Publications by authors named "A Gurney"

Objective: Cerebral blood flow (CBF) decline is increasingly recognized as an area of importance for targeting neurodegenerative disorders, yet full understanding of the mechanisms that underlie CBF changes are lacking. Animal models are crucial for expanding our knowledge as methods for studying global CBF and neurovascular coupling in humans are limited and require expensive specialized scanners.

Methods: Use of appropriate animal models can increase our understanding of cerebrovascular function, so we have combined chronic cranial windows with in vivo two-photon and laser speckle microscopy and ex vivo capillary-parenchymal arteriole (CaPA) preparations.

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Article Synopsis
  • Researchers studied early-onset urinary tract disorders like urofacial syndrome (UFS), which is caused by a mutation affecting bladder function and can lead to kidney failure.
  • Current treatments don't address the core issues of these disorders, prompting the exploration of a gene therapy approach using an adeno-associated viral (AAV9) vector to deliver the missing gene in neonatal mice.
  • The treatment successfully expressed the missing protein in the pelvic ganglia and improved bladder function, suggesting that AAV9 gene therapy may offer a potential cure for UFS and related neurogenic bladder issues.
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Currently, there exist no curative treatments for neurodegenerative disorders. Recently, there has been a resurgence of interest in the use of medicinal cannabis to improve neurological conditions. A 12-month, open label, dose-finding, safety and efficacy study was conducted including 48 subjects with a variety of neurodegenerative disorders.

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Introduction: Urofacial, or Ochoa, syndrome (UFS) is an autosomal recessive disease featuring a dyssynergic bladder with detrusor smooth muscle contracting against an undilated outflow tract. It also features an abnormal grimace. Half of individuals with UFS carry biallelic variants in , whereas other rare families carry variants in is immunodetected in pelvic ganglia sending autonomic axons into the bladder.

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Patients with pulmonary arterial hypertension (PAH) have a high burden of arrhythmias, including arrhythmias arising from sinus node dysfunction, and the aim of this study was to investigate the effects of PAH on the sinus node. In the rat, PAH was induced by an injection of monocrotaline. Three weeks after injection, there was a decrease of the intrinsic heart rate (heart rate in the absence of autonomic tone) as well as the normal heart rate, evidence of sinus node dysfunction.

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