Cochrane UK Stroke: easy to access blogshots

Make what you want of this, stroke references in Cochrane UK. If I had minions I would send them to summarize this stuff which should already be available in that public database of all stroke research, updated each time something new comes along. But NO, we have fucking failures of stroke associations instead, passing out lazy press releases as if that would help survivors at all. Why the fuck is stroke in their name anyway?
https://cochraneblogshots.tumblr.com/tagged/Stroke

Followup needed, which stroke research are you going to tackle?

If YOU don't work on these they will never get done. Our fucking failures of stroke associations don't even know what needs to be done to solve stroke, they are just getting in the way of actual solutions.  I don't have time, still not retired, need dozens of minions to work for me.
I've only been writing this blog since 2010 and only used followup as a indexing term since 2012 so there has to be thousands of other research needing followup.  Pure incompetency by all our stroke medical 'professionals'. Shades of  'Idiocracy'.
The ones listed are in the hyperacute category(immediate to one day according to my definition). The whole point is to prevent lots of dead and damaged neurons from occurring, thus not having to work on the 10% chance you will fully recover with rehabilitation.

Hibernating ground squirrels provide clues to new stroke treatments

Stem cells: A breakthrough in stroke treatment?

Traumatic brain injuries may be helped with drug used to treat bipolar disorder

Stroke treatment: Miracle drug limits brain damage and promotes repair

Effect of hypoxic-ischemic time on reduction of hypoxic-ischemic brain injury by sevoflurane postconditioning in neonatal rats

Can nicotine protect the aging brain?
 

Transcranial Ultrasound (TUS) for hyperacute stroke

Salvianolic acid A alleviates ischemic brain injury through the inhibition of inflammation and apoptosis and the promotion of neurogenesis in mice

Stroke treatment: Miracle drug limits brain damage and promotes repair

Effect of hypoxic-ischemic time on reduction of hypoxic-ischemic brain injury by sevoflurane postconditioning in neonatal rats
Or my two earlier lists;
My 31 ideas on hyperacute therapy I'm going to insist my doctor give me during the first week.

even without further research or real clinical trials. I will take the chance that more benefits accrue than danger by using these. But run them by your doctor. No knowledge of any of them and you need to fire that doctor immediately, practicing medicine with no knowledge. 

These 177 hyperacute therapies that need more research.    

Knockout of Silent Information Regulator 2 (SIRT2) Preserves Neurological Function after Experimental Stroke in Mice

We should be able to go to that public database of stroke research and its associated relevance to stroke recovery and interventions.  I could look at that and determine how important something like this is and if it needs to be followed up with human research. I can't do everything myself and our fucking failures of stroke associations take no responsibility for anything and are completely worthless in this regard. I need minions or a stroke association to be able to accomplish solving everything in stroke. It is all solvable if someone puts their mind to it. That is what's called LEADERSHIP. We have none in stroke right now.

Knockout of Silent Information Regulator 2 (SIRT2) Preserves Neurological Function after Experimental Stroke in Mice

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Lea Krey, Fred Lühder, Kathrin Kusch, ...

First Published July 29, 2015 Research Article

Download PDF	Article information

Abstract

Sirtuin-2 (Sirt2) is a member of the NAD+-dependent protein deacetylase family. Various members of the sirtuin class have been found to be involved in processes related to longevity, regulation of inflammation, and neuroprotection. Induction of Sirt2 mRNA was found in the whole hemisphere after experimental stroke in a recent screening approach. Moreover, Sirt2 protein is highly expressed in myelin-rich brain regions after stroke. To examine the effects of Sirt2 on ischemic stroke, we induced transient focal cerebral ischemia in adult male Sirt2-knockout and wild-type mice. Two stroke models with different occlusion times were applied: a severe ischemia (45 minutes of middle cerebral artery occlusion (MCAO)) and a mild one (15 minutes of MCAO), which was used to focus on subcortical infarcts. Neurological deficit was determined at 48 hours after 45 minutes of MCAO, and up to 7 days after induction of 15 minutes of cerebral ischemia. In contrast to recent data on Sirt1, Sirt2^−/− mice showed less neurological deficits in both models of experimental stroke, with the strongest manifestation after 48 hours of reperfusion. However, we did not observe a significant difference of stroke volumes or inflammatory cell count between Sirt2-deficient and wild-type mice. Thus we postulate that Sirt2 mediates myelin-dependent neuronal dysfunction during the early phase after ischemic stroke.

 

What is the logical course of action to solve all the problems in stroke?

The first action is to identify those problems as compared to our stroke associations who don't even acknowledge there are any problems in stroke. Don't you know that prevention press releases and F.A.S.T. are all that is needed? That leaves survivors totally screwed.
My assumption was that just stating the factual needs and problems of stroke survivors would lead to change. Obviously that is totally wrong, entrenched interests in keeping the status quo, stroke associations working only for doctors for example, and researchers going for the easy research, finding a new prediction point for stroke.
The stroke associations believe in not even addressing any of the problems in stroke, they do the lazy press release route and pat themselves on the back for that fucking pathetic nonhelp.

Obviously no one in the stroke medical world really cares about solving problems for survivors. You're screwed, deal with it and be happy you are alive.  

A stroke survivor like me should not be required to solve all my own stroke deficits along with all the incompetency in the stroke medical world. I don't have enough brain cells for that or any minions working for me.

Magnetic resonance imaging of local and remote vascular remodelling after experimental stroke

From this we should be able to get an objective damage diagnosis which we can then go to the stroke protocol database for solutions to recover from such damage. This is so fucking easy to setup that even a stroke addled person like me knows what needs to be done. And if my minions in the ASA, NSA and WSO would just do my bidding this could be fixed in  no time.
http://jcb.sagepub.com/content/early/2016/10/18/0271678X16674737.abstract?&

1. Pavel Yanev1
2. Peter R Seevinck1
3. Umesh S Rudrapatna1
4. Mark JRJ Bouts1
5. Annette van der Toorn1
6. Karen Gertz2,3
7. Golo Kronenberg2,4
8. Matthias Endres2,3,4,5,6
9. Geralda A van Tilborg1
10. Rick M Dijkhuizen1⇑

1. ¹Biomedical MR Imaging and Spectroscopy Group, University Medical Center Utrecht, Utrecht, The Netherlands
2. ²Department of Neurology, Charité – Universitaetsmedizin Berlin, Berlin, Germany
3. ³Center for Stroke Research Berlin, Charité – Universitaetsmedizin Berlin, Berlin, Germany
4. ⁴German Center for Cardiovascular Research (DZHK), Universitaetsmedizin Berlin, Berlin, Germany
5. ⁵German Center for Neurodegenerative Diseases (DZNE), Universitaetsmedizin Berlin, Berlin, Germany
6. ⁶Berlin Institute of Health (BIH), Berlin, Germany

1. Rick M Dijkhuizen, Center for Image Sciences, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. Email: r.m.dijkhuizen@umcutrecht.nl

Abstract

The pattern of vascular remodelling in relation to recovery after stroke remains largely unclear. We used steady-state contrast-enhanced magnetic resonance imaging to assess the development of cerebral blood volume and microvascular density in perilesional and exofocal areas from (sub)acutely to chronically after transient stroke in rats. Microvascular density was verified histologically after infusion with Evans Blue dye. At day 1, microvascular cerebral blood volume and microvascular density were reduced in and around the ischemic lesion (intralesional borderzone: microvascular cerebral blood volume = 72 ± 8%; microvascular density = 76 ± 8%) (P < 0.05), while total cerebral blood volume remained relatively unchanged. Perilesional microvascular cerebral blood volume and microvascular density subsequently normalized (day 7) and remained relatively stable (day 70). In remote ipsilateral areas in the thalamus and substantia nigra – not part of the ischemic lesion – microvascular density gradually increased between days 1 and 70 (thalamic ventral posterior nucleus: microvascular density = 119 ± 9%; substantia nigra: microvascular density = 122 ± 8% (P < 0.05)), which was confirmed histologically. Our data indicate that initial microvascular collapse, with maintained collateral flow in larger vessels, is followed by dynamic revascularization in perilesional tissue. Furthermore, progressive neovascularization in non-ischemic connected areas may offset secondary neuronal degeneration and/or contribute to non-neuronal tissue remodelling. The complex spatiotemporal pattern of vascular remodelling, involving regions outside the lesion territory, may be a critical endogenous process to promote post-stroke brain reorganization.

Magnetic resonance imaging of local and remote vascular remodelling after experimental stroke

From this we should be able to get an objective damage diagnosis which we can then go to the stroke protocol database for solutions to recover from such damage. This is so fucking easy to setup that even a stroke addled person like me knows what needs to be done. And if my minions in the ASA, NSA and WSO would just do my bidding this could be fixed in  no time.
http://jcb.sagepub.com/content/early/2016/10/18/0271678X16674737.abstract?&

1. Pavel Yanev1
2. Peter R Seevinck1
3. Umesh S Rudrapatna1
4. Mark JRJ Bouts1
5. Annette van der Toorn1
6. Karen Gertz2,3
7. Golo Kronenberg2,4
8. Matthias Endres2,3,4,5,6
9. Geralda A van Tilborg1
10. Rick M Dijkhuizen1⇑

1. ¹Biomedical MR Imaging and Spectroscopy Group, University Medical Center Utrecht, Utrecht, The Netherlands
2. ²Department of Neurology, Charité – Universitaetsmedizin Berlin, Berlin, Germany
3. ³Center for Stroke Research Berlin, Charité – Universitaetsmedizin Berlin, Berlin, Germany
4. ⁴German Center for Cardiovascular Research (DZHK), Universitaetsmedizin Berlin, Berlin, Germany
5. ⁵German Center for Neurodegenerative Diseases (DZNE), Universitaetsmedizin Berlin, Berlin, Germany
6. ⁶Berlin Institute of Health (BIH), Berlin, Germany

1. Rick M Dijkhuizen, Center for Image Sciences, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. Email: r.m.dijkhuizen@umcutrecht.nl

Abstract

The pattern of vascular remodelling in relation to recovery after stroke remains largely unclear. We used steady-state contrast-enhanced magnetic resonance imaging to assess the development of cerebral blood volume and microvascular density in perilesional and exofocal areas from (sub)acutely to chronically after transient stroke in rats. Microvascular density was verified histologically after infusion with Evans Blue dye. At day 1, microvascular cerebral blood volume and microvascular density were reduced in and around the ischemic lesion (intralesional borderzone: microvascular cerebral blood volume = 72 ± 8%; microvascular density = 76 ± 8%) (P < 0.05), while total cerebral blood volume remained relatively unchanged. Perilesional microvascular cerebral blood volume and microvascular density subsequently normalized (day 7) and remained relatively stable (day 70). In remote ipsilateral areas in the thalamus and substantia nigra – not part of the ischemic lesion – microvascular density gradually increased between days 1 and 70 (thalamic ventral posterior nucleus: microvascular density = 119 ± 9%; substantia nigra: microvascular density = 122 ± 8% (P < 0.05)), which was confirmed histologically. Our data indicate that initial microvascular collapse, with maintained collateral flow in larger vessels, is followed by dynamic revascularization in perilesional tissue. Furthermore, progressive neovascularization in non-ischemic connected areas may offset secondary neuronal degeneration and/or contribute to non-neuronal tissue remodelling. The complex spatiotemporal pattern of vascular remodelling, involving regions outside the lesion territory, may be a critical endogenous process to promote post-stroke brain reorganization.

Complying With the National Institutes of Health Guidelines and Principles for Rigor and Reproducibility

Our fucking failures of stroke associations should have enough employees that can monitor that stroke research meets these guidelines. But they won't, it would be too much like hard work. They would have to keep track of all research and do a better job than I can. If they were my minions they would accomplish that with no questions asked.
http://atvb.ahajournals.org/content/36/7/1303.extract?etoc

1. Alan Daugherty,
2. Robert A. Hegele,
3. Nigel Mackman,
4. Daniel J. Rader,
5. Ann Marie Schmidt,
6. Christian Weber

+ Author Affiliations

1. From the Saha Cardiovascular Research Center and Department of Physiology, University of Kentucky, Lexington (A.D.); Department of Medicine and Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada (R.A.H.); Department of Medicine, University of North Carolina at Chapel Hill (N.M.); Departments of Medicine and Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia (D.J.R.); Diabetes Research Program, Division of Endocrinology, Department of Medicine, New York University Langone Medical Center (A.M.S.); and Institute for Cardiovascular Prevention, and Department of Medicine, Ludwig-Maximilians-Universität (LMU) and German Centre for Cardiovascular Research (DZHK), partner site Munich Heart Alliance, Munich, Germany (C.W.).

1. Correspondence to Alan Daugherty, University of Kentucky, Saha Cardiovascular Research Center, 741 S Limestone - BBSRB Room 243, Lexington, KY 40536. E-mail Alan.Daugherty@uky.edu

In 2014, the National Institutes of Health (NIH) delivered a document that described the principles and guidelines for reporting preclinical research (https://www.nih.gov/research-training/rigor-reproducibility/principles-guidelines-reporting-preclinical-research). These principles and guidelines were developed in a workshop that addressed the concern of reproducibility of preclinical research and were built on previous NIH recommendations for transparency in reporting data.¹ A major driving force behind this effort stemmed from concerns voiced by the pharmaceutical industry that described their failure to replicate studies performed in academic laboratories^2,3 These issues have also attracted attention through commentaries in both scientific journals⁴ and the lay press.⁵

As guardians of a large investment of public funds, the NIH aspires to promote confidence in science through enhanced reporting of protocols and data in journals, focusing in particular on reproducibility of results of similar experiments performed in different laboratories. A wide spectrum of scientific leaders, including many journal editors, attended the meeting at which this document was developed. The consequent report emphasized the need for journals to modify their editorial processes in several respects. These included requirement that authors document a detailed description of statistical analyses and data reporting with the aim of increasing transparency, sharing of data and materials, and establishing best practices for reagent verification. An additional requirement was for journals to establish a standard mechanism for the reporting of refutations of published work. All American Heart Association journals, including ATVB, have endorsed these NIH guidelines.

The NIH guidelines state specifically that “the journal assumes responsibility …

[Full Text of this Article]

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What's this?

Hanlon’s Razor, never attribute to malice that which is adequately explained by stupidity.

Hanlon's razor is an adage, most commonly attributed to Robert J. Hanlon which is generally stated as: “”Never attribute to malice that which can be adequately explained by stupidity.
http://rationalwiki.org/wiki/Hanlon's_razor 
So we should be able to attribute the complete lack of progress in stroke to stupidity rather than malice. Which brings us to this quote:
'It's hard to win an argument with a smart person, but it's damn near impossible to win an argument with a stupid person.' 
So how the hell do we change the trajectory of stroke to solve all the problems in stroke? Rather than just sit around twiddling our thumbs and putting out more press releases? I'm obviously not smart enough to figure this out on my own. I need minions.

'You never suffer from a money problem, you always suffer from an idea problem."

My fortune from a Japanese, Chinese, Thai restaurant in NYC the other night. Well money is still ok even after losing half the assets in the divorce.  My idea problem is that I think way too large and I don't have the infrastructure or minions to accomplish those ideas.

African Plant May Be Possible Treatment for Aging Brain

Where does this fit in the strategy to solve stroke problems? ASA, NSA, WSO?  What is your considered opinion on this? You have hundreds, if not thousands of employees. Have them come up with an answer. I can't do everything until I get my minions.
http://www.biosciencetechnology.com/news/2014/08/african-plant-may-be-possible-treatment-aging-brain?
One paragraph here;
When Currais and Maher isolated different components of the plant, they found that the anti-inflammatory and neuroprotective effects of the plant were mostly due to one molecule, called voacamine. The compound hasn’t yet been tested in animal models but its performance in the assays suggests that it may have pharmaceutical potential for treating Alzheimer’s, Parkinson’s or stroke.

Traumatic brain injury patients with more education recover faster: Study

Who is going to fund and run a similar study for stroke? I'm probably alive today because of the significant brain reserve I built up. But my recovery has a long ways to go yet.
You're smarter - recover faster
You're smarter - more likely to get depressed post-stroke. I can't find my link to this study. This is a problem with my blogging, I have way too much information out there. Where are my minions?

Smarter People Tend To Drink More Alcohol

Can alcohol make men smarter? Study suggests yes

 

http://www.techtimes.com/articles/6030/20140424/traumatic-brain-injury-patients-with-more-education-recover-faster-study.htm
A new study shows that people who spend more time in school may recover faster and better from a moderate to severe brain injury compared to those with less years of education.
Johns Hopkins University scientists in Baltimore suggest that adults who earned at least one undergraduate degree were seven times more likely to fully recover from traumatic brain injuries than those who did not earn a high school diploma.

'You want to have minions, don't you?'

Why yes, I do. I don't have time to find and gather all the information needed to solve all of strokes' problems. I need minions to do my bidding. A friends comment to me the other day. She hit the nail directly on the head. Some day I will run the great stroke association I created. My arrogance knows no bounds.