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Perinatal Airway Management
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Pensée Wu, May M.C. Yaneza, Haytham Kubba, W. Andrew Clement, Alan D. Cameron
The incidence of lymphatic malformation is 1 in 6000 to 1 in 16 000 live births. This congenital malformation of the lymphatic system is thought to be due to failure of the jugular lymph sacs to join the lymphatic system. As well as an association with chromosomal abnormalities in 60% of cases, in particular Turner syndrome and Down syndrome, they are also linked to underlying genetic conditions, such as Noonan syndrome and multiple pterygium syndrome.2 Antenatal care therefore involves detection of other fetal structural anomalies, especially cardiac abnormalities, and the offer of prenatal karyotyping. There is a perinatal mortality rate of over 80% if fetal hydrops is detected. Postnatal intubation may be particularly difficult due to obstruction of the pharynx and larynx from very large lesions. Prognostic scores such as de Serres staging or Cologne Disease Score have been used to predict long-term outcome.13,14
Lymphatic disorders
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
The lymphatic system comprises lymphatic channels, lymphoid organs (lymph nodes, spleen, Peyer’s patches, thymus, tonsils) and circulating elements (lymphocytes and other mononuclear immune cells). Lymphatic endothelial cells are derived from embryonic veins in the jugular and perimesonephric areas from where they migrate to form the primary lymph sacs and plexus. Both transcription (e.g. Prox1) and growth (e.g. vascular endothelial growth factor-C (VEGF-C)) factors are essential for these developmental events.
Embryology of veins and lymphatics
Published in Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland, Manual of Venous and Lymphatic Diseases, 2017
Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland
Dilations of lymphatic channels form six primary lymph sacs at six to nine weeks. There are two jugular lymph sacs near the anterior cardinal veins, two iliac lymph sacs near the posterior cardinal veins, one retroperitoneal lymph sac in the root of the mesentery on the posterior abdominal wall and one that becomes the cisterna chyli dorsal to the retroperitoneal lymph sac at the level of the adrenal glands.
Daily and LPS-induced variation of endocrine mediators in cururu toads (Rhinella icterica)
Published in Chronobiology International, 2022
Priscilla Rachel Oliveira Bastos, Stefanny Christie Monteiro Titon, Braz Titon Junior, Fernando Ribeiro Gomes, Regina P. Markus, Zulma S. Ferreira
Fifteen days after the CORT and MEL diurnal rhythm determination, an LPS challenge was carried out with the toads. The animals were randomly divided into two groups (LPS and saline). At ZT15 (21 h) (dark phase), the toads were injected with LPS (2 mg/kg, Escherichia coli, Serotype 0127:B8, Sigma, St Louis, MO) or saline at their lymph sacs, according to (Gardner et al. 2018). Individuals were injected with an interval of 5 min, LPS, and saline, in sequence. Blood samples (~500ul, less than 5% of blood volume) were taken by cardiac puncture 2 h after the LPS or saline injection (ZT17, 23 h), and plasma was isolated, as described in section 2.3. Thereafter, animals were decapitated, and the eyes were removed and stored at a − 80°C freezer for further MEL assay (Wright et al. 1999).
Analysis between phenotypes and genotypes of inner ear malformation
Published in Acta Oto-Laryngologica, 2019
Suyang Wang, Wenjuan Ding, Chi Chen, Baicheng Xu, Xiaowen Liu, Panpan Bian, Yufen Guo
Most of the EVA patients were SNHL, and all the patients in this study were SNHL. No conductive deafness or mixed deafness was found. It is generally believed that VA enlargement is the main cause of SNHL in such patients, but the specific pathogenesis has not been clearly studied. Currently, there are three theories discussed as follows. (1) VA buffer theory: Normal VA can buffer the pressure of cerebrospinal fluid, while the pressure of cerebrospinal fluid in LVAS patients can be directly transferred to the membrane labyrinth through expanded VA and damage cochlear hair cells, leading to SNHL. (2) Circulating lymphoid reflux theory: The protein concentration in the inner lymphocytes is much higher than that in the membrane labyrinth and other parts, showing hypertonic state. LVAS patients often accompanied by lymphatic vessels in lymph sac or expand inside, when the increased intracranial pressure hypertonic liquid by expanding within the lymph sac of the VA reflux into the cochlear basal around, which affect the sensory nerve epithelial physiology function, producing SNHL. (3) Differential metabolism of the lymphocyst in memory: Studies have shown that LVAS patients have a thin membrane labyrinth wall, which causes the dysfunction of reabsorption function of the inner lymphocyst, leading to the mixing of internal and external lymphatic fluid, damaging the function of hair cells and leading to SNHL.