Ear Formation Research Articles

Desfolha, população de plantas e precocidade do milho afetam a incidência e a severidade de podridões de colmo

As relações entre fonte e dreno interferem sobre a ocorrência de podridões de colmo na cultura do milho (Zea mays). O estudo foi conduzido em Lages, SC, para avaliar o efeito da desfolha, população de plantas e híbridos sobre as podridões do colmo do milho. O delineamento experimental foi de blocos ao acaso com parcelas sub-subdivididas e três repetições. Os híbridos P32R21 (superprecoce), Premium (precoce) e C333B (tardio) foram testados sem desfolha e com 50% de desfolha no estágio de espigamento nas populações de 25.000, 50.000, 75.000 e 100.000 plantas ha-1. Avaliaram-se a incidência e a severidade das podridões do colmo causadas por Colletotrichum graminicola, Diplodia maydis e Fusarium moniliforme. O híbrido P32R21 foi o mais afetado pelos fungos causadores de podridões. Nos híbridos P32R21 e Premium, as plantas desfolhadas foram mais severamente infectadas pelos patógenos do que as intactas. O aumento da população de plantas aumentou a intensidade (incidência ou severidade) de podridões de colmo nas plantas intactas e diminuiu a ocorrência nas desfolhadas.

Zebrafish foxi one modulates cellular responses to Fgf signaling required for the integrity of ear and jaw patterning.

We identified four insertional alleles of foxi one (foo), an embryonic lethal mutation in zebrafish that displays defects in both otic placode and the jaw. In foo/foo embryos the otic placode is split into two smaller placodes and mutant embryos show a dorsoventral (DV) cartilage defect manifested as a reduced hyomandibular and reduced third and fourth branchial arches. We identified foxi one (foo), the zebrafish ortholog of Foxi1 (FREAC6, FKHL10, HFH-3, Fkh10) and a member of the forkhead domain transcriptional regulator family, as the gene mutated in foo/foo embryos. foo is expressed in otic placode precursor cells, and foo/foo embryos lack placodal pax8 expression and have disorganized otic expression of pax2.1 and dlx3. Third stream neural crest cell migration, detected by dlx2 and krox20 expression, is aberrant in that it invades the otic placode territory. foo is expressed in pharyngeal pouch endoderm and is required for pouch expression of pax8 and proper patterning of other markers in the pouch such as nkx2.3. In foo/foo embryos, we observed a failure to maintain fgf3 expression in the pouches, followed by apoptosis of neural crest cells in adjacent arches. We conclude that foo expression is essential for pax8 expression probably downstream of Fgf signaling in a conserved pathway jointly required for integrity of patterning in the otic placode and pharyngeal pouches. We propose that correct placement of survival/proliferation cues is essential for shaping the pharyngeal cartilages and that evolutionary links between jaw and ear formation can be traced to Fgf-Foxi1-Pax8 pathways.

Determination of the embryonic inner ear.

Inner ear induction, like induction of other tissues examined in recent years, is likely to be comprised of several stages. The process begins during gastrulation when the ectoderm is competent to respond to induction. It appears that a signal from the endomesoderm underlying the otic area during gastrulation initiates induction complemented by a signal from presumptive neural tissue. By the neural plate stage, a region of ectoderm outside the neural plate is "biased" toward ear formation; this process may be part of a more general "placodal" bias shared by several sensory tissues. Induction continues during neurulation when a signal from neural tissue (possibly augmented by mesoderm underlying the otic area) results in ectoderm committed to otic vesicle formation at the time of neural tube closure. Studies on several gene families implicate them in the ear determination process. Fibroblast Growth Factor (FGF) family members are clearly involved in induction: FGFs are appropriately expressed for such a role, and have been shown to be essential for inner ear development. FGFs also have inductive activity, although it is not clear if they are sufficient for ear induction. Activation of transcription factors in the otic ectoderm, for example, by Pax gene family members, provides evidence for important changes in the responding ectoderm beginning during gastrulation and continuing through specification at the end of neurulation, although few functional tests have defined the role of these genes in determination. The challenge remains to merge embryologic data with gene function studies to develop a clear model for the molecular basis of inner ear induction.

An algorithm for determining the optimal blank shape for the deep drawing of aluminum cups

In the deep drawing of cups, the earing defect is caused by planar anisotropy in the sheet and friction between the blank and punch/die. In the past, several incomplete research efforts have been directed toward predicting an optimal blank shape that will avoid the formation of ears. In this paper, we consider the problem of optimal blank design for deep drawing, including the effects of anisotropy and friction. The material considered for the simulations is aluminum 2048. A planar anisotropic yield function proposed by Barlat is used. The initial blank shape chosen is circular. A finite element analysis is performed to simulate the deep-drawing process. An error metric, to measure the amount of earing, is constructed for the resulting cup. This error metric is then used to re-design the initial blank shape. The cycle is repeated until the error metric satisfies a preset convergence criterion. This iterative design process leads to an optimal blank shape. Several different test problems are considered, including flanged and flangeless circular and square cups. Simulation results are very encouraging with reasonable number of iterations to arrive at the optimal blank shape.

The elongation factors Pandora/Spt6 and Foggy/Spt5 promote transcription in the zebrafish embryo.

Precise temporal and spatial control of transcription is a fundamental component of embryonic development. Regulation of transcription elongation can act as a rate-limiting step during mRNA synthesis. The mechanisms of stimulation and repression of transcription elongation during development are not yet understood. We have identified a class of zebrafish mutations (pandora, sk8 and s30) that cause multiple developmental defects, including discrete problems with pigmentation, tail outgrowth, ear formation and cardiac differentiation. We demonstrate that the pandora gene encodes a protein similar to Spt6, a proposed transcription elongation factor. Additionally, the sk8 and s30 mutations are null alleles of the foggy/spt5 locus, which encodes another transcription elongation factor. Through real-time RT-PCR analysis, we demonstrate that Spt6 and Spt5 are both required for efficient kinetics of hsp70 transcription in vivo. Altogether, our results suggest that Spt6 and Spt5 play essential roles of comparable importance for promoting transcription during embryogenesis. This study provides the first genetic evidence for parallel functions of Spt6 and Spt5 in metazoans and establishes a system for the future analysis of transcription elongation during development.

Expression ofPDS/Pds, the Pendred Syndrome Gene, in Endometrium

Expression of the Pendred syndrome gene (PDS/Pds) is thought to be responsible for the iodide transport in the thyroid as well as the formation and function of the inner ear. Its mRNA is also expressed in the kidney and placenta. We report here that PDS and its encoded protein (pendrin) are also expressed in the endometrium. The RNA levels of rat PDS in the endometrium and kidney were much higher than those of the thyroid, opposite of the pattern of RNA expression in humans. In human endometrium, pendrin localization changed from the basal to apical surfaces of the epithelium during progression of the menstrual cycle. This suggests a possible role for pendrin in cationic ion transport required to maintain the physiological function of the endometrium. Since there is no evidence of endometrial abnormalities in patients with Pendred syndrome, it suggests the existence of a compensatory mechanisms for pendrin's function in the uterus.

Histidine 90 function in 4-chlorobenzoyl-coenzyme a dehalogenase catalysis.

4-chlorobenzoyl-coenzyme A (4-CBA-CoA) dehalogenase catalyzes the hydrolytic dehalogenation of 4-CBA-CoA by attack of Asp145 on the C4 of the substrate benzoyl ring to form a Meisenheimer intermediate (EMc), followed by expulsion of chloride ion to form an arylated enzyme intermediate (EAr) and, finally, ester hydrolysis in EAr to form 4-hydroxybenzoyl-CoA (4-HBA-CoA). This study examines the contribution of the active site His90 to catalysis of this reaction pathway. The His90 residue was replaced with glutamine by site-directed mutagenesis. X-ray crystallographic analysis of H90Q dehalogenase complexed with 4-HBA-CoA revealed that the positions of the catalytic groups are unchanged from those observed in the structure of the 4-HBA-CoA-wild-type dehalogenase complex. The one exception is the Gln90 side chain, which is rotated away from the position of the His90 side chain. The vacated His90 site is occupied by two water molecules. Kinetic techniques were used to evaluate ligand binding and catalytic turnover rates in the wild-type and H90Q mutant dehalogenases. The rate constants for 4-CBA-CoA (both 7 microM(-1) x s(-1)) and 4-HBA-CoA (33 and 11 microM(-1) x s(-1)) binding to the two dehalogenases are similar in value. For wild-type dehalogenase, the rate constant for a single turnover is 2.3 s(-1) while that for multiple turnovers is 0.7 s(-1). For H90Q dehalogenase, these rate constants are 1.6 x 10(-2) and 2 x 10(-4) s(-1). The rate constants for EMc formation in wild-type and mutant dehalogenase are approximately 200 s(-1) while the rate constants for EAr formation are 40 and 0.3 s(-1), respectively. The rate constant for hydrolysis of EAr in wild-type dehalogenase is 20 s(-1) and in the H90Q mutant, 0.13 s(-1). The 133-fold reduction in the rate of EAr formation in the mutant may be the result of active site hydration, while the 154-fold reduction in the rate EAr hydrolysis may be the result of lost general base catalysis. Substitution of the His90 with Gln also introduces a rate-limiting step which follows catalysis, and may involve renewing the catalytic site through a slow conformational change.

The submental artery flap

The submental artery flap is a reliable source of skin of excellent color, contour, and texture match for facial resurfacing. This versatile flap was successfully used for various defects in 19 patients and all flaps have survived with a few minor complications: marginal necrosis, venous congestion, dog ear formation, and infection. Low morbidity and complication rates and constant pedicle diameter provide a wide range of applicability locally throughout the lower face and midface and also as a free flap all over the body.

Formation of the Middle Ear: Recent Progress on the Developmental and Molecular Mechanisms

The middle ear allows animals to hear while moving in an aerial medium. It is composed of a cavity harbouring a chain of three ossicles that transmit vibrations produced by airborne sound in the tympanic membrane into the inner ear, where they are converted into neural impulses. The middle ear develops in the branchial arches, and this requires sequential interactions between the epithelia and the underlying mesenchyme. Gene-inactivation experiments have identified genes required for the formation of different middle ear components. Some encode for signalling molecules, including Endothelin1 and Fgf8, probable mediators of epithelial–mesenchymal interactions. Other genes, including Eya1, Prx1, Hoxa1, Hoxa2, Dlx1, Dlx2, Dlx5, and Gsc, are most likely involved in patterning and morphogenetic processes in the neural crest-derived mesenchyme. Mechanisms controlling formation of a functional tympanic membrane are also discussed. Basically, the tympanic ring, which serves as support for the tympanic membrane, directs invagination of the first pharingeal cleft ectoderm to form the external acoustic meatus (EAM), which provides the outer layer of the membrane. Gsc and Prx1 are essential for tympanic ring development. While invaginating, the EAM controls skeletogenesis in the underlying mesenchyme to form the manubrium of the malleus, the link between the membrane and the middle ear ossicles.

Earing predictions based on asymmetric nonquadratic yield function

Abstract A nonquadratic yield function (Yld96; Barlat, F., Maeda, Y., Chung, K., Yanagawa, M., Brem, J.C., Hayashida, Y., Lege, D.J. Matsui, K., Murtha, S.J., Hattori, S., Becker, R.C., Makosey, S., 1997. Yield function development for aluminium alloy sheet. J. Mech. Phys. Solids, 45, 1727) which simultaneously accounts for the anisotropy of uniaxial yield stresses and r values was newly implemented in a finite element code. Yield surface shapes, yield stress and r-value directionalities of Yld96 were investigated and compared with those of the previous yield function, Yld91 (Barlat, F., Lege, D.J., Brem, J.C. 1991a. A six-component yield function for anistropic metals. Int. J. Plasticity, 7, 693). Complete formulations for Yld96 implementation and the calculation of coefficients were also discussed for the convenient use of Yld96. A 2090-T3 aluminum alloy sheet sample was modeled and earing formation during a cup drawing test was simulated using the FEM code. The results of earing and thickness strain profiles were compared with the results obtained with Yld91. Investigations were further carried out with a translated yield surface to account for the strength differential effect observed in this material. Computation results with the translated yield surface were in very good agreement with experimental results. It was shown that the yield surface shape and translation have a significant influence on the prediction of the cup height profile during the drawing of a circular blank.

Induction of inner ear fate by FGF3.

Loss-of-function experiments in avians and mammals have provided conflicting results on the capacity of fibroblast growth factor 3 (FGF3) to act as a secreted growth factor responsible for induction and morphogenesis of the vertebrate inner ear. Using a novel technique for gene transfer into chicken embryos, we have readdressed the role of FGF3 during inner ear development in avians. We find that ectopic expression of FGF3 results in the formation of ectopic placodes which express otic marker genes. The ectopically induced placodes form vesicles which show the characteristic gene expression pattern of a developing inner ear. Ectopic expression of FGF3 also influences the formation of the normal orthotopic inner ear, whereas another member of the FGF family, FGF2, shows no effects on inner ear induction. These results demonstrate that a single gene can induce inner ear fate and reveal an unexpectedly widespread competence of the surface ectoderm to form sensory placodes in higher vertebrates.

Aesthetic otoplasty with remodeling of the antihelix for the correction of the prominent ear: criteria and personal technique.

A brief account of some important aspects of the embryological formation of the external ear is presented. Family and patient motivations to correct the aesthetic aspect of the prominent ear caused by the lack of development of the antihelix are discussed. The criteria for the selection of the patients and the ideal age for the surgical procedure are analyzed. The objectives of otoplasty for the correction of this deformity and the personal technique of the author are described. Emphasis is placed on the author's original contributions to this procedure and the results. The possible postoperative complications are discussed. Arch Facial Plast Surg. 2000;2:57-61

A role for neural cell adhesion molecule in the formation of the avian inner ear

The inner ear forms by a series of folds within an ectodermal placode. Previous work has shown that changes in surrounding tissues play a more prominent role in invagination than changes in the cytoskeleton of the primordium. Interference with the integrity of the extracellular matrix causes abnormalities in the folding process, primarily related to abnormalities in the paraxial mesoderm which lies ventral to the placode. In this study, the role of the neural cell adhesion molecule (N-CAM) was investigated, based on the expression of this component of the plasmalemma at the time the otic placode begins to fold. Microinjection of blocking antibodies to N-CAM into the paraxial mesoderm adjacent to the otic placode resulted in two major classes of defects, detachment of the primordium from the neural tube and interference with formation of the folds. Microinjection of saline, control immunoglobulin, or antibody against cytoplasmic domain had no effect. These defects correlate with the pattern of N-CAM expression at the time of injection, along the neural ectoderm and otic epithelium and the mesenchyme cells ventral to the primordium. It seems likely that N-CAM is playing a role in heterophilic associations rather than through the homophilic binding domain during formation of the otic vesicle. Dev. Dyn.1998;213:359–369. © 1998 Wiley-Liss, Inc.

A role for neural cell adhesion molecule in the formation of the avian inner ear.

The inner ear forms by a series of folds within an ectodermal placode. Previous work has shown that changes in surrounding tissues play a more prominent role in invagination than changes in the cytoskeleton of the primordium. Interference with the integrity of the extracellular matrix causes abnormalities in the folding process, primarily related to abnormalities in the paraxial mesoderm which lies ventral to the placode. In this study, the role of the neural cell adhesion molecule (N-CAM) was investigated, based on the expression of this component of the plasmalemma at the time the otic placode begins to fold. Microinjection of blocking antibodies to N-CAM into the paraxial mesoderm adjacent to the otic placode resulted in two major classes of defects, detachment of the primordium from the neural tube and interference with formation of the folds. Microinjection of saline, control immunoglobulin, or antibody against cytoplasmic domain had no effect. These defects correlate with the pattern of N-CAM expression at the time of injection, along the neural ectoderm and otic epithelium and the mesenchyme cells ventral to the primordium. It seems likely that N-CAM is playing a role in heterophilic associations rather than through the homophilic binding domain during formation of the otic vesicle.

A triangular suture to simplify reduction mammaplasty.

A technique to facilitate correct preoperative marking for an en bloc resection in superiorly based mammaplasty is presented. A temporary triangular suture is placed to control the estimated resection lines for the removal of the medial and lateral tissue block. The described technique helps to avoid the formation of medial and lateral dog ears and the unpleasant and visible scars that result.

The variable expressivity and incomplete penetrance of the twist-null heterozygous mouse phenotype resemble those of human Saethre-Chotzen syndrome.

Most targeted gene mutations are recessive and analyses of gene function often focus on homozygous mutant phenotypes. Here we describe parts of the expression pattern of M-twist in the head of developing wild-type mice and present our analysis of the phenotype of heterozygous twist- null animals at around birth and in adults. A number of twist -null heterozygous mice present skull and limb defects and, in addition, we observed other malformations, such as defects in middle ear formation and the xyphoïd process. Our study is of interest to understand bone formation and the role of M-twist during this process, as within the same animal growth of some bones can be accelerated while for others it can be delayed. Moreover, we show here that expressivity of the mouse mutant heterozygous phenotype is dependent on the genetic background. This information might also be helpful for clinicians, since molecular defects affecting one allele of the human H-twist ( TWIST ) gene were identified in patients affected with Saethre-Chotzen syndrome (SCS). Expressivity of this syndrome is variable, although most patients present craniofacial and limb malformations resembling those seen in mutant mice. Thus the mutant mouse twist -null strain might be a useful animal model for SCS. The twist -null mutant mouse model, combined with other mutant mouse strains, might also help in an understanding of the etiology of morphological abnormalities that appear in human patients affected by other syndromes.

Effect of texture on earing in FCC metals: Finite element simulations

Abstract The effect of individual texture components on the development of ears in FCC metals was investigated using finite element modelling in conjunction with a texture-based sixth-order strain-rate potential. Five main FCC rolling and recrystallization texture components are considered: the cube, Goss (G), brass (B), S3 and copper (C). Also analyzed were mixed cube + B and B + S3 + C textures, as well as a typical rolling and a typical annealed aluminium texture. The shapes of cups drawn from sheets containing these textures are predicted, and the earing percentages are calculated. The contributions of individual texture components to ear formation are described. Some “ideal” textures that permit ear formation to be minimized are also discussed.

Influence of foam/glass-epoxy interface on the macroscopic compressive failure features

The effect on the macroscopic compressive failure features of introduction of two flexible foam layers, either together at mid-region or separately at two locations that are away from the mid-region, into a glass-epoxy (G-E) system is studied in this work. In this experimental approach an attempt to look at the possible influence the foam/G-E interface region has on the way the materials respond to compressive loading is made by involving an analyses of macrofractographic features. While foam-free samples fail by extensive ear formation and separation nearer to the mid-region, the foam bearing ones display pronounced interface separation. The positioning of the foam sheet(s) has a bearing on the failure features.

Asymmetric growth behavior of selectively grown InP on vicinal (1 0 0) surfaces by low-pressure metal-organic chemical vapor deposition

Shape changes in selectively grown InP mesas were studied at various wafer-tilting and stripe misalignment angles by low-pressure metal-organic chemical vapor deposition. Symmetric mesa structures were obtained irrespective of stripe misalignment when the wafers were not titled. However, asymmetric ear formation was observed when the wafers were tilted and stripes were misaligned. A model for the changes in step density with wafer tilting and stripe misalignment was proposed to explain the asymmetric ear formation. The effect of V III ratio on the asymmetric ear formation was also studied.

Retinoic Acid Disturbs Mouse Middle Ear Development in a Stage-Dependent Fashion

The mammalian middle ear contains a chain of three ossicles, the malleus, incus, and stapes, that transmit into the inner ear the vibrations produced in the tympanic membrane by aerial sound. I show here that retinoic acid interferes with the formation of the middle ear in a stage-specific fashion. The malformations produced are derived from a retinoic acid-induced inhibition of the formation and/or migration of the cranial neural crest that generates the middle ear skeletal elements and not from a respecification of neural crest identity to more posterior fates. I have used these effects of retinoic acid to analyze the temporal sequence of events involved in the morphogenesis of the middle ear. I show that the middle ear bones develop from several primordia that originate in a typical temporal sequence from Day 8 plus 4.5 hr to Day 8 plus 7.5 hr of pregnancy. Moreover, interactions between adjacent bones are not required for their proper formation. My results also suggest aHoxa-2-mediated patterning of the otic capsule in the region where the oval window is located.