Correction to: FDA Approval of Angiotensin II for the Treatment of Hypotension in Adults with Distributive Shock.

The author name that previously read.

FDA Approval of Angiotensin II for the Treatment of Hypotension in Adults with Distributive Shock.

Distributive shock is a subset of shock marked by decreased systemic vascular resistance, organ hypoperfusion and altered oxygen extraction. Despite the use of intravenous fluids and either higher dose of catecholamines or other additional exogenous vasopressors to maintain blood pressure in the target range, the rate of mortality remains higher in patients with septic shock. Therefore, there is clearly an unmet need for additional safe and effective treatments.

An α-synuclein AAV gene silencing vector ameliorates a behavioral deficit in a rat model of Parkinson's disease, but displays toxicity in dopamine neurons.

Effects of silencing ectopically expressed hSNCA in rat substantia nigra (SN) were examined as a novel therapeutic approach to Parkinson's disease (PD). AAV-hSNCA with or without an AAV harboring a short-hairpin (sh)RNA targeting hSNCA or luciferase was injected into one SN. At 9weeks, hSNCA-expressing rats had reduced SN dopamine (DA) neurons and exhibited a forelimb deficit.

A microRNA embedded AAV α-synuclein gene silencing vector for dopaminergic neurons.

Alpha-synuclein (SNCA), an abundantly expressed presynaptic protein, is implicated in Parkinson's disease (PD). Since over-expression of human SNCA (hSNCA) leads to death of dopaminergic (DA) neurons in human, rodent and fly brain, hSNCA gene silencing may reduce levels of toxic forms of SNCA and ameliorate degeneration of DA neurons in PD. To begin to develop a gene therapy for PD based on hSNCA gene silencing, two AAV gene silencing vectors were designed, and tested for efficiency and specificity of silencing, as well as toxicity in vitro.

Silencing of human alpha-synuclein in vitro and in rat brain using lentiviral-mediated RNAi.

Human alpha-synuclein overexpression and its toxic accumulation in neurons or glia are known to play key roles in the pathogenesis of Parkinson's disease and other related neurodegenerative synucleinopathies. Several single point mutations in the alpha-synuclein gene, as well as gene duplication and triplication, have been linked to familial Parkinson's disease. Moreover, genetic variability of the alpha-synuclein gene promoter is associated with idiopathic Parkinson's disease.

High-efficiency adenovirus-mediated in vivo gene transfer into neonatal and adult rodent skeletal muscle.

Several methodological limitations have emerged in the use of viral gene transfer into skeletal muscle. First, because the nuclei of mature muscle fibers do not undergo division, the use of strategies involving replicative integration of exogenous DNA is greatly limited. Another important limitation concerns the maturation-dependent loss in muscle fiber infectivity with adenoviral vectors.