A man who perished just yards from his home after driving a friend home on Christmas night died from a mixture of alcohol poisoning and hypothermia.The body of Bartley Doohan was found by his brother close to their home in Gortahork, Co Donegal on St Stephen’s Day, 2016. The 58-year-old machine operator had gone to the home of neighbour John Harkin, less than 500 yards away, for a couple of festive drinks.However, an inquest into Bartley’s death heard he never returned that night and was discovered face up in a ditch the following day.Donegal Coroner’s Court, held in Letterkenny, heard how Bartley’s Renault Laguna car was found partially in a ditch and his body was found in five inches of water a few yards away.A post mortem on the dead man’s body found that he had eight times the normal drink-driving limit of alcohol in his body when he was found.Mr Harkin gave evidence that he had been in Mr Doohan’s home earlier in the night at Curransport but he had left him home and the pair enjoyed a few hot whiskies together.Mr Doohan left after 1.30am but the next morning he was contacted by Bartley’s sister Ann asking if he had seen her brother.He went looking and came across Bartley’s brother Peter saying he had found him drowned and asked him to give him a hand taking him out of the ditch.A doctor from the NowDoc service arrived on the scene along with Gardai and Mr Doohan was pronounced dead at 11am and taken to Letterkenny University Hospital.Pathologist Dr Katriona Dillon said the dead man had no noticeable injuries either externally or internally apart from a small abrasion above one of his eyes and another on his toe.She said that in her opinion death was due to alcohol intoxication and exposure to a cold environment and that there was no evidence that Mr Doohan had died as a result of a road traffic accident.She said a reading of 403 milligrams of alcohol per 100 ml of blood of was found in Mr Doohan’s body.Coroner Dr McCauley remarked that he wouldn’t normally see as high a level as that noting that 50 milograms of alcohol was the drink-driving limit.He said “That alone could have been enough to cause his death.”The coroner agreed with Dr Dillon that death was due to alcohol intoxication and hypothermia and recorded a finding of death by misadventure.He added it was especially sad considering the time of year of Mr Doohan’s death.“It’s just very sad. It was miserable night and he wasn’t going to walk home and it resulted in a terrible accident which caused his death. It happened on Christmas night which adds to the sheer extra sadness,” he said.Man perished to death after leaving friend home on Christmas night was last modified: September 1st, 2017 by StephenShare this:Click to share on Facebook (Opens in new window)Click to share on Twitter (Opens in new window)Click to share on LinkedIn (Opens in new window)Click to share on Reddit (Opens in new window)Click to share on Pocket (Opens in new window)Click to share on Telegram (Opens in new window)Click to share on WhatsApp (Opens in new window)Click to share on Skype (Opens in new window)Click to print (Opens in new window) Tags:alcoholBartley DoohancarCHristmasdonegalGardaigortahorkhypothermiainquest
Source:http://www.upmc.com/media/NewsReleases/2018/Pages/parkinsons-stm.aspx Jul 26 2018A gene linked to 3 to 4 percent of people with Parkinson’s disease could play an important role in most, if not all, people with the disease, according to new study findings from the University of Pittsburgh School of Medicine and UPMC. The gene, called LLRK2, was previously thought to only cause disease when mutated, but researchers have found that it may be just as significant in the non-hereditary form of the disease, according to the study published today in the journal Science Translational Medicine. “This discovery is extremely consequential for Parkinson’s disease because it suggests that therapies currently being developed for a small group of patients may benefit everybody with the disease,” said senior author J. Timothy Greenamyre, M.D., Ph.D., Love Family Professor of Neurology in Pitt’s School of Medicine, chief of the Movement Disorders Division at UPMC and director of the Pittsburgh Institute for Neurodegenerative Diseases (PIND).Parkinson’s affects one million people in the U.S. and as many as 10 million worldwide and has no known cause, but is thought to involve both genetic and environmental factors. In 2004, researchers discovered that mutations in the LRRK2 gene (commonly pronounced as “Lark2″), overactivated the protein and caused Parkinson’s in a small group of people, often in a hereditary fashion. However, the LRRK2 protein is difficult to study because it is present in extremely small amounts in nerve cells that are affected in Parkinson’s.To overcome this problem, Greenamyre and his team engineered a molecular ‘beacon’ that attached to LRRK2 and glowed red under a microscope only if the protein was active. This allowed them to also reveal the nerve cells in which LRRK2 was active in the brain.The researchers applied the test to postmortem brain tissue donated to science by Parkinson’s patients, none of whom had mutations in LRRK2, and healthy individuals of approximately the same age.Related StoriesStudy provides new insight into longitudinal decline in brain network integrity associated with agingResearchers discover gene linked to healthy aging in wormsRevolutionary gene replacement surgery restores vision in patients with retinal degenerationRemarkably, the test indicated that in ‘dopamine neurons,’ which are the brain cells most commonly affected in Parkinson’s, LRRK2 was highly active in individuals affected by the disease, but not in the healthy individuals. This suggests that LRRK2 overactivity may be important in all people with Parkinson’s, not just those who have a mutation in the gene.A second major finding of the study was that it connected two proteins that have separately been recognized as important players in causing Parkinson’s – LRRK2 and alpha-synuclein. Accumulation of alpha-synuclein leads to the formation of structures called ‘Lewy bodies,’ a hallmark of Parkinson’s.While enormous efforts have been focused on alpha-synuclein, the cause of its accumulation is still poorly understood. Using a rodent model of Parkinson’s induced by an environmental toxin, Greenamyre and his team discovered that activation of LRRK2 blocked the mechanisms that cells use to clear excess alpha-synuclein, leading directly to its accumulation. The researchers then treated the animals with a drug currently being developed to treat familial Parkinson’s patients by blocking LRRK2 activity. The drug prevented the accumulation of alpha-synuclein and formation of Lewy bodies.”LRRK2 ties together both genetic and environmental causes of Parkinson’s, as we were able to show that external factors like oxidative stress or toxins can activate LRRK2, which can in turn cause Lewy bodies to form in the brain,” noted lead author Roberto Di Maio, Ph.D., an assistant professor in Greenamyre’s lab and a researcher at the Ri.MED Foundation.In the future, Greenamyre expects to build on these findings to discover how neurodegeneration caused by LRRK2 overactivation can be prevented, and identify how oxidative stress and environmental toxins cause LRRK2 activation.