Share Name Share Symbol Market Type Share ISIN Share Description
AstraZeneca LSE:AZN London Ordinary Share GB0009895292 ORD SHS $0.25
  Price Change % Change Share Price Bid Price Offer Price High Price Low Price Open Price Shares Traded Last Trade
  -45.50p -0.94% 4,788.00p 4,790.50p 4,791.50p 4,820.50p 4,756.00p 4,803.50p 1,710,049 16:35:24
Industry Sector Turnover (m) Profit (m) EPS - Basic PE Ratio Market Cap (m)
Pharmaceuticals & Biotechnology 16,632.7 1,648.8 175.5 28.6 60,626.69

AstraZeneca Share Discussion Threads

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Sterling going back to pre brexit level against the dollar probably hasn't helped either
Astras recent weakness likely as a result of Woodford going from 9% to 1 to help meet redemptions and of course invest inUk focused stocks , assuming you believe the latter. Redemptions more significant I suspect .
Surprisingly quiet board
buywell3 We have ALREADY had prion issues in this country! LOL What do you thing Mad Cow Disease was? You probably already have the prions in your brain. We all probably do. The illness was derived from sheep, which have carried this illness since time began. So, can you please stop posting on the AZN thread and create your own. Thanks.
Many BIG Pharmas have spent $ Billions trying to find a cure for Alzheimer's Prion disease is the whale passing through the room But it is soon to get recognised for what it is and the threats that it presents Deadly ... no cure UCLA researchers determine atomic structure of defective prions January 29, 2018 UCLA researchers have determined the atomic structure of part of a protein that causes certain neurodegenerative diseases. In a study published earlier in January, researchers in the lab of Jose Rodriguez, assistant professor of chemistry and biochemistry, determined the structure of a segment of prion, a protein that causes diseases such as mad cow disease, when it is defective. Visualizing the prion allows other researchers to understand the basis behind prion diseases and develop therapies toward preventing and treating them. Prions, which are found mainly in the brain, may randomly become defective and convert normal prions into additional defective prions, spreading the disease throughout the brain and resulting in death, according to the Centers for Disease Control. Individuals who come into contact with the flesh or fluids of animals with defective prions can contract them, spreading the disease. Prion diseases are particularly dangerous because defective prions aggregate into stable clumps of protein that the body cannot easily break down, Rodriguez said. “You can boil (a prion aggregate), dip it in acid, treat it (with harsh chemicals), and it still won’t lose its shape or break apart,” he said. Rodriguez said his lab decided to determine the structure of the defective prion in order to understand its extreme stability. Calina Glynn, a graduate student in Rodriguez’ lab, said they studied a segment of the prion of a small rodent called the bank vole. This segment behaved like a defective prion, so it served as a good model for studying prion diseases, Rodriguez said. While most animals usually do not contract prions from other species, the bank vole easily contracts defective prions from other animals, Glynn said. Marcus Gallagher-Jones, a postdoctoral researcher in Rodriguez’s lab, said studying the bank vole prion may explain why bank voles are so susceptible to prion diseases and inform further research on how defective prions spread. The researchers used a technique called MicroED to determine the protein’s structure, Glynn said. MicroED allowed the researchers to see fine details in the protein structure that would otherwise be invisible with traditional techniques like X-ray crystallography, she said. Gallagher-Jones said that using MicroED, the researchers could see the position of hydrogen atoms in the protein, a feat not normally possible with X-ray crystallography. Seeing the hydrogen atoms helped the researchers realize the hydrogen atoms form a network that helps glue prions together into an aggregate. “We’re very interested in seeing how the network of hydrogen bonding plays a role in the prion’s stability,” he said. Rodriguez said his lab’s work highlighted the advantages of MicroED and that a high resolution structure of the aggregated prion can help other researchers develop approaches to treating prion diseases. “MicroED (allowed us to determine) structures of proteins that have been challenging by traditional methods,” he said. “We’re now starting to get high-resolution structures of prions in their aggregated state. It’s a goal that was out of reach for a while.”
Good news here this morning
buywell3 11 Feb '18 - 17:54 - 2050 of 2050 (Filtered) Interesting but post somewhere else.
buywell3 All very interesting but can you just post the link. Thanks.
USA sell off still looking likely as Fund managers race for the exit RE vCJD and CJD which were caught by UK people eating Prion infected beef , BSE it was termed in cattle. Well now in the USA they have a prion infected problem with deer and Elk , they call it CWD over there ... it is also springing up in other countries too. It is going to be a big problem worldwide when those in the know admit that Prions are causing many brain disorders in humans Diseases that have been named many other names 50 to 100 years previously will get renamed as Prion diseases , with genetic mutations causing the various distorted shapes of prion proteins in the human brain Research: CWD may pose risk to humans FEB 4, 2018 Chronic wasting disease, a fatal brain illness killing area deer, may have the potential to infect humans, according to warnings from North American governments. And while there has not been a case of a human infection, local experts said they have been monitoring the illness with the same concerns. “We’re absolutely discussing things like that,” said Wayne Laroche, the Pennsylvania Game Commission’s special assistant for chronic wasting disease response. Last year, a branch of Health Canada — the Bureau of Microbial Hazards — issued a risk advisory opinion, warning that “the most prudent approach is to consider that CWD has the potential to infect humans.” That warning followed a series of tests performed by Canadian researchers on animals, including human-like macaque monkeys, which became infected with the disease. Officials at the U.S. Centers for Disease Control and Prevention also have referenced the tests, explaining macaques contracted the disease when they were fed muscle or brain tissue from infected deer and elk. Some of that meat, according to the CDC, came from asymptomatic deer — deer infected with chronic wasting disease that appear healthy and have not yet begun to show symptoms. “To date, there have been no cases of (chronic wasting disease) in people and no direct proof that people can get (the disease),” according to a CDC report. “Nevertheless, these experimental studies raise the concern that (the disease) may pose a risk to people and suggest that it is important to prevent human exposures to (it).” Chronic wasting disease is a resilient prion — an infectious protein — which attacks deer brains, eventually leading to a loss of motor functions and death. It is similar to but not the same as mad cow disease. In some cases, a deer doesn’t begin to show symptoms of chronic wasting disease until a year after contraction, according to the Game Commission. Symptoms include drastic weight loss, stumbling, listlessness and other neurologic symptoms. The disease was first detected in Blair and Bedford counties after the 2012 hunting season. A disease management area spanning more than 2,000 square miles has since been created, and it includes parts of Bedford, Blair, Cambria, Clearfield, Franklin, Fulton, Huntingdon and Somerset counties. The area is known as DMA 2. The disease likely got its start sometime in the 1960s at a feed testing facility in Colorado and was transported to other areas through infected deer. “They were trading deer,” Laroche said, hinting at a larger problem of humans spreading negative environmental factors from place to place. “It all boils down to people,” he said. “We’re moving everything around.” Chronic wasting disease has been detected outside of North America, including in Norway and South Korea. Locally, 25 deer tested positive for chronic wasting disease in 2016, Laroche said. All of the deer were in or near DMA 2, “the only area of the state where (the disease) has been detected in the wild,” according to Game Commission data. In 2017, 55 deer tested positive for the disease in Pennsylvania, Laroche said, revealing that the number could increase as 4,000-plus 2017 samples still have not been tested. Chronic wasting disease can be spread through direct physical contact or through bodily fluids, meaning if a deer expels excrement onto a surface and another deer comes in contact with that surface, it can become infected. That makes areas frequently populated by deer — bait piles, salt licks and deer pens — especially concerning, Laroche said. “Those are likely places where we might have a high enough dose for infection,” he said. And once an area is contaminated, it can remain that way for more than a decade, Laroche said. “This stuff can be on the landscape for at least 15 years and be infectious,” he said. To both study and eliminate the spread of chronic wasting disease in Pennsylvania, Game Commission officials have occasionally suggested culling deer. In early 2017, officials addressed a crowd gathered at Central High School, revealing a consideration of using sharpshooters to kill targeted groups of deer in areas where the disease is abundant. And just last month, officials announced a since-halted plan to kill about 40 deer in the Portage area to monitor the spread of chronic wasting disease. In both of those cases, plans to eliminate deer were met with much criticism from local hunters who are concerned the killings could drastically decrease the chances of bagging a buck during the following hunting seasons. “Of course everybody is worried about the deer (they’re) going to get next year,” Laroche said. Laroche said he has spoken with a number of hunters who believe the problem will go away or “burn itself out” without human intervention. “It may burn itself out, but there may be just smoke and ashes left,” Laroche said, explaining the disease has already decimated deer populations in Wyoming, where it is predicted that the animals “could be extinct in 40 to 50 years” if remedial action is not taken. “We absolutely need the support of the public,” Laroche said. “We are doing it for them, for their kids and for the future of hunting.” One thing is for sure: Now that chronic wasting disease is here, Pennsylvania hunting is going to change, said John Kasun — a longtime hunter, outdoors writer and columnist for the Mirror. “I don’t want to take a doomsday approach, but we are going to see a change,” he said. Kasun said he encourages hunters to strive to be part of the solution through engaging with officials, listening and responding with thoughtful feedback. He also said they should report any suspicious deer activity. Kasun also acknowledged a culture of conflicting information and opinions surrounding chronic wasting disease, calling the illness “a cauldron of misunderstanding and misinformation.̶1; “I think we have to increase our communications about the issue,” he said. “We should be focusing on what we can do to help. … Unfortunately nobody has that answer yet.” At least one Blair County deer meat processor, who asked not to be named, made sure to point out that there is no evidence that humans can surely contract the disease and said he is doubtful that they can. It seems it will be some time before that question can be answered, as “scientists expect the study to take many years before they will determine what the risk, if any, of CWD is to people,” according to the CDC. To date CWD infected animals exist in 24 states of the USA The spread to states is increasing
A little optimistic buywell? 7000 early this week I would have thought......?
I detect a run starting by Fund Managers getting out of FTSE 100 stocks as the USA looks like it is going to head lower DJIA to 20,000 in 12 weeks looks likely I think IMO FTSE 100 to 7,000 within 4 weeks
Astrazeneca's great leap into China: British drugs giant targets Asia's middle-class Http://
Yes good turnaround, far preferable to GSK imo but yet to see their results to confirm due on 7 Feb
Morgan Stanley said the conference call gave a very confident medium term outlook
Ah, I see. "Shares of AstraZeneca PLC (AZN.LN) reversed a morning fall after the company announced partnerships with two Chinese heavyweights, Alibaba Group Holding Ltd. (BABA) and Tencent Holdings Ltd., (TCEHY) alongside its fourth-quarter earnings. The Anglo-Swedish pharmaceutical company said it will work with Alibaba subsidiary Ali Health, using technologies such as artificial intelligence to help with patient diagnosis and treatment. The company said a major area of collaboration will be traceable codes on drugs that will give consumers more information about the medicine they use. In the second partnership, AstraZeneca will collaborate with Tencent to combat the online sale of counterfeit drugs. The announcement of the partnerships coincides with U.K. Prime Minister Theresa May's state visit to China."
No-one else commenting on a 6.6% rise from the lows of earlier today. Recovery was from US opening.
Interesting post-results volatility, having been way down initially but now nudging £50 again.
Inhaler trial breathes new life into Astrazeneca Https://
hTTps:// What Is Zombie Deer Disease? The CDC Is Warning That Humans Could Catch This Disease That’s Turning Deers Into Zombies Re the article Prions are now being found in vegatables
good news this am re COPD PIII trial
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