Publication date: Available online 24 November 2018
Source: Annals of Allergy, Asthma & Immunology
Author(s): Tiffany Jean, Su-Jau Yang, William W. Crawford, Scott H. Takahashi, Javed Sheikh
https://ift.tt/2AkK5EL
Publication date: Available online 24 November 2018
Source: Annals of Allergy, Asthma & Immunology
Author(s): Tiffany Jean, Su-Jau Yang, William W. Crawford, Scott H. Takahashi, Javed Sheikh
Publication date: Available online 23 November 2018
Source: Annals of Allergy, Asthma & Immunology
Author(s): Kathleen Rickard, Margot MacDonald-Berko, Robert Anolik, Neal Jain, Craig La Force, Richard L. Wasserman
Publication date: Available online 23 November 2018
Source: Archives of Oral Biology
Author(s): L.C. Pereira, J.C.R Nascimento, J.M.C. Rêgo, K.M. Canuto, M.E. Crespo-Lopez, J.I. Alvarez Leite, A. Baysan, R.B. Oriá
The association between cardiovascular and periodontal diseases is characterized by chronic inflammatory processes, with a high prevalence worldwide and complex genetic-environment interactions. Although apolipoprotein E4 (ApoE4), one of the isoforms coded by a polymorphic APOE gene, has been widely recognized as a risk factor for cardiovascular diseases and as an immunoinflammatory factor, but less is known regarding how ApoE4 affects atherosclerosis in periodontitis patients. The aim of this review was to investigate the potential underlying mechanisms related to APOE4 that could increase the risk of periodontal disease and, ultimately, of atherosclerosis. There have only been a few studies addressing apoE polymorphisms in patients with chronic periodontitis. To date, no studies have been performed that have assessed how ApoE4 affects atherosclerotic disease in chronic periodontitis patients. Although clinical studies are warranted, experimental studies have consistently documented the presence of periodontal pathogens, which are usually found in the oral cavity and saliva, in the atherosclerotic plaques of ApoE-deficient mice. In addition, in this review, the potential role of the APOE4 allele as an example of antagonistic pleiotropy during human evolution and its relation to oral health is discussed.
Publication date: Available online 23 November 2018
Source: Journal of the American Academy of Dermatology
Author(s): Rakesh Mehta, Deepak Jakhar, Ishmeet Kaur
Publication date: Available online 23 November 2018
Source: Journal of Allergy and Clinical Immunology
Author(s): Amy S. Paller, Heidi H. Kong, Patrick Seed, Shruti Naik, Tiffany C. Scharschmidt, Richard L. Gallo, Thomas Luger, Alan D. Irvine
As an interface with the environment, the skin is a complex ecosystem, colonized by many microorganisms that coexist in an established balance. The cutaneous microbiome inhibits colonization with pathogens such as S. aureus and is a crucial component for function of the epidermal barrier. Moreover, crosstalk between commensals and the immune system is now recognized, as microorganisms can modulate innate, as well as adaptive, immune responses. Host-commensal interactions also have an impact on the developing immune system in infants and subsequently the occurrence of diseases such as asthma and atopic dermatitis. Later in life, the cutaneous microbiome contributes to the development and course of skin disease. Accordingly, in patients with atopic dermatitis, a decrease in microbiome diversity correlates with disease severity and increased colonization with pathogenic bacteria such as S. aureus. Early clinical studies suggest that topical application of commensal organisms (e.g., S. hominis or R. mucosa) reduces atopic dermatitis severity and support an important role for commensals in decreasing S. aureus colonization in patients with atopic dermatitis. Advancing knowledge of the cutaneous microbiome and its function in modulating the course of skin disorders such as atopic dermatitis may result in novel therapeutic strategies.
Publication date: Available online 23 November 2018
Source: International Journal of Pediatric Otorhinolaryngology
Author(s): Hoda Mehregan, Marzieh Mohseni, Khadijeh Jalalvand, Sanaz Arzhangi, Nooshin Nikzat, Sussan Banihashemi, Kimia Kahrizi, Hossein Najmabadi
Hereditary hearing loss is the most common neurosensory disorder in humans caused by myriad mutations in numerous genes. Autosomal recessive nonsyndromic hearing loss (ARNSHL) accounts for 80% of hearing impairments of genetic origin and is quite prevalent in societies with a high rate of consanguinity. In the current study, we investigated the causes of sensorineural hearing loss in 24 unrelated Iranian families who were mainly consanguineous and had at least two affected children.
All probands were initially screened for GJB2 mutations, as the most common causes of ARNSHL in Iran. Verified GJB2-negative samples were subsequently subjected to whole exome sequencing (WES) to identify the underlying causes of hearing impairment, and the variants identified in each family were further confirmed by Sanger sequencing.
WES revealed three previously unreported mutations in MYO15A, the gene encoding the unconventional myosin 15 (Myo15). All variants identified, c.C6436T (p.R2146W), c.C9584G (p.P3195R) and c.G10266C (p.Q3422H), reside in the MYTH4 (myosin tail homology) and FERM (4.1 ezrin, radixin, moesin) domains of the protein.
Globally, mutations in MYO15A are considered to be among the most prevalent genetic causes of ARNSHL, and they rank as the third leading cause of hearing loss in the Iranian population, below GJB2 and SLC26A4. Yet again, these results endorse the importance of MYO15 screening in hearing impaired populations, particularly in Iran.
Publication date: Available online 23 November 2018
Source: International Journal of Pediatric Otorhinolaryngology
Author(s): Ahmed Mohamed Mehanna, Omneya A. Gamaleldin, Mohamed Fawzi Fathala
/Hypothesis— Evaluation of the clinical, electrophysiologic findings, the management plans of the misplaced cochlear implant electrode array and the possible causes of misplacement. Also to provide recommendations to prevent a repeat of cochlear implant electrode misplacement into abnormal sites.
—Retrospective study.
—Pediatric cochlear implant recipients implanted from January 2012 till January 2018 whose electrode arrays were misplaced outside the cochlea into the surrounding structures.
—Eight pediatric cochlear implant recipients, were identified to have a misplaced cochlear implant electrode array. Different sites of improper placement included one case in the eustachian tube, another one in the vestibule, one electrode array was found to be in the petrous apex lateral to the internal carotid canal, and another one in the internal auditory canal (IAC), and in three cases the electrode arrays were packed in the hypotympanum, and lastly an electrode array recoiled after perfect insertion and was found to be in the facial recess. Six cases were initially identified immediate because of their poor intraoperative implant testing which prompted imaging while in two cases, the one found in the petrous apex and the other one in the internal auditory canal (IAC) were diagnosed several months after surgery due to unsatisfactory auditory skills development or absent behavioral responses following implantation.
—Electrode array misplacement may be due to either failure to identify the anatomical landmarks during surgery specially the infracochlear air cell track or unidentified inner ear malformation. The routine use of intraoperative electrophysiologic testing and postoperative imaging should help to avoid such complications. Misplacement is a rare but still correctable complication after cochlear implant surgery. The diagnosis of misplacement can be delayed for years and in this occasion, it is suspected when benefit from the implant is limited or absent. Once misplacement is diagnosed revision surgery has to be done.