Advances in Skin-on-a-Chip Technologies for Dermatological Disease Modeling.

Skin-on-a-chip (SoC) technologies are emerging as a paradigm shift in dermatology research by replicating human physiology in a dynamic manner not achievable by current animal models. Although animal models have contributed to successful clinical trials, their ability to predict human outcomes remains questionable, owing to inherent differences in skin anatomy and immune response. Covering areas including infectious diseases, autoimmune skin conditions, wound healing, drug toxicity, aging, and antiaging, SoC aims to circumvent the inherent disparities created by traditional models. In this paper, we review current SoC technologies, highlighting their potential as an alternative to animal models for a deeper understanding of complex skin conditions.

Isolated Ulnar Neuropathy After Acute Angioedema.

Ulnar neuropathy commonly causes hand paresthesia, often associated with mechanical compression or repetitive movements across the elbow or wrist. There are a few cases that document ulnar nerve injury from rapid compression in the absence of trauma. We present a 30-year-old previously healthy male who developed bilateral hand and forearm swelling, numbness, and pain after an allergic reaction initially treated with epinephrine and steroids. Following treatment, swelling improved; however, paresthesia and weakness persisted. Electrodiagnostic studies performed two months later showed severe ulnar neuropathy prominent at the left proximal wrist, confirmed by ulnar motor inching studies. Signs of acute or subacute denervation and active reinnervation were noted in the left flexor digitorum profundus and abductor digiti minimi. Right-sided studies were unrevealing, although magnetic resonance imaging (MRI) showed an acute flexor pollicis longus tear. Given the timing of events, it was felt that the ulnar neuropathy and acute muscle tear were related to the rapid onset of angioedema. Further research should be conducted on how acute episodes of angioedema (allergy) can cause nerve compression in different extremities. There are very scant reports of different types of angioedema (such as vibratory or hereditary) associated with neuropathy; however, there are no reports of acute allergic angioedema associated with neuropathy. A more comprehensive understanding of the pathophysiology of neuropathy following acute angioedema will help guide treatment approaches both acutely and after symptom presentation.

Cutaneous T-cell Lymphoma Progression: A Potential Dupilumab Pitfall.

Dupilumab is a monoclonal antibody inhibiting key drivers in the inflammatory signaling cascade. It has been considered a saving grace for many patients suffering from severe atopic dermatitis and has quickly become a widespread treatment option for many inflammatory pathologies. However, recent reports have linked dupilumab with exacerbating symptoms and accelerated disease progression of cutaneous T-cell lymphoma (CTCL). This report presents the case of a 60-year-old African American female who was diagnosed with CTCL three months after her initial treatment with dupilumab for presumed atopic dermatitis. An appreciation of this unique relationship, as well as the morphological differences seen in patient presentation, is important for physicians to better guide timely diagnoses while working to uncover the true relationship between dupilumab and CTCL.

An Approach to Anesthetic Management of Venous Anomalies and Outflow Reconstruction in Liver Transplants.

Hepatic venous outflow is a pivotal factor in liver transplant. However, venous anomalies and the potential for hepatic venous congestion continue to remain major points of concern to ensure the viability of transplanted livers and maximize regenerative capacity. We present a 66-year-old patient undergoing liver transplantation who was found to have anomalous venous drainage requiring venous anastomoses. To ensure adequate venous flow and minimize the possibility of graft congestion and liver dysfunction, the anesthetic management of the patient's hemodynamic status was of utmost importance. The use of osmotic diuretics and intraoperative sonography was used to ensure adequate perfusion.

Testicular Rupture Following Motorcycle Accident.

Testicular rupture is a surgical emergency necessitating prompt diagnosis and intervention to prevent irreversible damage. Blunt trauma, including motorcycle collisions, is a common cause of testicular rupture. In the case of multi-trauma, the diagnosis of testicular rupture may be missed in the rush to surgical intervention of more grossly obvious injuries. We present a case of a 24-year-old male who suffered a motorcycle accident and subsequently presented with diffuse abdominal and hip pain. Physical exam and imaging at the emergency department showed multiple pelvic bone fractures, along with a small scrotal injury which was triaged below his pelvic injuries. His pelvic fractures were immediately operated on. Nearly 18 hours after his initial presentation, the patient received a scrotal ultrasound which demonstrated a rupture of the right testicle. Due to this long delay in diagnosis, his urological team opted for non-surgical management and instead employed a more conservative treatment regimen involving pain control, scrotal support, rest, and serial scrotal ultrasounds. This case highlights the importance of timely ultrasound examination for testicular pathology in the setting of multi-trauma and known scrotal injury. Another highlight of this case is the showcase of an uncommon treatment regimen utilizing conservative tactics as opposed to opting for surgical intervention.

A Case of Mistaken Identity: Varicella Zoster and Monkeypox.

Mpox, previously referred to as monkeypox, is a zoonotic virus originally endemic to West Africa which has recently garnered significant attention due to a global outbreak. It remains a challenging diagnosis due to varying clinical presentations and similarities with other infectious pathogens. While diligent monitoring of its prevalence remains crucial, clinicians should combat recency bias when forming differentials for viral illnesses with similar presentations. Here, we discuss the case of an immigrant child with self-reported vaccination history of Varicella Zoster who was diagnosed with Mpox in the emergency department but was subsequently found to have Varicella Zoster after further testing. To effectively manage outbreaks and provide optimal care, healthcare professionals should stay up to date on the latest advancements in diagnostic techniques and available interventions.

A possible mechanism underlying mood disorders associated with LUTS: Chronic bladder outlet obstruction causes NLRP3-dependent inflammation in the hippocampus and depressive behavior in rats.

AIMS: Reports link urinary dysfunction and mood disorders, such as depression, but a causative mechanism has never been postulated. Contemporary discoveries demonstrate a local inflammatory response in peripheral organs can trigger inflammation in the brain, particularly the hippocampus, mediated through the NLRP3 inflammasome. Critically, central inflammation causes depressive behavior. Since bladder outlet obstruction (BOO) evokes a local inflammatory response in the bladder, we hypothesize it will induce NLRP3-dependent inflammation in the hippocampus and depressive behavior. METHODS: There were four groups of rats: control, sham, BOO, or BOO + glyburide (an NLRP3 inhibitor). BOO was created by urethral ligation over a 1 mm catheter. Sham was tied loosely. Glyburide was provided by slow-release pellet (subcutaneous 50 mg, 21 day, replaced as needed). Rats were analyzed 12 weeks post-op for: hippocampal inflammation, microglial density, neurogenesis, and depression symptoms (open field and sucrose preference). RESULTS: BOO elicited hippocampal inflammation, accompanied by an increase in activated microglia (22%) and a decrease in neurogenesis (35%), which was blocked by glyburide. In addition, BOO rats displayed anxiety (57% decrease in exploratory behavior in the open field assay) and anhedonia (21% decrease in sucrose preference), two symptoms of depression. Like inflammation, these symptoms were diminished by glyburide to levels not statistically significantly different from controls. CONCLUSIONS: BOO, a bladder-localized event, stimulates NLRP3-dependent inflammation in the rat hippocampus after 12 weeks and this inflammation causes depressive behavior. This is the first mechanistic explanation of the link between BOO and depression and provides evidence for a distinct bladder-brain axis.