Relevant bibliographies by topics / Midline defects

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Midline defects'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Midline defects"

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Toriello, Helga V., James V. Higgins, John M. Opitz, and James F. Reynolds. "X-linked midline defects." American Journal of Medical Genetics 21, no. 1 (May 1985): 143–46. http://dx.doi.org/10.1002/ajmg.1320210121.

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Antonini, Sonir R. R., Alexandre S. Grecco Filho, Lucila L. K. Elias, Ayrton C. Moreira, and Margaret de Castro. "gene in midline cerebral defects." Journal of Pediatrics 139, no. 5 (November 2001): 754. http://dx.doi.org/10.1067/mpd.2001.118423.

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Winter, Robin M. "Diaphragmatic and multiple midline defects." American Journal of Medical Genetics 63, no. 2 (May 17, 1996): 411. http://dx.doi.org/10.1002/ajmg.1320630203.

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Ching, H. S., K. W. Lindsay, and B. F. O'Reilly. "Intracranial mucoceles with midline fusion defects." Journal of Neurology, Neurosurgery & Psychiatry 61, no. 4 (October 1, 1996): 428–29. http://dx.doi.org/10.1136/jnnp.61.4.428.

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Ruggiero, Antonio, Giuseppe Zampino, Pierpaolo Mastroiacovo, and Riccardo Riccardi. "Diamond–Blackfan Anemia and Midline Defects." Journal of Pediatric Hematology/Oncology 22, no. 5 (September 2000): 479–80. http://dx.doi.org/10.1097/00043426-200009000-00021.

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Parr, J. H. "Midline Cerebral Defects and Kallmann's Syndrome." Journal of the Royal Society of Medicine 81, no. 6 (June 1988): 355–56. http://dx.doi.org/10.1177/014107688808100620.

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Morales, J. Mark, Sanjeet G. Patel, James A. Duff, Roberto L. Villareal, and James W. Simpson. "Ectopia cordis and other midline defects." Annals of Thoracic Surgery 70, no. 1 (July 2000): 111–14. http://dx.doi.org/10.1016/s0003-4975(00)01388-6.

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Say, Burhan, and Donna P. Smith. "Midline field defects and Hirschsprung disease." American Journal of Medical Genetics 61, no. 3 (January 22, 1996): 293–94. http://dx.doi.org/10.1002/(sici)1096-8628(19960122)61:3<293::aid-ajmg17>3.0.co;2-o.

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Temple, I. K., H. Brunner, B. Jones, J. Burn, and M. Baraitser. "Midline facial defects with ocular colobomata." American Journal of Medical Genetics 37, no. 1 (September 1990): 23–27. http://dx.doi.org/10.1002/ajmg.1320370107.

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Zucchini, Stefano. "Pituitary abnormalities in midline brain defects." EClinicalMedicine 19 (February 2020): 100260. http://dx.doi.org/10.1016/j.eclinm.2020.100260.

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Dissertations / Theses on the topic "Midline defects"

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Webb, E. A. "Exploring the phenotypes of individuals with midline brain defects." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1417376/.

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Background The prevalence, aetiology and optimal management of the behavioural and cognitive difficulties, and circadian rhythm disturbances in children with midline brain abnormalities including isolated growth hormone deficiency (IGHD), isolated optic nerve hypoplasia (ONH) and septo-optic dysplasia (SOD) have to date not been adequately addressed. Aims and Methods This thesis aims to assess the prevalence of cognitive/behavioural problems and circadian rhythm abnormalities in children with midline brain abnormalities, and to further investigate any problems identified using high resolution MRI brain, actigraphy and melatonin profiling. Results Children with IGHD have significant impairments in motor skills and lower cognitive function scores, and children with ONH have significantly higher scores on the child behavioural checklist than controls. Children with SOD have significant sleep abnormalities. In IGHD corticospinal tract and corpus callosum fractional anisotropy (FA) and specific neural volumes are significantly lower than in controls, with neural abnormalities correlating significantly with IQ and motor skills scores. In ONH ventral cingulum, corpus callosum and optic radiation FA are significantly reduced, with right ventral 13 cingulum FA correlating significantly with behavioural assessment scores. In SOD melatonin production was absent in one child in association with a fragmented sleep pattern. Three children had normal melatonin profiles, one with an arrhythmic and two with fragmented sleep patterns. The remaining child had fragmented sleep and a modest increase in daytime melatonin concentrations. Conclusions These studies suggest that the GH-IGF-1 axis plays a role in brain and cognitive development. They also show that children with ONH require behavioural assessment, not previously part of routine clinical care, and that the behavioural abnormalities identified in children with ONH may be related to underlying whiter matter abnormalities. We have also demonstrated that the aetiology of the sleep disturbances found in SOD is complex, and not solely due to abnormal nocturnal melatonin production.
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Al, Deiri Mhd Bashar. "TGF-B signalling in the development of ventral embryonic structures." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/tgfb-signalling-in-the-development-of-ventral-embryonic-structures(7a337628-d26d-436b-b18c-62619bbbf130).html.

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Ventral body wall closure (VBW) defects are amongst the most common human congenital anomalies. They represent a wide and heterogeneous group of phenotypic defects that can present in isolation or as a component in a larger syndromic anomaly. In addition, the incidence of associated anomalies is high and reaches 75% of fetuses in some types of VBW closure defects. Nevertheless, the embryonic origin and the underlying cellular and molecular mechanisms between ventral closure defects and their associated congenital anomalies remain poorly characterised. This is in part due to the poor understanding of the physiological mechanisms that regulate the development of ventral organs and the lack of representative transgenic animal models allowing detailed in vivo analysis of defect formation. Transforming growth factor beta (TGF-ÃŽÂ2) signalling is essential for VBW closure and vascular and cardiac development. Yet, its mechanism of action and the responding cell(s) in the body wall remain largely unknown. In addition, in various cells TGF-B can induce the expression of Tagln, encoding for a cytoskeleton associated protein that enhances cell migration. No function has been ascribed to TAGLN in body wall development. I define here a role of TGF-B during a critical time window in embryonic development to fashion the ventral body wall, anterior diaphragm and parts of the circulatory system. I identify a population of TAGLN+ myofibroblasts that respond to a temporally regulated TGF-B signalling originating from the epithelium of the primary body wall. Deletion of TGF-B receptor in TAGLN+ cells leads to failure of ventral body wall closure, anterior diaphragmatic hernia, cardiac and outflow tract anomaly. Nevertheless, the descending aorta and the large aortic branches are spared. By using advanced transgenic methodology, I generated novel transgenic mouse lines that enabled me to fate map the cells that initiate the formation of important mesenchymal tissues. These studies revealed that the origin of aortic vascular smooth muscle cells can be traced back to a group of progenitor cells that reside in the wall of the dorsal aorta before the VBW closure. My studies provide intriguing evidence for spatially restricted role for TGF-B signalling in ascending but not descending aorta morphogenesis. I used a variety of techniques to characterise, analyse and quantify important mechanisms during mesenchymal and vascular development, their response to injury and repair. This thesis has been written in an alternative format, comprising the different areas which have been investigated. Collectively, the results presented here provide new insights into the role of migratory and mechanically stabilising cells in the development and maintenance of critical structures in the body and their common role in the development of concurrent congenital anomalies. A detailed understanding of the molecular signalling pathways and cells that drive VBW closure raises the hope that the related birth defects can in the future be treated by precise gene and cell therapies.
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Books on the topic "Midline defects"

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Giblin, Karen L. Eat to defeat menopause: The essential nutrition guide for a healthy midlife--with 150 recipes. Cambridge, MA: Da Capo Lifelong Books, 2011.

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Schreuder, Michiel F. Duplex, ectopic, and horseshoe kidneys. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0352.

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A duplex urinary tract, irrespective of the degree of duplication, is present in 0.8% at autopsy, of which about 20–35% is bilateral. The majority of duplex systems are incomplete, indicating that the ipsilateral ureters fuse before entering the bladder. A complete duplex system shows anomalies of the upper moiety, with associated ureterocele or ectopic ureter, and of the lower moiety, frequently associated with vesicoureteral reflux. Renal ectopia is a rare (1/1000) congenital defect where the kidney is not located in the renal fossa, and is associated with a high rate of hydronephrosis, vesicoureteral reflux, and abnormal contralateral kidney. In a horseshoe kidney (present in 1/400 to 1/1800), fusion of the two kidneys takes place, but the two renal moieties are still located on both sides of the midline. As the lower poles are fused in the midline, a horseshoe kidney is usually located lower than normal and orientation of the renal axis is shifted, which may guide diagnosis during abdominal ultrasound.
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Book chapters on the topic "Midline defects"

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Monuki, Edwin S., and Jeffrey A. Golden. "Midline Patterning Defects." In Developmental Neuropathology, 29–40. Oxford, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119013112.ch3.

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Voeller, Guy R. "Repair of Incisional Hernias and Midline Defects." In Abdominal Wall Hernias, 519–24. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4419-8574-3_79.

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Glees, P. "The Corpus callosum, an evolutionary and developmentally late crossing midline structure, malformations and functional aspects." In Spina bifida - neural tube defects, edited by P. Gless, J. Lorber, and D. Voth, 47–54. Berlin, Boston: De Gruyter, 1986. http://dx.doi.org/10.1515/9783110850307-007.

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Kelberman, Daniel, and Mehul Tulsidas Dattani. "Role of Transcription Factors in Midline Central Nervous System and Pituitary Defects." In Endocrine Involvement in Developmental Syndromes, 67–82. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000207478.

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Samandouras, George. "Congenital abnormalities." In The Neurosurgeon's Handbook, 704–19. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780198570677.003.0581.

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Chapter 13.1 covers congenital abnormalities, including abnormalities of cellular proliferation, heterotopias, dysgenesis of the corpus callosum (DCC), anterior midline defects, chiari malformations, Dandy-Walker malformation (DWM), and dysraphism.
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Medina, Pablo José, Guido Luis Busnelli, and Walter Sebastián Nardi. "Diastasis Recti and Other Midline Defects: Totally Subcutaneous Endoscopic Approach." In New Horizons in Laparoscopic Surgery. InTech, 2018. http://dx.doi.org/10.5772/intechopen.75653.

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Adelman, Ron A., and Patricia Pahk. "Visual Field Defects in Chorioretinal Disorders." In Visual Fields. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195389685.003.0012.

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Pathologic processes involving the retina or choroid can present with a wide variety of visual field defects. Usually visual field defects of retinal diseases directly correlate with the fundus findings. Visual field changes are often the result of damage to the retina or scarring but, in conjunction with other clinical findings, they may help narrow the differential diagnosis. Most of the macular lesions result in visual field defects that do not respect the vertical or horizontal midline. Occasionally inflammatory disorders result in visual field defects that do not directly correlate with the retinal findings. For example, patients with multiple evanescent white dot syndrome (MEWDS) may have an enlarged blind spot. Macular disorders can cause central or paracentral scotomas depending on the location of the lesion. Causes of macular pathology include drusen, atrophy from dry age-related macular degeneration (AMD), retinal hemorrhage, choroidal neovascular membrane, macular edema, macular hole, macular scar, pathologic myopia, and macular dystrophies of the retina or choroid. Central serous chorioretinopathy (CSCR) can show a relative defect that is anatomically correlated with the area of subretinal or sub RPE (retinal pigment epithelium) fluid accumulation. Residual pigmentary changes in inactive CSCR can also cause a relative depression in the corresponding visual field. Pathologic myopia can present with a variety of visual field defects depending on the retinal findings, such as posterior staphyloma or choroidal neovascular membrane. AMD may show nonspecific changes in the central or paracentral visual field that correlate with the structural damage to the retina and choroid. Geographic atrophy in dry AMD can cause a dense scotoma correlated with the pattern of the atrophy. Choroidal neovascular membranes can cause a depression in the correlating visual field due to edema or hemorrhage. Disciform scars in endstage AMD can also cause a dense scotoma. Macular holes may cause a small central scotoma. Pattern dystrophies are a family of disorders with a common pathology at the level of the RPE. Butterfly dystrophy, an autosomal dominant disorder, and Sjögren reticular dystrophy, an autosomal recessive disorder, are two examples of pattern dystrophies.
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Diprose, Paul. "Atrial assessment." In Focused Intensive Care Ultrasound, edited by Marcus Peck and Peter Macnaughton, 81–88. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198749080.003.0009.

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This chapter will describe the important anatomical features of both atria and how these can be identified using two-dimensional echo. It will explain how to recognize atrial dilatation and how to make inferences about atrial pressure from the position of the atrial septum. It will discuss atrial masses, including thrombus and tumour, and other more commonly seen structures that may be misinterpreted as such. The advanced section will introduce atrial volume assessment, as well as how colour Doppler and bubble contrast can be used to recognize midline septal defects.
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Kelly, Robert G. "Cardiac embryogenesis." In ESC CardioMed, edited by Miguel Torres, 33–36. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0004.

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The embryonic heart forms in anterior lateral splanchnic mesoderm and is derived from Mesp1-expressing progenitor cells. During embryonic folding, the earliest differentiating progenitor cells form the linear heart tube in the ventral midline. The heart tube extends in length and loops to the right as new myocardium is progressively added at the venous and arterial poles from multipotent second heart field cardiovascular progenitor cells in contiguous pharyngeal mesoderm. While the linear heart tube gives rise to the left ventricle, the right ventricle, outflow tract, and a large part of atrial myocardium are derived from the second heart field. Progressive myocardial differentiation is controlled by intercellular signals within the progenitor cell niche. The embryonic heart is the template for septation and growth of the four-chambered definitive heart and defects in progenitor cell deployment result in a spectrum of common forms of congenital heart defects.
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Kelly, Robert G. "Cardiac embryogenesis." In ESC CardioMed, edited by Miguel Torres, 33–36. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0004_update_001.

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The embryonic heart forms in anterior lateral splanchnic mesoderm and is derived from Mesp1-expressing progenitor cells. During embryonic folding, the earliest differentiating progenitor cells form the linear heart tube in the ventral midline. The heart tube extends in length and loops to the right as new myocardium is progressively added at the venous and arterial poles from multipotent second heart field cardiovascular progenitor cells in contiguous pharyngeal mesoderm. While the linear heart tube gives rise to the left ventricle, the right ventricle, outflow tract, and a large part of atrial myocardium are derived from the second heart field. Progressive myocardial differentiation is controlled by intercellular signals within the progenitor cell niche. The embryonic heart is the template for septation and growth of the four-chambered definitive heart and defects in progenitor cell deployment result in a spectrum of common forms of congenital heart defects.
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Conference papers on the topic "Midline defects"

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Millward, Dale. "Case Studies Highlighting Rapid Repair Methods of Pressurised Pipelines Damaged by Anchors." In 2018 12th International Pipeline Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/ipc2018-78105.

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Effective pipeline design and regular maintenance can assist in prolonging the lifespan of subsea pipelines, however the presence of marine vessels can significantly increase the risk of pipeline damage from anchor hazards. As noted in the Health and Safety Executive – Guideline for Pipeline Operators on Pipeline Anchor Hazards 2009. “Anchor hazards can pose a significant threat to pipeline integrity. The consequences of damage to a pipeline could include loss of life, injury, fire, explosion, loss of buoyancy around a vessel and major pollution”. This paper will describe state of the art pipeline isolation tooling that enables safe modification of pressurised subsea pipelines. Double Block and Bleed (DBB) isolation tools have been utilised to greatly reduce downtime, increase safety and maximise unplanned maintenance, providing cost-effective solutions to the end user. High integrity isolation methods, in compliance with international subsea system intervention and isolation guidelines (IMCA D 044 / IMCA D 006), that enable piggable and unpiggable pipeline systems to be isolated before any breaking of containment, will also be explained. This paper will discuss subsea pipeline damage scenarios and repair options available to ensure a safe isolation of the pipeline and contents in the event of an incident DNV GL type approved isolation technology enables the installation of a fail-safe, DBB isolation in the event of a midline defect. The paper will conclude with case studies highlighting challenging subsea pipeline repair scenarios successfully executed, without depressurising the entire pipeline system, and in some cases without shutting down or interrupting production.
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