CryoNet #31948 - #31953

CryoNet - Thu 10 Sep 2009

    #31948: abi freezer company [Leo]
    #31949: cas freezers [Leo]
    #31950: RE #31946 [Leo]
    #31952: Laser cooling [hrhirsch]
    #31953: Research could prevent stroke's damage [oberon]

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Message #31948
From: "Leo" <[email protected]>
Subject: abi freezer company
Date: Wed, 9 Sep 2009 20:37:38 +0200

the company site;

http://www.abi-net.co.jp/

translated more or less;

http://translate.google.nl/translate?prev=hp&hl=nl&js=y&u=http%3A%2F%2Fwww.abi-net.co.jp%2F&sl=ja&tl=en&history_state0=

Leo.




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Message #31949
From: "Leo" <[email protected]>
Subject:  cas freezers
Date: Wed, 9 Sep 2009 20:47:33 +0200

CI and Alcor beter order some off this to evaluate;

http://translate.google.nl/translate?prev=hp&hl=nl&js=y&u=http%3A%2F%2Fwww.abi-net.co.jp%2Fpro_freezer.html&sl=ja&tl=en&history_state0=

http://translate.google.nl/translate?prev=hp&hl=nl&js=y&u=http%3A%2F%2Fwww.abi-net.co.jp%2Fpro_cas.html&sl=ja&tl=en&history_state0=

Leo.


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Message #31950
From: "Leo" <[email protected]>
Subject: RE #31946
Date: Wed, 9 Sep 2009 20:22:39 +0200

Looks similar as something I posted years ago. I find a interesting old 2006 article here.

 

http://foodreview.ihs.com/news/2006/re-invention-freezer.htm

 

some parts of it .

 

One very simple demonstration of CAS freezing and how it prevents ice crystal formation is that it can freeze a full glass bottle of water. The water level remains the same, the glass does not break, and the water is crystal clear except for a few bubbles. 


ABI has been selling its systems in Japan for over ten years and it has recently started marketing abroad. CAS freezers can be retrofitted into existing infrastructure for the same price as conventional freezing equipment, with the benefits of reduced energy costs and superior preservation at higher temperatures. 


It has other applications, too, with five Japanese unlversities investigating it for human organ freezing. Progress so far indicates that although the CAS freezing process freezes to a high degree of perfection, the secret is in defrosting the organ as this is where some damage occurs. If this research is successful it will change the medical transplant business forever.

Google Search;



http://www.google.nl/search?hl=nl&newwindow=1&q=cas+freezing+ABI+&btnG=Zoeken&meta=

 

 

I found some patents to, and looking in to them.

 



 

Leo.


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Message #31952
Date: Wed, 09 Sep 2009 17:25:57 -0400
From: hrhirsch <[email protected]>
Subject: Laser cooling

Laser cooling has taken an important step toward such practical 
applications as reducing temperatures rapidly to values near absolute 
zero according to an article in "Wired Science": 
www.wired.com/wiredscience/2009/09/lasercooling/. Although I used to 
be a physicist, I really don't understand how this works. Can someone 
enlighten me? If practical, it might be just what we need for vitrification.

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Message #31953
Date: Wed, 9 Sep 2009 20:39:23 -0700 (PDT)
From: [email protected]
Subject: Research could prevent stroke's damage

[Suppressing TRPM7 eliminated neurological damage. Could thyme also eliminate stroke damage? Thyme contains carvacrol, which inihibits TRPM7.]


Snip: > "But the rats whose TRPM7 had been suppressed exhibited none of the expected damage. In fact, the treated rats performed just as well in memory tests as rats that had never been subjected to oxygen deprivation. And they exhibited no other side effects from the treatment."

http://www.theglobeandmail.com/news/national/research-could-prevent-strokes-damage/article1278339/

Research could prevent stroke's damage
New method from Canadian-led research team keeps rats' brain cells alive even when blood stops flowing

JILL COLVIN
>From Monday's Globe and Mail Last updated on Tuesday, Sep. 08, 2009 02:41AM EDT
A Canadian-led research team believes it has discovered a way to prevent the most devastating effects of stroke.
During a stroke, the brain is deprived of oxygen and nutrients, which strangles neurons, causing debilitating long-term impairment in motor function, memory and speech.
There are currently no drugs available to prevent the death of these cells and protect patients from their life-altering effects.
But a team of researchers, led by Michael Tymianski, a neurosurgeon at the Krembil Neuroscience Centre at Toronto Western Hospital, has found a method that protects neurons in rats, paving the way for new drugs that may keep cells alive even when blood stops flowing.
Previous studies in the field have focused mainly on finding new ways to restore blood to the brain as quickly as possible or on trying to block toxic chemicals that build up when cells experience stress, said Tony Hakim, a director of the Canadian Stroke Network, which supported the study.
But the current research, reported yesterday in the journal Nature Neuroscience, takes a new approach, focusing on an ion channel named TRPM7 ("Trip-M7").
TRPM7 is found in cells throughout the body and the researchers had a hunch that the channels play a key role in cell death following oxygen deprivation.
To test their theory, Dr. Tymianski's team took healthy rats and injected a virus that suppressed the expression of TRPM7 directly into the hippocampus - the delicate brain region that is crucial for learning and memory.
They then cut off blood flow to the rats' brains for 15 minutes and compared the extent of damage days later to rats whose brains had not been treated before deprivation.
As expected, untreated rats with intact TRPM7 suffered severe neurological damage, with long-term impairment, including difficulty learning and remembering how to navigate a maze.
But the rats whose TRPM7 had been suppressed exhibited none of the expected damage. In fact, the treated rats performed just as well in memory tests as rats that had never been subjected to oxygen deprivation. And they exhibited no other side effects from the treatment.
"To the best of our knowledge, our results are the first to demonstrate that suppressing TRPM7 in adult mammals is feasible and that this markedly reduces delayed neuron death after ischemia," they write.
Because TRPM7 is found in virtually every tissue of the body, the team thinks they may have discovered the key to preventing cell death caused by reduced oxygen and nutrient supply, not just in neurons, but in other cells as well.
"It has tremendous implications," Dr. Tymianski said. "It is conceivable that the same types of processes occur in other tissues where there's ischemia as well."
This means the findings could apply to cell death seen in heart attacks, diabetes-related kidney and retinal problems, glaucoma, Parkinson's disease and Alzheimer's disease.
The next step, he said, will be to develop drugs that target TRPM7 channels that can eventually be administered to stroke patients to stave off the devastating effects of oxygen deprivation.
Dr. Tymianski said he hopes to have drugs ready for testing on other animals in a year or two.
But University of Calgary neurologist and Heart & Stroke Foundation spokesman Michael Hill urged caution in interpreting the results. This is not the first time, he said, that receptors found to be crucial in cell death in the lab have failed to translate into viable therapies.
"Whether it can be translated to humans remains to be seen," he said.

____________________________________________

Free text:>
http://www.nature.com/neuro/journal/vaop/ncurrent/pdf/nn.2395.pdf

Nature Neuroscience
Published online: 6 September 2009 | doi:10.1038/nn.2395
Suppression of hippocampal TRPM7 protein prevents delayed neuronal death in brain ischemia
Hong-Shuo Sun1, Michael F Jackson2,3, Loren J Martin4, Karen Jansen5, Lucy Teves1, Hong Cui1, Shigeki Kiyonaka6, Yasuo Mori6, Michael Jones1, Joan P Forder1, Todd E Golde5, Beverley A Orser2,4,7, John F MacDonald2,3 & Michael Tymianski1,2,4,8

Abstract
Cardiac arrest victims may experience transient brain hypoperfusion leading to delayed death of hippocampal CA1 neurons and cognitive impairment. We prevented this in adult rats by inhibiting the expression of transient receptor potential melastatin 7 (TRPM7), a transient receptor potential channel that is essential for embryonic development, is necessary for cell survival and trace ion homeostasis in vitro, and whose global deletion in mice is lethal. TRPM7 was suppressed in CA1 neurons by intrahippocampal injections of viral vectors bearing shRNA specific for TRPM7. This had no ill effect on animal survival, neuronal and dendritic morphology, neuronal excitability, or synaptic plasticity, as exemplified by robust long-term potentiation (LTP). However, TRPM7 suppression made neurons resis
 tant to ischemic death after brain ischemia and preserved neuronal morphology and function. Also, it prevented ischemia-induced deficits in LTP and preserved performance in fear-associated and spatial-navigational memory tasks. Thus, regional suppression of TRPM7 is feasible, well tolerated and inhibits delayed neuronal death in vivo.

_______________________________
Cell Calcium. 2009 Mar;45(3):300-9. Epub 2009 Jan 9.
Carvacrol is a novel inhibitor of Drosophila TRPL and mammalian TRPM7 channels.
    Parnas M, Peters M, Dadon D, Lev S, Vertkin I, Slutsky I, Minke B. Department of Physiology, Kuhne Minerva Center for Studies of Visual Transduction, Faculty of Medicine, The Hebrew University, Jerusalem 91120, Israel.
    Transient receptor potential (TRP) channels are essential components of biological sensors that detect changes in the environment in response to a myriad of stimuli. A major difficulty in the study of TRP channels is the lack of pharmacological agents that modulate most members of the TRP superfamily. Notable exceptions are the thermoTRPs, which respond to either cold or hot temperatures and are modulated by a relatively large number of chemical agents. In the present study we demonstrate by patch clamp whole cell recordings from Schneider 2 and Drosophila photoreceptor cells that carvacrol, a known activator of the thermoTRPs, TRPV3 and TRPA1 is an inhibitor of the Drosophila TRPL channels, which belongs to the TRPC subfamily. We also show that additional activators of TRPV3, thymol, 
 eugenol, cinnamaldehyde and menthol are all inhibitors of the TRPL channel. Furthermore, carvacrol also inhibits the mammalian TRPM7 heterologously expressed in HEK cells and ectopically expressed in a primary culture of CA3-CA1 hippocampal brain neurons. This study, thus, identifies a novel inhibitor of TRPC and TRPM channels. Our finding that the activity of the non-thermoTRPs, TRPL and TRPM7 channels is modulated by the same compound as thermoTRPs, suggests that common mechanisms of channel modulation characterize TRP channels.
PMID: 19135721

[Thyme oil contains carvacrol.]

Br J Nutr. 2000 Jan;83(1):87-93.
Effect of thyme oil and thymol dietary supplementation on the antioxidant status and fatty acid composition of the ageing rat brain.
    Youdim KA, Deans SG. Aromatic and Medicinal Plant Group, Scottish Agricultural College, Auchincruive, Ayr, UK.
The present study measured changes in antioxidant enzyme activity in, and the phospholipid fatty acid composition of the ageing rat brain and tested whether dietary supplementation with thyme oil or thymol could provide beneficial effects. There were significant declines in superoxide dismutase (EC 1.15.1.1) and glutathione peroxidase (EC 1.11.1.9) activities and the total antioxidant status in the untreated rats with age, while thyme-oil- and thymol-fed rats maintained significantly higher antioxidant enzyme activities and total antioxidant status. The proportions of 18:2n-6, 20:1n-9, 22:4n-6 and 22:5n-3 in the brain phospholipids resulting from all three dietary treatments were significantly higher in 28-month-old rats than in 7-month-old rats. Only 20:1n-9 levels in 28-month-old thyme-o
 il- and thymol-treated rats were significantly higher than in the age-matched control. The proportion of 22:6n-3 in brain phospholipids, which declined with age in control rats, was also significantly higher in rats given either supplement. This latter finding is particularly important as optimum levels of 22:6n-3 are required for normal brain function. These results highlight the potential benefit of thyme oil as a dietary antioxidant.
PMID: 10703468

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