Pathogenesis and progression of anosmia and dysgeusia during the COVID-19 pandemic.

Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is the causative agent of COVID-19 which was detected in late 2019 in Wuhan, China. As of September 2022, there have been over 612 million confirmed cases of COVID-19 with over 6.5 million associated deaths. In many cases, anosmia and dysgeusia have been identified as primary symptoms of COVID-19 infection in patients. While the loss of smell (anosmia) and loss of taste (dysgeusia) due to COVID-19 infection is transient in most patients, many report that these symptoms persist following recovery. Understanding the pathogenesis of these symptoms is paramount to early treatment of the infection. We conducted a literature review of Google Scholar and PubMed to find and analyze studies discussing anosmia and dysgeusia in the context of COVID-19 to understand the progression and management of these symptoms. The mechanism for dysgeusia is largely unknown; however, pathogenesis of anosmia includes inflammation and cytokine release resulting from the infection that alters neuronal signaling, thus inducing the loss of smell that patients experience. Anosmia may be managed and potentially resolved sooner with a combination therapy of olfactory training and budesonide irrigation of the nasal cavity. It is important to note that the variants of SARS-CoV-2 are genetically distinguished from the original virion due to a mutation in their spike proteins, giving them a different symptom profile regarding anosmia and dysgeusia. This variability in symptomatology is an area of study that needs to be further explored.

Limiting Mrs2-dependent mitochondrial Mg2+ uptake induces metabolic programming in prolonged dietary stress.

The most abundant cellular divalent cations, Mg2+ (mM) and Ca2+ (nM-µM), antagonistically regulate divergent metabolic pathways with several orders of magnitude affinity preference, but the physiological significance of this competition remains elusive. In mice consuming a Western diet, genetic ablation of the mitochondrial Mg2+ channel Mrs2 prevents weight gain, enhances mitochondrial activity, decreases fat accumulation in the liver, and causes prominent browning of white adipose. Mrs2 deficiency restrains citrate efflux from the mitochondria, making it unavailable to support de novo lipogenesis. As citrate is an endogenous Mg2+ chelator, this may represent an adaptive response to a perceived deficit of the cation. Transcriptional profiling of liver and white adipose reveals higher expression of genes involved in glycolysis, ß-oxidation, thermogenesis, and HIF-1α-targets, in Mrs2-/- mice that are further enhanced under Western-diet-associated metabolic stress. Thus, lowering mMg2+ promotes metabolism and dampens diet-induced obesity and metabolic syndrome.

Arthroereisis: Treatment of Pes Planus.

Arthroereisis is a surgical procedure primarily used to treat flexible pes planus (flatfoot) in pediatric and young adult patients. The principal goal of subtalar arthroereisis is to relieve pain and restore function. This is primarily done by restoring the medial foot arch without fusing the subtalar joint and without requiring a long recovery period needed after osteotomies. Although the procedure can be performed in isolation to treat flexible flatfoot, it can also be performed as an ancillary in the treatment of tarsal coalition, posterior tibial tendon dysfunction, and accessory navicular syndrome. Various implants and multiple surgical techniques exist for arthroereisis, such as the sinus tarsi implant and calcaneo-stop. The type of device and the surgical approach to proceed with are based on the surgeon's discretion rather than an evidence-based protocol. Multiple complications can arise from subtalar arthroereisis, most commonly sinus tarsi pain. Currently, there is a dearth of quality clinical data and evidence on the long-term outcomes and complications of arthroereisis. This lack of literature for a commonly performed procedure validates the need for future studies to better guide a standard protocol, reach consensus on well-defined indications and contraindications, provide expected complications, and improve the practice of evidence-based medicine.