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We can pretty confidently say that we can eliminate mosquitoes these days and we're almost 100% sure that our last practice run didn't create zika.

I worked in vector borne disease surveillance for decades, I can say with equal confidence there is no technology known or proposed that has the potential of completely eradicating a mosquito population from any region larger than a thousand acres or so. Even those genetically modified mosquitoes you've been hearing so much about only reduce an infected population in a limited area short term. That reduction will last, at most, for a matter of months; in many situations mere weeks. Still, even that could be useful in reducing anthroponotic (human-to-vector-to-human) transmission.

And by the way yes, human activities didn't create Zika, but they were a big factor in its global emergence. 70 years ago it likely existed only in a small population of rhesus monkeys in a forest on the shores of Lake Victoria, where it no doubt had persisted for thousands of years. Human encroachment offered an alternative host for the primate virus, and human trade and migration patterns carried across the entire tropical world, with anthroponotic outbreaks spreading into temperate climates. That same combination of human incursion on isolated animal populations and global emergence through migration and trade routes is behind SARS, Ebola, Marburg, MERS, Lassa Fever among others in modern times, and are likely the sources of influenza and measles.

I reiterate: life always finds a way, but given a rapid rate of global change it's not going to be a way we'll be happy about.

I'll take "things that never happened" for $590, Alex.

Detection of Vancomycin-Resistant Enterococcus Spp. (VRE) from Poultry

Persistence of Vancomycin-Resistant Enterococci in New Zealand Broilers after Discontinuation of Avoparcin Use

BENEFITS OF DIETARY ANTIBIOTIC AND MANNANOLIGOSACCHARIDE SUPPLEMENTATION FOR POULTRY which says: The specific vanA gene cluster that encodes for vancomycin resistance has been isolated from Enterococcus faecium in farm animals destined for human consumption (Bates et al., 1994; Klare et al., 1995).

This article describes the purpose of CD163:

https://www.ncbi.nlm.nih.gov/p...

It is a receptor for hemoglobin, and is involved in hemoglobin clearance after intracerebral hemorrhage. It is elevated for anyone with myelo-monocytic leukaemia and infection.

http://jvi.asm.org/content/91/...

2018 study

There's my authority, published Feb 2018. AFAIK, Dyson's aren't heated, and that study dealt with "hot air hand dryers." Doesn't make sense that it would be funded by a Dyson competitor.

But feel free to provide your proof that the study was funded by a Dyson competitor.

Seem to remember a few decades ago that they found live Y-P in a couple of plague pits from the 1500's(might have been 1800's been a long time since I read the article) in the UK. It had survived by living inside other bacteria, and did so rather happily. There's an article this for anyone interested in reading about it.

> I challenge you to find any scientific study that uses raw, unfiltered data.

Im a mycologist and when doing spore measurements we measure the length and width or many spores. Then average the length and average the width. Providing largest measurements, smallest measurements, and average. We don't "adjust" our actual measurements to make sure the spore size meets the expected size.

Possibly you should, since other mycologists do make corrections. Here are some corrections factors noted by Smith et al: "Sources of Variability in the Measurement of Fungal Spore Yields": http://aem.asm.org/content/54/...

"Quantification of the sources of experimental error in spore
production measurements provided a basis for recommendations
concerning the necessary degree of replication"

"to ensure that these precise counts are also
accurate, checks must be made for interference from nonspore
particles in the same size range as spores and for the
clumping of spores. The degree of clumping that we encountered
necessitated a correction factor that was much larger
than that expected from the coincidental passage of conidia
through the aperture, which should have been less than 2% if the
conidia were all separate. Also, our correction factor was
only approximate and probably varied with culture age, as
did the mean weight per spore. "

see also Chapels: "Spore size revisited: Analysis of spore populations using an automated particle sizer" http://www.zobodat.at/pdf/Sydo...

Homeless shelters have been in the news lately because they are far from safe. Kids are developing anemia because they are so drained by bedbugs. And it's not just kids either. There are also numerous other complications.

And shelters are dangerous.

Once someone gets that low, how does anyone expect them to get back on their feet? Far better to prevent it in the first place. The people who rant on about how it's somehow wrong better hope that karma doesn't bite their ignorant asses.

My understanding from a very quick skim of the paper (open access, here) is that they are not using microarrays. They have a mixture of a very large (2 million) number of probes to match DNA/RNA sequences of all known viruses which infect vertebrates. They use these to amplify viral sequences and then use normal high throughput DNA sequencing (Illumina, in this case) to see what they've got. They claim that it is sensitive to both DNA and RNA viruses (and all the variations - double, single stranded etc.) Being able to detect both DNA and RNA in a single test mildly surprises me, but I'm only slightly familiar with DNA sequencing technology, so maybe it isn't a big deal.

They do say "A biotinylated oligonucleotide library was synthesized on the NimbleGen cleavable array platform and used for solution-based capture of viral nucleic acids present in complex samples containing variable proportions of viral and host nucleic acids." Perhaps that translates to say the microarray you talk about was used to make the 2 million probes.

As a complete aside, I'm a little surprised this isn't a Nature or Science paper.

This really intrigues me because it never struck me that this could be a mechanism for antibiotic resistance. It is even more interesting to me knowing the first CRE (Carbapenem-resistant Enterobacteriaceae)

clearly arose in India [source]

but the reasons weren't clear to me and I just naively assumed it was a random mutation. India, also according to to that same paper has quite a problem with antibiotic resistance which one wouldn't expect as there isn't so much of a problem with antibiotic overuse as there seems to be in the West. So, maybe not so random and maybe we have honed in on a legit reason for growing resistance.

The other problem in India and similar places is that the dosage wasn't what the label said. The doctor may have prescribed 500 mg of amoxicillin, and the patient bought capsules in a bottle labeled 500mg amoxicillin, but what was in those capsules was a fraction of the prescribed dosage.

Case in point is Ranbaxy who sold millions of doses of what they knew was non-performing anti-retroviral drugs.
http://www.bloomberg.com/apps/...
And more like this:
http://fortune.com/2013/05/15/...
http://fortune.com/2013/01/10/...

The bad part is Ranbaxy only got caught because one of their executives was an American who ratted them out.
Ranbaxy only got into trouble because they tried to sell their crap in the USA, otherwise nothing would have happened to them.
There are numerous other drug companies with the same ethics, but they don't try to sell in the USA or Europe, so they'll never get caught.

Another thing I did not know is that the FDA almost never test drugs for efficacy.
What happens is the drug company does the tests and the FDA looks at the drug companies documentation and procedures and signs off on that. This is why cheaters don't get caught - they are grading their own papers, so to speak.

BTW, Ranbaxy was bought by Sun Pharma, so Who Knows where their drugs are going now.

This really intrigues me because it never struck me that this could be a mechanism for antibiotic resistance. It is even more interesting to me knowing the first CRE (Carbapenem-resistant Enterobacteriaceae)

clearly arose in India [source]

but the reasons weren't clear to me and I just naively assumed it was a random mutation. India, also according to to that same paper has quite a problem with antibiotic resistance which one wouldn't expect as there isn't so much of a problem with antibiotic overuse as there seems to be in the West. So, maybe not so random and maybe we have honed in on a legit reason for growing resistance.

It was discovered in 95 by an African doctor who just guessed and saved 7 out of 8 people;

http://jid.oxfordjournals.org/...

something wasn't right about this though.

http://jvi.asm.org/content/75/...

the who was skeptical and it's only been in the last few months when it's been approved, when it was used out of desperation that the protocol has gained any traction. there are billions at stake with an EBOV vaccine, just as there was in 1948 with the polio vaccine.

"Klenner's paper (Klenner FR. The treatment of poliomyelitis and other virus diseases with vitamin C. J. South. Med. and Surg., 111:210-214, 1949.) on curing 60 cases of polio in the epidemic of 1948 should have changed the way infectious diseases were treated but it did not." - Robert Cathcart

Now look at these three:

http://en.ird.fr/the-media-cen...
http://orthomolecular.org/libr...
http://ajcn.nutrition.org/cont...

There's a reason there's no HIV vaccine and it's the same reason there never will nor can be an EBOV vaccine - Coxsackie viruses are different and if you ignore their RNA encoding and subsequent biochemical expression you're gonna have a really bad day. The second paper above explains why they cannot work, see Keshen's disease in Wikipedia, it's the Coxsackie virus disease we figured this out from.

http://en.wikipedia.org/wiki/K...

There's no need to mess around with blood, honest and antibodies are not the reason it works - what do antibodies need to do their job - think!. Look at recent work in the field, Google (scholar) "selenium" with words like "hiv", "ebola", "cancer" and pay attention to the work of the last 4-5 years and especially THAT 1995 Zaire paper - the only time Pauling ever posted to the net. Thanks for the warning Linus, you clever clever boy. Now there was a Doctor.

http://scarc.library.oregonsta...

I kinda already did?

As for the 'Ted Talks' I kind of ignored them for a number of reasons:
1. No reason to believe that they're peer reviewed.
2. Audio would be incredibly rude where I was at the time.
3. I'm a visual learner - listening to youtube lectures is painful for me.
4. My conclusion from the earlier 3 was that the latter 3 would be more the same. On reaching home, I confirmed this.

Anyways, some more articles on antibiotic growth promotion:
It improves growth, but not enough to justify the cost in chickens grown in clean & sanitary environments
The Mode of Growth Promotion by Antibiotics
The European ban on growth-promoting antibiotics and emerging consequences for human and animal health. link
Alternatives to Antibiotic Use for Growth Promotion in Animal Husbandry link
Effect of Abolishment of the Use of Antimicrobial Agents for Growth Promotion on Occurrence of Antimicrobial Resistance in Fecal Enterococci from Food Animals in Denmark link
Antibiotic Usage in Animals link

Conclusion: The cattle industry isn't feeding billions of dollars of antibiotics to their animals for fun.

When you're sick enough to (feel you) need medication, stay at home. Don't spread germs all over the workplace / auditorium / public mass transport.

Nice idea, but almost useless....

The typical incubation period for influenza is 1—4 days (average: 2 days). Adults shed influenza virus from the day before symptoms begin through 5—10 days after illness onset. However, the amount of virus shed, and presumably infectivity, decreases rapidly by 3—5 days after onset in an experimental human infection model. Young children also might shed virus several days before illness onset, and children can be infectious for 10 or more days after onset of symptoms.

What this basically means is that you are infectious the day before you show symptoms.....therefore you will not be able to ever stop the flu, at least not without a better vaccine (no, don't go pulling that Jenny McCarthy shit or I'll have to slap you); we can just mitigate some of the spread. It is incumbent upon the uninfected to keep from getting infected, as those who are will not know they are until its too late.

The science is that fever is an adaptive response to an infection. Yes, fever is what makes you feel like crap, but it changes the kinetics of viral (and bacterial replication). Ever notice that microbiological (especially bacterial) incubators are set to 37 deg C? That's the sweet spot for replication....change it and you put the invader at a disadvantage. Modern medicine unfortunately has taken on the dogma that: "If it ain't right, it needs to be fixed", a few (and growing) are starting to learn that not all that is wrong is bad....I continually rally against treating fevers less than 40 deg C (above that is concern for brain injury), but I have an uphill fight against an entrenched culture.

My personal strategy? I take the anti-pyretics so i can sleep or function, but reintroduce the elevated temperature by bundling up and keeping my core above 37 deg C. This is not scientific, just what works for me, YMMV and I won't be held responsible if you up and die from the flu as this is not my official advice.

the "anti-bacterial" ingredients are chlorinated organics, they just poison bacteria. they are not in any way related to antibiotics and thus do not in any way conribute to resistance to antibiotics any more than your chlorinated kitchen cleanser does.

All antibiotics poison bacteria in some way, and several are chlorinated hydrocarbons, e.g. vancomycin, clindamycin, clofazimine, chloramphenicol, thiamphenicol, etc. Antibiotics are widely varied category of chemicals, and while triclosan isn't directly related to any families I'm aware of, that doesn't mean that resistance to it would be useless against antibiotics that operate on the same system.

A mutation capable of resisting the effects of one class of chemicals can often be useful for resisting very different chemicals that have the same effect. Triclosan works at higher, lethal concentrations by disrupting bacterial cell membranes. At lower concentrations it also suppresses fatty acid formation necessary for cell membrane creation by binding up two enzymes necessary for the process: ENR and NAD+. (This prevents reproduction but doesn't kill.)

Isoniazid is one of our first-line treatments for tuberculosis. Interestingly, it also works by binding to NADH and then binding to ENR and blocking fatty acid synthesis. Studies have shown that some strains of isoniazid-resistant mycobacteria are also pretty resistant to triclosan as a result. Others aren't, because they developed mutations that affected other parts of the process of the drug's interaction. These are unrelated compounds, but a mutation that affects an enzyme they both act on can promote resistance to both.

There is also evidence that evolution of triclosan resistance can increase resistance to ciprofloxacin. In that case, the mutation was to increase the expression of certain efflux pumps, used to pump toxic chemicals out of the cell. Turns out in that case that the same pump was used as part of the processes to eliminate both toxins.

So, in summary, while there isn't any evidence that triclosan is responsible for anywhere near the damage that usage in livestock has done, it's probably not a good idea to keep using a chemical that has risks in a situation where it has little benefit because it can aid in the development of resistance for some antibiotics.

There are already fungi that eat plastic. But just like wood doesn't get digested that fast, neither is plastic going to be digested that fast even if the fungi become widespread.

http://news.bbc.co.uk/2/hi/science/nature/1402533.stm
http://aem.asm.org/content/77/17/6076

First, there's no evidence that UN has started the cholera epidemic. No bacterial strain genotyping has been performed. Second, in such cases a cholera epidemic is more-or-less a certainty - it makes no sense to search for the index case, especially because choleric bacteria occur naturally.

O Rly?

For those too lazy:

Wolbachia is a genus of parasitical/symbiotic micro-organisms that infect arthropods, including most insects

Many species of insect that have intimate contact with plants and plant juices harbor this parasite. including aphids

Now, asking if that is "a good idea" or not? That's an entirely different question!

The capsid doesn't enter the cell, but it is produced there.

There are many possible lines of defense against viruses. Ignoring natural innate/adaptive immunity, you can block viral binding to cells (target receptors). You can interfere with replication of viral genomes (reverse transcription inhibitors, a big one for HIV). You can prevent assembly of new viruses (capsid inhibitors: http://jvi.asm.org/content/82/20/10262.full, note the way they used structure to guide their work). Or you can prevent viral capsid maturation (protease inhibitors, also big with HIV).

So while you can't target live (enveloped) virus with a capsid inhibitor (at least easily), you can prevent the formation of new virus. Here's a picture of what actually happens: http://jvi.asm.org/content/82/20/10262/F6.expansion.html. There should be nice tidy spheres of new capsids, and instead you get blobs of virally-useless junk.

The capsid doesn't enter the cell, but it is produced there.

There are many possible lines of defense against viruses. Ignoring natural innate/adaptive immunity, you can block viral binding to cells (target receptors). You can interfere with replication of viral genomes (reverse transcription inhibitors, a big one for HIV). You can prevent assembly of new viruses (capsid inhibitors: http://jvi.asm.org/content/82/20/10262.full, note the way they used structure to guide their work). Or you can prevent viral capsid maturation (protease inhibitors, also big with HIV).

So while you can't target live (enveloped) virus with a capsid inhibitor (at least easily), you can prevent the formation of new virus. Here's a picture of what actually happens: http://jvi.asm.org/content/82/20/10262/F6.expansion.html. There should be nice tidy spheres of new capsids, and instead you get blobs of virally-useless junk.

Whoops, wrong paper. Try this one:

http://aac.asm.org/content/45/2/428.abstract

You can find more if you like. Sublethal exposure to antimicrobials like triclosan has been shown to select for drug resistant bacteria. If that scares people, good.

The summary and its linked article are both unclear as to what "misconduct" is being discussed. Fortunately, clarity is available through the original paper:

. . . we found that misconduct is responsible for most retracted articles and that fraud or suspected fraud is the most common form of misconduct. Moreover, the incidence of retractions due to fraud is increasing, a trend that should be concerning to scientists and non-scientists alike.

The study is looking into why scientific papers are being retracted and what trends there are in the retractions.

It's too bad that the summary was so generic it could have meant anything from nosepicking to marital infidelity to fabricating data. This is an interesting topic, and it's sad that the frequency of fraudulent publications is increasing.

Increasing? That's expected. the population of humans is doing the same thing. And even if it is not due to population size, detection could just be getting better.

The summary and its linked article are both unclear as to what "misconduct" is being discussed. Fortunately, clarity is available through the original paper:

. . . we found that misconduct is responsible for most retracted articles and that fraud or suspected fraud is the most common form of misconduct. Moreover, the incidence of retractions due to fraud is increasing, a trend that should be concerning to scientists and non-scientists alike.

The study is looking into why scientific papers are being retracted and what trends there are in the retractions.

It's too bad that the summary was so generic it could have meant anything from nosepicking to marital infidelity to fabricating data. This is an interesting topic, and it's sad that the frequency of fraudulent publications is increasing.

Another problem with replication is that very few replication articles will get published. Although reproducibility is a critical component of the scientific process, good luck getting your replication study published in a top journal. Or even in a crappy one. Editors just aren't interested in that sort of thing. It is so pervasive that the net result has a name: Publication bias.

Good scientists will often cooperate with those attempting to replicate their results. We just saw this in medicine with a controversial finding relating XMRV to Chronic Fatigue Syndrome. The original investigators cooperated with a more rigorous study of XMRV that disproved their initial findings. That's how science is supposed to work.

antibiotics (which remain in the meat, even after cooking

Citation needed.

http://pubs.acs.org/doi/abs/10.1021/jf00047a035

http://mbioblog.asm.org/mbiosphere/2012/08/antibiotic-residues-in-fermented-sausage-meat-target-beneficial-bacteria-leave-pathogens-alone.html

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2134130/

These and other references were brought to my attention at a time I had recently recovered from, yet another Streptococcus throat infection, where I could scarcely swallow for three days. I decided to give up beef, chicken, pork and rely only on fish caught in the lakes or ocean. Over a period of two years I did notice the severity of respiratory infections decline and when I did take antibiotics they actually worked. Though anecdotal, I did recall antibiotics had little to no effect before I changed my diet. Eventually a dairy allergy would remove all cheese, yoghurt, milk from my diet and I find the period from initial detection of a respiratory infection to recovery to be down to less than a week, where I once would suffer these occurances for up to two weeks. I believe there is merit to these studies, particularly regarding the constant presence of low levels of antibiotics in the body creating a breeding ground for resistant strains (which are on the rise) and leaving my immune system impared to some degree, as all antibiotics are toxins which target certain organisms, but also have a degree of collateral damage (killing non-bacterial cells.)

I'm a PhD student in biochemistry and microbiology and would like to point out that nothing in the parent post makes sense. Consuming low levels of antibiotics would not have an effect on the incidence and severity of respiratory infections. Also antibiotics are not generally toxic to humans at prescribed doses, particularly those fed to livestock, and especially not at the very low levels that could be encountered from food. Some antibiotics can cause organ damage with chronic exposure but would not have an effect on respiratory infections.

In summary, the issue of chronic low level exposure to antibiotics is a concern at the population level and their effects can not be teased out at the individual level from an anecdotal point of view.

antibiotics (which remain in the meat, even after cooking

Citation needed.

http://pubs.acs.org/doi/abs/10.1021/jf00047a035

http://mbioblog.asm.org/mbiosphere/2012/08/antibiotic-residues-in-fermented-sausage-meat-target-beneficial-bacteria-leave-pathogens-alone.html

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2134130/

These and other references were brought to my attention at a time I had recently recovered from, yet another Streptococcus throat infection, where I could scarcely swallow for three days. I decided to give up beef, chicken, pork and rely only on fish caught in the lakes or ocean. Over a period of two years I did notice the severity of respiratory infections decline and when I did take antibiotics they actually worked. Though anecdotal, I did recall antibiotics had little to no effect before I changed my diet. Eventually a dairy allergy would remove all cheese, yoghurt, milk from my diet and I find the period from initial detection of a respiratory infection to recovery to be down to less than a week, where I once would suffer these occurances for up to two weeks. I believe there is merit to these studies, particularly regarding the constant presence of low levels of antibiotics in the body creating a breeding ground for resistant strains (which are on the rise) and leaving my immune system impared to some degree, as all antibiotics are toxins which target certain organisms, but also have a degree of collateral damage (killing non-bacterial cells.)

antibiotics (which remain in the meat, even after cooking

Citation needed.

http://pubs.acs.org/doi/abs/10.1021/jf00047a035

http://mbioblog.asm.org/mbiosphere/2012/08/antibiotic-residues-in-fermented-sausage-meat-target-beneficial-bacteria-leave-pathogens-alone.html

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2134130/

And not getting sick one year is hardly such an odd event that it is reasonable to assume that your immune system has been affected. That's why anecdotes of this sort are pretty much worthless

I used to get colds or viruses every winter. Lots of them, every winter without fail. For the multiple years that I took flu shots (>3), prior to getting sick with CFS, I did not get any symptoms of illnesses for the rest of the winter after receiving the flu vaccine. That's not a single coincidence, that's an established pattern with a clear demarcation point. Now that my immune system has partially recovered, I get normal colds/virus infections and symptoms regularly again.

And you are specifically blaming thimerosal, even though the amount is very small (and we now know that this particular form of mercury is rapidly eliminated), and the symptoms of your illness do not resemble the symptoms of mercury toxicity

Nope. I said some additive in the flu shot seems to have been the trigger, and that thimerosal was a possible (even leading) candidate. I also used to have lots of amalgam fillings which are known to slowly leach mercury into the body, so they may have contributed in setting up a sensitivity, or not. However I'm not dead set on it being thimerosal, just that something in the vaccine affected my immune system. If you're willing to propose a different additive in those vaccines as the root cause then I would be willing to listen, but if you completely discount my experiential evidence from the get go, then we're not going to get anywhere - which was the point in my original post.

Although it is not known whether chronic fatigue syndrome is immune related

CFS, particularly as used in the US, has no conclusive test, and is basically an umbrella category of common symptoms which may or may not have different causes. The Canadian definition is somewhat more narrow. Now here's the interesting thing: as my condition gradually improved over a number of years, I was able to notice that fatigue attacks (which initially were not associated with any other standard immune response symptoms other than dull muscle pain), gradually came to be associated with increasingly stronger immune response symptoms, starting with just pain in throat lymph glands, but eventually normalizing to more typical such as runny noses at the same time that the fatigue attack levels decreased. My system still gets messed up if I do anaerobic exercise and I have manage aerobic exercise levels carefully so I'm not completely recovered. Generally I'm much more sensitive to all kinds of stimulants including adrenaline. It's possible that elevated levels of adrenaline from those years with full-blown CFS may have created a sensitivity (sort of the opposite of insulin-tolerance in diabetics).

There have also been indications that many people with CFS have elevated levels of cytokines and that a common cause may be cytokine dysregulation. So maybe not everyone with a CFS diagnosis in the US has an immune system component, but I'm pretty certain that for myself, and many (most?) other CFS patients, there is a significant immune system component.Seriously, your attitude to CFS is very 20th century. There has been a lot of progress on research of this disease in the last 12 years and, while carefully controlled exercise has place in a rehabilitation program, much progress seems to be achieved by people who pay attention to immunological factors.

...actually, terrifyingly, humans can be involved in horizontal gene transfer, too. So sorry about your nice clean object model.

Not at all what I pictured from a link to 'human horizontal gene transfer'.

What?! I figured it was something new on urban dictionary...

...actually, terrifyingly, humans can be involved in horizontal gene transfer, too. So sorry about your nice clean object model.

China and India. Fraud and plagiarism are pretty prevalent in both.

Of course, they don't get much fraudulent or plagiarized work into big journals, and the big journals prefer researchers with a good reputation

congrats being the citizen of a reputable country.
TFA: http://www.nytimes.com/2012/04/17/science/rise-in-scientific-journal-retractions-prompts-calls-for-reform.html?_r=1&adxnnl=1&adxnnlx=1334958458-PxivQM3BpvGZR636Xup/Qw&pagewanted=all
QUOTED: http://iai.asm.org/content/79/10/3855.full

QUOTE in asm: "Of more than 28,000 articles in its 40-year history, Infection and Immunity has issued only 15 retractions. Six of these were issued this year and arose from a single laboratory (52,–,55, 87, 89). ..."
lets check what these bad bad chindians are doing:
ARTICLE: (52-55, 89):
RESEARCHERS: (Naoki Mori1,*, Kazunori Oishi2, Borann Sar2, Naofumi Mukaida3, Tsuyoshi Nagatake2, Kouji Matsushima4 and Naoki Yamamoto1)
Affiliations:
Department of Preventive Medicine and AIDS Research1 and Department of Internal Medicine,2 Institute of Tropical Medicine, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523,
Department of Pharmacology, Cancer Research Institute, Kanazawa University, 13-1 Takaramachi, Kanazawa 920-0934,3 and Department of Molecular Preventive Medicine, School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-0033,4 Japan

(found to contain digital figures that had been inappropriately manipulated)
ARTICLE: (78):
RESEARCHERS: (Junghee J. Shin1, Anton V. Bryksin1, Henry P. Godfrey2 and Felipe C. Cabello1,*)
Affiliations:
1Departments of Microbiology and Immunology
2Pathology, New York Medical College, Valhalla, New York 10595

(two were unable to confirm their original results (42, 67))
Awdhesh Kalia1, Mark C. Enright2, Brian G. Spratt3 and Debra E. Bessen1,*
A Reynaud, M Federighi, D Licois, J F Guillot and B Joly
- Author Affiliations
Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut,1 and
Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY,2 and Department of Infectious Disease Epidemiology, Imperial College School of Medicine, University of London, St. Mary's Campus, London W2 1PG,3 United Kingdom
Laboratoire d'Analyses Vétérinaires et Biologiques Département du Puy de Dôme, Clermont-Ferrand, France.

(and three found a critical reagent to be impure (19, 49, 61). The remaining article was retracted due to extensive plagiarism (43))
19, 49 and 61:
D R Cue and P P Cleary
Paola Marcato, George Mulvey and Glen D. Armstrong*
I M Orme, S K Furney, P S Skinner, A D Roberts, P J Brennan, D G Russell, H Shiratsuchi, J J Ellner and W Y Weiser
Biswajit Khatua, Angana Ghoshal, Kaushik Bhattacharya, Chandan Mandal, Paul R. Crocker and Chitra Mandal
- Author Affiliations
Department of Microbiology, University of Minnesota Medical School, Minneapolis 55455, USA.
Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada
Department of Microbiology, Colorado State University, Fort Collins 80523.
Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada
Infectious diseases and Immunology Division, Indian Institute of Chemical Biology,
College of Life Sciences, University of Dundee, Dundee, DD1 5EH, UK

so, 1 indian of all these and no chinese!!!
i think someone should listen to you and ban indians ad chinese from publishing - right?

You've put some words in my mouth, and I disagree with some of your other points.

No argument here: varied diets with low to moderate intake of cholesterol, fats, and refined sugars are the way to go.

Cholesterol is important because it's what the hormones are made out of. There's a nice graphic on the "Progestogen" wikipedia page... Refined sugar isn't nearly as bad as starch. HFCS is undesirable because it's made from corn, and there can be significant contaminates.

Raw food diets are for idiots that want to spend money following trends. But eating uncooked meat is not good for you either.

I used to eat a lot of raw meat, and it never caused me any trouble, but neither did I notice much of a benefit. Agree that many ppl spend a lot of money on the "raw" trend...

To be fair; people that want to lose weight need to eat fewer calories than they burn. It doesn't matter if they eat cardboard or drink nothing but Mountain Dew. To lose weight healthfully is a bit more complicated.

Disagree. People can put on weight with 800 calories/day if they have poor thyroid function, for example. The thyroid gland does not respond favorably to the polyunsaturated oils.

Palm oil increases the risk of esophageal cancer. Asia has proven an wealth of information about how bad for us processed food is and palm oil is no exception; rates of esophageal cancer went from negligible to as-problematic-as-the-West as soon as it was introduced.

Palm oil comes from Asia and Africa, so it was never "introduced". Basically: Citation Required.

(For those that don't know, anything labeled "vegetable oil" probably contains palm oil.)

In the United States, Vegetable oil is always made from corn, soy, rapeseed, safflower, or a blend.

Polyunsaturated oils are not even remotely toxic in moderation.

Says who? I gave a link to "lipid peroxidation", which CANNOT happen when the fat is Saturated.

They are readily oxidized fats, making them a preferred energy source for bacteria in the gut.

IF you're an ruminant that has four stomachs, then your digestive system has time and space to biohydrogenate those nasty oils. If you're a single-stomach'd animal, your body fat composition generally reflects the type of fats in your diet

In return for eating these fats, they secrete all sorts of beneficial metabolites.

Never heard of this. Link?

Here is a link to an abstract on how to harvest the bacteria. Ochrobactrum anthropi YZ-1 If anyone has any other info on harvesting or economically growing the bacteria please post it here.

Even better, the The American Society for Microbiology could change their URL to www.org.asm. I imagine that'd get them a few extra page hits.

*facepalm*

My first though was "You mis-spelled 'organism'".

How about www.com.apple?

Even better, the The American Society for Microbiology could change their URL to www.org.asm. I imagine that'd get them a few extra page hits.

Like this or this? Nearly every major historic scientific publication can be found on the internet nowadays. Biology is not my area though, so I will not try to dig deeper in this.

Nylonase-generating organisms are merely speculated to have evolved a gene change via a beneficial mutation. None has been observed

Your information is out of date. After the discovery of natural evolution of nylonase in the wild, controlled laboratory experiments were conducted. We have in fact observed the evolution of nylonase in controlled experiments. Read the paper that was published on it.

the mutation has not been observed through gene sequencing before- and after-mutation populations, nor a mutagen identified. Indeed, until sequencing is perhaps a milllon times faster than today, such observation is virtually impossible.

First of all, I have no idea why you would expect some mutagen to be identified. Mutations naturally occur all the time. If a mutagen is applied it merely inflates natural mutation rates.

Secondly, you appear to be posting from a "today" which is some time in the mid 1980's or early 1990's. The speed and cost of gene sequencing has already improved by a factor in the ballpark of a million. There are commercial labs where you can get your entire human genome sequenced for a few thousand dollars. So yes, scientists obviously have been sequencing these genes, and they have identified the exact origin gene sequence, and identified the simple mutations that occurred in the evolution of nylonase. In one case a T was inserted into a largely repetitive gene sequence resulting in a frame shift.

Eventually it will be possible to conduct such experiments. Not today.

Yep, eventually. In like the late 1990's or early 2000's. Some time far far in the future when we have actual experimental proof of evolution in action, lol. Eventually we might even have personal computers and some sort of internet-thingie where we'll be able to go to some magical search engine-invention-thingie where we can find out stuff and all check what sort of evidence exists.

Eventually it may be possible. But not today. Because you're posting from like 1981.

-

This is a Government-funded paper, but it's behind a paywall. The price is $20.

There are lots of biotech schemes for digesting cellulose into something more useful, but so far, none of them are cheap enough.

Answering my own question:
"Results of the present study show for the first time that C. parvum oocysts exposed to undiluted laundry bleach for as long as 120 min are infectious for animals. Although bleach is widely used as a bacterial and viral disinfectant, the present findings indicate that under practical conditions it is not an effective disinfectant for C. parvum oocysts."
http://aem.asm.org/cgi/reprint/61/2/844.pdf

Based on a few papers I found and a few quick, back-of-the-envelope calculations, it should help at least 10.3% of the infected population and at best will help 96%. The huge amount of variability comes from not knowing much about superinfection in HIV. I'd also like to know what strains VRC01 and VRC02 specifically /don't/ target; if the researchers are referring to HIV-1M, O, and N and HIV-2, then "over 90%" means 23/25 is covered, so I'm betting HIV-1N [see http://commons.wikimedia.org/wiki/File:HIV-SIV-phylogenetic-tree.svg ]---but, who knows.

Anyway---for every 100 person-years, there will be a few HIV reinfections in HIV-positive individuals, sometimes by viruses of the same exact subtype, sometimes by viruses of differing subtypes. Sometimes the viruses are more virulent than the original infecting strain of HIV. The time elapsed since the original HIV infection does not seem to make an impact on the distribution of times of second HIV infections. (Yes, I know that sentence could use re-wording, but exactly how is eluding me atm.)
http://jama.ama-assn.org/cgi/content/full/292/10/1177 suggests 5.0 reinfections per 100 person-years (population size 78) in SoCal, http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.0030177 suggests 3.7% reinfections (population size 36) per 100 person-years in Kenya, and http://jvi.asm.org/cgi/content/full/79/16/10701?ijkey=30fccead91569e63031af4357a242da634620d52#SEC3 suggests 10.3 reinfections per 100 person-years (population size 20). A weighted average of these numbers, where the weights are the population sizes (not the best approach, but given the sparse amount of data found in the literature about this particular topic in general, it's better than no weighting, perhaps), comes out to 5.0 reinfections [reinfection or superinfection is very hard to define for HIV---see the methodology in the second article for more information about this] per 100 person-years. So if we look at http://en.wikipedia.org/wiki/File:HIV_time.png a timeline...

If we assume the number of reinfections a year is simply the reinfection rate (5.0/100 to get per-year) multiplied by the HIV-positive population that year, and guess that none of the population in 1980 (where the timeline starts) was superinfected, we get 22.7 million in 2008. If the population in 1980 had all been superinfected, we get 30.0 million in 2008.
On the other hand, if we assume that only the increment in HIV-positive population is eligible for reinfection (a lousy assumption, but with how little is known, it's as good as any---actually, I'm partly going off of the notes in the introduction of the second article about the known information about reinfection rates), and just multiple the difference from year-to-year in the HIV-positive population by the reinfection rate, we get 1.31 million. (It would not make sense to include the 1980 population here, based on the assumption made.)

We don't really know enough to guess, but we can probably assume there would be at least an easily noticeable impact. A 10% drop in HIV population would be very obvious---that's a few million people.

What is life, apart from very complex chemistry? If you belief there is some "magical" ingredient (something like Élan Vital), then you're going to have problems imagining life coming from complex chemical interactions alone - who gets to put the "magic" in? :-)

Personally, I like this answer from the first of the two papers I linked above: a very simple definition of a living system might be: compartments separated from their surroundings that spontaneously multiply with energy gleaned through self-contained, thermodynamically favourable redox reactions. (Martin and Russell, 2003)

It's not just complex chemistry. It is self-organizing, self-contained complex chemistry. The standard biological definition of "life" requires the following 7 characteristics:

1.) organization - in which the cell is the fundamental unit of organization. The self contained compartments from the above definition.

2.) metabolism - both anabolism and catabolism

3.) homeostasis - maintaining its own internal balance

4.) growth - defined as "anabolism > catabolism"

5.) response to stimuli - very wide open definition, could be as simple as an enzyme changing conformation in the presence of a substrate

6.) adaptation - changing to fit ones surroundings, both in the sense of acclimation and evolution

7.) be the product of reproduction - this used to be "be able to reproduce" but it would be nonsense to argue that a mule is not alive.

For a very good look at what it takes to be a living cell, I recommend this paper for a fascinating read:

Molecules into Cells: Specifying Spatial Architecture - Harold, Microbiology and Molecular Biology Reviews, December 2005, p. 544-564, Vol. 69, No. 4

Anyway, for those following along, these ideas are what biologists are talking when they talk about life and the formation of life. (Not disagreeing with the parent post... simply clarifying, expanding, and explaining). :)

and the article glosses over that MOST water supplies in the USA are so heavily chlorinated, that the chance of this happening are nearly ZERO.

Au contraire. Truth is not arrived at by listening to the voices in your head,* but by rigorous scientific study. For example, let's have a look at Chlorine Susceptibility of Mycobacterium avium and Effect of Growth in Biofilms on Chlorine Susceptibility of Mycobacterium avium and Mycobacterium intracellulare, two entirely independent studies.

It would appear that those published, peer-reviewed studies disagree with you. In particular, a quote from the former:

. . . M. avium has been isolated from a variety of sources, including municipal drinking water systems . . .

Whether M. avium is worth any worry is up for debate. Whether it exists in our water supplies is not. It probably isn't a great cause for concern, although it's nice to know that it's being looked into with more thoroughness than someone waving vaguely and going "naaaaah".

* Which I assume also whisper to you that the best way to denote emphasis is by capitalizing words in their entirety. They're wrong about that, too.

This article is misleading in supposing that the nucleic acid sequence represents the only information in encoded in a virus. A naked nucleic acid strand wouldn't make it very far in the wild. Here are some extra sources of information applicable to influenza:

1) RNA modifications

2) protein modifications

3) 8 different strands (the cut points are information)

4 - n) The tiny matter of the structure and organization of the virus, its proteins counts and arrangements, and the way that its RNA strands are packaged (see the wikipedia article for more on this).

So, the information contained in a single virus is far higher than its nucleic acid sequence. I'm not dead yet.

I'm not one to throw out the word "impossible" very quickly, since people who have used that word have been proven wrong so many times in the past. However, I read an argument back in...Jr. High?...that claimed that a truly rotational structure on a biological organism was at the very least highly improbable. There aren't biological structures that can rotate infinitely, because biological mechanisms require plumbing (blood, etc.) and muscle attach points on both halves of the rotating structure.

How far down the size scale are you looking?

Take a peek at this and see if it's what you're thinking of.

I'm a biochem post-doc working in a molecular-microbiology lab. We're studying E.coli O157:H7 and attempting to inhibit intimin formation.

intimin is a protein on the surface of the cell membrane which allows the bacteria to adhere. no intimin and the bacteria stay in solution, therefore no more quorum sensing, no more bio-film and no infection! voila!

Sounds easy, right? Those little critters just won't cooperate though!

But, back to papers. At the institutions I've been at it's quantity first, quality 2nd, and brand-name distant 3rd. Quantity is easy. Quality is harder - it's best judged over time by the number of cites. If your peers cite your papers as the basis for their work, you're doing something right. Scientists are being rated by their citations now.

As for brand - no one really cares if you publish in Cell, Journal of Bacteriology, Molecular Microbiology or PLoS Pathogens. (unless, of course it's top-tier Science/Nature/PNAS, etc. any guess as to what percentage of submitted papers those top tiers represent?)

Why would you give your work away to some publisher so they can make a buck? What do you get out of it? You give them your paper. Signing the copyright over to them. You work for them for free, peer-reviewing papers so they can have a peer-reviewed journal. And then they make $$$ money selling them, restricting their audience, and give you nothing. That seems right to you? Just so you can say your insignificant little paper [>90% are] was published in XXX journal?

I don't care if I never make a major discovery, but if the guy/gal who "cures" EHEC cites my work on intimin formation my scientific dreams would have been fulfilled. I will have participated in what Newton described with "If I have seen further it is by standing on the shoulders of giants".

rho

http://jvi.asm.org/cgi/content/abstract/JVI.01649-07v1

Of course, I want to see something more rigorous and objective (i.e.,
not my own anecdotal confirmation bias) to justify my conjectured link
between the two.

I was thinking this same thing: the wording seems odd. After reading several other posted stories (such as http://www.npr.org/templates/story/story.php?storyId=93381622) I think that the phrase "The Flask" seems to be casual lab term that was used to relay the information from the investigators on the ground to those that report the story to the news and courts etc. In the same way that a mechanic might casually refer to a window regulator that was replaced on a car. It's not common terminology, but specific to those who work on those systems, and despite our vocabularies, it's a very handy way to refer to the motor and stuff that makes your window go up and down.

These sites:
http://www.bellcoglass.com/searchcategoryresult.aspx?keyword=culture%20flask
and
http://iai.asm.org/cgi/reprint/58/2/303.pdf would support my statements to some extent. I can't yet find anything noteworthy about there being only a single flask of this culture. It seems like a single flask is identified because of the four markers found in all the attack samples and the flask Ivins had control of. There were probably many flasks of the spores but only this one matched to the spores used in the attacks. At least that is how I read all this, despite the questions that remain unanswered.

... Martian Dechloromonas overlords.
http://microbewiki.kenyon.edu/index.php/Dechloromonas_aromatica
http://jb.asm.org/cgi/content/abstract/187/15/5090

Assuming it's really influenza, and not some other virus, time will kill it. Influenza can't survive for extended periods of time on dry surfaces. Most influenza viruses only last a several hours on a hard dry surface. Under the right conditions they may last up to 72 hours, but they'll still die off over time.

http://aem.asm.org/cgi/reprint/73/6/1687.pdf

Of course, 3 days is a long time to not have a laptop, but you can safely handle it. You won't get re-infected now that your body is surging with antibodies targeting that specific strain. Just wash your hands afterward so you don't spread it to the non-immune.

If that's not good enough, you could try wiping the case with a cloth *very* lightly dampened with some kind of benzalkonium chloride based disinfectant (i.e.: well squeezed out lysol wipes or something similar). I don't know if that will damage the plastics or not (ie: the screen), it shouldn't but I've never tried it, so be careful here. And of course you have to be careful not to get any liquid into any of the vents.

Belief does not require accepting the evolutionary interpretation of the evidence either. Both sides examine the same evidence, but interpret it differently. Evolutionists merely substitute time and probability (chance randomness) for an intelligent designer God.

Evolution is not caused by random chance. Evolution is caused by harmful mutations tending to cause death while helpful mutations conferring an advantage to those who possess it. Random chance merely triggers some of the mutations. Not all mutations are random, though, and indeed, most helpful mutations are not.

I would also argue that literal creationists don't merely interpret the evidence differently. They ignore the evidence and instead base their judgment on the hypothesis that something written four or five thousand years ago is an accurate representation of reality. Basically, literal creationism is begging the question.

I could not, would not, on a boat.
I will not, will not, with a goat.
I will not eat them in the rain.
I will not eat them on a train.
Not in the dark! Not in a tree!
Not in a car! You let me be!
I do not like them in a box.
I do not like them with a fox.
I will not eat them in a house.
I do not like them with a mouse.
I do not like them here or there.
I do not like them ANYWHERE!