Graves' Disease Exacerbation with Impending Thyroid Storm After SARS-CoV-2 Infection: A Case Report.

BACKGROUND Since the COVID-19 pandemic, several cases of COVID-19 have been linked to the development of autoimmune disorders, including of the thyroid. Graves' disease (GD) is a rare complication that can occur following SARS-CoV-2 infection. Reports have linked COVID-19 to new onset and exacerbation of GD. We present a case of a 42-year-old woman with a history of GD presenting with impending thyroid storm 3 weeks following a diagnosis of COVID-19. CASE REPORT A 42-year-old woman with a history of GD presented to the Emergency Department (ED) for an acute exacerbation of hyperthyroidism 3 weeks after SARS-CoV-2 infection was diagnosed on a home test. Symptoms included daily headaches, increased bilateral eye pressure, fatigue, muscle weakness, episodes of confusion and agitation, persistent heart palpitations, and goiter. Elevated free T4 of 5.57, free T3 of 15.68, total T3 of 4.43, and near-absent thyroid stimulating hormone were noted. The Burch-Wartofsky scale was 40, which was concerning for an impending thyroid storm; however, at the time of admission, she was not in a thyroid storm. Treatment included propylthiouracil, potassium iodide oral solution, and propranolol, with symptom improvement. Due to prior history of intolerance to antithyroid medications and recent exacerbation, a thyroidectomy was performed once she was in a euthyroid state. CONCLUSIONS Our case demonstrates the importance of recognizing COVID-19 as an etiology or a trigger for new onset or exacerbation of GD. Our case highlights that being vigilant to recognize the association between COVID-19 and thyroid abnormalities for early diagnosis and treatment is imperative.

Cortical Brain Injury Causes Retrograde Degeneration of Afferent Basal Forebrain Cholinergic Neurons via the p75NTR.

Traumatic brain injury (TBI) elicits neuronal loss at the site of injury and progressive neuronal loss in the penumbra. However, the consequences of TBI on afferent neurons projecting to the injured tissue from distal locations is unknown. Basal forebrain cholinergic neurons (BFCNs) extend long projections to multiple brain regions including the cortex, regulate many cognitive functions, and are compromised in numerous neurodegenerative disorders. To determine the consequence of cortical injury on these afferent neurons, we used the fluid percussion injury model of traumatic brain injury and assessed the effects on BFCN survival and axon integrity in male and female mice. Survival or death of BF neurons can be regulated by neurotrophins or proneurotrophins, respectively. The injury elicited an induction of proNGF and proBDNF in the cortex and a loss of BFCNs ipsilateral to the injury compared with sham uninjured mice. The p75NTR knock-out mice did not show loss of BFCN neurons, indicating a retrograde degenerative effect of the cortical injury on the afferent BFCNs mediated through p75NTR. In contrast, locus ceruleus neurons, which also project throughout the cortex, were unaffected by the injury, suggesting specificity in retrograde degeneration after cortical TBI. Proneurotrophins (proNTs) provided directly to basal forebrain axons in microfluidic cultures triggered retrograde axonal degeneration and cell death, which did not occur in the absence of p75NTR. This study shows that after traumatic brain injury, proNTs induced in the injured cortex promote BFCN axonal degeneration and retrograde neuron loss through p75NTR.

Excess cerebellar granule neurons induced by the absence of p75NTR during development elicit social behavior deficits in mice.

Introduction: Recently, the cerebellum has been implicated with non-motor functions, including cognitive and emotional behavior. Anatomical and functional studies demonstrate bidirectional cerebellar connections with brain regions involved in social cognition. Cerebellar developmental abnormalities and injury are often associated with several psychiatric and mental disorders including autism spectrum disorders and anxiety. The cerebellar granule neurons (CGN) are essential for cerebellar function since they provide sensorimotor, proprioceptive, and contextual information to Purkinje cells to modify behavior in different contexts. Therefore, alterations to the CGN population are likely to compromise cerebellar processing and function. Previously we demonstrated that the p75 neurotrophin receptor (p75NTR) was fundamental for the development of the CGN. In the absence of p75NTR, we observed increased proliferation of the granule cell precursors (GCPs), followed by increased GCP migration toward the internal granule layer. The excess granule cells were incorporated into the cerebellar network, inducing alterations in cerebellar circuit processing. Methods: In the present study, we used two conditional mouse lines to specifically delete the expression of p75NTR in CGN. In both mouse lines, deletion of the target gene was under the control of the transcription factor Atoh-1 promotor, however, one of the lines was also tamoxifen-inducible. Results: We observed a loss of p75NTR expression from the GCPs in all cerebellar lobes. Compared to control animals, both mouse lines exhibited a reduced preference for social interactions when presented with a choice to interact with a mouse or an object. Open-field locomotor behavior and operant reward learning were unaffected in both lines. Lack of preference for social novelty and increased anxiety-related behavior was present in mice with constitutive p75NTR deletion; however, these effects were not present in the tamoxifen-inducible mice with p75NTR deletion that more specifically targeted the GCPs. Discussion: Our findings demonstrate that alterations to CGN development by loss of p75NTR alter social behavior, and contribute to the increasing evidence that the cerebellum plays a role in non-motor-related behaviors, including social behavior.

Can smart nutrient applications optimize the plant's hidden half to improve drought resistance?

Global agriculture is challenged with achieving sustainable food security while the climate changes and the threat of drought increases. Much of the research attention has focused on above-ground plant responses with an aim to improve drought resistance. The hidden half, that is, the root system belowground, is receiving increasing attention as the interface of the plant with the soil. Because roots are a sensing organ for nutrients and moisture, we speculate that crop root system traits can be managed using smart nutrient application in order to increase drought resistance. Roots are known to be influenced both by their underlying genetics and also by responses to the environment, termed root plasticity. Though very little is known about the combined effect of water and nutrients on root plasticity, we explore the possibilities of root system manipulation by nutrient application. We compare the effects of different water or nutrient levels on root plasticity and its genetic regulation, with a focus on how this may affect drought resistance. We propose four primary mechanisms through which smart nutrient management can optimize root traits for drought resistance: (1) overall plant vigor, (2) increased root allocation, (3) influence specific root traits, and (4) use smart placement and timing to encourage deep rooting. In the longer term, we envision that beneficial root traits, including plasticity, could be bred into efficient varieties and combined with advanced precision management of water and nutrients to achieve agricultural sustainability.

A Contemporary View of Respiratory Syncytial Virus (RSV) Biology and Strain-Specific Differences.

Respiratory syncytial virus (RSV) is a human respiratory pathogen which remains a leading viral cause of hospitalizations and mortality among infants in their first year of life. Here, we review the biology of RSV, the primary laboratory isolates or strains which have been used to best characterize the virus since its discovery in 1956, and discuss the implications for genetic and functional variations between the established laboratory strains and the recently identified clinical isolates.