OCCULT MACULAR DYSTROPHY WITH MUTATIONS IN THE RP1L1 AND KCNV2 GENES.

Purpose: To report a case of occult macular dystrophy associated with mutations in the RP1L1 and KCNV2 genes.

Methods: Case report. Multimodal retinal imaging and the results of genetic testing are described.

Prostaglandin-induced cystoid macular edema following routine cataract extraction.

To our knowledge, we are reporting the first case of a 59-year-old man who developed recurrent CME with three separate trials of three different prostaglandin class drugs following uncomplicated phacoemulsification with intraocular lens implantation. Despite multiple reports of individual prostaglandin (PG) analogues being suggested as the cause of CME, there are no recommendations regarding withholding these medications in the perioperative period. Our patient first developed CME OD 4-months post uncomplicated cataract extraction.

Coarctation of the aorta presenting as spontaneous subarachnoid haemorrhage in the absence of cerebral aneurysm: a report of a rare clinical entity.

Subarachnoid haemorrhage (SAH) is a common neurologic event characterised by bleeding into the space immediately surrounding the brain. In non-traumatic SAH, the predominant cause is aneurysmal rupture of the cerebral vasculature. A significant number occur in the absence of vascular anomalies.

Thrombin-mediated increases in cytosolic [Ca2+] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells.

Thrombin is a procoagulant inflammatory agonist that can disrupt the endothelium-lumen barrier in the lung by causing contraction of endothelial cells and promote pulmonary cell proliferation. Both contraction and proliferation require increases in cytosolic Ca(2+) concentration ([Ca(2+)](cyt)). In this study, we compared the effect of thrombin on Ca(2+) signaling in human pulmonary artery smooth muscle (PASMC) and endothelial (PAEC) cells.

Molecular biology of chronic thromboembolic pulmonary hypertension.

Recent efforts have seen major advances in elucidating the mechanisms underlying pulmonary arterial hypertension. However, chronic thromboembolic pulmonary hypertension (CTEPH) often has been excluded from these studies. Consequently, whereas the clinical, radiographic, and hemodynamic characteristics of CTEPH have been well described, there remains a deficit in our understanding of the cellular, molecular, and genetic mechanisms underlying CTEPH.