8 results on '"Waters, Karen Ann"'
Search Results
2. Snoring in children
- Author
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Chawla, Jasneek and Waters, Karen Ann
- Published
- 2015
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3. Sleep disordered breathing and its treatment in children
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Waters, Karen Ann
- Subjects
Sleep disorders in children ,Respiratory organs -- Obstructions -- Treatment ,Achondroplasia ,Sleep apnea syndromes - Abstract
The establishment of a dedicated paediatric sleep unit over the past three years has allowed detailed investigation of a large number of children with sleep associated upper airway obstruction. This thesis explores the characteristics of upper airway obstruction and sleep associated breathing control abnormalities, in children who have been investigated in that unit. The "unit" began with three or four people performing children’s sleep studies at the Sleep Unit (for adults) at RPAH; the results presented here include those studies. The methods used in this thesis have evolved through practical experience acquired in caring for children with breathing disorders in sleep. This thesis is presented in two parts. The studies in the first section provide an overview of the presentation and treatment of the syndrome of obstructive sleep apnoea (OSA) as it occurs in infants and children. The second section is a more detailed exploration of OSA and its treatment in achondroplasia. These latter studies provide further insights into the disorder in this specific group, and therefore into some aspects of OSA in the broader population of children.
- Published
- 1993
4. Brain-derived neurotrophic factor mRNA and protein in the piglet brainstem and effects of Intermittent Hypercapnic Hypoxia
- Author
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Peiris, Tanya Shyami, Machaalani, Rita, and Waters, Karen Ann
- Subjects
- *
MESSENGER RNA , *PROTEINS , *HYPOXEMIA , *PIGLETS - Abstract
Brain-derived neurotrophic factor (BDNF) is a neurotrophin essential for the development of normal respiratory rhythm and ventilatory control. Chronic exposure to Intermittent Hypercapnic Hypoxia (IHH) has been shown to alter ventilatory responses of piglets. This study investigated changes in BDNF distribution and expression in seven nuclei of the caudal medulla, from piglets exposed to IHH for 1, 2, 3, or 4 days before death, using non-radioactive in situ hybridisation (for mRNA) and immunohistochemistry (for protein). Compared to controls, BDNF mRNA was markedly increased across the entire medulla of the brainstem, after all durations of IHH (1–4 days). In contrast, BDNF protein expression increased after 1 day of exposure to IHH (p=0.003), but, thereafter, was not different to controls. Amongst individual nuclei, neurons of the dorsal motor nucleus of the vagus (DMNV) showed increased BDNF mRNA (p<0.01), but decreased protein expression (p=0.05) after all durations of IHH. In the ION, both mRNA and protein for BDNF were significantly increased after 1 day IHH (p<0.01 and p=0.001, respectively), but these increases were not sustained. This study is the first to investigate changes in BDNF expression in response to environmental challenges during postnatal development in the brainstem. Implications of the wide distribution of BDNF in the piglet caudal medulla and increased expression after IHH exposure are discussed, with particular reference to roles for BDNF-dependant neurons at this stage of development. [Copyright &y& Elsevier]
- Published
- 2004
- Full Text
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5. Chapter 65 - Sleep-Disordered Breathing
- Author
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Waters, Karen Ann
- Full Text
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6. Contributors
- Author
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Abman, Steven H., Adler-Shohet, Felice C., Allen, Julian Lewis, Anselmo, Mark A., Asher, M. Innes, Berg, Marc D., Berg, Robert A., Berlinski, Ariel, Brody, Alan S., Brown, Mark A., Buchanan, Ann M., Burgner, David, Bye, Michael R., Carlsen, Kai-Håkon, Carroll, John L., Clément, Annick, Collins, Rachel A., Colombo, John L., Covar, Ronina A., Crawford, Susan E., Crotty, Eric, Daum, Robert S., de Iongh, Robbert, Denjean, André, Deterding, Robin R., Devadason, Sunalene G., Doerschug, Kevin C., Donnerstein, Richard, Duke, Trevor, Elliott, Sean P., Esther, Charles R., Jr., Everard, Mark L., Fan, Leland L., Fauroux, Brigitte, Gabbay, Eli, Gaultier, Claude, Grant, Cameron C., Green, Christopher G., Gripp, Karen Webster, Gutierrez, Juan A., Hammerschlag, Margaret R., Hay, Thomas C., Helfaer, Mark, Henning, Robert, Holinger, Lauren D., Holt, Patrick G., Hunninghake, Gary W., Inselman, Laura S., Jennings, Lance C., Jobe, Alan H., Jones, Marcus Herbert, Kang, J. Brian, Kemp, Andrew S., Kotecha, Sailesh, Kumar, Swati, Laberge, Jean-Martin, Landau, Louis I., Lands, Larry C., Larsen, Gary L., Lee, Rees L., Leigh, Margaret W., Le Souëf, Peter N., Lieberman, Jay M., Liu, Andrew H., Marostica, Paulo José Cauduro, Martinez, Fernando D., Mayer, Oscar Henry, McCoy, Karen S., Meyer, Robyn J., Montgomery, Gregory S., Moodley, Yuben, Morgan, Lucy, Morgan, Wayne J., Morton, Alan R., Moss, Richard B., von Mutius, Erika, Nadkarni, Vinay M., Oberwaldner, Béatrice, Panitch, Howard B., Pattemore, Philip Keith, Pillow, J. Jane, Condessa Pitrez, Paulo Márcio, Poets, Christian F., Puligandla, Pramod S., Rajasekaran, Surender, Ray, C. George, Redding, Gregory J., Robinson, Philip, Rosenfeld, Margaret, Rubin, Lewis J., Rutland, Jonathan, Sandhaus, Robert A., Schidlow, Daniel V., Shehab, Ziad M., Sheikh, Shahid Ijaz, Shingadia, Delane, Sly, Peter D., Smevik, Bjarne, Snell, Gergory I., Soep, Jennifer B., South, Mike, Spahn, Joseph D., Stein, Renato T., Steinfeld, Jonathan, Stick, Stephen M., Stokes, Dennis C., Sulman, Cecille G., Szefler, Stanley J., Tauber, Danna, Taussig, Lynn M., Thomas, Heather M., Tiddens, Harm A.W.M., Upham, John W., Wagener, Jeffrey S., Wall, Michael A., Wamboldt, Frederick S., Wamboldt, Marianne Z., Waters, Karen Ann, Weinberg, Geoffrey A., Weiner, Daniel J., Weintraub, Robert G., Westall, Glen, White, Carl W., Williams, Trevor J., Wilson, Andrew, Wittman, Brenda J., Beck Wohl, Mary Ellen, Wood, Robert E., Yorgin, Peter D., Zach, Maximilian S., and Zar, Heather J.
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7. Letter Re: Butyrylcholinesterase is a potential biomarker for sudden infant death syndrome.
- Author
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Harrington CT, Hafid NA, and Waters KA
- Subjects
- Biomarkers, Butyrylcholinesterase, Humans, Infant, Syndrome, Sudden Infant Death diagnosis, Sudden Infant Death etiology
- Abstract
Competing Interests: Declaration of interests CH, NA, and KW declare no competing interests.
- Published
- 2022
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8. Butyrylcholinesterase is a potential biomarker for Sudden Infant Death Syndrome.
- Author
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Harrington CT, Hafid NA, and Waters KA
- Subjects
- Biomarkers, Butyrylcholinesterase, Case-Control Studies, Child, Child, Preschool, Cholinergic Agents, Humans, Infant, Infant, Newborn, Risk Factors, Sudden Infant Death diagnosis, Sudden Infant Death etiology
- Abstract
Background: Autonomic dysfunction has been implicated in the pathophysiology of the Sudden Infant Death Syndrome (SIDS). Butyrylcholinesterase (BChE) is an enzyme of the cholinergic system, a major branch of the autonomic system, and may provide a measure of autonomic (dys)function. This study was undertaken to evaluate BChE activity in infants and young children who had died from Sudden Infant Death or Sudden Unexpected Death., Methods: In this case-control study we measured BChE activity and total protein in the eluate of 5μL spots punched from the dried blood spots taken at birth as part of the newborn screening program. Results for each of 67 sudden unexpected deaths classified by the coroner (aged 1 week-104 weeks) = Cases, were compared to 10 date of birth - and gender-matched surviving controls (Controls), with five cases reclassified to meet criteria for SIDS, including the criterion of age 3 weeks to 1 year., Findings: Conditional logistic regression showed that in groups where cases were reported as "SIDS death" there was strong evidence that lower BChE specific activity (BChEsa) was associated with death (OR=0·73 per U/mg, 95% CI 0·60-0·89, P=0·0014), whereas in groups with a "Non-SIDS death" as the case there was no evidence of a linear association between BChEsa and death (OR=1·001 per U/mg, 95% CI 0·89-1·13, P=0·99)., Interpretation: BChEsa, measured in dried blood spots taken 2-3 days after birth, was lower in babies who subsequently died of SIDS compared to surviving controls and other Non-SIDS deaths. We conclude that a previously unidentified cholinergic deficit, identifiable by abnormal -BChEsa, is present at birth in SIDS babies and represents a measurable, specific vulnerability prior to their death., Funding: All funding provided by a crowd funding campaign https://www.mycause.com.au/p/184401/damiens-legacy., (Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.)
- Published
- 2022
- Full Text
- View/download PDF
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