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Published in Calver Pang, Ibraz Hussain, John Mayberry, Pre-Clinical Medicine, 2017
Calver Pang, Ibraz Hussain, John Mayberry
This question’s focus was around the lymphatic tissue of the neck. Waldeyer’s tonsillar ring refers to the collection of lymphatic tissue surrounding the upper pharynx. The palatine tonsils are part of this ring and can become inflamed due to a viral or bacterial infection. If an infection spreads to the peritonsillar tissue, it can cause an abscess to form. This is known as quinsy. It is treated with draining of the abscess and antibiotics. Quinsy can potentially cause obstruction of the pharynx.
Measles Virus
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Rory D. de Vries, Rik L. de Swart
An alternative route for MV to enter a susceptible host would be via direct infection of CD150+ cells in Waldeyer’s tonsillar ring, consisting of tonsils and adenoids. Tonsils and adenoids are lined by CD150− epithelial cells, but at sites of damage or in tonsillar crypts direct infection of CD150+ cells at the luminal surface might be possible. In the aerosol infection model, tonsils and adenoids were directly exposed to a high dose of nebulized virus, but a consistent level of infection was only detected at 4 and 5 d.p.i., after onset of viremia.68 These data suggest that MV cannot easily penetrate the epithelial barrier to initiate MV infection in respiratory tract lymphoid tissues.
Cancer-Causing Viruses
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Satya P. Gupta, Vertika Gautam
After exposure, EBV establishes a persistent infection in the host and is intermittently shed in oropharyngeal secretions. In uncomplicated EBV infections, the main target cells are B lymphocytes that express CD21, which along with HLA class II molecules serve as the viral entry receptor and coreceptor, respectively. Infected B lymphocytes resemble antigen-activated B cells. The virus can also infect epithelial cells and may initially replicate in the oropharynx before infecting B cells. Naive B cells become infected in local lymphoid tissue, most often Waldeyer’s tonsillar ring, and establish latent infected memory B-cell pools that migrate to other lymphoid tissues. Periodic reactivations of latently infected memory B cells are thought to facilitate infection of epithelial cells in the oropharynx that permits shedding of virus into saliva for transmission to new hosts. Latently infected memory B cells are long-lived and, due to low levels of expression of viral proteins, they escape detection by CD8+ cytotoxic T cells (Kutok and Wang 2006); thus, persistence of EBV in the body is lifelong. EBV gene expression in these cells is limited to a B-cell growth program, termed Latency III, that includes nine latency-associated viral proteins, including six nuclear antigens (Epstein–Barr nuclear antigen [EBNA]-1, -2, -3A, -3B, -3C, and -LP) and three membrane proteins (latent membrane protein [LMP]-1, -2A, and -2B) that include LMP-1 and LMP-2a/b; EBNA-1, -2, -3a, -3b, -3c, and -LP; miRNAs; BamHI A Rightward Transcripts, BamHI: a type II restriction endonuclease from Bacillus amyloliquefaciens, having the capacity for recognizing short sequences (6 b.p.) of DNA and specifically cleaving them at a target site (BARTs); and EBV-encoded RNAs (EBERs) (Gruhne et al. 2009). These cells are eliminated by a robust immune response to EBNA-3 proteins, resulting in Latency I, a reservoir of latently infected resting memory B cells expressing only EBNA-1 and LMP-2. The differentiation of memory cells to plasma cells results in reactivation of the replication phase of the viral life cycle that includes expression of Latency III gene products. In addition, there is likely another amplification step by reinfection of the epithelial cells followed by shedding virus in the saliva to the next host (McLaughlin-Drubin and Munger 2008). Apart from B cells, which are known to be primarily infected by EBV, other non-B-cell NHLs associated with EBV infection include T-cell lymphoproliferative disorders that include a subset of peripheral T-cell lymphomas such as extranodal nasal-type NK/T-cell lymphoma.
Nose-to-brain delivery of antipsychotics using nanotechnology: a review
Published in Expert Opinion on Drug Delivery, 2020
Madeleine S. A. Tan, Harendra S Parekh, Preeti Pandey, Dan J. Siskind, James R. Falconer
The olfactory and respiratory regions are pertinent to systemic drug absorption due to their high vascularization [24]. However, the respiratory mucosa has more blood vessels than the olfactory mucosa. The ophthalmic artery delivers blood to the olfactory mucosa while the respiratory mucosa receives its blood supply from the maxillary artery. The nasal lymphatics passes through the cribriform plate near the olfactory nerves and drain CSF to the cervical lymph nodes [26]. Waldeyer’s tonsillar ring, which is part of the mucosa-associated lymphoid tissue (MALT), is a ring located in the pharynx. It serves a similar function to the Peyer’s patches in the gastrointestinal tract. The Waldeyer’s tonsillar ring produces lymphocytes and acts as a defense mechanism against inhaled foreign particles [24]. Table 2 shows the parameters of the nasal cavity.
Neuroanniversary 2021
Published in Journal of the History of the Neurosciences, 2021
Heinrich Wilhelm Gottfried von Waldeyer-Hartz (1836–1921) was a German anatomist known for summarizing the neuron theory and introducing the term “neuron” in a series of article in the main medical German journal, Deutsche Medizinische Wochenschrift, in 1891. He synthesized discoveries by neuroanatomists and later Nobel Prize winners Camillo Golgi (1843–1926) and Santiago Ramón y Cajal (1852–1934). He is also known for naming the chromosome in 1888. And he is remembered by anatomical structures named after him: Waldeyer’s tonsillar ring (the lymphoid tissue ring of the naso- and oropharynx) and Waldeyer’s glands (of the eyelids).