Rud istvan

Wuhan Coronavirus–a WUWT Scientific Commentary
Guest Blogger / February 10, 2020

Guest post by Rud Istvan

Introduction

The Wuhan coronavirus potential pandemic has been much in the news recently. ctm discussed my doing an update to a rather long comment a few weeks ago. I first agreed but then demurred until now.

The reasons for agreeing were the numerous analogies (below) to climate change ‘science’ and ‘prognostications’—albeit on usefully shortened testable time frames like this year, not 2100. Examples below include assuming we know what we actually don’t based on models, and reporting worst case but unlikely scenarios as ‘likely” because ‘if it bleeds, it leads’.

First reason for originally demurring was that the factual situation was too fluid for rational qualitative analysis—alarmist rumors were flying all over, like from ‘reputable’ UK research groups who modeled an R0 near 4 (horrible, as defined below). Pure unsubstantiated alarmism, just like AGW prognostications.

Second reason (ironically), I came down with a wicked, likely coronavirus (less runny nose, more sore throat and cough) cold last week and am still recovering at day nine. So was too sick to even think about a guest post until yesterday evening day 8. Finishing this draft today merely proves that I am finally recovering on day 9 and that it probably was a human common cold corona virus since the typical rhino duration is ‘only’ 5 days, not 9-10.

Qualifications

None, if you are a CAGW ‘believer’. I am not a microbiologist, a virologist, or an infectious disease MD. A CAGW/skeptic ‘critique’ all too familiar at WUWT.

But, I served as CEO for a decade of a small private company that attempted (unsuccessfully for reasons beyond the scope of this post) to commercialize a novel topical antimicrobial PERSISTENT against all bacteria, all fungi, and many viruses including all colds, influenza and pinkeye. I had to teach myself the topic and its medical ramifications in order not to mislead my investors or misuse their several million dollars. Plus, we formed a pre-eminent science advisory board on infectious disease. Plus, in the 2009 swine flu scare, my corporate board forced interactions with NIH (Dr. Fauci), CDC, the FDA, and even the National Security Council (special briefing in the EOB at the WH, 2 hours, spooky)—because our FDA regulatory guy DIED in June 2009 from the swine flu contracted while on a cruise vacation to Mexico with his family (more below).

Those not interested in the background science sections can skip to the last sections of this longish comment, where the intervening basic science is applied to Wuhan coronavirus without further explanation.

Basic Virology

What follows perhaps oversimplifies an unavoidably complex topic, like sea level rise or atmospheric feedbacks to CO2 in climate science.

There are three main types of human infectious microorganisms: bacteria, fungi, and viruses. (I skip important complicating stuff like malaria or giardia.) Most human bacteria are helpful; the best example is the vast gut biome. In human disease some bacteria (typhoid, plague, tetanus, gangrene, sepsis, strep) and certain classes of fungi (candida yeasts) can cause serious disease, as do some human viruses (polio, smallpox, measles, yellow fever, Zika, Ebola).

There are two basic forms of bacteria (Prokaryotes and Archaea, neither having a genetic cell nucleus). Methanogens are exclusively Archaean; most methanotrophs are Prokaryotes. Membrane bound photosynthetic organelle containing cyanobacteria are the evolutionary transition from bacteria to all Eukaryotes (cells having a separate membrane bound genetic nucleus) like phytoplankton, fungi, and us. Both Prokaryote and Eukaryote single cell (and all higher) life forms have a basic thing in common—they can reproduce by themselves in an appropriate environment.

Viruses are none of the above. They are not ‘alive’; they are genetic parasites. They can only reproduce by infecting a living cell that can already reproduce itself. The ‘nonliving’ viral genetic machinery hijacks the reproductive machinery of a living host cell and uses it to replicate virions (individual virus particles) until the host cell ‘bursts’ and the new virions bud out in search of new hosts.

There are two basic virus forms, and two basic genetics.

Form

1. Viruses are either ‘naked’ or ‘enveloped’. A naked virus like cold causing rhino has just two structural components, an inner genetic whatever code (only the two basic types–DNA and RNA–are important for this comment) and an outer protective ‘capsid’ protective viral protein coat. An example is cold producing rhinovirus in the family picornavirus (which also includes polio).

2. Enveloped viruses like influenza and corona (Wuhan) include a third outer lipid membrane layer outside the capsid, studded with partly viral and partly host proteins acquired from the host cell at budding. These are used to infect the next host cell by binding to cell surface proteins. The classic example is influenza (internal genetic machinery A or B) designated HxNy for the flavor of the (H) hemagglutinin and (N) neuraminidase protein variants on the lipid membrane surface.

Conceptual images of both virion forms follow from CDC.

Naked Rhino Enveloped Influenza

clip_image002[1] clip_image004[1]

Genetic Type

The second major distinction is the basic genetics. Viral genetic machinery can be either RNA based or DNA based. There is a huge difference. All living cells (the viral hosts) have evolved DNA copy error machinery, but not RNA copy error machinery. That means RNA based viruses will accumulate enormous ‘transcription’ errors with each budding. As an actual virology estimate, a single rhinovirus infected mucosal cell might produce 100000 HRV virion copies before budding. But say 99% are defective unviable transcription errors. That math still says each mucosal cell infected by a single HRV virion will produce about 10 infective virions despite the severe RNA mutation problem. The practical clinical implication is that when you first ‘catch’ a HRV cold, the onset to clinical symptoms (runny nose) is very fast, usually less than 24 hours.

There is a related epidemiological consequence of great concern. It has been proven possible for a single mucosal cell to be infected ‘simultaneously’ by more than one viral seriotype. That is a simple math probability of virions and host cells Example: you have an easily transmissible ‘normal’ coronavirus cold already (defined below), go to Wuhan and also contract Wuhan. In your body those two different coronaviruses can now both be replicating in the same host cells, and because of RNA replication are indiscriminately exchanging genetic material. So you might end up with an attenuated virulence Wuhan, or a more virulent Wuhan—but most likely both.

The history of the 2009 Swine flu scare showed this. The novel new H1N1 seriotype started in Mexico, where my guy contracted his early fatal infection. For reasons explained below, flu is strongly seasonal. It was winter in South America, so the first hard hit country was Argentina. The mortality data were horrific (5.5%). But, this in hindsight meant the most virulent strains were already burning themselves out, since dead people cannot replicate virions. By the time swine flu reached the North American winter several months later, it was already significantly less virulent (1-2%, still very bad). What actually saved the situation was that based on Argentina, the world appropriately panicked, commandeered global conventional flu vaccine production, and crashed through a swine flu vaccine in just under 6 months at the expense of the normal next year stockpile.

Upper Respiratory Tract viral infections.

So-called URI’s have only two causes in humans: common colds, and influenza. Colds have three distinguishing symptoms–runny nose, sore throat, and cough—all caused not by the virus but by the immune system response to it. Influenza adds two more symptoms: fever and muscular ache. Physicians know this well, almost never test for the actual virus seriotype, and prescribe aspirin for flu but not colds. Much of what follows in this section is based on somewhat limited actual data, since there has been little clinical motivation to do extensive research. A climate analogy would be sea surface temperature and ocean heat content before ARGO. Are there estimates? Yes. Are there good estimates? No.

Common cold URI’s stem from three viral types: RNA rhinovirus (of which there are about 99 seriotypes but nobody knows for sure) causing about 75% of all common colds, RNA coronaviruses, for which (excluding SARS, MERS, and Wuhan) there are only 4 known human seriotypes causing about 20% of common colds, and DNA adenoviruses (about 60 human seriotypes, but including lots of non-cold symptom seriotypes like conjunctivitis (pink eye and pharyngoconjunctivitis) causing about 5% of common colds.

Another climate change related analogy. The internet (including Wikipedia) gets the previous paragraph’s facts mostly wrong. For example, Wiki distinguishes picornviruses from rhinoviruses without realizing the later is a subset of the former, so double counts.

Available data says rhinovirus seriotypes are ubiquitous but individually not terribly infective, coronavirus seriotypes are few but VERY infective, and adenoviruses are neither. This explains, given the previous RNA mutation problem, why China and US are undertaking strict Wuhan quarantine measures.

This also explains why there is no possibility of a common cold vaccine: too many viral targets. You catch a cold, you get temporary (RNA viruses are constantly mutating) immunity to that virus. You next cold is simply a different virus, which is why the average adult has 2-4 colds per year.

This also explains why adenovirus is not very infective. It is a DNA virus, so mutates slowly, so the immune memory is longer lasting. In fact, in 2011 the FDA approved (for military use only) a vaccine against adeno pharyngoconjuntivitis that was a big problem in basic training. (AKA PCF, or PC Fever, highly contagious, very debilitating, and unlike similar high fever strep throat untreatable with antibiotics.) In the first two years of mandatory PCF vaccine use, military PCF disease incidence reduced 100 fold.

These data expanded to influenza also explain why the annual flu shot is so hit or miss. The intent is to match the most common HxNy A or B types from end of this season for vaccination next season. That guess is never perfect. Plus, RNA based influenza mutates rapidly. So even IF the annual flu shot was a good initial match, the flu that spreads by the end of the vaccinated season will be the bits the guess missed—basic Darwinian evolution at work explaining the limited efficacy of the annual flu shot.

A clinical sidebar about URI’s. Both are worse in winter, because people are more indoors in closer infectious proximity. But colds have much less seasonality than flus. Summer colds are common. Summer flus aren’t.

There is a differential route of transmission explanation for this empirical observation. Colds are spread primarily by contact, while flus are spread primarily by inhalation. You have a cold, you politely (as taught) cover your sneeze or cough with a hand, then open a door using its doorknob, depositing your fresh virions on it. The person behind you opens the door, picking up your virions, then touches the mouth or nose (or eyes) before washing hands. That person is now probably infected. This is also why alcohol hand sanitizers have been clinically proven ineffective against colds. They will denature enveloped corona and adeno, but have basically no effect on the by far more prevalent naked rhinos.

There is an important corollary to this contact transmission fact. Infectivity via the contact route of transmission depends on how long a virion remains infective on an inanimate surface. This depends on the virion, the surface (hard doorknob or ‘soft’ cardboard packaging), and the environment (humidity, temperature). The general epidemiological rule of thumb for common colds and flus is at most 4 days viability. This corollary is crucial for Wuhan containment, discussed below.

The main flu infection route is inhalation of infected aspirate. This does not require a cough, merely an infected person breathing in your vicinity. In winter, when you breathe out outside below freezing ‘smoke’ it is just aspirate that ‘freezes’ and becomes visible. Football aficionados see this at Soldier and Lambeau Fields every winter watching Bears and Packers games. The very fine micro-droplet residence time in the air depends on humidity. With higher humidity, they don’t dry out as fast, so remain heavier and sink faster to where they don’t get inhaled, typically minutes. In typical winter indoor low humidity, they dry rapidly and remain circulating in the air for much longer, typically hours. This is also why alcohol hand sanitizers are ineffective against influenza; the main route of flu transmission has nothing to do with hands.

Wuhan Coronavirus

As of this writing, there are a reported 37500 confirmed infections and 811 deaths. Those numbers are about as reliable as GAST in climate change. Many people do not have access to definitive diagnostic kits; China has a habit of reporting an underlying comorbidity (emphysema, COPD, asthma) as cause of death, the now known disease progression means deaths lag diagnoses by 2-3 weeks. A climate analogy is the US surface temperature measurement problems uncovered by the WUWT Surface Stations project.

There are a number of important general facts we DO now know, which together provide directional guidance about whether anyone should be concerned or alarmed. The information is pulled from reasonably reliable sources like WHO, CDC, NIH, and JAMA or NEJM case reports. Plus, we have an inadvertent cruise ship laboratory experiment presently underway in Japan.

The incubation period is about 10-14 days until symptoms (fever, cough) evidence. That is VERY BAD news, because it has been demonstrated beyond question (Germany, Japan, US) that human to human transmission PRECEDES symptoms by about a week. So unlike SARS where all air travelers got a fever screening (mine was to and from a medical conference in Panama City). Since transmission did not precede symptoms, SARS fever screening sufficed; with Wuhan fever screening is futile. That is why all the 14-day quarantines imposed last week; the only way to quarantine Wuhan coronavirus with certainty is to wait for symptoms to appear or not. Quarantine is disruptive and expensive, but very effective.

Once symptoms appear, disease progression is now predictable from sufficient hundreds of case reports—usual corona cold progression for about 7-10 days. But then there is a bifurcation. 75-80% of patients start improving. In 20-25%, they begin a rapid decline into lower respiratory pneumonia. It is a subset of these where the deaths occur with or without ICU intervention. And as whistleblower Dr. Li’s death in Wuhan proves, ICU intervention is no panacea. He was an otherwise healthy 34 years old doctor.

There are two (really now three) key epidemiological numbers: R0 pronounced medically as ‘Rnaught’ (or, as we now know, R0 before and after symptoms). R naught is how many naïves will a single infected individual infect? We know from the Japanese cruise ship Diamond Princess quarantine that R0 is at least ~2. (As of now, 63 diagnosed out of 2667 passengers and ~1100 crew). Since Japan has moved the 63 symptomatic patients to hospital isolation, that same cruise ship may in the next 14 days also provide an experimental symptomless Wuhan R0 estimate. Late revision update, now 69, so asymptomatic R0 is unfortunately above 1.

The second important number is mortality, a virulence metric. We don’t know the mortality rate yet even given 811 deaths/37500 diagnosed. That is because of the multi-week disease progression, even if there were no other data issues. SARS was about 10% in the end (774 deaths from about 8000 diagnosed). The “Spanish flu’ of 1918-19 was also ~10% or perhaps a bit higher (CDC guesstimate is 40-60 million died out of about 500 million infected). BTW, for those wanting to deep dive that last lethal viral pandemic, I highly recommend the NYT best selling book THE GREAT INFLUENZA by John Barry. Wuhan is very unlikely to reach anywhere close to that mortality; otherwise we would already have seen many more deaths.

We also now know from a JAMA report Friday 2/7/2020 analyzing spread of Wuhan coronavirus inside a Wuhan hospital, that 41% of patients were infected within the hospital—meaning the ubiquitous surgical masks DO NOT work as prevention. The shortage of masks is symptomatic of panic, not efficacy.

Scientists last week also traced the source. There are two clues. Wuhan is now known to be 96% genetically similar to an endemic Asian bat corona. Like SARS and ‘Spanish flu’, it jumped to humans via an intermediate mammal species. No bats were sold in the Huanan wet market in Wuhan. But pangolins were, and as of Friday there is a 99% genetic match between pangolin corona and Wuhan human corona. Trade in wild pangolins is illegal, but the meat is considered a delicacy in China and Vietnam and pangolins WERE sold in the Wuhan wet market. This is is similar to SARS in 2003. A bat corona jumped to humans via live civets in another Chinese wet market. Xi’s ‘simple’ permanent SARS/Wuhan coronavirus solution is to ban Chinese wet markets.

This is similar to what is now known about the 1918-19 H1N1 ‘Spanish flu’. It started as a 1917 avian H1N1 (wild duck, Mississippi flyway, fall migration) influenza. It was hosted and incubated in an intermediary species, hogs, in Haskell County, Kansas for the rest of that year. A country doctor tending surprisingly many severe flu cases among hog farmer families as winter 1918 began raised an alarm, but his public health warnings were ignored. Then it jumped from Haskell County, Kansas hog farmers to Camp Funston, Kansas soldiers during winter 1918, where doughboys were training then deploying to Europe to finish the great war. The rest was history, with an R0 guesstimated between 2 and 3.

Conclusions

Should the world be concerned? Perhaps.

Will there be a terrible Wuhan pandemic? Probably not.

Again, the analogy to climate change alarm is striking. Alarm based on lack of underlying scientific knowledge plus unfounded worst case projections.

Proven human to human transmissibility and the likely (since proven) ineffectiveness of surgical masks were real early concerns. But the Wuhan virus will probably not become pandemic, or even endemic.

We know it can be isolated and transmission stopped with 14-day quarantine followed by symptomatic clinical isolation and ICU treatment if needed.

We know from infectivity duration on surfaces that it cannot be spread from China via ship cargo. And cargo ship crews can simply not be given shore leave until their symptomless ocean transit time plus port time passes 14 days.

Eliminating Chinese wet markets and the illegal trade in pangolins prevents another outbreak ever emerging from the wild, unfortunately unlike Ebola.
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phones sigh

i wotever, sounds like your calls are actually going through voicemail. Take alook at the following and try the disable codes on your phone.

Here’s how it’s done:

To enable voicemail:
*61*101**30# Divert to 101 when unanswered after 30 seconds
*62*101# Divert to 101 when unreachable
*67*101# Divert to 101 when busy
*21*101# Divert all calls to 101

To disable voicemail:
#61# Cancel divert when unanswered
#62# Cancel divert when unreachable
#67# Cancel divert when busy
#002# Cancel all diverts

I spent many hours searching for this last night. This thread was the #1 result in Google searches for “Telstra Call Forward codes”, and many of the pages on the Telstra site which deal with call forwarding didn’t show up on Google until the 6th or 7th page. So I thought it would be best to post the actual forward codes in this thread to help anyone else in the future.

To summarize:

Turn on Call Forward: **code*(phone number to forward calls to, including area code)*10#
Turn off call Forward: ##code**10#
Check if forwarding is on: *#code#

Where: “code” is:
21 for “All calls”
61 for “No answer”
62 for “Unreachable”, ie “out of coverage”
67 for “Busy”

Specifically for “no answer”, you can set the duration your phone rings before it diverts using the the following:
**61*(phone number to forward calls to, including area code)**(number of seconds)#

This was compiled from the following Telstra pages (though I will point out that none of the pages mention the “unreachable” diversion – this oversight should be corrected):

https://go.telstra.com.au/helpandsupport/-/turn-call-forward-on
https://go.telstra.com.au/helpandsupport/-/turn-call-forward-off-on-your-mobile
https://go.telstra.com.au/helpandsupport/-/check-if-call-forward-is-turned-on-or-off-on-your-mobile

https://go.telstra.com.au/helpandsupport/-/change-ring-time-before-calls-divert-to-messagebank-on-yo…

View solution in original post

Italian Story

C’era una Volta tre animale si trovano perduto nella bosca. C’erano un cangaru,un wombat u una rana verde dell’alberi.
“Il mio boomerang non ha ritornato” lamentarsi il cangaru con lacrime nel suoi occhi.
“Non fretta “ dice il wombat. “Comprero un nuovo quando torniamo a casa“
“Ma dov’e i nuoi casa“ urlo la piccola rana.”Non la vedo “

“Non ti fretta” dice il wombat ancora.” Stai placida”.
“di un piano”.
“Guarda questa collina davanti” ha detto.
“Cercheriamo di la.
Ma i alberi hanno bloccato il suo visione.
“Fammi aiutare”ha preghato il wombatche era scimmiando sul spalle del cangaru, ma i rami e fogli erano nella via.
La piccola rana ha salvuto il giornata.
Ha saltato nel capo del wombat e ha veduto il tetto rossa della loro casa lontano fa.
“Andiamo”.

Il messagio e semplice quello.
Senta alla rana sempre.

Other endings are possible but hard to say.
We can see further standing on the shoulders of giants.
Three heads are better than one.
Things work out when everyone helps.
Etc.
Can you make up a moral for this story as well?

Italian Story Corrected
C’erano una volta tre animali si trovavano perduti nel bosco. C’erano un cangaro, un wombat e una raganella verde.
“Il mio boomerang non è ritornato” lamentava il cangaro con lacrime agli occhi.
“Non c’è fretta “ disse il wombat. “Ne comprerò uno nuovo quando torniamo a casa“.
“Ma dov’è la nostra casa“ urlò la piccola rana. ”Non la vedo “
“Non c’è fretta” disse il wombat di nuovo.
”Stai calma”
“Ho un piano”.
“Guarda questa collina davanti” disse.
“Cercheriamo là
Ma gli alberi bloccavano la sua veduto.
“Aiutami” ha preghato il wombat che si era arrampicato sul spalle del cangaro, ma i rami e le foglie ostacolavano la veduta.
La piccola rana salvò la giornata.
È saltata sul capo del wombat e ha veduto il tetto rosso della loro casa lontana. “Andiamo”.
Il messagio è semplice.
Ascoltare sempre la raganella.
I cannot think of an Italian saying that would have the same meaning (Lelia)
Other endings are possible but hard to say.
We can see further standing on the shoulders of giants.
Three heads are better than one.
Things work out when everyone helps.
Etc.
Can you make up a moral for this story as well?

Once upon a time there were three animals who found themselves lost in the woods. There were a kangaroo, a wombat and a green tree frog.
“My boomerang didn’t come back” complained the kangaroo with tears in it’s eyes.
“Don’t worry”” said the wombat, I will buy you a new one when we get back home.
“But where is our house?”cried the little frog. “I do not see it”.
“Dont worry” said the wombat again.”Stay calm. I have a plan”
“See that hill in front” he said.
We will search [from] there””.
But the trees blocked his view [blocked him from seeing it?].
Help me” he asked the wombat who climbed on the shoulders of the kangaroo, but the branches and leaves blocked the view.
The little frog saved the day.
He jumped on the head of the wombat and saw the red roof of their house far away.
The message is simple.
Always listen to the tree frog.
or
Don’t go into the woods without a back up frog.
Boomerangs do not always return.
Jump around a lot when you get into trouble.
Have a house that you can easily identify [Isle of Burano story.]
It wont surprise you that Burano is famous for seafood.
The most popular place to eat seafood in Burano is Trattoria al Gatto Nero on Via Giudecca 88.

Are you looking for Causation or Blame?

I get the point that there are
Events caused by Anthropogenic effects
Events caused by Anthropogenic Climate Change
and that the general effect of the latter will cause more harm than the more localised effect of the former.

Attribution of either is complicated leading to a moral and scientific issue.
Are you looking for Causation or Blame?
One is a scientific approach and one a moral approach.

One can of course do both, find a cause and find blame in the same event.
This is helped by using story line approaches as they incorporate a moral lesson in their very definition.
“given that an event has occurred, how might climate change have influenced this event?”

“The claim is that in trying to separate the human influence from the natural variability of weather, extreme event attribution creates a new nature-culture divide.”
People have looked for causation in weather for ever. A rare event, did something I did cause that weather effect? People have always wanted to attribute causation and blame their actions or lack of them to explain misfortunes and occasionally good luck.
Once you attribute Blame or Causation to human action you open a divide between those who want to believe [naturalists] and those who want to understand [culture/science].

“The problem here is that extreme event attribution typically tries to understand how the event might be different because of anthropogenic-driven climate change,”
Even here what you are saying is that extreme events are natural and that in your view human causation might make it worse.
I say worse because if human causation ever made things better you would not feel concerned to investigate it further.
Hence the problem of trying to prove that rare extreme events are ever capable of offering proof of climate warming.
“if we don’t distinguish between natural and anthropogenic influences, how do you then avoid people simply concluding that it’s natural, or using this to argue that it’s natural?”
Hence the crux of the matter, do we tell them a story line to emphasis how bad we believe it may be and only choose, always, the bad side of that story line for emphasis?
– Or do we tell them the truth.

There will be a number of consequences that will become self evident in time.
We cannot prove this conclusively now but believe it to be so.
We are working on improving our attribution to everyone’s satisfaction.
We are not looking to blame or shame anyone.

Probability

angech says:
Your comment is awaiting moderation.
June 6, 2020 at 11:35 pm
ATTP are we reading this the same way?

“The key results are that for long-timescales (many decades) internal variability contributes little to the total uncertainty (essentially, it averages out).”

I do not see this as the key finding, rather a statement of the parameters being put in.
By definition internal variability is defined as fluctuations around some predetermined real value.
As time goes by the fluctuations balance out and the true value is revealed shed of dross. In other words it must always reduce to zero

Atomsk’s Sanakan @AtomsksSanakan. May 27
“Update thread citing published studies, along with comments debunking Judith Curry’s cherry-picking in the service of ideologically-motivated denialism on hydroxychloroquine:“

Missing in action. Why?
Lancelet study Chloroquine Debunked
New England Journal of medicine. Debunked same author

Most of the studies you quote have been extremely hastily put together with pal not peer review and rushed into print.
They all have massive flaws consequent.
As they fall apart, one by one, will you guarantee to return here and issue a mea culpa for your mudslinging?

The fact that you’re still willfully ignoring the fact that previously reputable Journals have thrown science out the window is expected from a committed ideologue.

How to redeem a scrap of integrity, if you ever wanted.
Be more skeptical in the right way.
Put up lists of both sides.
Just for fun and fairness.
There are papers out there for hydroxychloroquine.
Give their references too.

As an aside, Atom, I was extremely unbelieving at first based on my medical training. Chloroquine was an antimalarial drug. And a cramp treatment.
Viruses and bacteria or parasites are extremely different and require different mechanisms of treatment.
The medications being for totally different reasons would normally never treat both types of life forms.
My rationale for non belief was based on science, what I had been taught up until that moment.

That changed when I learnt of the mechanisms of interfering with viral RNA reproduction in cells. Scientifically proven.
Are you aware of that?
Of course you are, petal.
Research dating back to 2004 or earlier as an antiviral.
Are you aware of that?
If not, why not?

Why knock the study of it as a helpful treatment when we have precious little else?
You show a great interest in scientific topics.
You certainly have a skeptical mind, with blinkers on.

Ideology.
If the drug does work you would have to thank Trump for helping promote it.
Guess your attitude is best summed up by better millions die than Trump gets any credit, even if vicarious ( He did not invent it though he might take credit).
What a great and commendable attitude, man.

WordPress.com / Gravatar.com credentials can be used.

Arctic Ice


I find the the trend in sea ice age over the last ten years or so a conceptually difficult metric.
Ine of the problems as I have mentioned before is that the less ice you have to start with the less the percentage of multi year ice appears to be in a good recovery year.
Counter intuitively this means that years with low percentage multi year ice are actually making good recoveries.
This might help explain the contradiction between a 10 year pause in ice volumes, sought of a recovery in a way from the previous high falls and a downwards trend in multi year ice for 10 years which also fits in with recovering, not diminishing ice in the Arctic?

In defense of Roger Pielke jun

Atomsk,
I get the drift that the scenario itself is not the outcome
and that the scenario does not have to be real.
and that therefore, a scenario may not be a prediction, only a conditional prediction.

The problem is that you cannot usefully cleave [split] a scenario and a prediction in this way without losing the meaning of both words.

For your analogy I agree that one does not usually try to prove the precept is wrong to show that the outcome is wrong.
That is because a precept or scenario is not falsifiable, You determine the input.
If one uses a different input one would would have to put up a different output.
A scenario can only be a scenario if it is predicating [and hence predicting] a future outcome.

If the situation the scenario is attempting to mimic is shown by time to be different to the assumptions you used that is not a failure of the scenario.
Reality is a different scenario and you cannot falsify either by comparing the outcomes.

RP and I have never tried ” to claim a conditional projection failed, since they claim a predicted scenario didn’t occur.”
It is wrong to say that.
A more apt analogy would be that the child placed it’s hand on the hot stove and it did not burn.

In this case the fact that you claimed the stove was hot enough to burn the child’s hand is wrong.
You did not put enough wood in the fire [wrong assumptions] or did not light the match [check the starting conditions were as you said] or did not run it long enough [dodgy thermometers].

I do not mind people bagging my arguments but I do mind people bagging their opponents unjustly.
Fair enough with me, i make misunderstandings.
Roger Pielke is a true scientist, brought up in a scientific family and background and does not make basic misunderstandings of concepts.like scenario’s and it is just plain wrong to say that he does.

ATTP
“If there’s warming then I think you still need some kind of flux imbalance. My understanding is that quite soon after a perturbation (say, an increase in atmospheric CO2) the LW fluxes can return to balance, but the cloud feedback leads to an imbalance in the SW fluxes, which then dominates the subsequent warming.”
izen “The increase in surface temperature is a result in the greater thermalisation of OLR from the surface in the lower layers of the atmosphere, not in a imbalance in the energy flux for the whole system.”

“If there’s warming then I think you still need some kind of flux imbalance” This bit is very true but emphasises the problem raised by Izen.
If warming is occurring there must be a flux imbalance.
We see this every day when the sun comes up. The GHG concentration does not change **[much] but the atmosphere heats up and the radiating layer goes much further outward.
So some energy has been garnished from the sun and thermalised.

But what happens when the heat input stabilizes say just after midday[** more provisos].
For a short period of tome the energy in equals the energy out as everything is in balance.
Then the radiating layer contracts as the atmosphere cools.

Does the CO2 level affect this pattern? No [* more provisos].
What it does affect though is the amount of atmospheric thermalisation that day.
The atmosphere will be warmer with more CO2 in it.
Not in 100 years but at that lovely moment of equibrilation.
Which occurs every day, usually after midday, though it might occur several times around that time due to albedo cloud changes.

ATTP “quite soon after a perturbation (say, an increase in atmospheric CO2) the LW fluxes can return to balance,”
OK
” but the cloud feedback leads to an imbalance in the SW fluxes, which then dominates the subsequent warming.”

Not sure of this. Feedbacks occur including clouds which is more part of the expected imbalance due to the change in incoming heat.
The SW fluxes can only be variable due to the variable albedo? They temporarily alter the actual heat input which is why you might have several moments of equilibrium usually after midday. The longterm feedback effect amplification is more due to increased GHG [water vapour] in the air raising the ECS not the SW effects.

What responsibility, Doc

Joshua says:
“At any rate – the point being to respect the uncertainty, until we have better data.”
Why start now?
It is a bit late.
Plus it is more than the data,
Every Pandemic presents something novel so past experience does not guide future results.
What was that story about the fellow with the lion on the loose.
Sometimes you have to respect the uncertainty,
Sometimes you have to run. April 28, 2020 at 3:31 am

Mal Adapted
What responsibility, Doc? What are your expectations of scientists? What do you expect from yourself, your family, your neighbors, your country? Just who is responsible for AGW?
IMO, your comment reveals how alien the culture of science is to you.

The line
” d) maintaining research practices that normalize careless use of scenarios in a vacuum of plausibility,” came from Bete Noir, R.P. Who also said,
“As a consequence, the climate research community is presently off-track. Attempts to address scenario misuse within the community have thus far not worked.”

I added “Not to mention a vacuum of responsibility.”.
I fail to see the difference between what he is saying and what I appended, if something is used in a non plausible fashion it is being used irresponsibly.

Very difficult to answer questions about responsibility. It tends to get conflated with blame [responsibility for doing something wrong].
Do you want me to be responsible? I.e. Do things the way you want me to do them.
Do you want me to be responsible . I.e. the cause of AGW? [ or Collectively with skeptics or with humanity?].

I think you have asked a very important question epistemologically.
I do understand where you are coming from, a genuine care for the world.