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AZN Astrazeneca Plc

11,938.00
-88.00 (-0.73%)
Last Updated: 13:30:15
Delayed by 15 minutes
Share Name Share Symbol Market Type Share ISIN Share Description
Astrazeneca Plc 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
  -88.00 -0.73% 11,938.00 11,926.00 11,946.00 12,144.00 11,910.00 12,070.00 518,633 13:30:15
Industry Sector Turnover Profit EPS - Basic PE Ratio Market Cap
Pharmaceutical Preparations 45.81B 5.96B 3.8415 31.23 185.96B
Astrazeneca Plc is listed in the Pharmaceutical Preparations sector of the London Stock Exchange with ticker AZN. The last closing price for Astrazeneca was 12,026p. Over the last year, Astrazeneca shares have traded in a share price range of 9,461.00p to 12,210.00p.

Astrazeneca currently has 1,550,189,338 shares in issue. The market capitalisation of Astrazeneca is £185.96 billion. Astrazeneca has a price to earnings ratio (PE ratio) of 31.23.

Astrazeneca Share Discussion Threads

Showing 2176 to 2196 of 6150 messages
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DateSubjectAuthorDiscuss
16/2/2019
20:29
........... The Case for Transmissible Alzheimer's Grows ............


February 7, 2019

Last December research revealed that infectious, lethal proteins called prions have the potential to be transmitted on optical medical equipment because they are present throughout the eyes of victims.

Recently a study suggested that peptide aggregates – essentially sticky, self-propagating clumps of miss-folded protein bits collectively referred to as amyloid beta found in the brains of Alzheimer’s patients may be transmissible in the same ways that prions are.

A new paper has since been published that seems to take the evidence for the transmissibility of Alzheimer’s peptides from “circumstantial” to “experimentally produced”.

human prion transmission has happened when surgical instruments used on an infected patient were cleaned and reused on an uninfected one. Prions stick to steel like glue, are stable for decades at room temperature, and survive a bombardment of chemical and physical cleaning assaults that are more than sufficient to obliterate other pathogens.

Prions can and do survive current hospital cleaning , washing, sterilization processes. They can withstand temperatures of over 450 degrees Centigrade , which is way higher than autoclaving achieves in hospitals at around 200 degrees centigrade.

The vast majority of surgical instruments are not properly tested to measure that protein residue on the surface of 'cleaned instruments' meets NHS guidelines , in the USA NO GUIDELINE EXISTS.

By guideline I mean a stipulated amount of protein residue in Nano-grams measured on the surface of the surgical instrument AFTER the 'cleaning' process ie a pass or fail event before the instrument is bagged to go back into store for the next patient.

In the original Alzheimer’s transmissibility study, scientists examined the brains of eight patients treated with prion-contaminated human growth hormone as children who decades later died from prion disease ,out of over 30,000 people so treated, more than 200 died from acquiring a prion disease.

The growth hormone had become contaminated with prions because it had been extracted from cadavers some of which had presumably died of prion disease and processed in such a way that the prions still remained viable. Prions are not the only miss-folded proteins that lurk in the brains of cadavers.

Researchers discovered the brains of seven of the eight cadavers contained, in addition to prions, peptide aggregates called Amyloid Beta,Aβ .

Aβ is a collection of miss-folded peptides whose correctly folded versions are present in the human brain and perform a variety of mid-level tasks.

When the miss-folded versions form, they behave like prions, catalyzing the conversion of healthy forms into diseased ones and accumulating in clumps called plaques.

Past experiments have shown that injecting small amounts of human Aβ into the brains of primates or of mice bred to express a humanized form of the Aβ precursor protein generates Aβ plaques in these animals.

Aβ plaques are characteristic of and possibly the instigators of Alzheimer’s Disease when they accumulate around neurons in the brain.

Over the last 15 years many new drug compounds have been tested to Phase 3 clinical level in humans to try to eliminate Aβ plaques and thus find a cure for Alzheimer's.

NONE have worked , Tens of $ Billions have been spent by various big Pharma companies looking for a cure in this area of Aβ plaques ; money that has been wasted.


However, the seven brains from the cadavers did NOT have plaques.

The Aβ in these brains had built up in the walls of blood vessels, where such accumulations cause bleeding and dementia.

This condition is called cerebral amyloid angiopathy, and it co-occurs with most Alzheimer’s Disease but can also strike on its own.

The eight victims in the study had all still been young enough that their brains would not be expected to show any signs of Alzheimer’s or cerebral amyloid angiopathy unless they had genetic risk factors.

Alzheimer's generally being associated with people over 65 years of age. Therefore given the implications of these findings the scientists who studied their brains were very concerned.

The same group of scientists were involved in both studies, they managed to get the original vials of prion-contaminated growth hormone that had been put into safe secure storage for decades by Public Health England.

The scientists found when tested, the samples for both Aβ peptides and tau, another protein that builds up in the brains of Alzheimer’s patients and causes its other brain pathology: Tau tangles.

The two types of Aβ and Tau were still present in the vials

After more than three decades of room temperature storage.

Aβ and Tau proteins exist for over 30 years and like prion proteins are survivors.

The medical community needs to IMO re-classify them as Prion Proteins BUT this will open a big can of worms.

The group of scientists then took their study a step further by injecting a tiny samples from this decades old vintage vials into the brains of mice , that had been engineered to be susceptible to human Alzheimer’s.

Guess what ?

The mice developed both Aβ plaques and cerebral amyloid angiopathy, although they showed no signs of tau.

Aβ peptides had not only managed to survive decades of room-temeprature storage, they were also still transmissible.

Many neurological and eye surgeries, and perhaps certain kinds of medical examinations prion proteins have the potential to become lodged on or stick to the surgical instruments or examination equipment used.

The potential thus exists that prion diseases can be transmitted in this manner, indeed this has happened. Donations of dura mater, a tough brain covering, have also transmitted Aβ to young people in the past.

Alzheimer’s Disease is now very common, soon to become the 3rd cause of death in the USA. The rates AD occurs are increasing and the costs to Healthcare agencies are spiraling out of control.


Scientists have NOT been looking for Alzheimer's caused by surgical or other medical procedures that access eye or neural tissue,particularly in patients for whom the appearance of Alzheimer’s would not be surprising ie around 65 years of age or older.

Thus we are underestimating the transmission potential of this disease.

Alzheimer’s (AD) is not the only neurodegenerative disease in which aggregating miss-folded host proteins.

The class referred to as amyloid seem to propagate and wreak havoc in Parkinson’s Disease, there ,miss-folded alpha-synuclein proteins spread through the brain.

In the disease Amylotrophic Lateral Sclerosis (Lou Gehrig’s Disease), the miss-folded protein is TDP-43.

The need is obvious for scientists to investigate the transmission potential of these diseases.

All three are forms of Dementia , Alzheimer's being the most common followed by Parkinson's .

All three IMO are in fact forms of Prion Disease ... the exact nature of which is individual ie unique because of the muted genes and proteins that exist in each and every human.

Many thousands of different proteins have been identified in the human brain , as instrumentation and technology improves this number will rise.

buywell3
15/2/2019
22:30
Left in New York at £63-50 equivalent.

The shares go XD on the 28 Feb (147p equivalent at current Xrates).This combined with the follow through from the results and sterling weakness providing support, suggests that a new all time high of over £65 is achievable.

steeplejack
15/2/2019
11:44
In at 53.889 on 29th Jan out today at 61.855. Resistance at £62; but the likelihood is it will break through, maybe today. Just starting to look toppy for me. Was a risk off UKplc for me and got a 14% quick turn instead. I know....
I should run my winners.

stewart64
15/2/2019
11:39
Good to be holding yesterday's welcome gain so far.
patientcapital
15/2/2019
08:24
Yes,US left them £62-50 equivalent which won't be lost on the marketmakers as they try to shake out some profit takers.
steeplejack
14/2/2019
14:41
the americans certainly like the results. i wish id bought double the amount I did.
nimbo1
14/2/2019
13:58
It's fully vindicated their rebuff of PFE.
Have to admit I had my doubts, my take was too cautious.

essentialinvestor
14/2/2019
11:17
pondered over buying @ 54....silly me. in this am at 59.92 instead - the results are v good - divi and growth from azn so could get a proper rerate imo only. Their cancer drugs look fantastic.
nimbo1
14/2/2019
08:12
They're delighted...- Oncology Sales growth of 50% in the year (49% at CER) to $6,028m, including:- Tagrisso sales of $1,860m, representing growth of 95% (93% at CER), with increased use as a 2nd-line treatment for EGFR(6) T790M-mutated(7) NSCLC(8) patients and the 2018 approvals in the 1st-line EGFR-mutated (EGFRm) setting as a new standard of care (SoC). Tagrisso, based on the performance in FY 2018, is anticipated to be AstraZeneca's biggest-selling medicine in 2019- Imfinzi sales of $633m (FY 2017: $19m), reflecting ongoing launches for the treatment of patients with unresectable, Stage III NSCLC. The majority of sales of Imfinzi were in the US; the favourable impact of additional potential launches in other markets is yet to come- Lynparza sales of $647m, representing growth of 118% (116% at CER), driven by expanded use in the treatment of ovarian cancer and the medicine's first approvals for use in the treatment of breast cancer. The recent approval of Lynparza as a 1st-line treatment of patients with BRCAm ovarian cancer in the US is expected to support further expanded use
steeplejack
14/2/2019
08:05
Has anyone seen the poll on the ADVFN Twitter about Astra?
shiv1986
14/2/2019
07:22
Rns looks strong, seems to be saying put past behind us and blue skies all the way forward, 50% growth in cancer drugs bodes well
ayl30
13/2/2019
11:47
Will AstraZeneca get high on its own supply following Thursday’s full year results?

Given that the company said that it now expects a ‘period of sustained growth for years to come’ there is going to be a lot of pressure on Thursday’s full year results to show that the sales surge wasn’t a one-off. AstraZeneca is expecting a ‘low single-digit’ percentage increase in product sales for the full year, alongside core earnings per share of between $3.30 and $3.50. Its guidance for the new financial year could also be key.

Read what Spreadex analysts have to say, or watch a 60 second earnings preview video, here: hxxps://spreadex.com/?tid=386919

connorcampbell
12/2/2019
08:56
Is results 14th feb ta
stevenrevell
10/2/2019
20:02
I don't believe in coincidences ... when there are more than 3 examples


Hence I find it too hard to take that Alzheimer's can exist in 4 distinct sub-types of plain Alzheimer's (AD) ... number in (brackets below = years of age)

'' There are four subtypes of dementia in Alzheimer’s disease (AD):

Early onset Alzheimer dementia (< 65)
Alzheimer dementia with delayed onset (> 65)
Alzheimer dementia with atypical or delayed form
Alzheimer dementia without any specification. ''




This compares very much with CJD

Sporadic CJD. sCJD is the most common type.
Variant CJD. vCJD
Familial or inherited CJD fCJD
Iatrogenic CJD iCJD.

buywell3
10/2/2019
19:37
Objectives

To identify the misdiagnoses of patients with sporadic Jakob-Creutzfeldt disease (sCJD) during the course of their disease and determine which medical specialties saw patients with sCJD prior to the correct diagnosis being made and at what point in the disease course a correct diagnosis was made.



''The most common individual misdiagnoses were viral encephalitis, paraneoplastic disorder, depression, vertigo, Alzheimer disease, stroke, unspecified dementia, central nervous system vasculitis, peripheral neuropathy, and Hashimoto encephalopathy. ''

buywell3
10/2/2019
18:43
Wrong diagnosis of Alzheimer's is now a problem ... the question in the piece below that should have been asked

What were the other 50% of people suffering from ?

IMO it was CJD , which NO test exists for a living patient.

CJD is only identified by autopsy IF it is correctly tested for ... this is why Alzheimer's rates have soared 50 fold in recent years as autopsy rates on Alzheimer's patients have dropped alarmingly.

That is because within the medical community it is known that Neurosurgeons are 6 times likely to die from Alzheimer's themselves than ANY other cause.

That is because it isn't Alzheimer's it is form of CJD, a prion disease, and highly transmissible as well as 100% lethal ... no cure.


Some Alzheimer’s patients might have been misdiagnosed, study suggests
Jul. 20, 2017 , 10:45 AM

Alzheimer’s disease can be hard to definitively diagnose, but one study’s findings could make the process much easier and more accurate.

Interim results from a 4-year analysis suggest that a substantial number of patients being treated for the condition may not have it at all, The Washington Post reports.

The presence of amyloid plaque in the brain precedes Alzheimer’s and can be detected by costly positron emission tomography (PET) scans, which are not usually covered by insurance. Therefore, doctors often diagnose and treat patients for the disorder based on symptoms.

After administering PET scans to 4000 people previously diagnosed with either mild cognitive impairment (MCI) or dementia and treated for Alzheimer’s to test for the presence of amyloid plaque, only 53.3% of patients with MCI and 70.5% with dementia tested positive. Following the results, doctors changed the care plans of two-thirds of the patients involved in the study, presenters said at the Alzheimer’s Association International Conference in London. Researchers hope the results will move the Centers for Medicare & Medicaid Services to cover PET scans through Medicare.

buywell3
06/2/2019
05:44
Fuji99..I did make the bet last week that internationals were oversold and domestics overbought. A bit of a warning light for me was when TW had risen 34% in a matter of days due to Brexit optimism during which time majors like RDSB and AZN had fallen. They were two of my recent buys. Out went TW, SLA and Regional Reit, all of which have hit a brick wall on a falling pound and Brexit chaos.

Could all rotate back on a hand brake turn of course. Things usually go pear shaped once you think you're on a winning streak.

stewart64
30/1/2019
13:27
Sector rotation starting to take place.
The pharmas should have a good run for a while.

fuji99
29/1/2019
17:32
The XD date for that looks to be Thurs 28 Feb this year based on the record date of 1 Mar on their website
bountyhunter
29/1/2019
17:26
Final dividend scheduled to be announced in Annual Results on 14 Feb
call-logger
29/1/2019
17:25
XD was 15 Feb last year and will probably be 14 Feb this year as it tends to be on a Thursday
bountyhunter
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