The human gut is heavily colonized by a community of microbiota, primarily bacteria, that exists in a symbiotic relationship with the host and plays a critical role in maintaining host homeostasis. The consumption of a high-fat (HF) diet has been shown to induce gut dysbiosis and reduce intestinal integrity. Recent studies have revealed that dysbiosis contributes to the progression of cardiovascular diseases (CVDs) by promoting two major CVD risk factors—atherosclerosis and hypertension. Imbalances in host–microbial interaction impair homeostatic mechanisms that regulate health and can activate multiple pathways leading to CVD risk factor progression. Dysbiosis has been implicated in the development of atherosclerosis through metabolism-independent and metabolite-dependent pathways. This review will illustrate how these pathways contribute to the various stages of atherosclerotic plaque progression. In addition, dysbiosis can promote hypertension through vascular fibrosis and an alteration of vascular tone. As CVD is the number one cause of death globally, investigating the gut microbiota as a locus of intervention presents a novel and clinically relevant avenue for future research, with vast therapeutic potential.

No abstract

No abstract

Overall, average LOE remained relatively consistent between 2012 and 2016, with most abstracts classified as level III or level IV. There was a gradual, albeit minor, increase in the proportion of level I and level II evidence in 2015 and 2016, potentially indicating the increasing commitment to producing and disseminating high-level research in vascular surgery. Furthermore, a lack of a classification tool specific to vascular surgery research occasionally presented a challenge in assigning LOE, perhaps indicating a need for such a tool in this specialty.

Pulmonary langerhans cell histiocytosis (PLCH) is a diffuse lung disease that primarily affects young adults, with cigarette smoking playing a significant role in developing the disease [1,2]. Patients with PLCH present with characteristic CT chest findings of small irregular nodules and upper zone cysts [3][4][5]. Previously, larger nodules greater than 10 mm and cavitation have only been reported a few times in the literature [6][7][8][9]. We describe the case of a 69-year-old male who presented with dyspnea, non-productive cough and weight loss, who was found to have multiple cavitary nodules on CT imaging of the chest. Histopathologic sampling of the lung revealed Langerhans cells which stained positive for S100 and CD1a, consistent with a diagnosis of PLCH. The patient was counselled to quit smoking as the mainstay of treatment. In 3-month follow-up his symptoms had largely resolved, with evidence of decreased nodule size on repeat CT imaging.