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We generated a novel nanoparticle called PVAX, which has intrinsic antiapoptotic and anti-inflammatory properties. This nanoparticle was loaded with neuropeptide Y (NPY), an angiogenic neurohormone that plays a central role in angiogenesis. Subsequently, we investigated whether PVAX-NPY could act as a therapeutic agent and induce angiogenesis and vascular remodeling in a murine model of hind limb ischemia. Adult C57BL/J6 mice ( = 40) were assigned to treatment groups: control, ischemia PBS, ischemia PVAX, ischemia NPY, and Ischemia PVAX-NPY Ischemia was induced by ligation of the femoral artery in all groups except control and given relevant treatments (PBS, PVAX, NPY, and PVAX-NPY). Blood flow was quantified using laser Doppler imaging. On and posttreatment, mice were euthanized to harvest gastrocnemius muscle for immunohistochemistry and immunoblotting. Blood flow was significantly improved in the PVAX-NPY group after 14 days. Western blot showed an increase in angiogenic factors VEGF-R2 and PDGF-β ( = 0.0035 and = 0.031, respectively) and antiapoptotic marker Bcl-2 in the PVAX-NPY group compared with ischemia PBS group ( = 0.023). Proapoptotic marker Smad5 was significantly decreased in the PVAX-NPY group as compared with the ischemia PBS group ( = 0.028). Furthermore, Y receptors were visualized in endothelial cells of newly formed arteries in the PVAX-NPY group. In conclusion, we were able to show that PVAX-NPY can induce angiogenesis and arteriogenesis as well as improve functional blood flow in a murine model of hind limb ischemia. Our research project proposes a novel method for drug delivery. Our patented PVAX nanoparticle can detect areas of ischemia and oxidative stress. Although there have been studies about delivering angiogenic molecules to areas of ischemic injury, there are drawbacks of nonspecific delivery as well as short half-lives. Our study is unique because it can specifically deliver NPY to ischemic tissue and appears to extend the amount of time therapy is available, despite NPY's short half-life.

Introduction The Chiari network is an uncommon vestigial structure of the heart that is often clinically insignificant. We present an unusual case of infective endocarditis affecting only the Chiari network in a patient who presented with septic emboli to the lungs and brain. Case summary A 61-year-old man was admitted with a 2-month history of hemoptysis, pleuritic chest pain, and right upper extremity numbness and weakness. He was found to have multifocal bilateral pulmonary opacities and an abscess collection in the brain. Blood cultures grew Streptococcus intermedius and transthoracic echocardiogram (TTE) was normal. Subsequent transesophageal echocardiogram (TEE) revealed an 8.3 × 4.6 mm vegetation arising from the Chiari network, close to the right atrial appendage, without involvement of the tricuspid valve or any of the other valves. There were no atrial or ventricular septal defects. He was treated with appropriate antibiotics with improvement of symptoms. Repeat imaging showed improvement of the lung opacities, but not the brain abscess, warranting transfer to another hospital for neurosurgical intervention. Conclusion The diagnosis and management of isolated Chiari network endocarditis require a high index of clinical suspicion. A multidisciplinary approach incorporating both medical and surgical approaches where necessary is essential for optimal outcome.

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Takotsubo cardiomyopathy is also known as stress induced cardiomyopathy and transient left ventricular apical ballooning syndrome. There have been few case reports where hyponatremia was implicated as a trigger for stress-induced cardiomyopathy. We report the unusual case of a 79-year-old African American woman without any discernible recent stressors who presented atypically with generalized fatigue and was found to have severe hyponatremia (from chronic alcohol use and thiazide diuretics) and significantly elevated Troponin. Her echocardiogram and cardiac catheterization revealed typical features of apical ballooning syndrome.