Despite decades of research devoted to the study of inferior colliculus (IC) neurons' tuning to sound-source azimuth, there remain many unanswered questions because no previous study has examined azimuth tuning over a full range of 360° azimuths at a wide range of stimulus levels in an unanesthetized preparation. Furthermore, a comparison of azimuth tuning to binaural and contralateral ear stimulation over ranges of full azimuths and widely varying stimulus levels has not previously been reported. To fill this void, we have conducted a study of azimuth tuning in the IC of the unanesthetized rabbit over a 300° range of azimuths at stimulus levels of 10-50 dB above neural threshold to both binaural and contralateral ear stimulation using virtual auditory space stimuli. This study provides systematic evidence for neural coding of azimuth. We found the following: 1) level-tolerant azimuth tuning was observed in the top 35% regarding vector strength and in the top 15% regarding vector angle of IC neurons; 2) preserved azimuth tuning to binaural stimulation at high stimulus levels was created as a consequence of binaural facilitation in the contralateral sound field and binaural suppression in the ipsilateral sound field; 3) the direction of azimuth tuning to binaural stimulation was primarily in the contralateral sound field, and its center shifted laterally toward -90° with increasing stimulus level; 4) at 10 dB, azimuth tuning to binaural and contralateral stimulation was similar, indicating that it was mediated by monaural mechanisms; and 5) at higher stimulus levels, azimuth tuning to contralateral ear stimulation was severely degraded. These findings form a foundation for understanding neural mechanisms of localizing sound-source azimuth.

Telemedicine in its many forms has been utilized across numerous medical specialties to facilitate and expand access to medical care, optimize existing healthcare infrastructure to encourage patient–provider communication, reduce provider burnout, and improve patient surveillance. Since the emergence of the novel coronavirus (COVID-19) pandemic there has been widening of existing socioeconomic disparities in healthcare access for those with chronic respiratory diseases, sparking interest in expanding the use of telemedicine modalities to enhance access to pulmonology specialist care, pulmonary rehabilitation, symptom monitoring, and early identification of clinical exacerbations. Furthermore, the use of telemedicine has been expanded into the intensive care setting to improve patient outcomes and offset provider demands following the increase in critically ill patients due to COVID-19. While an invaluable modality by which to broaden healthcare access and increase the efficacy of care delivery, telemedicine must be used in conjunction with face-to-face physical evaluation and appropriate clinical testing to optimize its benefit. We present here our view of the benefits and disadvantages of the use of telemedicine in the management of chronic respiratory disorders from the perspective of practicing clinicians.

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Background Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are autoimmune diseases with chronically elevated inflammatory activity. Treatments typically have been aimed at decreasing inflammation. While RA and SLE are known to have a high incidence of congestive heart failure (HF), the mechanism behind this remains elusive. We sought to assess the outcomes of HF patients with either RA or SLE as opposed to HF patients without RA or SLE. Methods We conducted a retrospective analysis of the Healthcare Utilization Project-National Inpatient Sample Database from 2010 to 2015 (third quarter). Patients with a primary admitting diagnosis of HF were queried, and those with or without a diagnosis of either SLE or RA were separated into two groups. In-hospital mortality, total charges (TOTCHG), and length of stay (LOS) were analyzed with a multivariate regression model adjusted for demographical and comorbidity variables, using generalized linear models with family binomial, gamma, and negative-binomial, respectively. A p-value smaller than 0.05 was deemed statistically significant. All the statistical analyses were performed in R 3.5.5

INTRODUCTION:Magnesium toxicity can occur due to decreased excretion or overconsumption and is rare in the general population. Early-onset symptoms of toxicity are nausea, flushing, weakness, and urinary retention. However, severe toxicity and its management is not well-described. We present a case of magnesium overdose with intractable hypotension. CASE PRESENTATION:A 34-year-old male presented to the emergency department after he was found unresponsive in a restaurant in the presence of empty bottles of magnesium supplements and ibuprofen. He was hypotensive, hypothermic, and emergently intubated for airway protection. His serum magnesium level was 11.7mg/dl. He was treated with gastric decontamination, intravenous calcium and admitted to the intensive care unit. Continuous Renal Replacement Therapy (CRRT) was initiated and led to a reduction in the measured serum magnesium concentration. Despite aggressive volume administration and multiple vasopressors, he had refractory shock and severe acidosis. An echocardiogram revealed adequate cardiac function; hence, he was not a candidate for Extracorporeal Membranous Oxygenation (ECMO). A trial of hydrocortisone and methylene blue also yielded no benefit to his distributive shock. His hospital course was further complicated by abdominal compartment syndrome requiring a bedside exploratory laparotomy, aspiration pneumonia, acute respiratory distress syndrome, and disseminated intravascular coagulation. Ultimately, his family elected to transition to comfort care, and the patient passed away on hospital day 4.DISCUSSION: Magnesium competitively blocks the entry of calcium into presynaptic terminals of smooth muscle cells, inhibiting the release of acetylcholinesterase, causing smooth muscle relaxation. In the setting of an overdose, this translates to refractory vasoplegia. Magnesium also alters the polarization of the cytoplasmic membrane in cardiac myocytes, causing lengthening of the action potential, thus predisposing to arrhythmias. While iatrogenic magnesium toxicity has been reported at levels of 3-5mg/dL, a level of >10mg/dL is uncommon. There may be a dose-dependent refractoriness that has not been identified in the literature so far. Treatment of severe magnesium toxicity requires urgent dialysis in conjunction with IV calcium which acts as an antagonist. If there is catecholamine resistance, methylene blue may be used to restore systemic vascular resistance. CONCLUSIONS:Severe magnesium toxicity can present with shock & acidosis. Despite dialysis and aggressive resuscitation, the vasoplegia can be refractory and lead to fatal complications, including respiratory collapse and cardiac arrest. Even with early recognition and treatment, the mortality can be high, and further studies are needed to improve outcomes.