecular cloning, we conclusively demonstrate that NO synthesis in normal human airways is due to the continuous expression of the inducible NOS (iNOS) isoform in airway epithelial cells. Although iNOS mRNA expression is abundant in airway epithelial cells, expression is not detected in other pulmonary cell types, indicating that airway epithelial cells are unique in the continuous pattern of iNOS expression in the lung. In situ analysis reveals all airway epithelial cell types express iNOS. However, removal of epithelial cells from the in vivo airway environment leads to rapid loss of iNOS expression, which suggests expression is dependent upon conditions and/or factors present in the airway. Quantitation of NOS activity in epithelial cell lysates indicates nanomolar levels of NO synthesis occur in vivo. Remarkably, the high-level iNOS expression is constant in airway epithelium of normal individuals over time. However, expression is strikingly decreased by inhaled corticosteroids and beta-adrenergic agonists, medications commonly used in treatment of inflammatory airway diseases. Based upon these findings, we propose that respiratory epithelial cells are key inflammatory cells in the airway, functioning in host defense and potentially playing a role in airway inflammation.

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Research on the psychological impact of women's fashion has focused on fashion's negative influence over how women think and feel about themselves. Several studies have examined the relationship between fashion and women's self-appraisals (Martin & Gentry, 1997; Pinhas, Toner, Ali, Garfinkel, & Stuckless, 1999; Tiggemann, Polivy, & Hargreaves, 2009), although few investigations have explored the range of viewpoints that arise when women interact with their own personal style or with other forms of fashion media. This paper presents a narrative review of what has been written about fashion in clinical research. I briefly discuss why this is an important topic and why fashion has psychological meaning. Cognitive behavioral therapy (CBT) is considered in the exploration of fashion's impact on conjuring unproductive and productive schemas (Beck, 1976; Wright, Basco, & Thase, 2006). This discussion includes a presentation of interviews with female consultants, hypothetical examples, my own accounts, and feminist perspectives. While emphasizing the potential biases of women's interactions with fashion, I discuss matters of gender performance and reflections on clinical work. The purpose of this article is to present a pro-social defense of fashion. I do this by acquiring personal chronicles, applying those findings to the current body of research, and adding to the continued investigation of why women's fashion is still important in a postfeminist world.

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Gender differences in anthropometric and athletic properties (e.g. strength) as well as the different net heights (2.24 vs. 2.43 m) on the same field size (8x16 m) would be reflected in the game. The literature about differences between male and female playing characteristics in beach volleyball is scarce. Therefore, the aim of this study was to analyse the differences by gender in the use of offensive zones. Study participants were 20 players (10 female and 10 male) who took part in the European Beach Volleyball Championship 2005 and 2006. Video recordings were made of the 659 points in eight matches played. The beach volleyball court was divided into six zones (z1 to z6). The results showed that men and women use different offensive zones and also were different in the percentages of ball out (15.53 and 27.38% respectively). Concretely, men players used more 1, 2, 4 and 5 zones and women 1 and 5 zones. A few differences were observed in the percentage the ball to the net (7.73 and 5.35% respectively). An understanding of the use of offensive zones is relevant to establish specific tactical training patterns for beach volleyball.