Total artificial heart implantation for biventricular failure due to eosinophilic myocarditis.

Idiopathic hypereosinophilic syndrome is a condition of unknown etiology characterized by proliferation of eosinophils and their infiltration into tissues. Although cardiac involvement is rare, eosinophilic myocarditis can lead to life-threating fulminant congestive heart failure. Treatment of patients with eosinophilic myocarditis is challenging as heart failure can be caused by biventricular dysfunction. To our knowledge, this is the first case reported in the literature describing a patient with acute severe biventricular heart failure caused by eosinophilic myocarditis with mural left ventricular apical thrombus who was successfully treated with implantation of a total artificial heart as a bridge to heart transplant.

Another Case of Lisinopril-Induced Acute Pancreatitis.

Lisinopril as a cause for acute drug-induced pancreatitis is an emerging phenomenon that due to its generally low-risk profile often goes unnoticed. The true incidence of drug-induced pancreatitis is unknown, probably because of its nonrecognition among differential diagnosis. Only a handful of lisinopril-induced pancreatitis has been discussed in the literature, and little epidemiological evidence exists to establish true causality. Additionally, many of these reports have been met with skepticism claiming that it is difficult to isolate a true cause since many of these patients had comorbidities or were concomitantly taking other medications that may have contributed to the pancreatitis. Here, we report a case in which a generally otherwise healthy patient presented with acute drug-induced pancreatitis caused by an angiotensin-converting enzyme (ACE) inhibitor taken eight weeks prior to the onset of symptoms. The drug was immediately stopped, and the patient recovered well, with no complications.

Brain derived neutrophic factor (BDNF) coordinates lympho-vascular metastasis through a fibroblast-governed paracrine axis in the tumor microenvironment.

It has long been known that the tumor microenvironment contributes to the proliferation and survival of neoplasms through the constant interaction with the stromal and immune compartments. In this investigation, we explored the role of cancer-associated fibroblasts (CAFs) in the regulation of the tumor microenvironment in head and neck squamous cell carcinoma (HNSCC) though a complex intercellular BDNF-TrkB signaling system. Our studies show that conditioned media derived from patient-derived CAFs promoted HNSCC cell proliferation, in vitro cell migration, cell invasion and chemotherapy resistance, compared to normal fibroblasts. Furthermore, examination of the in vivo impact of CAF pathophysiology in the tumor microenvironment in animal xenograft models revealed that HNSCC cell lines in combination with CAFs promoted tumor growth and increased incidence of lymphovascular metastasis as compared to injection of tumor cells or CAF cells alone. Using pharmacological and genetic alterations, we mechanistically demonstrate the critical importance of BDNF-TrkB signaling in the tumor microenvironment. These investigations further support the rationale for BDNF/TRKB targeted therapy against in the treatment of HNSCC.