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2.
Laryngoscope ; 131(6): E2013-E2017, 2021 06.
Article in English | MEDLINE | ID: covidwho-969763

ABSTRACT

OBJECTIVES/HYPOTHESIS: Intracellular entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) depends on the interaction between its spike protein with the cellular receptor angiotensin-converting enzyme 2 (ACE2) and depends on Furin-mediated spike protein cleavage and spike protein priming by host cell proteases, including transmembrane protease serine 2 (TMPRSS2). As the expression of ACE2, TMPRSS2, and Furin in the middle and inner ear remain unclear, we analyzed the expression of these proteins in mouse ear tissues. STUDY DESIGN: Animal Research. METHODS: We performed immunohistochemical analysis to examine the distribution of ACE2, TMPRSS2, and Furin in the Eustachian tube, middle ear spaces, and cochlea of mice. RESULTS: ACE2 was present in the nucleus of the epithelium of the middle ear and Eustachian tube, as well as in some nuclei of the hair cells in the organ of Corti, in the stria vascularis, and the spiral ganglion cells. ACE2 was also expressed in the cytoplasm of the stria vascularis. TMPRSS2 was expressed in both the nucleus and cytoplasm in the middle spaces, with the expression being stronger in the nucleus in the mucosal epithelium of the middle ear spaces and Eustachian tube. TMPRSS2 was present in the cytoplasm in the organ of Corti and stria vascularis and in the nucleus and cytoplasm in the spiral ganglion. Furin was expressed in the cytoplasm in the middle ear spaces, Eustachian tube, and cochlea. CONCLUSIONS: ACE2, TMPRSS2, and Furin are diffusely present in the Eustachian tube, middle ear spaces, and cochlea, suggesting that these tissues are susceptible to SARS-CoV-2 infection. LEVEL OF EVIDENCE: NA Laryngoscope, 131:E2013-E2017, 2021.


Subject(s)
Angiotensin-Converting Enzyme 2/genetics , COVID-19/pathology , Ear, Inner/pathology , Ear, Middle/pathology , Eustachian Tube/pathology , Furin/genetics , Gene Expression/genetics , Serine Endopeptidases/genetics , Animals , Cochlea/pathology , Epithelium/pathology , Immunohistochemistry , Mice , Mucous Membrane/pathology , Organ of Corti/pathology , Spiral Ganglion/pathology , Stria Vascularis/pathology , Temporal Bone/pathology
3.
Preprint in English | bioRxiv | ID: ppbiorxiv-164335

ABSTRACT

ObjectivesIntracellular entry of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) depends on the interaction between its spike protein to a cellular receptor named angiotensin-converting enzyme 2 (ACE2) and depends on Furin-mediated spike 23 protein cleavage and spike protein priming by host cell proteases including 24 transmembrane protease serine 2 (TMPRSS2). Tmprss1, Tmprss3, and Tmprss5 are expressed in the spiral ganglion neurons and the organ of Corti in the inner ear; however, Ace2, Tmprss2, and Furin expression profiles in the middle ear remain unclear. Therefore, this study aimed to analyze Ace2, Tmprss2, and Furin expression in the middle and inner ear of mice. Study DesignAnimal research. SettingDepartment of Otolaryngology and Head and Neck Surgery, University of Tokyo. MethodsWe performed immunohistochemical analysis to examine the distribution of Ace2, Tmprss2, and Furin in the eustachian tube, middle ear space, and cochlea of mice. ResultsAce2 was expressed in the cytoplasm in the middle ear epithelium, eustachian tube epithelium, stria vascularis, and spiral ganglion. Tmprss2 and Furin were widely expressed in the middle ear spaces and the cochlea. ConclusionCo-expression of Ace2, Tmprss2, and Furin in the middle ear indicates that the middle ear is susceptible to SARS-CoV-2 infections, thus warranting the use of personal protective equipment during mastoidectomy for coronavirus disease (COVID-19) patients.

4.
Preprint in English | medRxiv | ID: ppmedrxiv-20076703

ABSTRACT

BackgroundHypercoagulability is becoming widely recognized as a major complication of COVID-19 infection as evidenced by high levels of fibrinogen degradation products and microthrombi identified within the lungs and kidneys of autopsy specimens from these patients. We report thromboelastography (TEG) testing on a cohort of patients with suspected COVID-19 infection at the time of admission to the intensive care unit. MethodsTEG testing was performed using the TEG 6s analyzer near or at the time of ICU admission. We also report the results of other coagulation or inflammatory related indices such as platelet count, prothrombin time, fibrinogen, D-dimer, C-reactive protein, ferritin, and procalcitonin. All laboratory testing was performed at the discretion of the attending physician in the course of normal patient care and retrospectively reviewed. ResultsWe found that maximum clot strength was consistently elevated in COVID-19 patients while normal in all patients found to be negative. We did not encounter significant prolongations of coagulation assays outside of those expectedly prolonged by heparin therapy nor was meeting the criteria for disseminated intravascular coagulation encountered. ConclusionsWe postulate that elevated maximum clot strength by TEG testing is predictive of COVID-19 status as within our cohort this perfectly predicted patients COVID-19 status despite a high level of suspicion in negative patients with normal TEG results. While these results require a larger cohort for confirmation, we feel that TEG testing could improve confidence in COVID-19 testing results in suspected patients possibly allowing for earlier de-escalation of infectious precautions and personal protective equipment utilization.

5.
Preprint in English | medRxiv | ID: ppmedrxiv-20021584

ABSTRACT

BackgroundSevere ill patients with 2019 novel coronavirus (2019-nCoV) infection progressed rapidly to acute respiratory failure. We aimed to select the most useful prognostic factor for severe illness incidence. MethodsThe study prospectively included 61 patients with 2019-nCoV infection treated at Beijing Ditan Hospital from January 13, 2020 to January 31, 2020. Prognostic factor of severe illness was selected by the LASSO COX regression analyses, to predict the severe illness probability of 2019-CoV pneumonia. The predictive accuracy was evaluated by concordance index, calibration curve, decision curve and clinical impact curve. ResultsThe neutrophil-to-lymphocyte ratio (NLR) was identified as the independent risk factor for severe illness in patients with 2019-nCoV infection. The NLR had a c-index of 0.807 (95% confidence interval, 0.676-0.38), the calibration curves fitted well, and the decision curve and clinical impact curve showed that the NLR had superior standardized net benefit. In addition, the incidence of severe illness was 9.1% in age [≥] 50 and NLR < 3.13 patients, and half of patients with age [≥] 50 and NLR [≥] 3.13 would develop severe illness. Based on the risk stratification of NLR with age, the study developed a 2019-nCoV pneumonia management process. ConclusionsThe NLR was the early identification of risk factors for 2019-nCoV severe illness. Patients with age [≥] 50 and NLR [≥] 3.13 facilitated severe illness, and they should rapidly access to intensive care unit if necessary.

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