Sex differences in myocarditis hospitalizations: Rates, outcomes, and hospital characteristics in the National Readmission Database.

Inflammation of the myocardium, or myocarditis, presents with varied severity, from mild to life-threatening such as cardiogenic shock or ventricular tachycardia storm. Existing data on sex-related differences in its presentation and outcomes are scarce. Using the Nationwide Readmission Database (2016-2019), we identified myocarditis hospitalizations and stratified them according to sex to either males or females. Multivariable regression analyses were used to determine the association between sex and myocarditis outcomes. The primary outcome was in-hospital mortality, and the secondary outcomes included sudden cardiac death (SCD), cardiogenic shock (CS), use of mechanical circulatory support (MCS), and 90-day readmissions. We found a total of 12,997 myocarditis hospitalizations, among which 4,884 (37.6 %) were females. Compared to males, females were older (51 ± 15.6 years vs. 41.9 ± 14.8 in males) and more likely to have connective tissue disease, obesity, and a history of coronary artery disease. No differences were noted between the two groups with regards to in-hospital mortality (adjusted odds ratio [aOR] 1.20; confidence interval [CI] 0.93-1.53; P = 0.16), SCD (aOR:1.18; CI 0.84-1.64; P = 0.34), CS (aOR: 1.01; CI 0.85-1.20;P = 0.87), or use of MCS (aOR: 1.07; CI:0.86-1.34; P = 0.56). In terms of interventional procedures, females had lower rates of coronary angiography (aOR: 0.78; CI 0.70-0.88; P < 0.01), however, similar rates of right heart catheterization (aOR 0.93; CI:0.79-1.09; P = 0.36) and myocardial biopsy (aOR: 1.16; CI:0.83-1.62; P = 0.38) compared to males. Additionally, females had a higher risk of 90-day all-cause readmission (aOR: 1.25; CI: 1.16-1.56; P < 0.01) and myocarditis readmission (aOR:1.58; CI 1.02-2.44; P = 0.04). Specific predictors of readmission included essential hypertension, congestive heart failure, malignancy, and peripheral vascular disease. In conclusion, females admitted with myocarditis tend to have similar in-hospital outcomes with males; however, they are at higher risk of readmission within 90 days from hospitalization. Further studies are needed to identify those at higher risk of readmission.

Clinical and Radiological Features of Menetrier's Disease: A Case Report and Review of the Literature.

We present a case report describing the diagnosis and management of a patient who presents with a rare diagnosis of Menetrier's disease. This condition poses a diagnostic challenge to clinicians due to its nonspecific clinical presentation and is oftentimes misdiagnosed for more common gastric disorders. Menetrier's disease is characterized by gastric mucosal hypertrophy and subsequent protein loss, resulting in gastric symptoms and widespread edema. While the etiology remains unclear, notable associations have been observed with Helicobacter pylori (H. pylori) infection and overexpression of transforming growth factor-alpha (TGF-a). The management often involves supportive measures with medical and surgical interventions for refractory cases and when necessary. This report includes a comprehensive review of the literature on the clinical presentation, diagnostic approach, and management of this rare disease. By documenting such cases in the medical literature, we aim to enhance the clinician's ability to recognize and manage this disorder, thereby preventing the development of more severe manifestations such as gastric carcinoma.

Novel Model of Oxalate Diet-Induced Chronic Kidney Disease in Dahl-Salt-Sensitive Rats.

Diet-induced models of chronic kidney disease (CKD) offer several advantages, including clinical relevance and animal welfare, compared with surgical models. Oxalate is a plant-based, terminal toxic metabolite that is eliminated by the kidneys through glomerular filtration and tubular secretion. An increased load of dietary oxalate leads to supersaturation, calcium oxalate crystal formation, renal tubular obstruction, and eventually CKD. Dahl-Salt-Sensitive (SS) rats are a common strain used to study hypertensive renal disease; however, the characterization of other diet-induced models on this background would allow for comparative studies of CKD within the same strain. In the present study, we hypothesized that SS rats on a low-salt, oxalate rich diet would have increased renal injury and serve as novel, clinically relevant and reproducible CKD rat models. Ten-week-old male SS rats were fed either 0.2% salt normal chow (SS-NC) or a 0.2% salt diet containing 0.67% sodium oxalate (SS-OX) for five weeks.Real-time PCR demonstrated an increased expression of inflammatory marker interleukin-6 (IL-6) (p < 0.0001) and fibrotic marker Timp-1 metalloproteinase (p < 0.0001) in the renal cortex of SS-OX rat kidneys compared with SS-NC. The immunohistochemistry of kidney tissue demonstrated an increase in CD-68 levels, a marker of macrophage infiltration in SS-OX rats (p < 0.001). In addition, SS-OX rats displayed increased 24 h urinary protein excretion (UPE) (p < 0.01) as well as significant elevations in plasma Cystatin C (p < 0.01). Furthermore, the oxalate diet induced hypertension (p < 0.05). A renin-angiotensin-aldosterone system (RAAS) profiling (via liquid chromatography-mass spectrometry; LC-MS) in the SS-OX plasma showed significant (p < 0.05) increases in multiple RAAS metabolites including angiotensin (1-5), angiotensin (1-7), and aldosterone. The oxalate diet induces significant renal inflammation, fibrosis, and renal dysfunction as well as RAAS activation and hypertension in SS rats compared with a normal chow diet. This study introduces a novel diet-induced model to study hypertension and CKD that is more clinically translatable and reproducible than the currently available models.

Toward Development of Neuron Specific Transduction After Systemic Delivery of Viral Vectors.

Widespread transduction of the CNS with a single, non-invasive systemic injection of adeno-associated virus is now possible due to the creation of blood-brain barrier-permeable capsids. However, as these capsids are mutants of AAV9, they do not have specific neuronal tropism. Therefore, it is necessary to use genetic tools to restrict expression of the transgene to neuronal tissues. Here we compare the strength and specificity of two neuron-specific promoters, human synapsin 1 and mouse calmodulin/calcium dependent kinase II, to the ubiquitous CAG promoter. Administration of a high titer of virus is necessary for widespread CNS transduction. We observed the neuron-specific promoters drive comparable overall expression in the brain to the CAG promoter. Furthermore, the neuron-specific promoters confer significantly less transgene expression in peripheral tissues compared with the CAG promoter. Future experiments will utilize these delivery platforms to over-express the Alzheimer-associated pathological proteins amyloid-beta and tau to create mouse models without transgenesis.