PubMed Health⌕ Search

Biomedical subjects

Jonathan Fox

Publications and source records attributed to Jonathan Fox.

6 recordsLinked to original sources
PubMed2006

Modifications to advanced life support in renal failure.

The outcome of cardiopulmonary resuscitation (CPR) has been reported to be worse in patients with renal failure compared with those with normal renal function. It is likely that this increased mortality may be at least partly attributable to sub-optimal and highly variable treatment strategies used in cardiac arrest in patients with renal failure, but this issue has not previously been explored. Such patients undoubtedly pose a challenge to advanced life support (ALS) providers, and renal unit staff are not trained to provide specialist advice after a patient has sustained a cardiac arrest. There are few studies investigating the epidemiology, safety or outcome of cardiac arrest in patients with renal failure and there are no generally accepted resuscitation guidelines for this special circumstance. In this article we discuss the unique problems of resuscitating patients with renal failure and propose a suitable management strategy.

Advance Directives↗
PubMed2006

Discovery of bioactive small-molecule inhibitor of poly adp-ribose polymerase: implications for energy-deficient cells.

Poly (ADP-ribose) polymerase (PARP1) is a nuclear protein that, when overactivated by oxidative stress-induced DNA damage, ADP ribosylates target proteins leading to dramatic cellular ATP depletion. We have discovered a biologically active small-molecule inhibitor of PARP1. The discovered compound inhibited PARP1 enzymatic activity in vitro and prevented ATP loss and cell death in a surrogate model of oxidative stress in vivo. We also investigated a new use for PARP1 inhibitors in energy-deficient cells by using Huntington's disease as a model. Our results showed that insult with the oxidant hydrogen peroxide depleted cellular ATP in mutant cells below the threshold of viability. The protective role of PARP1 inhibitors against oxidative stress has been shown in this model system.

Adenosine Triphosphate↗
PubMed2004

Anti-inflammatory treatment with acetylsalicylate or rofecoxib is not neuroprotective in Huntington's disease transgenic mice.

Inflammatory mechanisms have been implicated in the pathogenesis of Huntington's disease (HD). Possible benefits of anti-inflammatory treatments include improved folding of mutant huntingtin mediated through chaperones, reduction of destructive cellular and humoral inflammatory pathways, and reduction of proapoptotic signaling mediated by NF-kappaB or other transcription factors. This study was performed to investigate the therapeutic potential of anti-inflammatory drugs as treatments for Huntington's disease by examining whether two compounds in widespread human use can ameliorate the phenotype of HD transgenic mouse models. We examined the effectiveness of acetylsalicylate and rofecoxib as treatments for the R6/2 and N171-82Q transgenic mouse models of Huntington's disease. Both drugs were administered from weaning. To monitor the effectiveness of the treatment, we analyzed the mice for weight loss, behavioral changes, and gross cerebral and striatal atrophy. The studies showed that neither drug benefited the animals at doses comparable to those tolerated by humans.

Acoustic Stimulation↗
PubMed2003

Neuronal ceroid-lipofuscinosis in a Labrador Retriever.

An 8-year-old Labrador Retriever with an 11-month history of progressive partial seizures and necropsy examination findings characteristic of the lamellar form of canine neuronal ceroid-lipofuscinosis (NCL) is presented. The clinical, light microscopic, and ultrastructural features of this case most closely resemble human adult-onset NCL (Kufs disease). This is the first report of NCL occurring in the Labrador Retriever breed.

Animals↗