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jz_

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Two things that carry negative sentiment in relation to HP:

HP acquired Palm for $1.2 billion in 2010, stumbled with a mobile product launch that was killed without much runway or developer investment: https://news.ycombinator.com/item?id=44270709 (article archived: https://www.thelayoff.com/t/1jxp06mns) - This no doubt soured people who cared about Palm.

HP were known for carrying Intel's Itanium business, for which few tech people have nostalgia for (the second hand market prices have always been eye-watering too), compared to the older PA-RISC line.

I'll agree their consumer/business laptops were always been perfectly usable and long lasting. I dumpster dived an excellent condition pentium 3 laptop from a HP Office that was probably thrown out because of a password locked BIOS (which was not resettable by battery removal, only by getting access to someone who had the bios password serial->keygen tool). It was a great daily driver with Debian, and wifi worked fine with ndiswrapper.

Historically speaking, GHC has had C backend option to facilitate porting.

https://downloads.haskell.org/~ghc/9.4.2/docs/users_guide/co...

-fvia-C

Use the C code generator. Only supposed in unregisterised GHC builds.

This is the oldest code generator in GHC and is generally not included any more having been deprecated around GHC 7.0. Select it with the -fvia-C flag.

The C code generator is only supported when GHC is built in unregisterised mode, a mode where GHC produces “portable” C code as output to facilitate porting GHC itself to a new platform. This mode produces much slower code though so it’s unlikely your version of GHC was built this way. If it has then the native code generator probably won’t be available. You can check this information by calling ghc --info (see --info).

Gnome supports Google Drive, or at least used to, directly in Nautilus. I don't use Gnome, so I can't comment.

I'm using it right now. It is not particularly responsive (perform an operation and it looks like no operation is happening until the remote end responds) but works well enough for copying files in and out via nautilus if you don't expect instant feedback.

are there any limits around the number of files? The official linux client starts to bug out somewhere over 250k files and gets stuck on "syncing". Dropbox support have said they don't recommend more than 100k files.

n=1

I use an intel nuc i3-7100U as a wifi to ethernet bridge for a Windows 10 machine (HP Elitedesk 8300 Core i5-3470). The nuc also serves as a htpc running libreelec.

Why? I tried 4 different USB WiFi dongles with different chipsets spanning ~11 years and each one would end up being the cause of intermittent blue screen of death. The dump file backtrace repeatedly pointed to the usb-wifi stack.

"Free" - terms and conditions say only for personal, non-commercial use. http://www.kunstderfuge.com/notes.htm#Limitations%20of%20Use

Personal use. You may use and play everything from the kunstderfuge.com web site and from its Services for your personal, non-commercial, use only. you agree not to reproduce, retransmit, distribute, disseminate, sell, broadcast, make available to third parties or circulate the musical content downloaded through the Service to anyone, or to exploit any such content for commercial or non-commercial purposes without the express prior written consent of kdf.

What I don't get is how they are marketing their honey around containing higher amounts of something which has putatively negative qualities?

Methylglyoxal, a highly reactive dicarbonyl compound, is inevitably formed as a by-product of glycolysis. Methylglyoxal is a major cell-permeant precursor of advanced glycation end-products (AGEs), which are associated with several pathologies including diabetes, aging and neurodegenerative diseases. In normal situations, cells are protected against methylglyoxal toxicity by different mechanisms and in particular the glyoxalase system, which represents the most important pathway for the detoxification of methylglyoxal. While the neurotoxic effects of methylglyoxal and AGEs are well characterized, our understanding the glyoxalase system in the brain is more scattered

https://www.frontiersin.org/articles/10.3389/fnins.2015.0002...

On Old Age 6 years ago

If anyone here is giving, don't forget to check if your employer provides a matching fund. Many large companies do, so you can effectively double your donation.

They do.

Can be used it to interact with the execution of the current program. It is simple as appending further code with a label and jumping to it using goto. I first noticed it in 2007 started using it in production.

I'll answer the question two parts:

Are there any facilities that map all or most of those areas to full diagnostics of a person

Not exactly, it's all very much an underdeveloped area of research. Biomarkers of biological aging are still being developed, and what has to happen is "translation" into the clinic before any hospital or medical practice can really claim to offer treatment.

On mapping/diagnosing:

Although telomere attrition is a hallmark, leukocyte telomere length has long been criticised as unreliable, which is popularly available as direct to consumer testing companies are capitalising on ignorance.

https://onlinelibrary.wiley.com/doi/abs/10.1002/ajhb.22906

[Telomeres, Aging and Exercise: Guilty by Association? (2017)](http://www.mdpi.com/1422-0067/18/12/2573)

[Salk scientists find that for stem cells to be healthy, telomere length has to be just right (2016)](http://www.salk.edu/news-release/goldilocks-effect-aging-res...)

['This test is garbage': Experts in telomere biology and former employees allege that a Silicon Valley startup gives bogus 'cellular ages' based on a flawed blood test](https://www.thisisinsider.com/silicon-valley-telomere-blood-...)

I think the current more promising biomarker is epigenetic age:

https://www.nia.nih.gov/news/epigenetic-age-estimated-change...

https://en.wikipedia.org/wiki/Epigenetic_clock#Properties_of...

Horvath spoke at a conference last year recorded here: https://www.youtube.com/watch?v=uw1J0UqWSjo

Direct to consumer testing: https://www.mydnage.com/services

The high level view is that whatever rejuvenation therapy versus one or more hallmarks does, should also reverse epigenetic age to validate it.

On a less theoretical level, any intervention would also have functional outcomes that reflect things like cognition, strength, balance, immune system function, and follow up monitoring for disease incidence and decline.

In terms of reversal, again - we have to wait for things to progress through the stages of clinical trials. No one wants to be pushing unverified snake oil, given the long history of that around aging and health.

part two of your question:

and try to mitigate the aging effects from chronic issues?

The only consolation currently I think is that for those that can exercise, should based on what's known about the benefits:

* [Aging Hallmarks: The Benefits of Physical Exercise (2018)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5980968/)

* [Exercise Attenuates the Major Hallmarks of Aging (2015)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340807/)

Most of them just look at diet

Some biogerontologists do think that it's possible to slow the effects of aging with short dietary intervention, such as Valter Longo, who designed a 5-day low protein (as protein inhibits autophagy) calorie restricted diet based on animal research and success in humans. The 'Fasting Mimicking Diet' or FMD. Before anyone asks - no it has not been validated against epigenetic age. That would be a good line of inquiry. Yes, anyone can do it with basic ingredients from a supermarket. There's a subreddit for it: https://www.reddit.com/r/FMD

Selected research on fasting and the FMD:

Longo and Mattson, 2014. [Fasting: molecular mechanisms and clinical applications](https://www.sciencedirect.com/science/article/pii/S155041311...). Cell metab, 19(2), pp.181-192. Cheng et al, 2014. [Prolonged fasting reduces IGF-1/PKA to promote hematopoietic-stem-cell-based regeneration and reverse immunosuppression](https://www.sciencedirect.com/science/article/pii/S193459091...). Cell stem cell, 14(6), pp.810-823. Brandhorst et al, 2015. [A periodic diet that mimics fasting promotes multi-system regeneration, enhanced cognitive performance, and healthspan](https://www.sciencedirect.com/science/article/pii/S155041311...). Cell metab, 22(1), pp.86-99. Longo and Panda, 2016. [Fasting, circadian rhythms, and time-restricted feeding in healthy lifespan](https://www.sciencedirect.com/science/article/pii/S155041311...). Cell metab, 23(6), pp.1048-1059. Di Biase et al, 2016. [Fasting-mimicking diet reduces HO-1 to promote T cell-mediated tumor cytotoxicity](https://www.sciencedirect.com/science/article/pii/S153561081...). Cancer cell, 30(1), pp.136-146. Choi et al, 2016. [A diet mimicking fasting promotes regeneration and reduces autoimmunity and multiple sclerosis symptoms](https://www.sciencedirect.com/science/article/pii/S221112471...). Cell rep, 15(10), pp.2136-2146. Wei et al, 2017. [Fasting-mimicking diet and markers/risk factors for aging, diabetes, cancer, and cardiovascular disease](http://l-nutra.com/wp-content/uploads/2017/02/science-transl...). Sci trans med, 9(377), p.eaai8700. Cheng et al, 2017. [Fasting-mimicking diet promotes Ngn3-driven β-cell regeneration to reverse diabetes](http://www.celprogen.com/uploads/product/14902320845.pdf). Cell, 168(5), pp.775-788. Guidi N, Longo VD, 2018 [Periodic fasting starves cisplatin-resistant cancers to death](https://www.ncbi.nlm.nih.gov/pubmed/29875131)

Fontana et al, 2013. [Dietary protein restriction inhibits tumor growth in human xenograft models of prostate and breast cancer](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926840/). Oncotarget, 4(12), p.2451. Mirzaei et al, 2014. [Protein and amino acid restriction, aging and disease: from yeast to humans](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4254277/). Trends Endocrin Metab, 25(11), pp.558-566. Levine et al, 2014. [Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population](https://www.sciencedirect.com/science/article/pii/S155041311...). Cell metab, 19(3), pp.407-417. Shim and Longo, 2015. [A protein restriction-dependent sulfur code for longevity](https://www.sciencedirect.com/science/article/pii/S009286741...). Cell, 160(1-2), pp.15-17. Mirzaei et al, 2016. [The conserved role for protein restriction during aging and disease](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4807119/). Curr op clin nut metab care, 19(1), p.74. Song et al, 2016. [Association of animal and plant protein intake with all-cause and cause-specific mortality](https://jamanetwork.com/journals/jamainternalmedicine/fullar...). JAMA in med, 176(10), pp.1453-1463. Wei et al, 2017. [Fasting-mimicking diet and markers/risk factors for aging, diabetes, cancer, and cardiovascular disease](https://www.ncbi.nlm.nih.gov/pubmed/28202779)