Friday, May 19, 2017

Wood, weed and phones: a No Trump Friday

Yeah, posting about the decrepitude of POTUS and the Republicans gets a bit boring, so let's try to avoid that today and instead note:

*   Hey, did you know wood was actually a pretty good material with which to construct big buildings?  An article at Nature, about a revival of wood for large construction, notes this:

....wood has developed a bad reputation over the centuries, because of catastrophic blazes that levelled cities such as London, New York and Chicago before modern fire-suppression strategies emerged. In fact, in case of fire wood maintains its structurally integrity much better than the non-flammable alternatives favoured by modern building codes. It chars at a predictable rate, and doesn't melt like steel or weaken like concrete. “The fact that it actually can withstand fire better than steel took a long time for people to realize,” says Guido Wimmers, who chairs a master's programme in wood engineering at UNBC....

The science of safety and engineering has also advanced. Douglas fir — the exposed layer at the UNBC centre — chars at 39 millimetres per hour. The provincial building code requires that the structure be able to endure at least one hour of fire on any given storey, so Green's team opted for floors made of a 5-layer panel that could afford to sacrifice a portion without losing its structural integrity.
And it is pretty good in earthquake prone regions:
Asif Iqbal, a civil engineer who is working on the project, came to UNBC from New Zealand, where he saw the damage from the 2011 earthquake in Christchurch at first hand. Most of the steel-reinforced concrete buildings in the city remained standing, but around 1,800 were irreparably damaged owing to cracked concrete and warped steel. Iqbal says that many of the replacement buildings are being constructed from wood, precisely because it is more likely to survive another major earthquake and the steel connectors can be replaced relatively easily if damaged.
 Some large wood buildings have been built recently:
 Norway set a world height record in late 2015 with a 52.8-metre tower block; that was edged out in September 2016 by a 53-metre student dormitory at the University of British Columbia in Vancouver. This year, Austria will take the lead with the 84-metre HoHo building in Vienna, comprising a hotel, apartments and offices. The United States saw its first tall wooden building go up in Minneapolis, Minnesota, in 2016, and others are in the works in Portland, Oregon, and in New York City.
 And I had been meaning to post about this months ago - a tall wood office building is to be built in Brisbane - on the showgrounds which I hang around most Saturdays:
Standing at more than 52 metres, the 14,000 square metres of nine storeys of engineered timber on the A-grade site, with retail space at ground level, is targeting a 6 Green Star Design & As Built rating:


Neat.

*   Dementia wards might soon smell of marijuana?   (Well, probably not, but still, it's a funny idea):
Memory performance decreases with increasing age. Cannabis can reverse these ageing processes in the brain. This was shown in mice by scientists at the University of Bonn with their colleagues at The Hebrew University of Jerusalem (Israel). Old animals were able to regress to the state of two-month-old mice with a prolonged low-dose treatment with a cannabis active ingredient. This opens up new options, for instance, when it comes to treating dementia.

*  The Samsung S8, the phone I would love to own, is selling very well, it seems:
It's been less than a month since the Galaxy S8 hit store shelves, but the curved flagship phone is apparently already a huge success. Samsung has already sold over 5 million units of the phones worldwide, according to the Korean site The Investor....

And the sales could keep on rolling in. The phone is expected to come to 120 countries by the end of the month including China, says The Investor.

According to the report, some analysts predict the S8 to reach 50 to 60 million in annual sales. Not bad at all for a comeback phone.

4 comments:

John said...

Mol Pharm. 2006 Nov-Dec;3(6):773-7.
A molecular link between the active component of marijuana and Alzheimer's disease pathology.
Eubanks LM1, Rogers CJ, Beuscher AE 4th, Koob GF, Olson AJ, Dickerson TJ, Janda KD.
Author information


Abstract
Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients and reduce the health care costs attributable to Alzheimer's disease. Here, we demonstrate that the active component of marijuana, Delta9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid beta-peptide (Abeta) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Abeta aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.
PMID: 17140265 PMCID: PMC2562334 DOI: 10.1021/mp060066m
[Indexed for MEDLINE] Free PMC Article




Cell Mol Neurobiol. 2014 Jan;34(1):31-42. doi: 10.1007/s10571-013-9984-x. Epub 2013 Sep 13.
Cannabinoid effects on β amyloid fibril and aggregate formation, neuronal and microglial-activated neurotoxicity in vitro.
Janefjord E1, Mååg JL, Harvey BS, Smid SD.
Author information


Abstract
Cannabinoid (CB) ligands have demonstrated neuroprotective properties. In this study we compared the effects of a diverse set of CB ligands against β amyloid-mediated neuronal toxicity and activated microglial-conditioned media-based neurotoxicity in vitro, and compared this with a capacity to directly alter β amyloid (Aβ) fibril or aggregate formation. Neuroblastoma (SH-SY5Y) cells were exposed to Aβ1-42 directly or microglial (BV-2 cells) conditioned media activated with lipopolysaccharide (LPS) in the presence of the CB1 receptor-selective agonist ACEA, CB2 receptor-selective agonist JWH-015, phytocannabinoids Δ(9)-THC and cannabidiol (CBD), the endocannabinoids 2-arachidonoyl glycerol (2-AG) and anandamide or putative GPR18/GPR55 ligands O-1602 and abnormal-cannabidiol (Abn-CBD). TNF-α and nitrite production was measured in BV-2 cells to compare activation via LPS or albumin with Aβ1-42. Aβ1-42 evoked a concentration-dependent loss of cell viability in SH-SY5Y cells but negligible TNF-α and nitrite production in BV-2 cells compared to albumin or LPS. Both albumin and LPS-activated BV-2 conditioned media significantly reduced neuronal cell viability but were directly innocuous to SH-SY5Y cells. Of those CB ligands tested, only 2-AG and CBD were directly protective against Aβ-evoked SH-SY5Y cell viability, whereas JWH-015, THC, CBD, Abn-CBD and O-1602 all protected SH-SY5Y cells from BV-2 conditioned media activated via LPS. While CB ligands variably altered the morphology of Aβ fibrils and aggregates, there was no clear correlation between effects on Aβ morphology and neuroprotective actions. These findings indicate a neuroprotective action of CB ligands via actions at microglial and neuronal cells.
PMID: 24030360 DOI: 10.1007/s10571-013-9984-x
[Indexed for MEDLINE]

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Steve said...

So, they seem to be taking a very long time to get around to human trials on this?

I note that in the mouse study, the does was supposed to be so low as to have no intoxicating effect. Given the widespread use of it recreationally means its very very unlikely to have any surprise detrimental effects, it's a bit hard to see why it hasn't been trialled earlier, on people with early signs of dementia in particular...

Steve said...

the dose, not "does"

John said...

Political interference doesn't help. Clinical trials cost gazillions, Pharma pays for 90% of all trials, no money in cannabis.

V. low dose is worth thinking about but I'm not particularly confident about it because the pathology is often too advanced. It may slow the decline but it damaged brains it may cause other problems.

Perhaps more importantly it casts light on pathological processes and how these can be addressed. So eventually it may be possible to create drugs that have like effects but with much greater efficacy. It often works out that way ... herb X does have effect Y but we tweaked it so now effect Y is much larger.