13 research outputs found
More Than Smell - COVID-19 Is Associated With Severe Impairment of Smell,Taste, and Chemesthesis
Recent anecdotal and scientific reports have provided evidence of a link between COVID-19 and chemosensory impairments, such as anosmia. However, these reports have downplayed or failed to distinguish potential effects on taste, ignored chemesthesis, and generally lacked quantitative measurements. Here, we report the development, implementation, and initial results of a multilingual, international questionnaire to assess self-reported quantity and quality of perception in 3 distinct chemosensory modalities (smell, taste, and chemesthesis) before and during COVID-19. In the first 11 days after questionnaire launch, 4039 participants (2913 women, 1118 men, and 8 others, aged 19-79) reported a COVID-19 diagnosis either via laboratory tests or clinical assessment. Importantly, smell, taste, and chemesthetic function were each significantly reduced compared to their status before the disease. Difference scores (maximum possible change +/- 100) revealed a mean reduction of smell (-79.7 +/- 28.7, mean +/- standard deviation), taste (-69.0 +/- 32.6), and chemesthetic (-37.3 +/- 36.2) function during COVID-19. Qualitative changes in olfactory ability (parosmia and phantosmia) were relatively rare and correlated with smell loss. Importantly, perceived nasal obstruction did not account for smell loss. Furthermore, chemosensory impairments were similar between participants in the laboratory test and clinical assessment groups. These results show that COVID-19-associated chemosensory impairment is not limited to smell but also affects taste and chemesthesis.The multimodal impact of COVID-19 and the lack of perceived nasal obstruction suggest that severe acute respiratory syndrome coronavirus strain 2 (SARS-CoV-2) infection may disrupt sensory-neural mechanisms
Posterior Vertebral Column Resection for VATER/VACTERL Associated Spinal Deformity: A Case Report
The VATER/VACTERL association is a syndrome notable for congenital vertebral malformations, anal atresia, cardiovascular anomalies, tracheoesophageal fistula, esophageal atresia, and renal or limb malformations. Vertebral malformations may include the entire spectrum of congenital spinal deformities, including kyphosis, as was seen in this case. A 14-year-old girl presented to our institution with severe rigid sagittal deformity in the thoracolumbar spine that had recurred following three prior spinal fusion surgeries: the first posterior only, the second anterior and posterior, and the third a posterior only proximal extension. These surgeries were performed to control progressive kyphosis from a complex failure of segmentation that resulted in a 66° kyphosis from T11 to L3 by the time she was 9 years old. Our evaluation revealed solid arthrodesis from the most recent procedures with resultant sagittal imbalance, and surgical options to restore balance included anterior and posterior revision spinal fusion with osteotomies, multiple posterior extension osteotomies with circumferential spine fusion, and posterior vertebral column resection with circumferential spine fusion. She was advised that multiple posterior extension osteotomies would likely be insufficient to restore sagittal balance in the setting of solid arthrodesis from anterior and posterior surgery, and that the posterior-only vertebral column resection would provide results equivalent to revision anterior and posterior surgery, without the morbidity of the anterior approach. She successfully underwent posterior vertebrectomy and circumferential spinal fusion with instrumentation and is doing well 2 years postoperatively. Severe rigid sagittal deformity can be effectively managed with a posterior-only surgical approach, vertebrectomy, and circumferential spinal fusion with instrumentation
The conserved interaction of C7orf30 with MRPL14 promotes biogenesis of the mitochondrial large ribosomal subunit and mitochondrial translation
Quality control of mitochondria: protection against neurodegeneration and ageing
Dysfunction of mitochondria has severe cellular consequences and is linked to ageing and neurodegeneration in human. Several surveillance strategies have evolved that limit mitochondrial damage and ensure cellular integrity. Intraorganellar proteases conduct protein quality control and exert regulatory functions, membrane fusion and fission allow mitochondrial content mixing within a cell, and the autophagic degradation of severely damaged mitochondria protects against apoptosis. Here, we will summarize the current knowledge on these surveillance strategies and their role in human disease