You're right about radiative cooling - I didn't consider that radiative cooling would be that much easier.

I asked claude.ai a bunch of questions.below According to it, purely radiative cooling of a device in space (40-60C) is roughly as effective as very crude conductive cooling of a similar device on earth (internal temp 49 C).

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Consider a 1 m radius spherical object in LEO. One direction, bathed in direct sunlight is coated with solar panels. The electricity generated runs computers internally - the computers are capable of running regardless of the internal temperature of the enclosure. The reverse side is exposed to the 2.7 K of the CMB and had small metal radiative panels.

Compare it to another similar size sphere stored in a room at a constant 22C on earth. Instead of solar panels, the same amount of electricity is pumped in.

In which case would the internal temperature of the sphere be higher?
Make a few assumptions about the other parameters. All power generated by the solar panels in space, or fed in by power lines on earth is immediately used for computation.

Give me rough internal temperatures for both cases

Now assume the sphere on earth is (a) suspended on a thread (b) half buried (c) fully buried , and it has a metal body.
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Answers from Clause.ai
LEO. 40-60 C
Earth.a 95 C
Earth.b 75 C
Earth.c 49 C

Yeah! And the frozen person shatters into smithereens when hit by a protagonist with a hammer.

" Demands for cooling could also be cut because of the vacuum of space."

How does that work? Vaccum makes cooling harder, not easier, doesn't it?

There only so much oil and hydel power to go around.

When demand ourpaces supply, prices go up

As time goes by, I hope programming editors and IDEs start doing language translation via AI.

Say, someone needs to edit a C program but is not very skilled in it. They could use their favourite language (say, C#), to quasi-edit the source program (which would be presented as C# to them). C# code changes would be auto-translated to C in a manner that fits the source codebase's conventions. Aspects of the C program that have no C# equivalent could summarised and edited by AI dialog.

I wonder how TIOBE would measure this sort of work. As activity in the source language (C)? Editing language (C#)? Or both?

Like so?

select * from Citizens
CTRL+A
CTRL+C
ALT+TAB
CTRL+V

This news says all lupus cases may be caused by the EBV virus. Link:
https://www.nbcnews.com/health...
The Epstein-Barr virus was found to reprogram immune B cells to wrongly attack the nucleii of other cells with 'anti-nuclear antibodies'

Past research has also liked scleroderma and EBV. So I feel lupus and scleroderma may both have be triggered by EBV.
  EBV hides in immune B cells. This has also been linked to scleroderma. So the question is how to flush out these bad cells, called *auto-reactive B cells*.

Some more ideas:

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- Could a blood transfusion help? I am O+ ... Universal donor. Just kidding.. I am rolling my sleeves just yet. But worth investigating with the help of AI and doctors. Remember, Leviticus 17:11 states, "For the life of the flesh is in the blood...".

- There is also a treatment called autopheresis. It seperates out blood into its various components (plasma, platelets) and returns the desired components back to you. Perhaps B cells count can be reduced this way.

- Photopheresis. This is an immune-modulating treatment. Here your immune blood cells are separated and exposed to UVA light. It is used for scleroderma to help with skin thickening, joint involvement, and other symptoms, particularly in patients with refractory disease.

- UVA1 phototherapy. This is a topical, non invasive treatment that involves shining the UVA1 band of ultraviolet light, which is longer than UVA and penetrates deeper. UVA1 phototherapy can lead to softening and a reduction of sclerotic plaques, with benefits such as increased skin elasticity and a reduction in skin thickness

- Rituximab: This is a well-studied antibody therapy that eliminates B cells by binding to the CD20 protein on their surface. It has shown favorable results in many patients, including those with scleroderma and lupus resistant to other treatments.

- CAR T-cell therapy: This cutting-edge approach modifies a patient's own T-cells to specifically target and destroy auto-reactive B cells.

- Reduction of unhealthy immune b cells in blood by infusion of cultured healthy autologous b cells (your own B cells) That's so the good B cells crowd out the bad ones. This may be done in combination with either autopheresis, apheresis, transfusion of other blood fractions and simple blood-letting (phelobotomy)

- Autologous Hematopoietic Stem Cell Transplantation (AHSCT). AHSCT is a more intensive treatment that first uses high-dose immunosuppression to wipe out the existing, dysfunctional immune cells, including B cells. The patient's own (autologous) stem cells are then transplanted to rebuild a new, healthier immune system that is re-established as self-tolerant.

- Natural killer (NK) cells play a crucial role in the immune system's defense against Epstein-Barr virus (EBV) by targeting and eliminating EBV-infected B cells. Food to boost NK cells include mushroom, garlic, turmeric, and green tea. [Mushrooms]: Varieties like shiitake and maitake contain beta-glucans, compounds that have been shown to stimulate NK cell activity in studies. [Garlic]: Contains sulfur compounds like allicin that can stimulate various immune cells, including NK cells. [Turmeric]: The active ingredient, curcumin, has anti-inflammatory properties and can enhance NK cell function. [Green Tea]: Rich in the antioxidant EGCG, which may stimulate NK cell activity.

- light exposure - you need vitamin D, but high intensity sunlight exposure can worsen scleroderma flares. So some amount of daily sun exposure (to be quantified; perhaps early mornings) and this light therapy called UVB-NB (narrowband UVB) shows promise for scleroderma. https://www.odermatol.com/oder...

- Vitamins D. scleroderma patients typically need high-dose vitamin D3 (cholecalciferol) due to high deficiency rates and potential malabsorption. To ensure effective use and prevent soft tissue calcification, cofactors like magnesium and vitamin K2 are generally recommended, while zinc and boron may also be beneficial due to common deficiencies and their role in immune function. Regular monitoring of serum vitamin D, calcium, and PTH levels is essential to achieve a target range

This is some info regarding scleroderma that I have shared with my friend with scleroderma over the years. I suspect some relationship to Lupus. Maybe this can help someone.

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Take a look at this article on autoimmune diseases.
https://www.lifeextension.com/...
It suggests vitamin D and Omega-3s:

_The daily supplemental dose was 2,000 IU of vitamin D3 and 1,000 mg of omega-3 fatty acids._

https://journals.plos.org/plos...
Here the core paper behind this article. They induced and cured an MS- like condition in animals by deactivating something called an 'aryl hydrocarbon receptor' in T cells. The receptor makes T cells overactive. This is what triggers sclerosis
Interestingly
- the receptor is sensitive to hydrocarbons (petrol, benzene, dry cleaning, cleaning chemicals)
- the receptor is sensitive to blue and UV light (getting a sunburn or tan)
So this should help:
- removing sources of volatile hydrocarbons
- avoiding blue/UV light and substituting with red light therapy (which energises mitochondria)

This paper seems promising.
https://www.ncbi.nlm.nih.gov/p...
I believe skin sclerosis occurs in scleroderma, correct? This paper basically says UV light that's normally used to treat skin sclerosis may be too damaging to certain tissue components. Instead, Red Light therapy is a promising treatment for skin sclerosis as it does not have these side effects. The paper recommends investigating its use in treatment.

*Excerpts:*
_Ultraviolet (UV) phototherapy is a non-invasive modality that has been used to treat several diseases associated with skin fibrosis including morphea, systemic sclerosis, chronic graft versus host disease, and nephrogenic systemic fibrosis [5–7]. However, UV phototherapy causes thymidine dimer DNA damage that is associated with an increased incidence of skin cancers and premature photoaging [8–10]. In addition to these safety concerns, UV phototherapy units are often prohibitively expensive for home use and require fluorescent or incandescent bulbs that limit portability. Therefore, UV phototherapy requires frequent office visits that patients often find burdensome [11, 12]. In contrast, light-emitting diode-generated red light (LED-RL) phototherapy is a safe, non-invasive, inexpensive, and portable treatment that may be combined with existing treatment modalities. Furthermore, the visible red light spectrum has superior depth of penetration, when compared to UV light, that allows it to penetrate the epidermis and reach the dermis to affect fibroblast function [13]. LED-RL is not known to cause thymidine dimer DNA damage or to be associated with an increased incidence of skin cancer [14]. However, the underlying biochemical mechanisms and clinical effects of visible light photobiomodulation of skin fibrosis are not well characterized._

*_Conclusions_*
_Visible light phototherapy is an emerging therapeutic modality for treatment of skin fibrosis. There is a growing body of evidence demonstrating that visible red light is capable of modulating key cellular characteristic associated with skin fibrosis. We believe that further laboratory research may elucidate the underlying mechanisms and effects involved in visible light photobiomodulation. LED-based devices are the optimal devices for red visible light phototherapy. There is a current lack of clinical trials investigating the efficacy of LED-RL to treat skin fibrosis. Randomized clinical trials are needed to demonstrate visible red light’s clinical efficacy on different types of skin fibrosis._

"The technique, called transcutaneous auricular vagus nerve stimulation (tVNS), which involves electrical stimulation to the vagus nerve through the skin on the outer ear and can be done at home, also resulted in lower levels of IL-6, an inflammatory molecule with a known role in SSc"
  https://sclerodermanews.com/ne...

https://wholefamilyproducts.co...
There is a Japanese supplement called serrapeptase. It dissolves unwanted protein and is used by silkworms to free themselves from their cocoon.
It is useful for scleroderma.

  https://www.inspire.com/groups...
This thing called natto, a Japanese fermented soy food, may be good for you. See this enzyme extracted from it is "fibrolytic" - dissolves clots and scars.

https://chatgpt.com/share/67a7...
can you have a read of the attached AI session and then ask your specialist about rhubarb extract containing rhein?

This is a very interesting supplement. small amounts reboot mitochondria, and increase energy
https://youtu.be/qdN3q8MFJIM?s...

https://youtu.be/MBXBpm1Y5J0?s...
This seems useful: a video on diet in managing scleroderma. At 15:57 he makes a very interesting point that 50% of calories must come from Omega fats. He says carnivore diet helps by eliminating carbs that feed harmful gut bacteria. But he recommends the carnivore diet only during scleroderma flares. In the main, he recommends a customised 'phyto-diet' based on plant foods

https://youtu.be/vmBHj-5SUWY?s...
This video lists different useful natural supplements for Sjogren's syndrome - a somewhat related autoimmune disorder that overlaps with scleroderma 20% of the time. The recommendations here each target specific different pathologies and root causes (the CMV and EBV viruses). I feel these will be useful for you. He talks about supplements including wormwood and cordyceps mushrooms

My friend has Scleroderma and his mother died of lupus.
Both are auto-immune conditions . From what I read online, both conditions are somewhat related: "around 20% of people with scleroderma also have lupus as a cross-over condition or 'overlap syndrome'".

I wonder if both my friend and his mother had the same virus trigger their conditions

Yes, the problem with 'end-to-end encrypted traffic' is one end is the device, and the other end is the manufacturer. The supposed owner gets no look at the data 'his' device is sending

If (say) the bus services a naval base, very sensitive information may be transmitted (stop location, duration, schedule, internal fuel level...)

If only a strange hybrid of John Deere and Tesla built buses, those would not have this problem, right?

Right?

I don't know why large buyers, in particular, allow end-to-end encrypted traffic between the vendor and the products the buyer ostensibly owns.

At the very least, the traffic should be open to inspection by the buyer, who should be able to selectively turn off or disable aspects of it.

I agree completely. AIs can do that already. There are even some prompts supposed to enhance the interaction. Something like this:
  "You are an advanced so and so... You teach using the Socratic method".

Coupling AI to licensed course content chopped up for focussed instruction delivery will make it even more powerful. It should also reduce the chance of misinstruction or hallucination.

It can do a passable simulacrum of that :-).

Won't using 1Password - as opposed to using a local credential store - also risk compromise of the enterprise?

My impression of 1Password is that it is centralised store of encrypted passwords - isn't that a hacker magnet? Hackers could obtain the encrypted store and attempt to decrypt at leisure. Or hack 1Password's communication interfaces and endpoints.

I'd be much more comfortable if all 1Password did was enable the syncing of credential stores directly between devices, never keeping a copy . That way I gain a distributed master record. Basically, a signal to say "hey, a credential has changed; sync up with such and such device". If my devices happen to sync directly, the vendor may never even see an encrypted copy of my passwords, much less store it.

If a centralized master copy is essential, 1password should deploy software that centralizes credentials at the organisation level... The software should be owned by the customer. instead, right now the 1Password architecture has them hosting hundreds of millions of credentials on their servers. While the data is encrypted from their eyes, doesn't centralization make them a hacker magnet? Hackers could obtain encrypted stores with hundreds of millions of credentials and attempt to decrypt them at leisure. Or they focus their hacking efforts on 1Password's communication interfaces and endpoints. That make me queasy.

With 1 billion terminal sessions made per week to its mainframe cloud, IBM spins off its thriving hosted mainframe business. The IPO is valued at 1 Trillion dollars.

Then the microprocessor and PC revolution breaks.