Obesity is associated with metabolic perturbations including liver and adipose tissue inflammation, insulin resistance, and type 2 diabetes. Omega-6 fatty acids (ω6) promote and omega-3 fatty acids (ω3) reduce inflammation as they can be metabolized to pro- and anti-inflammatory eicosanoids, respectively. 12/15-lipoxygenase (12/15-LO) enzymatically produces some of these metabolites and is induced by high fat (HF) diet. We investigated the effects of altering dietary ω6/ω3 ratio and 12/15-LO deficiency on HF diet-induced tissue inflammation and insulin resistance. We examined how these conditions affect circulating concentrations of oxidized metabolites of ω6 arachidonic and linoleic acids and innate and adaptive immune system activity in the liver. For 15 weeks, wild-type (WT) mice were fed either a soybean oil-enriched HF diet with high dietary ω6/ω3 ratio (11∶1, HFH), similar to Western-style diet, or a fat Kcal-matched, fish oil-enriched HF diet with a low dietary ω6/ω3 ratio of 2.7∶1 (HFL). Importantly, the total saturated, monounsaturated and polyunsaturated fat content was matched in the two HF diets, which is unlike most published fish oil studies in mice. Despite modestly increased food intake, WT mice fed HFL were protected from HFH-diet induced steatohepatitis, evidenced by decreased hepatic mRNA expression of pro-inflammatory genes and genes involved in lymphocyte homing, and reduced deposition of hepatic triglyceride. Furthermore, oxidized metabolites of ω6 arachidonic acid were decreased in the plasma of WT HFL compared to WT HFH-fed mice. 12/15-LO knockout (KO) mice were also protected from HFH-induced fatty liver and elevated mRNA markers of inflammation and lymphocyte homing. 12/15-LOKO mice were protected from HFH-induced insulin resistance but reducing dietary ω6/ω3 ratio in WT mice did not ameliorate insulin resistance or adipose tissue inflammation. In conclusion, lowering dietary ω6/ω3 ratio in HF diet significantly reduces steatohepatitis.
Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a complex clinical syndrome that is characterized by evidence of acute myocardial infarction in the absence of significant epicardial coronary artery disease on angiography. The term “MINOCA” encompasses a group of heterogeneous diseases with varying underlying mechanisms and each with its own pathophysiology. Overlooked plaque rupture or erosion and coronary vasospasm are the most common causes of MINOCA and can be diagnosed by routine intracoronary imaging and vasoreactivity testing, respectively. Coronary microvascular dysfunction is a less recognized, albeit an important cause of morbidity in patients presenting with MINOCA. Although MINOCA is a rare presentation of acute coronary syndrome, it is not a benign disorder and can have adverse consequences if untreated. In this article, we aim to review the pathogenesis, clinical characteristics, and finally propose a systematic approach in the diagnosis and management of patients with MINOCA.
Pulmonary arterial hypertension (PAH) is a rare, life-threatening disease with poor survival despite recent advances in management. Pulmonary Function Testing (PFT) with diffusing capacity for carbon monoxide (DLCO) are used to assess severity in patients with PAH; however, cardiopulmonary exercise testing (CPET) remains the clinical standard for multi-organ assessment and severity of exercise limitation. We hypothesized that DLCO correlates with PAH severity as measured by CPET, and potentially characterized high-risk phenotypes. METHODS: A single-institution, retrospective evaluation from 2000 to 2019 was performed at the Liu Center for Pulmonary Hypertension (Harbor-UCLA Medical Center) in patients with PAH. Baseline and serial PFT/CPET were collected in 80 PAH patients followed for an average length of 3.9 years. The data was compared between PAH subtypes. The subtypes included Idiopathic (IPAH), and PAH associated with: connective tissue disease (APAH/CTD), drugs/toxins (APAH/D&T), congenital heart disease (APAH/CHD), HIV (APAH/HIV), and portal hypertension (Porto-PH). Differences in baseline demographics, PFT/ CPET were assessed by Fisher's exact test or exact Wilcoxon rank sum test. Pearson or Spearman correlation coefficients were used for correlations between changes in DLCO (%) and PFT/CPET. Repeated mixed models were used to estimate the association of risk factors with change in DLCO (%), adjusting for differences in baseline and number of follow-up years.
Vaping or e-cigarettes use has been previously marketed as a safe alternative to smoking. However, the outbreak of e-cigarette, or vaping, product use-associated lung injury (EVALI) has become a public health disaster leading to the hospitalization of thousands of young, healthy individuals. Currently there is limited data available on the residual lung disease that develops after EVALI. CASE PRESENTATION: The case series included 8 patients, ages 21-46, hospitalized in the Southern California region during 2019. They presented with symptoms of unexplained dyspnea that were found to be responsive to corticosteroid treatment. All met the CDC surveillance case definition for severe pulmonary disease associated with e-cigarette use (1).
INTRODUCTION: Cryptococcus neoformans is an ubiquitous endemic organism that is frequently acquired during early childhood and maintained in a state of latency with no evidence of clinical disease. Reactivation primarily occurs in the lungs and can lead to dissemination in immunocompromised hosts. We present a rare case of disseminated cryptococcosis manifesting as empyema and acute suppurative cholangitis, in a non-HIV patient who developed immunosuppression from critical care illness.
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