Watching it as one of the very common types, and our favorite brands of laughter, university love and life, I decided I Would supply it with a whirl. Before stopping to see with sleep immediately connected, I check out 50 parts. Task function to continuing it and however I'd been bogged down with soon and that I never got around. I continued when it comes to a-4-month didn't have occasion for anime or manga during those times and break. However, recently the stars along with summer arranged that I'd occasion to consider and started.
The bill isn't unique, or may it's a masterpiece. However, it really is its merits. The faculty romcom genre was already more lucrative, which isnot the 1st time that folks've discovered one along with abnormal. Moreover, it's not the 1st time that individuals've seen an anime. Plus the results inside the harem (my evaluation, others think that harem isn't right) aren't among the most unique both. But I'll reach that. The adventure, with information from the title as well as the first incident, is targeted around our personality, the faculty, Ore to Kawazu-san no Isekai Hourouki Manga Ryu's delinquent. To Shiraishi Urara, whom I believe about the feminine identity, we are also released upon his release. Unlike Yamada, whois a severe delinquent, Shiraishi may be known as an ideal scholar: interesting, and studious calm. Essentially, they are opposites. The portion happens once the ways causes Shiraishi and walks up. They both journey slide the steps down and though achieving this. After blacking out, Yamada gets up inside the infirmary, in order to realize that he is today in Shiraishi's body within the host to their particular. After a while, they recognize that switching devices is completed using a hug. Around the basis of the title, we're ready to guess you will find each utilizing their own electricity, 7 witches. The ability inside the story isn't the piece however its distribution. It's nothing we'venot viewed as the bit is definitely interesting. However, so just how it truly is executed is what sets it apart. The anime doesn't consider itself. And yes it understands when to become generally an even more extreme, good thriller story, while it should really be a laughter it recognizes. Standard, the item is exciting which is delivered effectively, but isn't masterpiece.
In drawing manga-type figures I dabble somewhat, but I'm no judge of great art. However, really I'll inform this point looks good. the colors are often energetic, and in addition all the capabilities are well-driven and Pop Out. However the key level of this graphics report could be the personality design. The numbers therefore are designed specifically and thus are merely separated from another. Most of the numbers are manufactured with techniques helping to make them hard to forget, and perhaps they are unique inside the other individuals to point their meaning towards the history.
Once I said before, the results aren't just special. The progress occurs forced considering that the series is lowered into 12 problems and even faster and sometimes looks uneasy. The only two witches who in my opinion get any type of advancement that's important are Shiraishi Urara and Odagiri Nene, whois separately my own favorite of the lot. Having a single-position, that's usually just presented in place of explained, their causes are often described for that rest. Because of this, the results are pleasant, but generally lack amount beyond this one level.
I don't are the best critic, and you'll discover merits for this anime. If you don't feel a great deal of while viewing and continue in utilising the right targets, you'll arise content and likely content though you will find problems. The final handles every one of the problems, even though that I truly might really notice returning a distance away. Good, it anticipated and is slogan, but there is a great deal of satisfaction available here. Select what it is: unpleasant romcom having a scattering of bill, a satisfying. You will probably wind-up miserable should you assume more out of this.
Yamada-Kun to 7-nin no Majo was a satisfying watch and had me laughing occasionally. It'd been that I can happily suggest that it is probably worth your time, and a terrific information. It ranks very highly among my anime that is considered, even though that I'venot considered that numerous recently. Should you demand a hefty, plan this is simply not for you -driven situation. I recommend it to everyone who like manga.


The nutshell explanation of how a digital camera works is that light lands on a sensor, which converts the light into electrical signals.
Depending on the kind of camera you're using, how the light reaches the sensor may seem different but the sensor fundamentals stay the same.
The sensor is where most of the megapixel stuff comes from. When you press the shutter button, the sensor (like film in old-school cameras) is exposed to light for however long you have the exposure time set for, which for many ordinary camera users is automatically preset.
Generally, the more pixels packed onto a sensor, the higher the resolution of the images it can produce. A megapixel is 1 million pixels, so a 12-megapixel photo has a resolution of about 12 million pixels. The most recent crop of point-and-shoot digital cameras from manufacturers like Canon, Nikon, Sony etc seem to establish 10-12 megapixels as the new norm for everyday pocket cameras, and some crazy phone manufacturers like Sony Ericsson crammed a 12-megapixel into their Satio mobile phone, the same as Canon's entry-level XSi DSLR and Nikon's D700 pro DSLR. DSLR stands for Digital Single-Lens Reflex, which for the purpose of this article should simply mean a professional camera, like the ones those professional photographers use.
Obviously, there's a world of difference between the image quality you're going to get out each of those. Most of it comes down to the size of the sensor and the pixels. You can fit a much bigger sensor inside of a DSLR than you can inside of a mobile phone, which not only means you can fit more pixels on the sensor, but also fit much bigger ones. Sure enough, the sensors inside of DSLRs are huge compared to the ones in mobile phones. To get really high-resolution smaller cameras and phones, manufacturers pack as many teeny pixels as tightly as they can onto tiny sensors.
The pixels in standard point-and-shoots are not the same kind of high-quality pixels found on DSLRs. So, on a given sensor size, a lower megapixel count with bigger pixels will produce cleaner images hence the professional Canon or Nikon having only 12 megapixels with way better pictures than your 12 megapixel camera phone.
When it comes down to buying cameras for regular people, just keep in mind that more megapixels isn't necessarily more better. It's how good those pixels are that matters.


text:
Q: golang producer consumer number of messages received I have written producer-consumer pattern in golang. Reading multiple csv files and processing records. I am reading all records of csv file in one go.
I want to log percentage of processing completion in interval of 5% of total records including all csv files. for e.g I have 3 csv to process & each have 20,30,50 rows/records (so in total 100 records to process) want to log progress when 5 records are processed.
func processData(inputCSVFiles []string) {
    producerCount := len(inputCSVFiles)
    consumerCount := producerCount

    link := make(chan []string, 100)
    wp := &sync.WaitGroup{}
    wc := &sync.WaitGroup{}

    wp.Add(producerCount)
    wc.Add(consumerCount)

    for i := 0; i < producerCount; i++ {
        go produce(link, inputCSVFiles[i], wp)
    }

    for i := 0; i < consumerCount; i++ {
        go consume(link, wc)
    }
    wp.Wait()
    close(link)
    wc.Wait()
    fmt.Println("Completed data migration process for all CSV data files.")
}

func produce(link chan<- []string, filePath string, wg *sync.WaitGroup) {
    defer wg.Done()
    records := readCsvFile(filePath)
    totalNumberOfRecords := len(records)
    for _, record := range records {
        link <- record
    }
}

func consume(link <-chan []string, wg *sync.WaitGroup) {
    defer wg.Done()
    for record := range link {
        // process csv record
    }
}

A: I have used atomic variable & counter channel where consumer will push count when record is processed & other goroutine will read from channel & calculate total processed record percentage.
var progressPercentageStep float64 = 5.0
var totalRecordsToProcess int32

func processData(inputCSVFiles []string) {
        producerCount := len(inputCSVFiles)
        consumerCount := producerCount
        link := make(chan []string, 100)
        counter := make(chan int, 100)
        defer close(counter)
        wp := &sync.WaitGroup{}
        wc := &sync.WaitGroup{}

        wp.Add(producerCount)
        wc.Add(consumerCount)

        for i := 0; i < producerCount; i++ {
            go produce(link, inputCSVFiles[i], wp)
        }

        go progressStats(counter)

        for i := 0; i < consumerCount; i++ {
            go consume(link, wc)
        }
        wp.Wait()
        close(link)
        wc.Wait()

    }

    func produce(link chan<- []string, filePath string, wg *sync.WaitGroup) {
        defer wg.Done()
        records := readCsvFile(filePath)
        atomic.AddInt32(&totalRecordsToProcess, int32(len(records)))
        for _, record := range records {
            link <- record
        }
    }

    func consume(link <-chan []string,counter chan<- int, wg *sync.WaitGroup) {
        defer wg.Done()
        for record := range link {
            // process csv record
            counter <- 1
        }
    }

func progressStats(counter <-chan int) {
    var feedbackThreshold = progressPercentageStep
    for count := range counter {
        totalRemaining := atomic.AddInt32(&totalRecordsToProcess, -count)
        donePercent := 100.0 * processed / totalRemaining
        // log progress
        if donePercent >= feedbackThreshold {
            log.Printf("Progress ************** Total Records: %d, Processed Records : %d, Processed Percentage: %.2f **************\n", totalRecordsToProcess, processed, donePercent)
            feedbackThreshold += progressPercentageStep
        }
    }
}

redpajama_set_name: RedPajamaStackExchange


Did you know that being a dog owner can make you healthier and give you a longer life? Our canine friends help to lower stress, anxiety, and even blood pressure. Obviously, you want to return the favor and make your dog's life as long and healthy as you can. Dogs need exercise to be healthy. So do you. Why not exercise together? Here are some ideas.
It's a great form of exercise for you and your dog. Plus it is a great time to talk with your spouse! If you have a dog that likes to stop frequently and sniff everything in sight, though, this may not be as beneficial to you as it is for her, but it's still a lot of fun. Walking or running is natural and easy for both of you. Keep in mind that your dog doesn't wear sneakers, and hot pavement or walking through the woods might damage the pads on his feet. Be sure to find somewhere clean and clear to exercise, and if you're in a public place, keep your dog on a leash so that he doesn't get into trouble.
If you live near a river or a stream, or even if you have your own pool, you and your pooch will have a great time swimming together. Swimming is low-impact, so it's easy on your joints and hers. Be careful with short-legged dogs, though – they're often not good swimmers and they can get tired out easily.
Frisbee, Fetch, ball, and other games where your dog can chase things will get both of your hearts pumping. Put some extra effort into jumping when you throw or even chase the toy with her. You'll both enjoy the game and get a healthy workout in. Again, be careful where you are throwing – it's very easy for a dog to get overly excited and run in front of a car after a toy.
If you live near an obedience course, this can be extra fun for both of you. Run and jump over the hurdles with your dog and you'll both feel the burn. You never know – your old dog may even teach you some new tricks!
Keep in mind that dogs are a lot like humans – they need to build up to an exercise routine. Don't expect your dog to run a marathon with you if he's never left the yard. Make sure you're both well hydrated, take the proper precautions, and you'll both be on your way to being the healthiest dog and owners in the dog park!
How do you exercise with your pet?
I love to exercise with my dog. Last summer I would put the baby in a stroller, leash the dog, and walk 2 miles a day. I can't wait for the warm weather to get here again!
Oh, I love walking with my dog in the warm weather, Amber. I really hate cold weather, and rarely get her out and about. Is it summer yet?
I took my dog to the vet to make sure he could run with me. He is only 7.5 lbs and I am training for a marathon so I wanted to see what distance would be safe for him. Our vet said as long as he is happy and I am not dragging him let him run. He is now out running me and well it is quite embarrassing when I have to stop and he is impatiently waiting, lol. I love having him as my running partner. They need exercise to stay healthy too.
That is hilarious, Jennifer! I wish my dog could run with me. She is a beagle, and is VERY easily distracted. She'll see a squirrel and go in one direction then she smells something and stops cold << not conducive to running!
Great ideas.....I'm pretty allergic so no exercise with pets for me, but I imagine it's great for both owner & pets!!
I don't have pets but we always had outside dogs when I was growing up. It's amazing they always got plenty of exercise themselves.
I have 2 small dogs and they have not received the exercise they should. We started to do long walks each day. That is a great step in the right direction.


text:
Thoughts on Antibody Persistence and the Pandemic
By Derek Lowe 22 June, 2020
The fundamental challenge of dealing with this pandemic is uncertainty. There are just too many important things that we don't know – and what's more, they aren't easy to find out, either. We've seen that with the waves of optimism and pessimism about various therapies, just to pick one. As everyone has been learning (if they didn't know it before!), getting solid clinical data is not easy. The good numbers don't come quickly and they don't come cheaply, and data that are fast and cheap tend not to be any good.
That uncertainty extends deep into the biology of the disease. Let's illustrate that with a look at a paper that's come out recently that has shaken a lot of people up. It's a valuable look at a controversial topic: people who have definitely been infected with the coronavirus, but who are asymptomatic. There are very important questions about this situation, among them how infectious such patients are and for how long, what might be different in their immune response as compared to people who become more overtly ill, and how the longer term effects on immunity might differ as well. And not least: how many such asymptomatic patients are there in general, and are they more common among some parts of the population than others? All of these questions are very important to our understanding of the pandemic and our responses to it, and none of them are as well-worked-out as we need them to be.
This group (from China) looked at 37 patients who tested positive (by RT-PCR) for coronavirus infection, but who had not displayed symptoms before testing (and continued to show none during subsequent monitoring), and compared them to the more well-studied symptomatic patients. One thing that stands out from a public health perspective is that the asymptomatic group had a much longer period of viral RNA shedding. That is not what one would have wanted to hear, since these are the people who are walking around without realizing that they're sick at all.
But it's also important to realize that this report, as with so many reports of viral shedding, it looking at it by detection of viral RNA. That does not mean that there is infectious virus present. (This distinction has confused a great number of reports about the persistence of the virus on surfaces as well). We still don't know how long infected patients (symptomatic and asymptomatic) are shedding infectious virus – those are far harder data points to obtain than just detecting viral RNA. I should note that this goes for the recent reports, which were all over the media, about the possibility of spreading coronavirus through flushing toilets. Now, I think that closing the toilet lid is a pretty good precaution, because it's an easy enough thing to do. But the spread of infectious virus through toilet aerosols has not been proven, to the best of my knowledge. You can find viral RNA in sewage, and monitoring it could be a useful public health measure in water-treatment plants. But infectious virus is something else again.
Now, when you hear of patients who are infected but are showing no symptoms, you could have a mental picture of a stronger immune response that's keeping the virus knocked down more. But it's clearly not that simple: this paper shows that the asymptomatic patients had a weaker antibody response that tended to disappear during the convalescent phase. That's the result that's gotten a lot of attention – as it should – although it's important to not run with it too quickly. Remember, there is more than one type of immune response – you have T cells pitching in as well. That response is one of the great unanswered questions of the epidemic, from what I can see. We already have data about some of the T cell responses in symptomatic infected patients as compared to uninfected ones, and one of the most intriguing things about that earlier work was the finding that 40 to 60% of those uninfected people had CD4+ T cells that appear to already recognize the new coronavirus. The speculation is that this could be immune memory of past infections with other coronaviruses (such as the ones that can cause common-cold illnesses), and that they are cross-reacting with the current pathogen. (Update: from the comments, this work that raises the possibility that the T-cell response is from zoonotic coronavirus infections that we hadn't appreciated). That's very much in contrast to the antibody situation in uninfected patients – it seems clear that the human population had raised no circulating antibodies to the new coronavirus before the advent of this pathogen. Prior infection with other coronaviruses does nothing for you on the antibody side.
And that's the missing piece from this new work. It is possible that these asymptomatic patients are showing a weak antibody response because they already had a more robust T-cell response ready to go. Now, this hypothesis could be wrong, but it has to be tested. In the same way, it's possible that there is a percentage of the population that, because of their T-cell profile, are more likely to have only such an asymptomatic infection or perhaps to not become infected at all. That's a very important thing to clear up, but it's unfortunately a lot more labor-intensive to profile CD4+ and CD8+ T cells in people than it is to profile their antibody responses. This applies to the vaccines under development as well: T cell effects are an important component of vaccine efficacy, but there's a lot that we don't understand about how various vaccines raise such responses. There have been many reports of recovered patients who never seem to have raised much of an antibody response at all, and it's not yet clear how they cleared the virus: was it the innate immune response that did the job before the adaptive system kicked in, particularly in younger patients? Was it the T-cell response instead? We just don't know yet.
So my advice is not to panic, but not to be complacent, either. The complexities of the immune system mean that we have a whole range of possible situations in how this pandemic is unfolding. At the most optimistic end, it is possible that a larger percentage of the population than we realize might already be protected (to some degree) from the coronavirus. Unfortunately, it's also possible that almost everyone is, in fact, still vulnerable and that we just haven't seen the virus run through most of the population yet. Everyone will have seen the various population surveys with antibody testing that have suggested, in most cases, that a rather small percentage of people have been exposed. Think of the various ways you could get such a result: (1) it's just what it looks like, and most people are unprotected because they have so far been unexposed. (2) the antibody results are what they look like – low exposure – but people's T-cell responses mean that there are actually more people protected than we realize. (3) the antibody results are deceiving, because (as this latest paper seems to show) the antibody response fades over time, meaning that more people have been exposed than it looks like. And that means you can split that into (3a) the antibody response fades, but the T-cell response is still protective and (3b) the antibody response fades and so does the T-cell response. That last one is not a happy possibility.
You can extend this thinking to the effects of the coming vaccines. The protective effects of the antibody response versus the T-cell response are going to be important to figure out, of course. And keep in mind, the timelines that we're seeing do not allow for time to see how quickly either of these responses might fade. So we could be in a situation where people would have to get re-vaccinated with a different agent after a few months when some of this comes into better focus. There's no particular reason why the first workable vaccine to make it through trials should be the best long-term answer, but we also don't know how much these things are going to vary, either.
So we need to take this new paper and its results about antibody persistence seriously, but we also need to keep our eye on the T-cell situation as well. We're not going to know the whole picture until we know more about both of those. And in the end, we're not going to know about the protective effects of recovery from a coronavirus infection, or the protective effects of being vaccinated against it, until enough time has passed in a large population of both cohorts. You'd want a faster, less difficult readout for those things, but I'm just not sure that there is one.
94 comments on "Thoughts on Antibody Persistence and the Pandemic"
David Borhani says:
Derek, you're missing a "not":
This group (from China) looked at 37 patients who tested positive (by RT-PCR) for coronavirus infection, but who had *NOT* displayed symptoms before testing (and continued to show none during subsequent monitoring)…
Jeez, I sure am. Gotta whack the forebrain into not doing that sort of thing.
Sue Fics says:
Please, whatever you do, don't whack your forebrain! World needs you as you are!
I think the virus whacks the forebrain for you…seen the study about invasion through the nose and olefactory bulb into the forebrain…
Reverse axonal transport up the olfactory bulb has been studied off and on for decades. In his book on prions/slow encephalopathies Deadly Feasts, Richard Rhodes repeates an anecdote Carleton Gajdusek told about having terminal cancer patients volunteer to snort atropine to dry out their nasal passages, then inhale fine gold dust through their noses… on autopsy the gold dust was found to have traveled up through the olfactory bulb in those patients… so all sorts of things can travel that way, if they're the right size.
Derek, I find a good, strong medium or dark roast breakfast blend, 2 cups, repeat prn helps me with typos.
Then again, I grew up in the marshes outside New Orleans drinking that. It's the only way I know…. 🙂
But when I try to use HTML, all bets are off.
Might be my problem, because I don't even drink coffee. My wife can't figure out how I walk around on two legs without it.
Md Saiful Islam Roney says:
I don't drink coffee, tea. I'm an Aquaman.
still here says:
There cannot be that many coonass chemists outside of the oil industry. I'm from Thibodaux.
Minored in chemistry at LSU, finished up in tech writing at La Tech. I'm from St. Charles Parish, not far from Thibodaux.
Chris Boeres says:
The caffeine intake noted in the comments has been very effective for me too though it does effect blood pressure so be advised. A questing from the peanut gallery anything out there yet on sarscov2 effecting patients on calcium blockers particularly on CD4+T leukocytes ? Asking for a friend
Name * says:
"This group (from China) looked at 37 patients who tested positive (by RT-PCR) for coronavirus infection, but who had displayed symptoms before testing"
Should probably be "who had NOT displayed symptoms"
I noticed that too
Any thoughts on whether vaccines (mostly Chinese) using the original Chinese virus virus will work on the mutated European virus?
Dumb question. They pulled these patients from people living with another confirmed case. Does it stand to reason that if I lived with a person who had an active infection, and they did a nasal swab — they would find viral material but in reality no infection?
Charlie,
The virus has *barely* changed globally, so the idea that there's a European version/strain and a Chinese one (Or an American one or … etc) is wrong. Our ability to track viral lineages is based around precise observation of minor variations, not meaningful differences between the virus across regions. It is highly likely that a vaccine developed anywhere would work anywhere else, because as yet there is no evidence the virus is meaningfully different.
Culturing nasal swabs on a lawn of human (HeLa?) cells in culture is slow and expensive, but it would distinguish the persistence of viral RNA (in neutralized virions) from an active infection.
Kevin Law says:
Damn! That Henrietta Lacks just keeps on giving and giving.
Yes, that's basically how it's done. Plate a bunch of easy-to-culture but infectible cells (Vero monkey cells are typically used, instead of HeLa), then add dilutions of your viral sample, and then count the number of "plaques" formed when an infectious virus kills a cell, spreads to its neighbors, and kills them too.
In principle, any old cell culture lab could do this all day long, if nobody cared about biosafety. But since this kind of assay inherently produces a lot of highly concentrated and definitely infectious virus in the process, it has to be done using biosafety level 3 containment. And right now, all the BSL3 labs and personnel are already running well beyond their normal capacity, trying to research the coronavirus and discover potential treatments.
Why'd you want to bring HeLa into your lab if you didn't absolutely have to? As I understand it, the precautions needed to keep HeLa from spreading into other cultures are part of why working with it is so expensive.
Of all the human coronaviruses. What are the T-cell and antibody response longevity time frames?
In other words, for each human coronavirus, how long does immunity last?
Note that "T-cell and antibody response" does not imply immunity.
What I've seen on studies on human corinaviruses, infection gives you immunity for a year or less from infection with the same virus.
daksya says:
I posted this earlier but it's relevant here:
An interesting preprint in this regard is at
https://www.biorxiv.org/content/10.1101/2020.05.26.115832v1.full.pdf
"For the management of the current pandemic and for vaccine development against SARS-CoV-2, it is important to understand if acquired immunity will be long-lasting. Therefore, we tested if individuals who recovered from SARS 17 years ago still harbor memory T cells against SARS-CoV-1. Hence, their PBMC (n=15) were stimulated directly ex vivo with peptide pools covering SARS-CoV-1 NP (NP-1 and NP-2), NSP7 and NSP13 (Figure 3A). This revealed that 17 years after infection, those individuals still possess virus-specific memory T cells, and similar to COVID-19 recovered patients, we detected T cells reacting almost exclusively to NP and not to the NSPs (Figure 3B/C). Subsequently, we tested if the NP-specific T cells detected in SARS recovered patients could cross-react with SARS-CoV-2 NP peptides (aa identity = 94%). Indeed, although at lower frequency, T cells in all 23 individuals tested reacted to SARS-CoV-2 NP (Figure 3D, 4A). In order to test whether these T cells could expand after encounter with SARS-CoV-2 NP, their PBMC were stimulated in vitro with the whole battery of NP, NSP7 and NSP-13 peptides and the quantity of T cells responding to SARS-CoV-2 NP, NSP7 and NSP13 was analyzed after 10 days of cell culture. A clear and robust expansion of NP-specific T cells was detected in 7 out of 8 individuals tested (Figure 3E). Importantly, and in sharp contrast to the T cell response to NP peptides, we could not detect any T cells reacting to the peptide pools covering NSP13 and only 1 out of 8 reacted to NSP7, despite in vitro expansion. Thus, SARS-CoV-2 NP-specific cross-reactive T cells are part of the T cell repertoire of individuals with a history of SARS-CoV-1 infection and are able to robustly expand after encounter with SARS-CoV-2 NP peptides. These findings demonstrate that virus-specific memory T cells induced by beta coronanvirus infection are long-lasting, which supports the notion that COVID-19 patients would develop long-term T cell immunity. Furthermore, our findings also raise the intriguing possibility that infection with related viruses can also protect from or modify the pathology caused by SARS-CoV-2 infection."
Elane Imgoven says:
Until we have more widespread testing (both for viral presence, and for antibodies), we won't really know what the infection rates are, will we. I have just enough background in statistics to be aware of the pitfalls in population sampling.
Thanks as always for an illuminating explanation of stuff that this mining engineer would otherwise not grasp.
/Elane
In New York City around 20% of the population had antibodies in late April. 20% is large enough to avoid some of the statistical pitfalls.
The 1% fatality rate back from Wuhan times is still a surprisingly good way to estimate past infections, multiply the number of deaths in a region with 100 to get a reasonable rough estimate of the cumulative number of infections 2-3 weeks ago.
For countries like the US or Canada this gives you the estimate that around 3% (US) or 2% (Canada) of the population already had a COVID-19 infection. This has to be taken with a grain of salt, but any hopes for numbers already > 5% wouldn't sound realistic to me.
I definitely wouldn't count on higher numbers (in terms of making any decisions based on the hope that more people are protected).
But there does seem to be some evidence of protection of some form other than antibodies — e.g. the comparative rarity of serious (or even symptomatic, maybe?) infection in children.
And extrapolating based on a 1% fatality rate would require that the age profile of the infected population is the same. COVID fatality rates vary so sharply with age that this can make a huge difference (see Singapore, which has an anomalously low CFR since nearly all infections are in a worker population, therefore younger).
My "reasonable rough estimate" does not apply in populations that exclude the COVID-19 risk groups because everyone is under 50 and not obese, like in your example or on Navy ships.
But it's not quite that simple… I mean, there are people over 50 in Singapore. It's a matter of who gets infected, not just who is present in the population. And lots of things could affect that; actual government measures as in Singapore, but also individual behavior and pre-existing demographics (population density, age of working population, % of single-person households, % of multigenerational households, etc. etc.)
I wouldn't expect to see the more-than-order-of-magnitude difference between Singapore and places like Lombardy/NYC very often, but even in more "normal" situations (say Texas versus New York) the difference could be large enough to make extrapolating based on a fixed IFR problematic.
Lorry Turner says:
Thanks DL.
To add another dimension: should we worry about the possibility that 65+ vaccine recipients are less likely to have the capacity to mount a good response to a vaccine? Or that mounting a good response to the vaccine correlates with existing immune response (ie. those who would have combatted the infection fairly well anyway). Guess the vaccine could still be beneficial in preventing transmission from younger/healthier individuals to others, but then how would you convince those to take it beyond relying on civic duty?
"We already have data about some of the T cell responses in symptomatic infected patients as compared to uninfected ones, and one of the most intriguing things about that earlier work was the finding that 40 to 60% of those uninfected people had CD4+ T cells that appear to already recognize the new coronavirus."
I'm not sure why this hasn't gotten more press since its discovery. In theory this could change _everything_ about the way the disease has been modeled.
nobody says:
Cross-immunity from other coronaviruses also opens up the prospect of using minimally hazardous (e.g. common-cold level danger) coronaviruses as a stopgap vaccine.
This is old news, and no one is assuming that there would be immunity against COVID-19 after infection with a different coronavirus.
The idea has been around for months that recent infection with a different coronavirus might increase the chances that the infection is mild if catching COVID-19, but the effect seems small enough that this is hard to prove (or disprove) and barely relevant in practice.
At the most optimistic end, it is possible that a larger percentage of the population that we realize might already be protected (to some degree) from the coronavirus.
that->than?
Please delete.
Thanks for the work that goes into this blog.
Steve Scott says:
Many concerns have been raised over a vaccine's ability to protect the elderly with their less efficient immune systems. It has been suggested that some vaccines may not work well for 65+ and others might, eliciting a stronger immune response. But the best ones for seniors might not be the first to be released.
I think the timeline for any vaccine based on a modified active virus (SARS-COV2 or any other virus modified to present SARS-COV2 proteins) is going to run into big delays. I can see how these vaccines could offer short term protection and very little if any long term protection. Showing protection for a few months is very different than showing protection for 12.
To go progressively further out on a limb. Nuclear Factor-kappa Beta hyper-activation is likely critical for the overimmune responses to coronaviruses.
By extension the use of effective NF-kB inhibitors should be explored with more urgency than currently seems to be the case.
Most of those individuals with co-morbidities (diabetes, hypetension, Alzheimer's disease, etc.) have high activation of NF-kB to begin with so they are more likely to be susceptible to the virus and to its damaging effects.
NF-kB activation via oxidative stress and inflammation may inhibit T cell activation. This may explain in part why NF-kB inhibition also appears to limit viral loads.
P.S. my caption test was two + 2=
Wish it were that easy.
Bali is still having great resistance and no one knows why.
asiatimes.com/2020/06/us-scientists-seek-answers-to-balis-covid-19-secret/
Big Mystery says:
The secret is to count covid cases as dengue cases.
They might just have had few initial cases when they went into lockdown.
In Europe most countries went into lockdown at the same time, and the different numbers of infections and deaths in these countries can be largely explained by the number of cases at that point (in Italy COVID-19 has spread for months, in other countries there were very few cases).
"40 to 60% of those uninfected people had CD4+ T cells that appear to already recognize the new coronavirus. The speculation is that this could be immune memory of past infections with other coronaviruses (such as the ones that can cause common-cold illnesses), and that they are cross-reacting with the current pathogen".
Well this supports an idea of mine of a month ago. Stop the pandemic in its tracks by giving everyone in the world an infection with the 4 coronaviruses known to cause the common cold. People reading that post were worried about something called immune enhancement as seen with Dengue, but I'm not.
For details please see https://luysii.wordpress.com/2020/05/24/a-way-to-end-the-pandemic-an-update/
Andrew P says:
Do you really think the 4 known common cold coronaviruses are the only ones circulating? I can't believe that. Lots of new viruses must have come from China over the years. As long as there isn't a lot of death, nobody will notice. I mean, how often is the virus that causes a cold, cough, or sinus infection sequenced in a lab? Unless the person is serious enough to be hospitalized, the probability is next to nil.
Among the coronaviruses found in homes is feline coronavirus. From the wikipedia article:
"Feline coronavirus is typically shed in feces by healthy cats and transmitted by the fecal-oral route to other cats. In environments with multiple cats, the transmission rate is much higher compared to single-cat environments. The virus is insignificant until mutations cause the virus to be transformed from FECV to FIPV. FIPV causes feline infectious peritonitis, for which treatment is generally symptomatic and palliative only. The drug GS-441524 shows promise as an antiviral treatment for FIP, but at the moment it's only available on the black market and still requires further research."
There are also infectious coronaviruses affecting pigs and dogs in the same species Alphacoronavirus 1
as feline coronavirus. While we think SARS_CoV2 was originally spread zoonotically from an animal host in China to humans, elsewhere the virus jumps from humans to pet cats and other animals (including mink herds in the Netherlands).
No news on whether feline or canine coronaviruses spread zoonotically to humans, even asymptomatically. Some researchers have found antibodies to coronaviruses which are not the four known to cause "common colds". More work's needed to see what coronavirus(es), exactly, those antibodies are associated with.
There's also the possibility that they saw longer viral shedding just due to starting the clock sooner. From the cases that became symptomatic while being studied (and were then excluded), we can presume that some people in this population entered the study up to 17d before they would have started showing symptoms if they were going to, while studies of symptomatic patients don't enroll people 17d before they are symptomatic patients. I don't see anything to suggest that they tried to correct for this (or how you would, aside from getting a big population of infected people, studying them all, and splitting them into symptomatic and asymptomatic groups to compare retrospectively).
BigSky says:
The exclusion of IgA and emphasis (and this reported subsequent "loss over time") in blood prick IgG really doesn't add much to the field does it???
The unusual focus on a blood Ig that is incidental to a respiratory infection to the exclusion of a respiratory Ig integral to the entire dance points to the importance/ease of blood vs. sputum recovery and reagents to report IgG vs IgA measurement.
Has anyone seen good data on the IgA levels in various patients and infections over time 'cause that would be interesting to read.
Just saw an interesting pre-print that addresses IgA!
https://www.medrxiv.org/content/10.1101/2020.06.22.20137141v1.full.pdf+html
"In asymptomatic patients, we show an early burst of IgA that may rapidly and effectively eliminate the virus in the respiratory mucosa and prevent a full adaptive immune reaction. Accordingly, IgG is produced in low amounts and becomes undetectable after 6-8 weeks. An intermediate response is observed in patients with mild disease without the early IgA peak and characterized by a late, but modest IgG and IgA production, suggesting a minor adaptive immune response. Further studies are necessary to establish whether specific memory persist and for how long after asymptomatic and mild disease. "
That's very interesting!
Not to be alarmist, but before taking a vaccine that raising IgG and not IgA, I'd very much like to know what the course is of SARS-CoV-2 in that immunological situation. Hopefully a cold with no systemic involvement.
Yes, I agree. My guess is that rasing IgG without IgA will lead to most being protected from severe invasive respiratory disease, but not mild infections….but if those mild respiratory infections flare, will you still see the weird, likely post-infectious inflammatory sequelae in a subset of patients…i.e. MIS-C in kids? Hopefully raising IgG will protect from that, but I don't know if we understand enough to say that. And from a broader population health point of view, it seems like the current vaccine approaches will allow the vaccinated to spread the virus. Imagine telling people who get the vaccine that they still need to wear masks and socially distance to protect others…letdown of the century! Is anybody looking at any inhaled or other approaches to raise IgA or innate defenses in the respiratory mucosa? This is the "frontline" of viral entry into the body and it seems like there is little attention to strategies to fortify it!
TB is not covid 19, of course. But we know that in case, the BCG vaccine elicits IgG without much IgA and although it protects from miliary TB( infection be the same organism of non-lung tissues) it fails utterly to protect from infection on the lung surface (the common infection)
By the time we have an effective covid 19 vaccine, we may know a lot more about how to make an effective TB vaccine
(danger: layman speculation below)
The recent Italian retrospective wastewater PCR testing results point to the emergence of SARS-CoV-2 in parts of Italy in mid-December. Given how quickly SARS-CoV-2 spreads in the population, it's very hard to square a December introduction with the very low levels of antibodies detected in population-level sampling in Italy. It seems to me that either our understanding of R0 is vastly wrong, or antibodies fade so quickly that many historical infections cannot be detected by antibody tests and we have no idea how many people have been infected.
I have no explanation for why it took several months for the Italian outbreak to go from levels of population infection large enough to be detectable in wastewater to causing a spike in excess mortality. There's no obvious way to reconcile these data points.
If unmitigated R0 in Italy was at or slightly below 2 the data would match nicely.
Such an R0 value would be within the range of previous estimates.
Exactly. The sky-high ROs early on were mainly a function of testing coming on board to finally detect transmission that had already been ongoing for weeks or months.
Additionally , apparent high ROs are largely driven by cluster events ( nursing homes , meat packing plants , etc. ) , and early transmission in many countries could have been largely non-cluster in nature , for example if the first people infected were at some international event and then carried the virus to scattered places around the globe , only later to find their way to other cluster hotspots.
We don't even know for sure that patient zero was in China , much less Wuhan , and we seem to have constructed roadblocks to discover the answer to this important question :
https://www.latimes.com/california/story/2020-06-21/babies-children-december-deaths-join-the-wait-for-covid-19-testing
Do we know whether antibody-dependent cytotoxicity requires COV2-specific anti-spike/RBD antibodies? If not, could this be the basis of protection against serious COV2 infection and disease provided by antibodies to other coronaviruses?
Valdis Andersons says:
According to this pre-print, the cross reactivity is not from other HCoVs but from some other zoonotic CoV(s):
https://www.biorxiv.org/content/10.1101/2020.05.26.115832v1
If I understood the paper right, then they basically went T cell hunting and found some. Then they tried to map them back to the pathogens they're for and came up empty when comparing with the 4 Common Cold ones. They did not investigate what the animal CoVs could be, just noted that there could be a number of them that match the T cell targets.
Another intersting bit was that the pre-existing T cells (from 2 years ago) had a potentially better target recognition against SARS-cov-2 than the actual T cells from recovered SARS-cov-2 patients.
Now, that's interesting. Just added a link inside the body of the post – thanks!
Jeffrey L Bell says:
Shades of CowPox.
>>>You can find viral RNA in sewage, and monitoring it could be a useful public health measure in water-treatment plants. <<<
https://www.biobot.io/covid19
Early on, my county did this, bought testing of the sewage to see if the virus was more widespread then the meager testing showed. But now the state is on a push to TEST, TEST, TEST and if they use all of the kits they bought they will have tested 25% of the population!
Too many scientific geeks around here, everything seems to be data driven.
Papers from that group…
https://medium.com/@biobotanalytics/testing-for-covid-19-beyond-the-clinic-using-wastewater-epidemiology-to-proactively-detect-ede0cbf81e49
Dreamed up by MIT people.
Don't know about spreading infectious virus, but the spread of bacterial pathogens in infectious form to all the surfaces in a bathroom by aerosol is well demonstrated. Not DNA/RNA, infectious material to plates which showed colony growth. Not only that, but for pathogens that managed to form a biofilm in the toilet, multiple flushes did not eliminate the tendency to spread infectious particles.
Proving that that particular method was what spread an actual infection from human to human is much, much harder, but the possibility is certainly there.
The oral-fecal route is critical for a bunch of diseases (polio, cholera, typhoid…) Sanitary sewers, potable water, and hand-washing remain crucial for the Public Health. But in the case of Covid19, infection seems to be overwhelmingly air-borne respiratory-tract to respiratory tract, unmediated.
FlushingMeadows says:
Re. spreading coronavirus through toilet flushing and subsequent aerosol dispersion of infected fecal particles. This was shown for the original flavour SARS CoV at the Amoy Gardens apartment complex in Hong Kong:
An unusual plumbing configuration was the culprit, but it's definitely possible …
Thanks for an interesting post. I do wonder whether the concern about these weak circulating IgG responses in asymptomatics is as bad as some are speculating and this is more an issue of inadequate measurement of the immune response. If they remained asymptomatic the entire time, their immune system collectively (i.e. innate, t-cell, IgA, IgM, IgG, etc) must be doing something right…it's just not doing something right that we are measuring when we focus almost exclusively on circulating IgG! If it were shown that these asymptomatic positives with declining IgG levels got re-exposed and then became symptomatic or seriously ill, then I would worry! The abstract says "These data suggest that asymptomatic individuals had a weaker immune response to SARS-CoV-2 infection." Um, how can you knock their "immune response" as "weak" when they stayed asymptomatic! Would we not all want that immune response? Is IgG level synonymous with the entire immune response? Don't forget to actually look at the patient, not just one of their test results!!!
The prevailing paradigm is that a robust IgG response is "good," the marker of a strong, protected immune response to COVID-19. But maybe in some people, the other parts of their immune systems make a big, lasting IgG response unnecessary….and that is not a bad thing if they stay asymptomatic!!!!
On the flip side, I wonder if in some patients, especially those who get severely ill, a robust IgG response should not be knee-jerk celebrated as "good" but rather viewed in context as the result of the failure of the non-IgG immune response that made all that IgG production necessary. After all, the severe forms of the disease are associated with an out-of-control immune response!!! "I went to the ICU and all I got were these lousy (yet Robust!) antibodies!"
I wonder if the fact that vaccines are not producing sterilizing immunity in monkeys goes along with view. Maybe an intramuscular vaccine will produce strong IgG responses that help prevent severe invasive disease…but won't stop recipients from getting a mild respiratory tract infection, perhaps asymptomatic. So, just like a mild resp infection in someone with strong non-igG immune response produces little IgG, producing strong IgG through IM vaccination will do little to stop those mild resp infections. As some have noted, perhaps you need a way to increase mucosal IgA (something inhaled) in order to sterilize. But since that is not going to happen, we could have a situation where people who get vaccinated are mostly protected from severe disease…but those who refuse vaccines or don't mount an adequate response to them might face continued risk because even the vaccinated and partially protected will be able to spread the virus to them…especially if they shed as long as those in this study!
It seems like prisons such as Marion and Pickaway in Ohio would be ideal research populations since most of the inmates there tested positive in April. Why didn't all test positive? How many have antibodies? What are the true asymptomatic and fatality rates?
Have researchers been able to study these groups?
Inmates as research populations are ethically problematic, because consent is problematic; they are powerless.
That would be the case for research in which various treatments would be studied and compared, but mere compilation of biostatistics surrounding COVID-19 in the prison setting, in which inmates' risk of morbidity or mortality didn't vary whether they took part in the research or not… it's hard to see an ethical conundrum there.
All you'd be doing is tabulating prisoners' previous experience with COVID-19, and existing antibody titers, not varying their treatment or other risk factors for the disease.
It's my understanding that even a blood-draw constitutes a "search" and requires consent or a warrant
I assume that any reputable CRO or researcher would obey the Helsinki Declarations on biomedical research and obtain an informed consent from all subjects, incarcerated or not.
Aidan chappuis says:
I have a con-law background, not a bioethics one, but isn't the definition of a search there (including blood draws) for fourth amendment purposes? I.E., police need a warrant for a blood draw for say a DUI. I didn't know/don't think the fourth amendment is that relevant to prison bioethics, and it doesn't really apply at all in prisons anyway.
Not commenting on the (lack of) ethics of U.S. prisons, just the law
Another problem is you'd be depending on the prison medical system, and in the US at least prisons have a very bad reputation when it comes to correctly identifying medical problems.
White science says:
That's all very interesting but I would ask an expert idiot. There is a consensus here, mainly carved by the likes of cravatt at scripps.
idiotraptor says:
To date, discussion about the role of innate and humoral immune mechanisms have dominated the focus of primary anti-SARS-CoV2 immunity to the near exclusion of adaptive T -cell mediated responses. It's been twenty-five years since I was actively involved in research studying anti-viral immunity to orthomyxo/paromyxovirus infection in mice and people. The experimentally-based paradigm for these and most other viral agents was that virus clearance and resolution of primary infection was principally T-cell mediated. Generation of virus-specific T cells always precedes production of protective antibody. Understanding the immune response to and the epidemiology of SARS-CoV2 in humans is complex and evolving. In vitro cellular immune assay and reagent development as well as patient lymphocyte procurement can require more time and technical complexity than development of antibody-based screens and assays. Still I find it curious that until recently comparatively little discussion of SARS-Cov2 specific T cell responses in clearing primary infection has been apparent. Others better read than myself please feel free to comment.
Derek and readers, keep up the thoughtful and informative work.
Here is a simplified hypothesis: the coronavirus in severe cases disables t cells while overactivating other parts of the immune system (a cytokine storm).
Some potentially helpful research regarding T cells.
Daren Austin says:
When you want perspective, you need to step back. Only 10 subjects, but TWENTY YEARS of coronavirus infection monitoring says that immunity is unlikely and reinfection occurs about every 30 months.
Darby says:
I'm confused by that study – they seem to have defined "reinfection" by a rise in antibody levels, plus something about influenza-like symptoms (including fever, which is rare in colds) in some. Wouldn't a re-exposure cause a rise in circulating antibodies?
They measured virus-specific antibodies for each strain :
"…We used a relatively small part of the N protein as the antigen in our tests, to most specifically identify infections by each virus individually. "
One more critical finding:
"Additionally, upon discovering that COVID-19 patients had significantly higher concentrations of cytokines, The authors suggested that rather than directly attacking T cells, the COVID-19 virus triggers a cytokine storm, which then acts to drive down T cell numbers."
https://www.id-hub.com/2020/05/01/low-t-cell-counts-affect-outcomes-covid-19-patients/
TallDave says:
good point on uncertainty… remember the imminent ventilator crisis?
outcomes highly contingent… effective treatments may (or may not) reduce vaccine urgency
if we're fortunate, by the time vaccines are available COVID death rates may be so close to nil that the major challenge is persuading enough to vaccinate
catspyjamas says:
Nice article, thank you . Given the polyspecifity of T cells why are you assuming that prior exposure to coronas is what's needed. Maybe just a robust and diverse T cell repertoire does the trick. And would explain why the younger folks are generally more resistant
Does anyone know whether this preprint makes sense?
It's a tiny sample size, of course, but if valid, it would at least be an "existence proof" (that people can be infected, clear the virus, and still test negative for antibodies).
I don't think they proved the point. None of the "contact" patients (i.e. the group with the patients that presumably cleared the virus sans antibody response) tested positive by PCR. Only positive by "symptoms".
I'm not so sure that their T-cell assays adequately ruled out non-COV2 coronavirus reactivity , either.
That said , I think it's possible , if not likely , that some people clear a COV2 exposure before the development of a COV2-specific antibody response could be detected. To the extent that antibody is required , I think preexisting cross-reactive antibodies might do the job. I'd still expect the immune system to generate some level of COV2-specific antibody capability , however low.
A simple enough question for someone out there. Is the virus test specific for SARS-CoV-2, or does it return a positive result for any coronavirus infection? Presumably the antibody tests are also selective for the novel coronavirus?
Presently there are multiple antibody tests available and being used as allowed under FDA EUA. I don't know details, but I suspect they differ in sensitivity (limit of quantification) and possible their antigenic specificity as well.
Just wanted to say thanks for an incredibly informative article.
In case folks didn't see this today – a preprint of an NIH paper entitled, "Serologic cross-reactivity of SARS-CoV-2 with endemic and seasonal Betacoronaviruses." As far as I can tell (not an expert in this by any stretch) this is cross-reactivity of antibodies, not the T-cell cross reactivity most have been discussing.
It does corroborate the earlier preprint I linked to. They found two instances of cross-reactive antibodies dating from testing pre-2000. I don't think this should be viewed as surprising. Of course, does low antibody titre and cross reactivity generate any protection – or antibody dependent enhancement of infection? So much unknown.
What I am about to share is personal experience, it's not a scientific study, but I think sometimes eye-tests should also be considered.
Me and a student of mine both had COVID-19 back in the middle of March. It is most likely that I infected him back then, even though we had very minimal contact in a closed space on the day when I started developing very mild symptoms. He tested negative around April 1st. I had more severe symptoms, and was in hospital as a precaution for 16 days. He is a teenager and only had mild symptoms – fever and cough for a couple of days – much like a common cold. He donated blood plasma two weeks ago, so his level of antibodies was still high. A week ago he was in close contact for a couple of days with a person who turned out to be positive for the virus (The person had the virus for sure when they met). My student has not had any symptoms, he has been in close contact with many people since then, and none of them are feeling unwell either.
I know there is an incubation period, or that this person may not have been contagious at the time they met, but they did have more contact than when I possibly infected him a few months ago.
Joshua Roopchand says:
I think that it may be also a robust TLR (Toll like receptors) response which is clearing the virus without the asyptomatic patients serocoverting. T cell responses are also a possibbles infcetionsbut that may be delayed because thaere may not be as many memory T cells from previous coronaviru . Don't forget thet TLR3, TLR 7 and I believe TLR 9 can shut down protein synthesis in virus infected cells as soon as the viral RNA is detected and the type 1 IFN system gets activated. Long story short, TLRs clear the virus, B cells dont get activated ano seroconversion after virus infection. Innate immunity wins again. There also could be RNA silencing as well.
Antibody Responses to SARS-CoV-2 at 8 Weeks Postinfection in Asymptomatic Patients
Abstract : "We compared levels of severe acute respiratory syndrome coronavirus 2 neutralizing antibodies in recovery plasma from 7 completely asymptomatic coronavirus disease patients with those in symptomatic patients in South Korea. We found that serologic diagnostic testing was positive for 71% (5/7) of completely asymptomatic patients, but neutralizing antibody response occurred in all 7 patients."
The reported absence of antibody production in some patients may be due to time-of-sample issues or assay type ( i.e. conventional serology vs neutralization ).From the same report:
"… The difference in results from our study compared with the previous study might be caused by differences in the timing of the test. In the previous study, (neutralizing) antibody tests were performed 2–3 weeks after symptom onset, whereas we tested 2 months after symptom onset or laboratory diagnosis. Seroconversion in asymptomatic patients might take longer."
https://wwwnc.cdc.gov/eid/article/26/10/20-2211_article?deliveryName=USCDC_333-DM31489
New preprint with some more tantalizing T-cell cross-reactivity findings in unexposed donors, with this bit being especially intriguing with regard to "heterologous immunity" (exposure to virus A providing some native immunity to virus B). Really need to figure this stuff out.
"In our study we identified and characterized the exact T-cell epitopes that govern SARS-CoV-2 cross-reactivity and proved similarity to human common cold coronaviruses regarding individual peptide sequences, physiochemical and HLA-binding properties30,31. Notably, we detected SARS-CoV-2 cross-reactive T cells in 81% of unexposed individuals. To determine if these T-cells indeed mediate heterologous immunity and whether this explains the relatively small proportion of severely ill or, even in general, infected patients during this pandemic32,33, a dedicated study using e.g. a matched case control, or retrospective cohort design applying our cross-reactive SARS-CoV-2 T-cell epitopes would be required."*
https://www.researchsquare.com/article/rs-35331/v1
This related "viewpoint" article in the Journal of Clinical Investigation on innate immunity and priming it with various substrates was also interesting.
https://www.jci.org/articles/view/140530
Hi Derek! You have a very calming, yet analytical and objective voice. I enjoyed reading this a lot. I'm a student and have been following the latest articles on the pandemic – so, understandably I've had difficulty finding solid ground. I'm never sure what to believe. I really appreciate this article because of the assurances (but not certainties) that you provide, while educating the reader about all possibilities. I finished reading with a "well if he's not worried, I'm not worried" point of view, while still taking your advice of not being complacent either. Thanks for this! 🙂
Riah says:
Thanks for this very interesting info. Apologies I am coming in very late having just seen this blog. In response to your statement "That's very much in contrast to the antibody situation in uninfected patients – it seems clear that the human population had raised no circulating antibodies to the new coronavirus before the advent of this pathogen. Prior infection with other coronaviruses does nothing for you on the antibody side" I have just dug up a pre-print which claims to find antibodies cross reacting with Cov2 (buried at top of pg 8): "Coronovirus Protective Immunity is Short Lasting"
Would be interested to know what you make of this. Also what you think of this paper in general. Particularly re methodological rigour (which I'm not sure is great although this does not impact on the initial point above). Also, athough a 35 year time span and 2473 floow up months sounds impressive this only translates to less than 6 people, a very small sample and all male. I remember some other old studies showing that people do develop resistance to the same strain of cold coronoviruses which contradict this- will have to try and dig those out again -unless you have ready refs? Thanks
Thanks – I'll have a look!
Dave Engvall says:
Liked both the Blog and the comments. Bit of a struggle with a degree approaching 60 years in age. Still a good read. Played chemist for most of my working life. Keep it coming.
Brian Hastings says:
Great post! Thanks for sharing the knowledge and keep up the good work.
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I work within a wide range of academic disciplines but specialize in the arts, humanities (in particular, philosophy and literary theory), social sciences (in particular, political science and gender studies), education, and business and management studies.
Whatever your academic editorial needs, get in touch today to discuss your requirements. If you need a quick turnaround, enquire about my express service (subject to my availability).
Your writing, whether it be a piece of coursework, a thesis, a dissertation, or a research paper, should be evaluated based on the quality of your ideas and how well you understand the subject matter, without typos and poor English getting in the way. A professional proofreader can help eliminate these distractions so your writing is judged on its academic merit alone.
Academic integrity is my top priority, and it is crucial that your work remains your own. I will proofread student texts for spelling, grammar, punctuation, sense, and consistency, but I will never write, rewrite or substantially edit the content of your work. Please note that I require written proof from your department or supervisor that you have permission to use the services of an editorial professional before I will accept any work from you.
In the current "publish or perish" academic climate, having a regular output of innovative and clearly written academic writing has never been more important. An editorial professional can help ensure that typos, awkward wording, and inconsistencies don't undermine your ideas, and a fresh pair of eyes can give your research a better chance of being accepted in the top journals in your field.


text:
Q: Android facebook birthday error I am trying to use the login button for facebook and I am able to successfully login. I have set the permissions as -
loginButton.setReadPermissions(Arrays.asList(
            "public_profile","email","user_birthday"));

But the problem is that some people keep their birthday as private. And in such cases when I am trying to access the birthday, the app is going to the catch block -
try {
                        user = new User();
                        user.facebookID = object.getString("id").toString();
                        user.email = object.getString("email").toString();
                        user.name = object.getString("name").toString();
                        user.gender = object.getString("gender").toString();
                        PrefUtils.setCurrentUser(user, LoginActivity.this);
                        user.birthday = object.getString("birthday").toString();

                        Log.d("LoginActivity","in executeGraphRequest user.birthday = "+user.birthday);

                        //PrefUtils.setCurrentUser(user, LoginActivity.this);

                    } catch (Exception e) {
                        e.printStackTrace();
                    }

I can understand why it is going to the catch block. But I want to know how we can know in advance, before querying, that the information we are querying is private. This can apply not just to birthday but other fields too. Thanks in advance.

A: use something like this
if(object.has("birthday"))
    user.birthday = object.getString("birthday").toString();


text:
Q: Update map value in nested struct in pyspark I have a table with dates and comments.
dob        | comment
---------------------------
1960-12-01 | this is useful

And I want a new column with this type:
value_type = T.StructType(
    [
       T.StructField("extra",T.MapType(T.StringType(), T.StringType(), True), True),
       T.StructField("date", T.StringType(), True),
       T.StructField("from_date", T.StringType(), True),
       T.StructField("to_date", T.StringType(), True),
       T.StructField("value", T.StringType(), True),
    ]
)

I need to:

*

*put the df.date into the date field of the struct and

*put the df.comment into the extra map of the struct

thanks to blackbishop I figured out how to do the first part here - and i tried to use .withField() to update the map but it throws an error:
I tried:
(df
.withColumn("new_col",
            F.struct(*[F.lit(None).cast(f.dataType).alias(f.name)
                       for f in value_type.fields]))
.withColumn("new_col", (F.col("new_col")
                         .withField("date", F.col("dob"))
                         .withField("extra.value", F.col("comment")))))

But I get the following error:
AnalysisException: cannot resolve 'update_fields(update_fields(new_col, WithField(dob), WithField(dob)).extra, WithField(dob))' due to data type mismatch: struct argument should be struct type, got: map<string,string>;

I am confused as per why it would not work with the map inside the struct?
Thanks :)

A: I figured it out!
(df
.withColumn("new_col",
            F.struct(*[F.lit(None).cast(f.dataType).alias(f.name)
                       for f in value_type.fields]))
.withColumn("new_col", (F.col("new_col")
                         .withField("date", F.col("dob"))
                         .withField("extra",
                                    F.create_map(F.lit("my_key"), F.col("comment")))))

The problem was that I was not actually passing a map to a map type!


Sony goes new ways with the introduction of Xperia X series. The first topmobil in the series is Xperia X which offers quality in a compact format.
You should have the best and most advanced from Sony, was Mobile phones from Xperia Z-series until now the smart phone for you.
This year the company introduces instead a new series in the top of the company's line-up: X-series.
First X-Mobile is Xperia X, as the company's previous approach with vrager smartphones in different size for instead of creating the best possible mobile in 5-inch class.
Xperia X offers a new design for the company, change glass back out with aluminum and is in possession of the company's most advanced camera on the whole to date 23 megapixels.
Processor in the Xperia X not nearly as powerful as in the market's other phones-it is instead a more integrated experience that wagered on, with simpler and more responsive software as well as long operating time there together need to do to the best Sony Xperia X-Mobile ever.
See why with including, where our site takes Xperia X in use and gives the first impression after our initial tests.


text:
Q: Getting datepicker starting value after selecting another value from another datepicker So the idea is I have 2 datepickers. I want to get the second datepicker minDate value by selecting the first datepicker value.
For instance:
If I choose the first datepicker value to be 22-03-2015 the second datepicker value will start from 23-03-2015
or If I choose 13-05-2015 the second datepicker value will start from 14-05-2015. How do I achieve that. This is what i tried:
$(".datepicker").datepicker({
     minDate: 'today',
     yearRange: "2015:2016",
     dateFormat: 'dd-mm-yy'
});
$(".datepicker2").datepicker({
     minDate: 1,
     yearRange: "2015:2016",
     dateFormat: 'dd-mm-yy'
});

A: You can subscribe to the onSelect event assuming you are using 'jquery datepicker'
JQuery Datepicker onchange event help!

A: You can reset the minDate option for datepicker2 after datepicker1's value has changed:
HTML:
<input id="datepicker1" />
<input id="datepicker2" />

jQuery:
$("input").datepicker();

$("#datepicker1").change(function() {
   var minDate = $(this).val();
   $("#datepicker2").datepicker("option", "minDate", minDate);
});

http://jsfiddle.net/ke8LowuL/


text:
The Virtual Memories Show
A podcast about books & life — not necessarily in that order
Guests (Alphabetical)
Comics & Cartooning
Podcasts By Our Guests
Podcast Supporters
Support Artists & Creators!
The Guest List 2019
All the Books I've Read
Another Year, In The Books: 2011
Tag: Ernie Kovacs
Posted on July 18, 2016 December 17, 2017
Episode 177 – MK Brown
http://traffic.libsyn.com/virtualmemories/Episode_177_-_MK_Brown.mp3
Episode 166 – Ben Model
Virtual Memories Show #166:
Ben Model
http://traffic.libsyn.com/virtualmemories/Episode_166_-_Ben_Model.mp3
Subscribe: Apple Podcasts | Android | TuneIn | Spotify | RSS
"I'm trying to create music that's pretty enough to listen to but not interesting enough to pay attention to."
Ben Model has made a career for himself as a silent-film accompanist, playing for audiences throughout the US (and a city in Norway!). I was thrilled to have him on the show and ask him how he got his start and how he reached the top of his field. We talk about the not-exactly-secret society of his peers, the challenge of reading and adapting to audience and movie simultaneously, the importance of audience preservation, the differences between playing live and recording a score for a movie, the reasons young and old audiences get engaged by silent movies, why you need to city Chaplin's City Lights with a live orchestra, and more! Give it a listen!
"No film collector is going to hold up a 4tb hard drive and say, 'Look at all the movies I have!'"
Ben & I also discuss the difference between digital and "real" instruments, the way his style has evolved, the Kickstarter revolution and how it funds his DVD label, the Stan Laurel comedy that makes little kids lose their minds, his love for Ernie Kovacs, the awful and sometimes incomprehensible stereotypes of century-old comedy, his theory of Undercranking, where the next generation of accompanists is coming from, the multi-decade dearth of comedic filmmakers with distinct vision, the lost comic genius of Marcel Perez, and what it's like to create "music of momentary significance" (as his mentor described it). Go listen!
"Bringing the silent movie experience to a place where it doesn't usually get to happen is great fun for me."
Enjoy the conversation! Then check out the archives for more great episodes! You might like:
David Leopold
Kliph Nesteroff
Drew Friedman
David Jaher
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Ben Model is one of the nation's leading silent film accompanists, and performs on both piano and theatre organ. Ben works full-time presenting and accompanying silent films in a wide variety of venues around the USA and internationally, carrying on a tradition he learned from silent film organist Lee Erwin (1919-2000). Over the past 30+ years Ben has created and performed live scores for several hundred silent films, films lasting anywhere from one minute to five hours. Ben is a resident film accompanist at the Museum of Modern Art (NY) and at the Library of Congress' Packard Campus Theatre. His recorded scores can be heard on numerous DVD/Blu-Ray releases, on TCM and on his YouTube channel. His indie DVD label Undercrank Productions has released several discs of rare/lost silent films, including films preserved by the Library of Congress. Ben is a regular accompanist at classic film festivals around the U.S.A. and in Norway, and performs at universities, museums, and historic theaters. Ben is the producer and co-founder of The Silent Clowns Film Series, now in its 19th season in NYC. Ben has composed film scores for both orchestra and concert band for accompaniment to films by Chaplin and Keaton. These scores are performed around the U.S. every year by both professional and school ensembles. In his work as a programmer, Ben has co-curated a film series for MoMA, and co-programs a monthly silent film series at the Cinema Arts Center. As archivist of the Ernie Kovacs/Edie Adams collection, he also curated two recent DVD box sets of Ernie Kovacs television shows for Shout! Factory. He is currently a Visiting Professor of Film Studies at Wesleyan University.
Credits: This episode's music is Ben noodling on my friend's Steinway. The conversation was recorded at my friend's place in Manhattan on a pair of Blue enCORE 200 microphones feeding into a Zoom H5 digital recorder. B/W photo of Mr. Model by me; no attribution for the color photo.
This is a Gil Roth joint. You want more of me? Try these:
Virtual Memories Show
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text:
Q: probability density function (PDF) I have a function defined as:
P_{n}=p+ (n-1)beta.   where n={1,2, ....} and 0<=p<=1.
which condition can I impose on beta for this function to be a probability density function (PDF).

A: I don't think that it is possible in the way you have stated your problem: A PDF needs to represent a probability distribution, i.e. you need to impose that the sum of all the probabilities is exactly $1$.
In this case, you would have $1 = \sum_{n=1}^\infty (p + (n-1) \beta)$ which diverges no matter the value of $\beta$ (I assume beta is constant).
Even with $p=0$, you would end up with the Harmonic series, which is also divergent.
If you make $\beta = \beta(n)$ not constant, then you would need to have something which gets rid of $p$ and then imposes a convergent series (something like $1/n^2$ for instance).
Cheers


Following on from our debut at Carnegie Hall with the one & only Neil Gaiman, we are playing an exclusive "FourPlay proper" show at the legendary Joe's Pub. You don't want to miss this! Nor do we, for obvious reasons.
I'm from Washington, DC and would have made the trip to see you all.


text:
Marin-Epagnier je švýcarská obec v kantonu Neuchâtel. Nachází se na severovýchodním okraji Neuchâtelského jezera v nadmořské výšce 455 metrů. V roce 2007 zde žilo 4 087 obyvatel.

Pamětihodnosti
 Na okraji obce v katastru vesnice La Tène byla odkryta archeologická lokalita La Tène. Tato lokalita dala název keltské kultuře mladší doby železné, laténské kultuře.
 Papiliorama je nejstarší motýlárium v Evropě, zoologická zahrada specializovaná na chov motýlů, založena roku 1988.

Externí odkazy

 Marin-Epagnier

Vesnice ve Švýcarsku
Obce v kantonu Neuchâtel

redpajama_set_name: RedPajamaWikipedia


When is plastic surgery appropriate for young adults?
In the previous, apart from for some unusual cases, plastic surgery was limited to adults, typically older grownups. A latest development demonstrates that not only are plastic medical procedures clients acquiring youthful, the amount of teenagers in search of plastic surgical treatment is rising. When need to the answer be "of course" to plastic surgical treatment for youngsters? Below are a few frequent procedures asked for by teens along with recommendations, but every single situation ought to be regarded as independently.
Current figures show that plastic surgical procedure methods amid teenagers are on the increase, but not all of it is alarming. Typical techniques that teenagers ask for incorporate noninvasive skin processes like microdermabrasion, chemical peels and laser pores and skin resurfacing. These varieties of techniques can make zits scars and pores and skin discolorations considerably less apparent and can improve the total appearance of the skin.
Above the past 5 many years, dermal fillers have also manufactured a significant influence on how faces and lips are augmented, not only in teens but also in grown ups. Teens have observed their "Hollywood" position designs get overdone lips and cheeks and have followed fit. Sadly, many of these teenagers have been misguided and most plastic surgeons suggest against the use of dermal facial fillers during the teenager years.
Hyaluronic acid fillers are in a natural way transpiring substances that may be a much better alternative. In excess of a few months, they will slowly and safely be absorbed by the body. However a lot of men and women think it is as well early, some teenagers are getting Botox to inhibit the development of traces on the confront. In general, most experts do not recommend the use of Botox or fillers for beauty functions in teens, but the consequences of Botox are not long lasting and will fade more than time.
Cosmetic techniques necessitating surgical procedure for teenagers are exceptional. Breast enhancements for teens are generally executed for individuals seeking to enhance symmetry and harmony proportions for a sleeker, far more athletic and more all-natural appear. Some teenagers even find breast reductions to attain this objective. In boys, male breast reduction processes for gynecomastia are in need. Gynecomastia, or the development of male breast tissue, is regarded to be a "silent male condition" and may possibly be induced by treatment side results, weight problems or other factors.
Typically, when boys entirely experienced and slim down, the breasts will disappear on their own. Significant situations, even so, could demand from customers surgical attention to lower the psychological impact of excessive breast tissue in the teen male. In some cases, this can be carried out by way of minimally invasive techniques employing ultrasonic liposuction.
Otoplasty is a procedure that is commonly performed to reshape and right well known ears. It can be accomplished for the duration of the teen a long time but may possibly be done as early as age 6 or seven when the ears are virtually grownup-dimensions, especially if a child is currently being ridiculed at college with names like "Dumbo ears." The nose is also a frequent subject of teasing in school-aged children and teens. Rhinoplasty, or nose reshaping, is the most typical cosmetic surgical process for teens, and it is generally performed when needed for psychological causes. Both of these surgical procedures may consequence in spectacular enhancement for teens, each bodily and psychologically.
Some mother and father are continuing to give plastic surgical treatment as a "reward" for graduation or other events but several plastic surgeons may possibly be heaving a sigh of reduction as teenagers are trending towards a a lot more "natural" appear.
Above the earlier several a long time, upticks in plastic medical procedures prices may possibly have been pushed by celeb tendencies. The "selfie" has also been credited with escalating plastic surgical procedure rates but the development may be slowing. Escalating numbers of famous people who had "botched" techniques or who basically went also much could have lowered outrageous needs and teens are appearing to grow to be much more happy with small improvements.
Plastic surgeons who are faced with teens wanting plastic surgery should act as guides and help each teens and mother and father arrive to a affordable expectation. Medical professionals normally call for conversations with the teenager to ensure that they are mature sufficient to understand each the pitfalls and rewards of a prospective change, specifically if it is a long lasting, surgical process. In some cases, teenagers are encouraged to "hold out and see" since additional maturity may give the teenager what they want in excess of time.