How do you determine if donated, stored blood is viable? Think about stored donated blood; What should we check before transfusing it to a patient, to see if blood is still viable?
What methods to use?
What components should it have in what levels, to be counted as viable?
Detailed version of the question, including some background:
Since I'm a software engineer I'm not aware which kind of topics should I search to find answers that I need. Of course I have tried to find publications and books related directly to this topic. But I could not find any. What I need at the moment is some material to do "some reading/research". And of course, if possible (which I don't know if there are too many possible answers or not) direct answers would be extremely helpful.
Of course I have done some research on indirectly related topics. For example; I have read papers about results of blood storage on blood quality etc. But these papers just analyze the effects, while it is not clear for me if these analyzed materials represents viability of blood.
For more detail, things those analyzed in few papers that I have read are;

CBC: The CBC consisted of 10 parameters: white blood cell (WBC) count, red blood cell (RBC) count, hemoglobin (HGB), hematocrit (HCT), mean cell volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), red cell distribution width (RDW), platelet (PLT) count, and mean platelet volume (MPV).
Differantial: consisted of relative percentages (%) and absolute numbers (#) of neutrophils, lymphocytes, monocytes, eosinophils, and basophils.
Reticulocyte: The reticulocyte enumeration consisted of relative percentage (retic %) and absolute number of reticulocytes (retic #), and immature reticulocyte fraction(IRF).
The NRBC: enumeration consisted of NRBC per 100 WBC (NRBC %) and absolute number of NRBC.
Others: Factors V, VII, VIII, X, and XI, protein S (PS), a2-antiplasmin (AP), and fibrinogen; and the activated partial thromboplastin (APTT) and prothrombin (PT) times. Factors VIII and factor IX.

Still, I'm reading about each of these. What I'm in need is someone help and say; like:

"You are totally lost, these are not related to your case"
"You should check this paper which is related to your case"
"This, this and this ones in your list are what you are looking for. Focus on them."

Thanks

Blood can be stored as whole blood or packed red blood cells. The constituents of each are different. Which one will be used varies based on the patient, the availability and the situation. Whole blood (not necessarily warm) is used more often when there is massive blood loss, as it contains all the components of blood: clotting factors, platelets, plasma, etc. Packed red blood cells have had the white blood cells removed, most of the plasma, the platelets, etc. It is indicated for routine blood loss and to increase the oxygen carrying capacity of blood. The constituents of each are different.

The primary problems of stored blood viability are red blood cell deformability (red cells are normally very flexible in order to pass through capillaries) and red blood cell fragility (this results in fewer RBCs actually active in the recipient, as RBCs will break apart.) The viability of RBCs in storage depend on factors such as adequate ADP (the energy substrate). When RBSs are less viable for any reason (less deformable, more fragile, or hemolysis has started in the stored blood), this is termed red cell (or red blood cell/rbc) storage lesion.

Though there are probably many questions you may have about storage methods and viability, this will give you an idea of search terms for your reading. Good luck in your research efforts.

Fresh Warm Whole Blood (FWB
2012 Clinical Practice Guide on Red Blood Cell Transfusion
Blood Products
Deformability of stored red blood cells. Relationship to degree of packing
Microvascular perfusion upon exchange transfusion with stored red blood cells in normovolemic anemic conditions
Studies on the preservation of human blood. II. The relationship of erythrocyte adenosine triphosphate levels and other in vitro measures to red cell storageability
Nitric Oxide Scavenging by Red Blood Cell Microparticles and Cell-Free Hemoglobin as a Mechanism for the Red Cell Storage Lesion
Hemoglobin-driven pathophysiology is an in vivo consequence of the red blood cell storage lesion that can be attenuated in guinea pigs by haptoglobin therapy


Why do we encode information in DNA in binary and not in base 4? I recently read an article about Harvard scientists encoding 700Tb of data in DNA strands. But they encoded the information in base 2, so T and G was a 1 and C and A was a 0. But why binary? Why didn't they just use base 4? It would be much more efficient!

EDIT: here the link

In the research article on the effort, they give the following explanation for doubling up nucleotides, rather than have each nucleotide stand for two bits:

  This allows us to encode messages many ways in order to avoid sequences that are difficult to read or write such as extreme GC

In practice, they chose which base of the pair it was randomly (so a 50% GC content), while disallowing homopolymer runs greater than three.

Their scheme also uses barcodes and addresses as the "table of contents"/"index"/"page numbers". (The data wasn't stored on a single long piece of DNA, but on a large number of shorter fragments.) By having a slightly flexible coding scheme, this allows them to potentially avoid inserting those annotation elements within the contents.

Furthermore, a slightly flexible coding scheme would allow them to avoid accidentally encoding a text with part of a select agent's genome. (That is, you wouldn't want to synthesize part of the smallpox genome when you're storing your novel. If you can change the nucleotides used, you can avoid that.)


How does heat generated by metabolism differ compared with heat generated through exercise? I am from a mathematical background so I don't have much knowledge on biology. I'm building a mathematical model to predict heat generation with parameters of metabolic heat generation and exercise heat generation.

Metabolic heat generation as far as I understand is the heat produced through body's chemical processes, digestion of food, and elimination of waste.

In this article here, the value for metabolic heat generation is given as 33800$W/m^3$. But the exercise intensities as given here only has values of around $582 W/m^2$.

I think we produce more heat when we exercise than through metabolic activities alone. Is this correct?

If so, why does this huge difference in values of 33800 and 582? Why would the heat generated via exercise be such a low value? (Of course they are not measured in same units.)

Is there any other unit other than $W/m^2$ that measures the heat generated through exercises so that it gives a resonably at least closer value to metabolic heat generation?

First, you have to convert your numbers to the same units for any comparison to make sense. Consider that the average human body has a surface area of about 1.8m$^2$ and a volume of about 66L = 0.066m$^3$. Then your numbers are equivalent to 2230W metabolic heat and 1050W exercise heat for an average person.

The value 2230W for basal metabolic rate (from Table 1 of the Bagum et al paper) is nowhere near what's measured in practise. Basal metabolic rate ("metabolic equivalent", 1 MET) would be 105W for an average person according to the wikipedia page you cited, which equals 2150 kcal / day. That's about the recommended daily calorie intake, so it makes sense. I don't know where their value of 33,800 W/m$^3$ for "metabolic heat generation" comes from, perhaps it's meant represent something else (can't say I understand the article) but it's not the metabolic rate for an average human tissue.


Plasmolysis vs Flaccidity in cells When is a cell said to be flaccid and when is it called plasmolysed?
So far I found that there is a specific relation to osmosis.

Flaccidity in plant cells

  The failure to display turgidity especially as seen with plant cells.
  The suspension of cells from plants in isotonic solutions results in the state termed flaccidity. On a cellular level it represents a lack of pressure of the plasma membrane against the plant cell wall. A more extreme state, termed plasmolysis, is seen given suspension of cells in a hypertonic solution, i.e., as occurs with bacteria suspended in solutions containing high salt or sugar concentrations.

A flaccid cell is one which is in an isotonic solution, this means that the solution and the cell have an equal water conc.. Although there are always water molecules flowing into and out of the cell, they balance each other out. So a cell is referred to as flaccid when it is between being turgid and plasmolysed.

Plasmolysis in plant cells

  If a plant cell is placed in a hypertonic solution, the plant cell loses water and hence turgor pressure by plasmolysis: pressure decreases to the point where the protoplasm of the cell peels away from the cell wall, leaving gaps between the cell wall and the membrane and making the plant cell flaccid.

Sources:

http://www.biologyaspoetry.com/terms/flaccidity_cell_biology.html
http://study.com/academy/lesson/what-are-plasmolysis-deplasmolysis.html
https://en.wikipedia.org/wiki/Plasmolysis


In reconstructions, how are various shapes of facial features determined from skull only? I have seen reconstructions (with skin, eyes, muscles etc) of some first humans based on skulls and skeletons. But how can the shape of nose (protruding part), shape of eyelids, shape of eyebrow, hairline be determined base on the skull only?

Examples of these reconstructions:

Disclaimer: I am an evolutionary geneticist. I know nothing about anatomy and forensic methods....

You should just have a look at wikipedia > forensic facial recognition. There are a number of different facial reconstruction methods, one of which is the so-called Manchester method (see a review of the Machester method in Wilkinson 2010).

In any method of facial reconstruction, there is some part of artistic representation to fill the gap of what we fail to infer from the tissues available. It is typically not so uncommon esp. for recent(-ish) fossils to have remains of soft tissues as well. In absence of such soft tissue, the morphology of the mouth and ears are typically left to artistic interpretation.


Do these large spiders in Taiwan belong to different species? I see both of these spiders (and others) frequently on hiking trips outside of Taipei. Their large webs are often high overhead between trees but can be right across a hiking trail that hasn't been used in a few days, which can make for some excitement.

The two individuals shown in the photos were quite large; both had a body length of about 5 cm not counting legs.

They have similar body shapes but very different color. I don't know if they are completely different species, or different sex or different age.

I mostly see "Spider #2", and usually they are around 3-4 cm in body length. I see  "Spider #1" much less frequently, and I don't think I have ever spotted a smaller individual, but that could just be due to lower frequency.

Spider 1:

I spotted this on on this plant, but once disturbed he started climbing up a vertical thread back into the threes.

Spare photos: 1, 2

Spider 2:

I see these more often than Spider #1.

Adjusted brightness, contrast, sharpness to make the structure of the web more visible:

Spare photos: 1

The following is from Biogeography and Speciation Patterns of the Golden Orb Spider Genus Nephila (Araneae: Nephilidae) in Asia, Yong-Chao Su, Yung-Hau Chang, Deborah Smith, Ming-Sheng Zhu, Matjaž Kuntner and I-Min Tso, Zoological Science, 28(1):47-55. 2011., DOI: 10.2108/zsj.28.47 http://www.bioone.org/doi/full/10.2108/zsj.28.47

Spider 1 seems a good match for C in the images below, and Spider 2 matches A and B. So I propose that both spiders are Nephila pilipes but with different color patterns.

  Fig. 1. Nephila diversity in Asia and Australia and its extreme sexual size dimorphism: (A–E), N. pilipes; (A–B), female of the common color pattern, Taiwan; (C–D), female of the darker color pattern, Taiwan; (E), male (arrow) in copulatory pose on female, Singapore; (F–G), female N. antipodiana, Singapore; (H), female N. plumipes, Australia; (I–J), female N. clavata, Taiwan. Images by M. Kuntner (www.nephilidae.com).


Affinity isolated peptide What is affinity isolated peptides??(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

A peptide or protein can be purified by affinity chromatography. The principle is that the peptide has some substrate to which it will bind, retarding its progress through the column compared to the rest of the peptide population. A couple of typical examples are:

Using a His6 tag put on recombinant molecules, IIRC it binds to Ni2+ trapped in the chromatographic resin and is eluted with a chelator like EDTA.
Immunoaffinity chromatography, where you have a population of antibodies on the chromatographic resin which are specific to the protein that you want to purify (or alternatively having the immunogen bound to the resin so that you can purify the antibodies against it)

Mighty Wikipedia has a link about affinity chromatography here.


What is the lowest pressure at which plants can survive? What is the lowest pressure at which plants can survive? How the plants behave in a Martian-type atmosphere? Is there any plant that can survive such atmosphere?

Can a lichen grow at Martian pressure?

I like your question!

Low surface pressure on Mars (averaging 600 Pa or about 1/170 of Earth's at sea level) is only one difficulty that an organism would have to contend with. In addition, mean surface temperatures are ~210 K (- 63 °C), the surface ultraviolet flux is extremely high (no ozone layer) and an aridity comparable to the Atacama desert. On the plus side, a 95% CO2 atmosphere might promote photosynthesis.

So, higher plants are extremely unlikely to prosper on Mars. Purely in terms of pressure, experiments suggest that at 1/10 Earth atmospheric pressure vascular plant transpiration increases significantly. So much so that they enter into a drought response which often leads to plant death.

However, lichens may be another matter. These are often adapted to low precipitation/pressure environments such as high mountains. Indeed, this article addresses exactly your question (sadly it is not open access). The authors suggest that the lichen Xanthoria elegans experiences no loss in vitality after 22 days exposure to laboratory Mars-like conditions (low pressure, low temperature etc.)!

Having skimmed this article I am frankly amazed (and slightly dubious) at the result. However, it should be noted that they only ran the experiment for 22 days, applied no ionising radiation (to simulate the high UV flux) and make little mention of the precise metabolic state of the lichen. If it has entered into cryptobiosis (cessation of metabolic processes) then it can't exactly be regarded as prospering.

de Vera et al., 2010, Astrobiology, 10, 2, Survival Potential and Photosynthetic Activity of Lichens Under Mars-Like Conditions : A Laboratory Study


Virus-to-virus gene transfer via "sequences integrated into a common host organism" From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese:

  In addition to direct HGT between organisms as depicted in Figure 1, forms of indirect HGT have been observed, which involve an additional intermediary organism in gene transfer from a host organism to the final recipient organism. The most notable are virus mediated gene transfer (transduction) between bacteria (Weinbauer, 2004), retrotransfer of a plasmid to a second bacterium, acquiring host genes and returning to the original bacterium (Ronchel et al., 2000), the spread of donor genetic material between several different bacteria coexisting in complex communities or biofilms (Molin and Tolker-Nielsen, 2003; van Elsas et al., 2003; Wuertz et al., 2004); or from virus to virus via sequences integrated into a common host organism.

Does it mean that a viral gene or other DNA sequence gets integrated into the host's genome and then some other virus (that chanced to be in the same organism) manages to obtain this sequence and package it into its own DNA?

Keese's article has no reference for this statement, and perfunctory googling brought nothing to clear the matter for me.

Does it mean that a viral gene or other DNA sequence gets integrated
  into the host's genome and then some other virus (that chanced to be
  in the same organism) manages to obtain this sequence and package it
  into its own DNA?

Yup, that's what it means (although not all viral genomes are DNA-based).

A lot of genomes contain extensive content that is thought to arrive from viral transfer. Here's a reference to get you started:

Endogenous Viral Elements in Animal Genomes (by Aris Katzourakis , Robert J. Gifford; 2010; PLoS Genetics)

If much of an organism's genome originally derives from viral transfer, then any subsequent viral transduction represents a virus-to-virus transfer of genetic information.


Is the deep ocean fish look ugly because due to darkness there is no visual sexual selection? Is the deep ocean fish look ugly because due to darkness there is no visual sexual selection? If so, is there a common notion of beauty between humans and animals?

I suspect the deep ocean fish look ugly to you because they are unfamiliar.  The iconic fish species with which humans have coexisted forever are all surface fish, with common adaptations for surface living in the light.  When one thinks of a fish the salmon or cod is what we think of.

The deep fish have different selection pressures.  They do not need to be streamlined or svelte.  A deep fish might think a surface fish is ugly because it cannot make its own light - how plain and dull.  How can the surface worlders find a good mate if everyone is dark?


Can coding DNA be used for DNA fingerprinting? I am confused if coding DNA can be used for DNA fingerprinting because I have read that non-coding segments of DNA are used to identify and analyze DNA. I want to know if coding DNA segments are of equal length in all individuals?

When selecting sequences to use for DNA fingerprinting, you have to use sequences that are highly variable within the population.  Coding sequences mostly aren't, and they aren't going to vary much in size, the way tandem repeat sections do.


How can viruses have an incubation period of only 3 days? Cold viruses seem to typically have incubation periods of 3 days, but from a mechanical point of view, I wonder how this is possible?

For example, if we read this viral assay protocol document: https://www.virapur.com/protocols/Virus%20Plaque%20Assay%20Protocol.pdf we can see that when a viral plaque is grown, then the plaque becomes visible in "5-7 days". So, since viruses have reproductive cycle of 6 hours, then that would be about 24 generations. Presumably each generation can only infect cells immediately adjacent to the infected cells since viruses cannot move on their own. So, the virus spreads in rings emanating outwards from the initial innoculation site.

If the visible plaque is 4mm in diameter, then we presume each generation is growing by 4mm/24 = 0.17mm which in itself is kind of suprising because a cell is only about 0.005mm in diameter, so the virions would seem to be simultaneously spreading by 0.17/0.005 = 34 layers of cells per generation. It is hard to see how they could do that without moving in some way. Maybe diffusion of some kind is occurring?

In any case, from geometrical standpoint I don't understand how a viral plaque in the wild could spread fast enough in only 3 days given what we see in the lab.

A viral plaque assay is an artificial system which limits the physical dispersion of newly released virions. It is designed to count the number of infectious virions (plaque forming units) in a given sample, not to measure the rate of reproduction or spread. Since each plaque begins with a single infected cell, the number of new cells infected with each cell burst is going to be limited by the physical proximity of cells to the infected cell, not by the number of infectious virions released.

In a living system, a single cell burst from a viral infection can release anywhere from a few hundred to up to several tens of thousands of new virions which will then be carried in all manner of different bodily fluids to infect new cells, dramatically increasing the potential number of new cells infected after each replication cycle, compared to a plaque assay.

Another consideration is that some of the symptoms of the common cold are generally similar to those common in the prodrome phase of most viral infections, so it is probably difficult to distinguish its true incubation period from the onset of any acute viral infection.


Secondary/ Acquired lactose intolerance Acquired lactose intolerance may occur due to a sudden and high intake of milk-based diets. Lactase is an inducible enzyme.

So if lactase is an inducible enzyme then why increase intake of lactose is causing negative effect? Why more lactase isn't produced in more lactose intake conditions?

Searching for the quote you included led me to the original source.

I wouldn't spend too much time worrying about this particular source, and look at some other sources for more information on acquired lactose intolerance. I think there may be some translation/language issues with this section in this particular source. I believe what the author is trying to convey is not that the intolerance is coming from the increased intake, but that the symptoms of intolerance are coming from a sudden increase in lactose intake following a period of low/no lactose intake, where "sudden" essentially means "faster than lactase induction can occur."

That said, I think this is really more an issue of poor wording in a textbook. The whole section is a bit strangely worded, particularly the part on "flatulence" which this author describes as "characterized by increased intestinal motility, cramps, and irritation" - while these issues may certainly accompany flatulence, this definition of these symptoms characterizing flatulence is not correct, as one can certainly have flatulence with normal intestinal function.


copper spiral birth control not toxic? I Always thought that copper was toxic to the human body.
So how can it be safe to place a copper object (birth control spiral) into a uterus for a duration of 5 years?

Copper is toxic, however from a copper device insufficient levels enter the bloodstream to cause any harm. The released copper is however toxic to sperm. Nevertheless at the site of insertion, they can cause inflammation (especially in the first 21 days and during menstruation) and thus they also recruit white blood cells and the increase in levels of prostaglandins. However, this isn't that common.


Is "monosexual" still a valid term in biology? I read an older article where they talk about species being strictly monosexual as opposite of being hermaphrodite, etc [1]. After an extensive googling and reading about how everybody has to be at least a little bit homosexual, I am still not clear about this. Is monosexual still a valid term to be used in biology? If not, what is the correct term referring to a species that has separate sexes over the entire life-cycle?

I suspect "monosexual" is a term recruited in sociology, psychology and/or medicine. I haven't ever heard of it in application to biological questions. It's a behavioral habit and doesn't seem to be directly related to the (biological) opposition "separate sexes" vs "hermaphroditism".

In biology:

Animals can either be gonochoristic (separate sexes) or hermaphroditic. If an animal species reproduces without gametes it's called asexual (in animals asexual reproduction is rarely the only way of propagation), and if only females are present which give birth without fertilization, they are called parthenogenetic.

In some cases different modes of reproduction are utilized by different stages (alternate generations) or even phases (larva vs adult, young vs old). In other cases in populations coexist males and hermaphrodites or males and parthenogenetic females.

Mammals, including humans, are (nearly) perfect examples of gonochoristic animals: only a male and a female together can produce offspring. If someone is homosexual (it refers to behavior only), he is a dead end in this respect.


Who/where has the advocado genome been sequenced? I have read several places that the genome of the advocado has been sequenced in mexico but i am not sure at what university or persons involved.

You can search for genome sequences at the National Center for Biotechnology Information (NCBI) site.

Here is a link to Persea americana (avocado) from NCBI. It states on the page the submitter for the genome was Hainan University.


RT-qPCR for RNA quantification I'm really new to RT-qPCR and probably I've just a minor problem than I think.

So, what's my problem about.

I want to quantify a virus by a specific area within a gene on its genome. I've specific primer which are working fine with the extracted virus rna from my samples. But now I need a template for a dilution series to quantify this virus. And there's my little problem. And maybe you can help me.

So I know that the genome of my virus is a negative sense single stranded RNA, so -ssRNA, and moreover I know the virus strain and the gene, which RNA I want to synthesize for the quantification. So I looked it up on ncib and I found the sequence of the gene, but it is listed as the complete cds of the gene and not the RNA sequence. And as I'm right the cds is the same sequence as the positive sense RNA, with Us instead of the Ts?!? So is it right for synthesizing, that I have to translate the cds first in +ssRNA and then in -ssRNA and this -ssRNA sequence I have to synthesize to get a standard?

If the cds would be: ATG , the +ssRNA would be: AUG and therefore the -ssRNA would be: UAC and this UAC , I would have to synthesize? Sorry for this stupid question but I am a lil bit confused at the moment with the difference of - and + ssRNA regardind the RT-qPCR. Another question would be, whether the Reverse transcriptase with Random hexamer primer is specific for -ssRNA or +ssRNA. It isn't ? So my quantification would also work with the AUG as a template for a standard curve?

Thanks a lot!

dan

To start off with your last question, strandedness is something the reverse transcriptase does not care about. If you use random hexamers it will simply translate your -ssRNA into a + single stranded cDNA. Perhaps this diagram from Wikipedia makes things more clear, it is for an mRNA but the principle is the same:

This cDNA will then serve as a template for your primers in the qPCR which will turn it into a double stranded DNA molecule. In other words, after one round of amplication in a PCR reaction the DNA products of the + and the - RNA strand would be indistinguishable!

It therefore does not matter which strand you synthesise as DNA to make your standard curve. It will be double stranded so you just need to compensate for the other strand being a template in the PCR as well.


Causes of the stochastic behaviour of voltage-gated ion channels I came up with the following electro-mechanical model of a voltage-gated ion channel, resp. of its voltage sensor as described here and here. The voltage sensor is a bistable system with two local energy minima $E_1(V)$, $E_2(V)$, the first one indicating "closed", the second one "open":

From Bezanilla, The Voltage Sensor in Voltage-Dependent Ion Channels, p. 567. You can interactively explore a voltage-dependent energy surface here (schematically).

I created a spring model with Algodoo which looks like this (green: the voltage sensor (= a peptide subunit), white springs: keep it in place, blue: favours the closed state, red: simulates voltage, opens the gate):

(You can download the model here and explore it interactively with Algodoo.)

To behave stochastically - i.e. the probability of being open $p(V) \sim e^{-\Delta Q(V)/kT}$ which presupposes a thermal equilibrium - there must be fluctuations that can lift the system above the energy barrier between the two energy minima.

My question concerns the source of these fluctuations in the real ion channel: are these thermal (mechanical) fluctuations (e.g. other molecules hitting or tearing the sensor) or are these fluctuations of the membrane potential?

The fluctuations arise form thermal energy and can be described by the Eyring equation


Online resources for entomology? I'm going to teach a c ollege-level introductory entomology course soon, and I'm looking for free online entomology resources. Does anyone have any recommendations?

In particular I'm looking for phylogenetic resources, experiment ideas, images, topics, etc.

Ideally, I'd love to find a discussion forum consisting of other entomology instructors sharing their ideas.

Thank you!

The Entomological Society of America has dedicated page called Entomology Resources for Teachers, which might answer many of your questions. It compiles curated links to resources, universities,

Here are a couple of other entomological links/resources that I have saved from before:

Bugguide.net
Pictures, simple keys and taxonomical info. Also has a forum.
The Entomological Foundation: Education
Links, project ideas etc.
Kerbtier.de
Webpage on beetles found in Germny, but relevant for many European countries. Also has general pages on e.g. beetle morphology and a glossary that might be useful.


Is honey in hot green tea unsafe? I used Google to try to figure out what kind of mixture honey has with hot water, and I found several Ayurvedic sources claiming that honey in hot water is toxic.

For example:

Honey – NEVER Put It in Hot Water/Teas
5 Reasons You Should NEVER Cook With Honey
Honey: A Must Read For Those Who Eat It Regularly

What I would like to know is how does heating honey make it toxic?

Is there something that happens at the molecular level that changes the chemical properties of honey when it is heated? If so, are these chemicals harmful, as claimed?

Are there any other reasons other than heating that may make honey toxic?

Heated Honey and HMF

In this paper, Studies on the physicochemical characteristics of heated honey, honey mixed with ghee and their food consumption pattern by rats, by Annapoorani, et.al.;International Quarterly Journal of Research in Ayurveda, 2010 Apr-Jun; 31(2): 141–146.doi:  10.4103/0974-8520.72363, the report finds a statistically significant increase in the compound hydroxymethyl furfuraldehyde (HMF).

The compound was studied by the National Toxicology Program of the U.S. Department of Health and Human Services in Mice and Rats and the results were published in a report dated June of 2010.

  5-(Hydroxymethyl)-2-furfural is formed when reducing sugars such as fructose and sucrose are heated in the presence of amino acids. 5-(Hydroxymethyl)-2-furfural is ubiquitous in the human diet and occurs at concentrations greater than 1 g/kg in dried fruits, caramel products, certain types of fruit juices, and up to 6.2 g/kg in instant coffee. 5-(Hydroxymethyl)-2-furfural also occurs naturally and has been identified in honey, apple juice, citrus juices, beer, brandy, milk, breakfast cereal, baked foods, tomato products, and home cooking of sugar and carbohydrates.

- NTP toxicology and carcinogenesis studies of 5-(Hydroxymethyl)-2-furfural (CAS No. 67-47-0) in F344/N rats and B6C3F1 mice (gavage studies).; Natl Toxicol Program Tech Rep Ser. 2010 Jun;(554):7-13, 15-9, 21-31 passim.

HMF is a breakdown product of Fructose, Glucose, and Cellulose (hexoses) and is found in many products, especially high fructose corn syrup, after heating, and is excreted in the urine. However, it has not been correlated to any diseases in humans (4). In the NTF toxicology and carcinogenesis studies, the conclusions were that

  under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in male or female F344/N rats administered 188, 375, or 750 mg/kg. There was no evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in male B6C3F1 mice administered 188 or 375 mg/kg. There was some evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in female B6C3F1 mice based on increased incidences of hepatocellular adenoma in the 188 and 375 mg/kg groups. Administration of 5-(hydroxymethyl)-2-furfural was associated with increased incidences of lesions of the olfactory and respiratory epithelium of the nose in male and female rats and mice.

- NTP toxicology and carcinogenesis studies of 5-(Hydroxymethyl)-2-furfural (CAS No. 67-47-0) in F344/N rats and B6C3F1 mice (gavage studies).; Natl Toxicol Program Tech Rep Ser. 2010 Jun;(554):7-13, 15-9, 21-31 passim.

As is shown in the NTP report and the other sources above, HMF is not only found in honey. It will be found in any product that contained sugar or high fructose corn syrup that has been heated, such as baked goods. The reason you are likely to encounter it in honey is foremost that honey is 70-80% reducing sugars (5) and also that bee keepers often supplement HFCS for actual flower nectar when there is not enough flower nectar available for the bees to use to produce honey.

Toxic Honey

One thing to note is that there are toxic forms of honey, just as there are poisonous mushrooms and edible mushrooms. Honey derived from rhododendrons can contain Grayanotoxin, however it is rarely fatal in humans. If you are buying your honey from a supermarket or a reputable keeper, then there is almost no chance that your honey will contain grayanotoxin.

Why is Honey Harmful to Infants?

The issue with honey is that it can contain Clostridium botulinum spores. If the spores germinate, the resulting bacteria release botulinum toxin.

Botulinum toxin, which is the cause of botulism, is a neurotoxin that causes dystonia, and can be lethal in minute doses (ng/kg doses).

For most adults, the risk of botulism from the spores found in honey is minute. The gut microbiome and immune system proteins such as defensins will prevent C. botulinum colonization, so even if the spores germinate, they will not grow to a critical mass to produce enough toxin to do harm and will be excreted.

This however is not the case for infants less than six months of age. Their microbiome is still developing and their immune system is not fully formed. Also, as they have less mass, it takes a lesser absolute amount of the toxin to cause illness and death.

C. botulinum spores are heat resistant, though they can be killed by boiling (7), which means that the internal temperature of the spore needs to reach >85°C for over 5 minutes. Pasteurized honey should already have had this treatment, however you will still see the warnings to not feed to infants less than six months to one year of age, as commercial heat pasteurization may not kill all of the spores (7).

So unless you are immunocompromised, have no gut microbiome, are an infant less than six months of age, or your boiled water does not stay at a temperature greater than >85°C for longer than 5 minutes, and are using raw honey, then you shouldn't be at too much risk.

Edit

Information has been reorganized to better reflect edit to question.


possibly unusual spider behavior? In Cambridge UK there is this spider:

I know not what species but it is common - I think they look good.

But look at this behavior. What are they doing? I thought malting but do spiders do that? Why would they congregate like this?

Those appear to be Daddy Longleg spiders, and they are known for forming spider clusters, which is considered as gregarious behavior. Quoting Wikipedia:

  Many species of harvestmen easily tolerate members of their own species, with aggregations of many individuals often found at protected sites near water. These aggregations may number 200 individuals in the Laniatores, and more than 70,000 in certain Eupnoi. Gregarious behavior is likely a strategy against climatic odds, but also against predators, combining the effect of scent secretions, and reducing the probability of any particular individual being eaten.


Does anyone know a good pancreatic-cancer metastasis cell line? Researching about pancreatic cancer. We have mostly "main-tumor" cell lines in our lab, and I´m currently looking for cell lines originating from metastases (liver, lung, etc.).
Does anyone know a well-established pancreatic-cancer-metastasis-cell line?

SUIT-2 cell lines are derived from the liver metastases of Pancreatic Ductal Adenocarcinoma. The subline S2-007 is highly metastatic. The other sublines are S2-013, S2-020 and S2-028 which have decreasing metastatic capabilities.

You can probably refer these articles for more info :
1. https://www.ncbi.nlm.nih.gov/pubmed/3102439
2. https://link.springer.com/article/10.1007/s10585-017-9840-3


Can a dog run 150 km non-stop? In Werner Herzog's 2010 documentary Happy People: A Year in the Taiga, a dog is reported to run 150 km from the Taiga back to the owner's village, without any stop and seemingly at full speed as it is running next to a snowmobile.

I am skeptical of this. I cannot find any reports of dogs running a distance even close to this. This article on super-distance dogs does not mention any distances over 40 miles (64 km), which is still less than half the distance, and together with the owner running, so at much lower speed.

Can a dog really run 150 km at full speed?

There are 100, 200 and 1000 mile races for huskies, we can check the speeds of the winners of the races: http://www.eaglecapextreme.com/index.php/the-race/race-times

97 miles run in 17.23 hours, gives 5.6 miles an hour, 10 km/h, on a cold day, 12-16 dogs towing the musher and the sledge. without a sledge, a husky can probably run 150km at 15km/h average, so that's 10 hours of running.

there have been studies about husky mitochondria and their biology.


What causes feeling of feet falling asleep to be delayed? This answer explains the sensation of extremities "falling asleep" as a result of sustained pressure on a nerve. The answer links to an external web page that says that the feeling "quickly goes away once the pressure is relieved."

In my experience, however, it doesn't usually go exactly like this.  For me at least, usually what happens is I will start feeling a tingling sensation in my feet after sitting in an awkward position for an extended period of time. If I ignore the sensation for long enough, it continues to get worse until I finally do stand up.  But after I stand up, rather than the sensation quickly disappearing, I find that usually it suddenly gets much worse for a period of time.  What started as an annoying tingling when I was sitting quickly turns into something quite uncomfortable upon standing up, even to the point where I am not able to walk around properly until the sensation passes a few minutes later.

But once I am standing up, the nerve shouldn't be pinched anymore, so why does the sensation of my foot being "asleep" remain for a few minutes after standing up, and why does it actually seem to briefly get worse after I have already stood up and "unpinched" the nerve?

This paper, while mainly dealing with chronic nerve compression, appears to explain the effects of nerve compression on the blocking the transmission of neural impulses (causing the "sleeping limb" syndrome).

This paper describes how the application of pressure on a nerve causes a miniature case of compartment syndrome, where the pressure causes the intraneuron pressure to increase, leading to paresthesia. Edema also occurs within the neuron, causing pain signals to be sent out. In the experimental rats which were unable to relieve this pressure, permanent nerve damage resulted.

When the effects from the nerve compression exceeds a certain level, the pain/tingling will result in you releasing the pressure from the limb in order to prevent nerve damage.

However, the nerves are still blocked from transmitting their impulses due to the  compression blockage described in Paper 1. When the blockage is resolved, the neurons are now capable of transmitting their pain signals, which continue for a period of time until the pressure within the limb falls sufficiently below the pain threshold.


Is nucleosomal DNA ever degraded? A hallmark of apoptotic DNA fragmentation is the digestion of DNA into individual nucleosomes. In addition, in the following experiment that tried to isolate the components of the nucleosome, the micrococcal nuclease only cleaved the linker DNA and not the nucleosomal DNA.

I've tried searching the internet but I couldn't find a clear answer to my question. Is nucleosomal DNA ever degraded? Are there nucleases that degrade it, and if there are, are they common? If nucleosomal DNA is not degraded, what protects it? The histone proteins?

Nice question! Nucleosome is quite a stable structure because of electrostatic attractions between the phosphate group of DNA and Lysine or Arginine of histone octamer1. In fact, both histone and DNA are known to protect each other from degradation: histone protects DNA from some kinds of damage2 and DNA protects histone protein from proteolysis3. Also, the histone protein gets modified whenever there is damage to nucleosomal DNA, so that DNA repair machinery can be activated4. Thus, nucleosome is not only structurally stable, but also tries to maintain its stability by its constituents protecting each other.

source

This stability has also been taken to a whole new level. In a research paper, scientists predicted that the reason for discovery of thousands of years old DNA, in intact form, is due to the stability of nucleosome5. They have even predicted that nucleosomal DNA can remain readable for even millions of years, because the time when histones start degrading is also the time when proteases and nucleases degrade, leaving very few chances for DNA to degrade.

But, nucleosomal degradation is not impossible. In a research, scientists concluded that the enzymes Caspase Activated DNase (CAD) or DNA Fragmentation Factor 40 (DFF40), together called CAD/DFF40, are indirectly required for degradation of nucleosome6. See this paragraph (I only pasted the main points):

  We report here that in response to apoptotic signals from a death receptor (CD95 and tumor necrosis factor-$\alpha$) or mitochondrial (staurosporine) apoptotic stimulus, the core nucleosomal histones H2A, H2B, H3, and H4 become separated from DNA during apoptosis in Jurkat and HeLa cells and are consequently detectable in the cell lysate prepared using a non-ionic detergent. The timing of this histone release from DNA correlates well with the progression of apoptosis...Taken together, these data demonstrate that CAD/DFF40 functions indirectly in mediating nucleosomal destruction during apoptosis...In this study, we have found that core nucleosomal histones separate from chromatin in apoptotic cells, but that this is not simply a by-product of DNA fragmentation. This event is indirectly related to CAD/DFF40 in the sense that CAD/DFF40 is required but is insufficient for the apoptotic histone release.

Thus, though it was the only paper I could find, nucleosomal DNA can also degrade in the same way as linker DNA if larger amount of CAD/DFF40 is present to degrade it.

References:

Histone structure and nucleosome stability; Leonardo Mariño-Ramírez, Maricel G Kann, Benjamin A Shoemaker, and David Landsman
Nucleosomal histone protein protects DNA from iron mediated
damage; Helen U.Enright, Wesley J.Miller and Robert P.Hebbel
Actin and DNA Protect Histones from Degradation by Bacterial Proteases but Inhibit Their Antimicrobial Activity; Asaf Sol, Yaniv Skvirsky, Edna Blotnick, Gilad Bachrach, and Andras Muhlrad
Histone - Wikipedia
Degradation of ancient DNA; Zvi Kelman, Lori Moran
Apoptotic Release of Histones from Nucleosomes; Dongcheng Wu, Alistair Ingram, Jill H. Lahti, Brie Mazza, Jose Grenet, Anil Kapoor, Lieqi Liu, Vincent J. Kidd and Damu Tang


Is there a good site or software to see if a primer pair spans an exon junction? I am going to perform some RT-qPCR tests to validate an experiment.

I'm currently in the process of ordering primers, and I would like to get them from the Harvard Primer Bank since these have been validated before.

However, I would like to get primer pairs that span an exon junction (i.e., one primer on one exon, the other primer on another exon.)

Currently, I have to do a lot of steps to figure this out, since the Primer Bank only gives the positions of the primers on the CDS, and not on the entire mRNA molecule.

Does anyone have a quick way to check on which exons the primers belong?

Thank you!

Is there a good site or software to see if a primer pair spans an exon junction?

If there is a such a site, I have never encountered it. Since you say you have the genomic coordinates for each primer it seems to me like all you need is a list of the genomic coordinates of every transcribed exon in the human genome. Assuming that is correct then you are in luck because such lists do exist in the form of a GFF3 file. You should be able to obtain a comprehensive annotated GFF3 file of the human genome from the EnsEMBL website. It is possible that the UCSC browser has a similar file (except in their '.bed' format) but I  am less familiar with the contents of that site.


Is there a schema for how human behavior is genetically determined? It seem one can distinguish three different kinds of genetic determinism of common patterns of human behavior:

behavior that is directly wired into our nervous system, e.g. face-related mirror neurons and chewing,
behavior that is within reach of operand conditioning, i.e. that is predisposed by certain features of our bodies (and environment) and relatively easily discoverable by exploration, e.g. how to throw something,
behavior that is passed on culturally, e.g. tool use.

Does there exist something like this in the literature?

We can only observe correlations

Let's just talk about statistics. You can see a correlation between two things only if there is variation for these two things. It therefore, make no sense to look at a single trait that has no variance and ask "is it genetically coded?". The only thing that makes sense is to understand what variables explain the observed variance for the trait of interest. Here, in your question, you are interested in behavioural traits. This answer stands for behavioural traits as it stands for any other phenotypic traits.

What variables could explain variance in a given trait?

To make it easy, let's consider only two variables, genetics and environment. In reality, one should consider other variables such as epigenetic for example. The total variance in phenotype that you observe is the result of the addition of the variance of this phenotype that is due to genetics variance ($V_G$) and the variance of this phenotype that is due to environmental variance ($V_E$) and their covariance ($COV_{GE}$). In other words:

$$V_P≈V_E+V_G+COV_{GE}$$

It is very common to express the phenotypic variance as being the sum of the genetic and environmental variances (and some others such as epigenetic variance). However, you are free to make this partitioning as you feel it useful for you.

Let's investigate those variables a bit further

Of course, $V_E$ and $V_G$ can be further decoupled into a sum of variances (and covariances). And you are free to do the decoupling exactly as you want to. For example $V_E$ could be defined as the sum of the phenotypic variance that is due to variance in temperature ($V_T$), the phenotypic variance that is due to variance in water availability ($V_W$) and the phenotypic variance that is due to variance in the culture of the parents ($V_P$) (and all the covariance). $V_E = V_T + V_W + V_P + ... $

Similarly, the genetic variance $V_G$ can be further decoupled. It is standard to decouple this variance in dominance vs additive effects (relating to the genetic architecture underlying the trait) but this won't be of great help to you. How about talking about variance in the genes affecting brain morphology $V_B$ and variance in the genes affecting hormones concentration $V_H$ and their covariance (epistasis and pleiotropy) $V_G = V_B + V_H + ...$.

Common schema

To my knowledge there is no common schema in how to partition those variances for the specific study of the mechanistic of behaviour. I don't really understand what is the partitioning that you're suggesting in your post but I am hoping that this answer can help you to think further and eventually come up with a satisfying schema.


Can anyone remind me of the name for the inter-scapular space on the back? It's one of those names which are often said not to exist, like philtrum.

"Inter-scapular space" is defined as the space between the scapulae.  It was most likely created by doctors who had no name for the space.  Yet another expansion of the English language by those who have need of a word or phrase to describe something that has no word or phrase already.  I found no other definition.


Does prolonged exposure to low pitch but low volume noise affect hearing or stress? This is similar to another post but not quite the same... At work, our ventilation system produces a constant low pitched sound - like a rumble - as well as the sound of air blowing through the vents. It's not very loud, we can certainly talk, even whisper to each other, but when it shuts off, it's like a huge weight off my shoulders. My ears don't really pop but there's sort of a slight "tingling" sensation - like when the blood starts flowing to a hand or foot that fell asleep. You can usually hear several people in the same room say "Ahhh" as in we are all glad the noise has stopped. I have worked in this location for over 10 years and in that time I have developed tinnitus which is probably attributed to a number of bad behaviors as a youth. But I was wondering if this constant noise could contribute to the decline in hearing? Also, that sense of relief when the noise stops makes me wonder if the constant noise adds to our stress levels?

Basically you are asking: (1) does the low-pitch noise affect my hearing sensitivity; (2) has the noise aggravated hearing loss acquired earlier in life; (3) if the noise can induce stress and (4) if the noise may cause tinnitus (kind of a hidden question).

(1) Is the ventilator noise damaging?: Noise-induced hearing loss typically occurs at high sound levels. Occupational safe noise levels are set at around 85 dB SPL (Nat. Stand. Occupational Noise). This is comparable to listening to traffic on a busy road from 10 meters away for 8 hours/day for 5 days/week (see wiki on sound levels), or a diesel truck at 15 meters going 64 km/h. If you can still talk normally, the noise cannot be much more than 60 dB SPL, which is normal conversational level (see sound chart). So the ventilation noise is not bad for your ears as it is well below 85 dB SPL.

(2) Does the noise aggravates present damage?: Similarly to the answer under (1), the noise is not loud enough to be regarded damaging even with existing hearing loss.

(3) Does it cause stress? As @anongoodnurse suggested: yes it causes stress, apparently. Every unpleasant sensation will do so to a certain level.

(4) Effects of the noise on tinnitus: Typically, tinnitus is caused by hearing loss (see cause of tinnitus) and the pitch of tinnitus often coincides with the lost frequencies (see cause and effect of tinnitus). So if your "bad behaviors" at youth refer to loud music, then it is probably noise-induced hearing loss that has resulted in a dip at your hearing acuity at 4 kHz (the 4-kHz notch). In effect, the tinnitus you are experiencing will be around this frequency and therefore high-pitched. As the loudness of the ventilator is too low to cause damage, it is probably unrelated to your tinnitus.


Are black panthers the same as jaguars? I google the scientific name for black panthers. I get panthera onca. I google panthera onca, and I get jaguar. Can someone explain what is going on? Are they the same? What is the real scientific names for them? Because panthers are black and jaguars are yellow with black spots.

Black panther refers to melanistic examples of either leopards (Panthera pardus):

or jaguars (Panthera onca):

It is not typically used to refer to (the rare/historic/unconfirmed) examples of melanism or pseudo-melanism in other species of Panthera (e.g. black tigers).


When is strict sterile technique necessary? Cloning vs. protein expression Background: I have previously worked with RNA, and then we use laminar flow hoods for any work where we do plating or inoculation of cultures while applying sterile technique. I am now working in a biochemistry lab. I'm told that I can work on a lab bench, while doing basic cloning for production of plasmids in E.coli, and don't need to use a Bunsen burner as long as I apply sterile technique (and in most cases I don't see people sterilizing the bench with enthrall prior to work). However, if I do any work which relates to expression of proteins - then I should use the Bunsen-burner while applying sterile technique.

Question: Is it really so that you don't even have to use a Bunsen-burner while plating (normal E.coli: XL1-blue cells)? in this case, why? Are there not always something in the lab which can grow on kanamycin plates? We don't use white/blue screening, we simply spread XL1-blue cells onto LB plates with kanamycin - then pick a averaged sized colony to make a LB-culture. It seems to me that we are just lucky that we usually pick the right colony (which we do confirm by sequencing after mini-prep).

For most plasmid preparation, strict sterile technique is not necessary. The antibiotics in the media will select for bacteria which carry a resistant plasmid, so you don't usually have to worry about other organisms getting in.

However, when you're using several types of plasmid, you do need to be careful to avoid cross-contamination, because each plasmid is resistant, so bacteria transformed with plasmid A will live just fine on plasmid B's plate. When plating your cells, be sure to pass your cell spreader through a flame. It doesn't have to be an official Bunsen burner, I used an alcohol burner just fine.

If you make a big bottle of media and use small aliquots at a time, then the bottle should only be opened inside the hood.


How can Chronic myeloid Leukaemic drugs reduce the production of the Philadelphia genotype? How can Chronic Myeloid Leukaemic drugs (Tyrosine kinase inhibitors, e.g. imatinib, etc.) that act by inhibiting bind of ATP to the active site of the BCR-ABL1 protein actually reduce the prevalence of the Philadelphia chromosome? (For example, optimal response to TKIs in 3 months would be Ph+ <35% and/or BCR-ABL1 <10%.) What I am actually asking is how a drug that targets the result of the oncogene (the BCR-ABL1 protein) can have an effect on the source (ie. genotype of the cells), as CML is a clonal haematopoietic stem cell disorder?
An example Reference paper: Apperley JF. Chronic myeloid leukaemia. Lancet. 2015 Apr 11;385(9976):1447-59. doi: 10.1016/S0140-6736(13)62120-0. Epub 2014 Dec 5. PMID: 25484026.

The key is that TKIs, such as Imatinib, are a therapy rather than a cure
Per Wikipedia, Imatinib acts as a competitive inhibitor of the otherwise constitutively-active BCR-ABL fusion protein, rather than the fusion gene.  By binding the kinase domain, BCR-ABL is unable to phosphorylate downstream effectors that result in unchecked proliferation.  As long as a patient continues to take Imatinib, BCR-ABL activity should be blocked.

In the past few years (i.e, long after imatinib's discovery) there has been a lot of research into exactly how hematopoetic stem cells, which reside in the marrow and create leukemic blasts, work. Most HSCs remain in a quiescent state, but it's not particularly well-known how frequently they turn over.  Recent CML studies have shown that after ~5 years, a large portion of CML patients can safely taper the the drug.  Presumably this is related to HSC turnover, but frankly as a leukemia molecular biologist rather than a physician, I'm not the best font of clinical knowledge.


What determines when a virus becomes a "new strain"? The reason we cannot find a cure for the common cold is because viruses mutate rapidly. Where do the mutations occur in the DNA/mRNA of viruses and does this have any effect on the protein level? what has to change for the virus to be considered a new strain?

I don't know if this is a comprehensive enough answer, but viruses are taxonomically broken down into order (-virales), family (-viridae), subfamily (-virinae), genus (-virus) and species. This system was developed by the ICTV and is concurrently used with the Baltimore System.

A lot of species contain variations called virus strains. There are two types, serotype and genotype.

In serotypes, the differences are detected by variation in antigens. Genotypes are detected by differences in genome sequence.(1).

The reason a vaccine is difficult to create for the common cold, or upper respiratory tract infections is not only because of the frequency of mutation but also due to the large number of serotypes present.(2),(3).

Virology: Principles and Applications - Carter.
Princuples and Practice of Infectious Diseases - Mendell, et al.
E.g. Olszewska, et al. Development of vaccines against common colds. Br Med Bull. 2002. 62(1):99-111.


How to determine continental ancestry group (race) with transcriptome data obtained with RNA microarray? Say I have a whole genome expression data (transcriptome) for some sampled human tissue. Is this data sufficient to find out the continental ancestry group of a donor?

If you can call genomic variants from your data, depending on your coverage of the genome, you should be able to map ancestry. For example, if you have sequencing reads, you can align your reads to a reference genome and then call variants using existing pipelines.

Once you have variant calls, you could use ancestry-informative markers to infer the ancestry of your sample directly.

Or you could use existing software to map the ancestry of your sample in relation to other samples of known ancestry, using a program like ADMIXTURE, STRUCTURE, EIGENSOFT, or just principal components analysis. For reference samples, you could use a publicly available data set like HapMap 3 or the Human Genome Diversity Project.


how the coronavirus was distinguished? I have read a lot about the outbreak of the coronavirus, I know that in january scientists had already sequenced the viral genome.

How was the virus identified prior to the sequencing

Given that viruses are not like germs that you can see and distinguish readily in microscope, how could scientists know that there was something new about the new disease and how could they purify the pathogen that cause that disease without knowing what it is and without knowing its genetic code?

Where can I find information about procedures that are used to identify new viral pathogens?

Given that there is a group of people with suspicious desease, what are the laboratory procedures used to eliminate known pathogens and how you discover that you have a novel virus without knowing its genetic sequence (and without the ability to extract it - as far as I know you can not isolate virus particle with tweezers...).

Thank you!

This is basic epidemiology. When medical professionals notice that a group of people with some characteristic in common, are being seen for a similar disease, they ask if there's a connection. In this case, several people in Wuhan were diagnosed with severe pneumonia, and the doctors noticed that they worked in the same location.

  Three adult patients presented with severe pneumonia and were admitted to a hospital in Wuhan on December 27, 2019. ... Her occupation was retailer in the seafood wholesale market. ... He had been a frequent visitor to the seafood wholesale market.

--A Novel Coronavirus from Patients with Pneumonia in China, 2019

You're more likely to follow up when the disease is unusual or severe, and when the connecting factor is unusual or suspicious. In this case, the severe pneumonia was presumably unexpected, and live animal markets always have potential for disease transmission.

(In fact, it's quite possible that the virus had been circulating in the region for weeks before this cluster was noticed, and that previous cases had not been surprising enough to trigger the research needed to identify a new virus; though it's also likely that the medical personnel in Wuhan had noticed that there were an usually high number of pneumonia cases and were already looking for a connection.)

See also the answers to How did scientists discover HIV?. Old-fashioned epidemiology is always critical.

The same article explains how the virus was sequenced:

  Bronchoalveolar-lavage fluid samples were collected in sterile cups to which virus transport medium was added. ... RNA extracted from bronchoalveolar-lavage fluid and culture supernatants was used as a template to clone and sequence the genome. We used a combination of Illumina sequencing and nanopore sequencing to characterize the virus genome.

And isolated:

  ... supernatant from bronchoalveolar-lavage fluid samples was inoculated onto the apical surface of the cell cultures. ...  After three passages, apical samples and human airway epithelial cells were prepared for transmission electron microscopy. ...

So briefly, they took patient samples, grew them on cultured cells, used electron microscopy to check the kind of virus. They sequenced fluid (not cells, since the virus would be secreted into the fluid, making it a relatively pure source of virus RNA) and then sequenced using a standard high-throughput sequencing approach; knowing the likely kind of virus would make this easier but isn't essential. There would have been lots of human RNA in the sequence, but it's easy to bioinformatically separate that out and limit your analysis to the viral sequences. The virus isolate was also not essential for the identification; knowing the sequence is the critical information today. But having a virus isolate certainly makes all the subsequent work much easier.

This is pretty standard modern molecular biology, not an esoteric skill.


What is the difference between the evolution of fins in whales and fish? For a homework assignment I received the following question:

Which statement best explains the evolution of fins in whales and fish?

a. The common ancestor of whales and fish possessed genes for fins.

b. Whales and fish possess the same mutations in their genomes.

c. Fins evolved in whales and fish because they both use them to swim in water.

d. Fins evolved in whales and fish because of different mutations that occurred
in their genomes.

e. Fins evolved in whales and fish because their most recent common ancestor swam in water.

My answer is (c). Of the given options, it seems most accurate. I feel that the language is unclear as many organisms who do not have fins swim in water. That can be a logic against the option. But, the given answer is (d). That seems too bizarre as even humans and fishes have different mutations in their genomes. (c) seems more appropriate as it can exemplify convergent evolution.

I agree with you that the question is ambiguous, and also that the most sensible answer would be C.  However, one could make a more or less reasonable argument in favor of several other answers, too.

  a. The common ancestor of whales and fish possessed genes for fins.

Technically, this statement is true.  At least some of the fins of whales and fish are even distantly homologous, even though the lineages leading to tetrapods (including whales) and to ray-finned fishes diverged quite early in their evolutionary history.

(Specifically, the flippers of whales are modified tetrapod forelimbs, which are homologous to the pectoral fins of ray-finned fishes.  Whether one should also consider the tails fins of whales and fish to be homologous is a bit more debatable: the actual fin structures are very different, and presumably share few if any developmental pathways, but the tail and the spinal column which they attach to and are powered by is clearly a shared feature of both groups.)

However, while shared evolutionary history may explain why fish and whales have similarly placed flippers / pectoral fins, and why they both have a flexible spine that supports undulatory swimming with the help of a tail fin, it does not explain the convergent evolution of whales' forelimbs (which were formerly adapted for walking on land) into fin-like flippers.  So in that sense, while perhaps partially correct, this answer is also quite incomplete.

  b. Whales and fish possess the same mutations in their genomes.

It's hard to even tell what this statement means.  Insofar as it's a restatement of the fact that whales and fish share some of their evolutionary history (up to the divergence of the bone-finned and ray-finned fishes), it's no more or less correct than statement A above.

However, I suspect that the intended meaning of this statement is that whales and (ray-finned) fish would've separately evolved the same "fin-making" mutations after their lineages diverges, which is both clearly incorrect and also, even prima facie, statistically very unlikely.  So I would rule this one out.

  c. Fins evolved in whales and fish because they both use them to swim in water.

This statement is written using teleological language, which some may consider misleading, as it could be misinterpreted as implying that evolution was a directed process: it could be interpreted as saying that whales needed to be able to swim, so they chose to evolve fins (or that some guiding consciousness granted them fins).  This is, of course, incorrect — or, at least, we have no scientific evidence of there being any such conscious force guiding evolution, or of any organism (with the arguable exception of humans) being able to deliberately direct their own evolution.

However, it's quite possible to interpret this statement in a way that makes it perfectly correct: as both whales and fish move around by swimming, possessing fins (or something similar to fins) is an advantageous trait for them, and has thus been favored by natural selection.  If pressed, I would thus choose this one as the most correct answer out of the given options.

In particular, note that the argument made by AliceD that "they have to develop fins first before they can use them" is not really true: the ancestors of both whales and fish were swimming long before they evolved fins, and thus the selection pressure in favor of having fins (or fin-like structures) was already present before the fins themselves evolved.

In particular, the first aquatic ancestors of whales are believed to have swum much like modern-day otters and seals, using their flipper-like limbs as makeshift fins.  While there's no discrete transition point where one could definitely say that whale limbs turned into proper fins, it is clear that the fins, and their direct evolutionary predecessors, were being actively used for swimming, and that this fact directly drove their evolution into the actual fins that modern whales have.

  d. Fins evolved in whales and fish because of different mutations that occurred in their genomes.

While technically correct, this statement is so vague that it's all but meaningless.  All evolution is driven by mutations, and those mutations, being basically random, are rarely if ever the same in any two lineages.

Certainly, it would be silly to claim that "different mutations occurring in their genomes" is an explanation of why whales and fish evolved fins: humans also constantly have different mutations occurring in our genomes, but we clearly don't seem to be evolving fins.  Neither are pigs or bumblebees or sunflowers, even though all of those species (and, of course, all others too) are also constantly experiencing different mutations in their genomes.

Really, this answer reminds me of the story about a person in a car who gets lost and stops to ask a passerby where they are; the passerby, after a moment's thought, replies "you're in your car."  While technically correct, that answer is absolutely useless — and so is this one, too.

  e. Fins evolved in whales and fish because their most recent common ancestor swam in water.

Again, this answer could be interpreted as basically a restatement of answer A, and thus as being partially correct.  However, it completely ignores the convergent selection pressure described in answer C, which is responsible for the more recent evolution of whale flippers into something resembling fish fins more than, say, human hands or the feet of hippopotamuses (currently believed to be the closest living relatives of whales and other cetaceans).  Thus, I would not pick this answer, for the same reason that I wouldn't pick answer A.


Need help interpreting Western blot data So the paper I am reading (here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7094582/) uses densitometric units to quantify the western blots.
The authors mentioned that the unphosphorylated proteins were used as loading controls, and their quantities are represented by the densitometric graphs for each corresponding figure, but protein activity is measured by their phosphorylated counterparts which I believe is represented by the densitometric graph on the right of each corresponding figure.
Questions:

Did I interpret that correctly?
What exactly are loading controls?
I am trying to use these data for parameter estimation purposes. Is it possible to find the basal mass quantity of a particular protein?

Answers to each question:

Approximately, yes. In this case, phosphorylated Akt (p-Akt) is supposed to be the active form of the enzyme that goes around the cell doing its job, whereas non-phosphorylated Akt doesn't have activity that they are interested in. The authors do show that targets of Akt show characteristics of Akt activity when Akt is phosphorylated (Fig 2B, 2C).

Note that densitometry is just a way of measuring the intensity of some bands on immunoblots (westerns). In this case, it is normalized by the loading control (non-phospho Akt). So you could interpret the densitometry plots as showing the proportion of Akt that is phosphorylated. It is a little confusing because they subsequently normalize them to a specific timepoint. From the methods:

The results were quantitated by densitometric analysis (ImageQuant, Molecular Dynamics and PDSI, GE Healthcare). The ratio of phosphoprotein to its respective internal control was normalized to the control level at 0.5 h, arbitrarily set to 1.

Loading controls indicate how much protein of interest is present. For example, 1% of 100mg of protein is the same as 10% of 10mg protein (each is 1 mg). However the interpretation of 1% vs. 10% may be quite large. So if what you are interested in is a percentage or proportion, you need to have a loading control to allow unbiased comparison or normalization.

I don't really know what "basal mass quantity" means, but you could look into the molecular weight of proteins (usually measured in kilodaltons). For example the molecular weight of Akt is ~55kda. You can compute this from the protein sequence by adding up the weights of all the amino acids.


Growth on raspberry cane: What is it? I have raspberries growing in my garden.

One of the raspberry canes has some sort of growth on it.

Size: Approximately 2 inches long
Location: Zone 5; east of Toronto, Ontario, Canada
Date: April 4, 2019.

What is the growth? Is it insects, fungus, bacteria, a defect, or something else?

A botanist at a local university says it is most definitely Crown Gall.

He didn't provide any other information than that, so all I can do is quote Wikipedia:

  Agrobacterium tumefaciens (updated scientific name Rhizobium radiobacter, synonym Agrobacterium radiobacter) is the causal
  agent of crown gall disease (the formation of tumours) in over 140
  species of eudicots.

https://en.wikipedia.org/wiki/Agrobacterium_tumefaciens


Could alpha-numeric taxonomy of fungi make things simpler? Please feel free to construe this question broadly--I don't see why the question would not apply to branches of biology other than mycology.

If the goal of taxonomy is to create classification of fungi that reflect evolutionary relationships, and if this results in a more or less unmanageable proliferation of names, might it not be a good idea to use a numeric or alpha-numeric system instead of a verbal one? One author estimates there may be as many as 5 million species of fungi (and it may take 1000 years to catalog them). If we did manage to note them all would the result really be useable? The ease of storage and retrieval alone would seem to commend a numerical approach.

I assume someone has thought of this before and I guess viral taxonomy does this to some extent. Are there any proposals like this afoot?

Thanks for any insights.

This is actually already done in some contexts.

For instance: yeast (a fungus) is a pretty extensively studied organism, and this means that there are a vast number of yeast strains which are know/used by biologists.  Many of these strains are referred to simply by an alphanumeric string rather than a "verbal" name.  (some examples in link 1)

This is also the case for bacteria, and maybe most of microbiology.


Do mitochondria digest fats? I am a student and I'm currently using the IB biology Oxford textbook. A few weeks ago I had a test on biochemistry. I studied on my textbook and it stated the following: "Mitochondrion: (…) fat is digested here if it is being used as an energy resource in the cell" (page 22) "The energy store from them (Triglycerides) can be released by aerobic cell respiration" (page 78). My teacher told me that I was wrong to write these statements in my test. Is there something wrong? Is the term 'fat' too generic? Do different kinds of fats undergo either aerobic or anaerobic respiration? I am currently confused as I do not know who is right and who is wrong… Can someone answer my questions?

Thank you

You are not far off the mark I would say. Strictly speaking it's not correct to say that mitochondria oxidize fat. By "fat" we usually mean triacylglycerides, and these must first be hydrolyzed into free fatty acids (by enzymes known as lipases) that can be oxidized in the mitochondria. But many researchers and textbook authors are not always careful with this distinction.

Most fatty acids are indeed oxidized ("digested" sounds strange to me) in the mitochondria into acetyl-CoA units, in a process known as beta-oxidation. The acetyl-CoA units produced are then further oxidized into CO$_2$ by the TCA cycle. These processes generate NADH and FADH$_2$ which is converted into ATP by the respiratory chain.

There are exceptions though. Very long-chain or branched fatty acids are instead oxidized in peroxisomes, which contain enzymes specialized for this purpose.

There is no such thing as "anaerobic respiration": in animals, respiration always uses oxygen as the terminal electron acceptor. Mitochondrial beta-oxidation is coupled to the respiratory chain, and therefore requires oxygen. Peroxisomal oxidation is not directly coupled to respiration, but the process still requires oxygen, which in this case is reduced directly by the fatty acid oxidases. So there is no truly anaerobic form of fatty acid oxidation.


Is this a valid definition of independent assortment? "Allelic combinations separate randomly. I.e. a parent might be Aa and Bb for two traits but that doesn't necessarily mean the gametes will strictly be AB or ab but any of a number of combinations. I.e. blue eyes does not imply short height or something."

That's a valid explanation, but not definition. Mendel's law of independent assortments states that during the formation of gametes, the alleles for one trait segregate independently of the alleles of another trait.


How plasma cells switches secreting different Ig classes? In Type 1 hypersensitivity how do B lymphocytes switch Ig classes, from synthesizing IgG to IgE? What is the mechanism? I studied multiple pathology books, it says the same as for IgG secreting pathway. So how does the body know how to change the Ig secretions in response to allergens?

In T-dependent antigen recognition, the B cell can switch the isotype by first altering the heavy chain gene. This is driven by Tfh cells. The specific cytokine stimulating the class switch determines the isotype of the heavy chain to be synthesized. For your example, interleukin 4 (IL-4) drives the class switch to IgE. You also need a costimulatory signal from the CD40/CD40L interaction between the B cell and the Tfh cell. This induces activation-induced deaminase (AID), see bottom paragraph on this.

There are switch regions (denoted S) in the introns between J and C segments at the 5' end of each CH locus, and upstream of that is an I exon (region denoted I) w/ it's own promoter. Induction by CD40 and whatever cytokine is present starts transcription of the I exon, switch region and CH chain of the H-chain the B cell is meant to switch to. This germline transcript facilitates dsDNA breaks at the switch regions Sµ for the IgM (switch region mu) and the switch region for the class to be switched to, Sε in our case for IgE. The intervening DNA is deleted and the coding region Cµ is replaced by Cε coding for the IgE heavy chain BUT, it ends up with the same V domain as the B cell originally had!

Some enzymes involved are AID, which deaminates cytosines and allows the germline transcript to hybridize in the switch region, Uracil N glycoylase UNG which removes uracils from the DNA, and APE I endonuclease that generates a nick at the abasic sites generated. These nicks lead to dsDNA breakages in the switch regions. Text shows that the switch region DNA is G-C rich and can form stable RNA:DNA hybrids with the coding strand of the switch region and the germline transcript. This is what frees up the noncoding strand for alteration by UNG and cutting by APE. The result is that the V region becomes associated w/ a new constant region.

I'd also be careful with the terminology plasma cell as used in the title because we aren't yet at the high-affinity secreting stage when we're talking about class switching. This is mediated at the activation of the actual B cell by Tfh cells.

All information above is summarized from Cellular and Molecular Immunology, 8th ED


Can the human body enter "Power Save" mode? Once a year, I am fasting for 24 hours. No food or drink at all for whole 24 hours.

Recently I thought about what is happening to me during those 24 hours, and realized there might be something strange going on. I will try to describe the things I find strange:

I do not feel thirst or hunger at all. Not even after 20 hours.
I still urinate after 10, 15, and 20 hours, and unlike what I would expect from not drinking, the color is not very dark. (actually, same as when I drink normally)
I can still perform energy consuming tasks after 20 hours without eating or drinking anything. I'm not talking about running in the park or lifting weights, but I can walk, do house chores etc, and only after 20 hours or so the body starts to "protest" in the form of headache.

All of the above led me to think that maybe when knowing it's going to be deprived of energy, the body enters "Power Save" mode, allowing it to function as usual under those conditions? (to a limit of course, but still - I would expect hunger, thirst, and headaches to appear few hours into fasting)

If you are performing the fast for ritualistic or spiritual purposes, then that mental state likely overcomes the feeling of thirst or hunger, especially if you are an otherwise healthy person.

As for the physiological aspects. The Human Body is made up of 2/3 water, and as your kidneys are still functional, they are constantly filtering, and creating urine. The body can last a few days without water.

As for food, the body has about a one day supply of sugar, assuming limited exertion, that it can consume before it begins to break down other substances. Then there are the fat reserves. The average person will likely have on the order of 7 to 15 kilograms of fat in reserve. There are 9 calories per gram of fat, so roughly 63 to 135 thousand calories worth of energy. Since the average adult will use about 2000 calories a day, then you can see that burning body fat alone would allow about a months worth of energy.

I am not saying that these are optimal conditions, but the body of a healthy human adult can easily withstand a 24 hour fast with no adverse effects. You would likely encounter more problems if you tried to go without sleep for the same period of time than if you refrained from food or water.


How to batch convert gene names to protein IDs in Uniprot? I have a list of >1000 "ordered locus names" from the STRING database (also called gene numbers, ORF numbers, or CDS numbers by uniprot). They're in the form of 'b0014', 'b0015', etc. I'd like to convert them all to Uniprot protein IDs.

I know how to do it in a non-batch way, since searching Uniprot for 'b0014' returns what (I think) is a protein ID. However I'd like a batch solution since there are so many IDs that need converting.

ID mapping

This is called ID mapping. It used to be a headache as programmatic sequence comparisons were the only real way, but it is pretty trivial these days.

As mentioned in the comments, by far the most popular and easy method is to use Uniprot's list uploader for mapping. The corresponding publication can be found here.

Example

Programmatic access

The web user interface will work for thousands of IDs, but is like to result in errors for queries exceeding 10,000 IDs. In that case programmatic queries are probably better. I've slightly modified this from the Uniprot docs so that the IDs are queried 1 at a time to avoid any errors in exceeding query size. The python code would be:

import urllib,urllib2

list_to_convert = ["b0014", "b0015"]
url = 'http://www.uniprot.org/mapping/'

print "From To"
for genename_id in list_to_convert:
    params = {
    'from':'GENENAME',
    'to':'ACC',
    'format':'tab',
    'query':genename_id
    }

    data = urllib.urlencode(params)
    request = urllib2.Request(url, data)
    contact = "" # Please set your email address here.
    request.add_header('User-Agent', 'Python %s' % contact)
    response = urllib2.urlopen(request)
    page = response.read(200000)
    print page.splitlines()[1] #Ignores the header line returned by uniprot

The output from this looks like:

From    To
b0014   P0A6Y8
b0015   P08622

Web GUI

b0014 and b0015 aren't actually STRING IDs. They are IDs referred to as gene names and are used across a variety of databases including Uniprot.

The mapper:

Note in section 2 of the ID mapping that I have set the left option to "gene name". "STRING" won't work.

The result is below:


Are mesophyll cells the same as parenchyma cells? I read in my biology textbook that ground tissue is constituted by parenchyma, collenchyma and sclerenchyma.It was also mentioned that, in leaves the ground tissue was made up of thin walled chloroplast containing cells called mesophyll cells.

Despite countless sites and other resources saying otherwise, Mesophyll is not a tissue technically speaking. It's just a place, a specific area. Or you can even think of it as the set of all tissues in a given area.

And that given area is easy to define: the "filling" of the leaf, between the upper and lower epidermis. According to Mauseth (2012), that with Raven is my favourite book on Botany:

  Mesophyll: All tissues of a leaf except the epidermis.

Actually, this is easy to see if you understand the Greek origin of the term: μέσος, meaning "in the middle", and φύλλον, meaning "leaf". Therefore, mesophyll means "in the middle of the leaf".

In a common, regular leaf, most of the mesophyll is made of parenchyma, be it palisade or spongy. As I said before several sources treat these terms (mesophyll and parenchyma) as synonyms, but they are not.

Just for completeness, this is a very simple list of the plant tissues. You'll see that mesophyll is not on it:

Meristems
Dermal tissues

Epidermis
Peridermis

Ground tissues

Parenchyma
Collenchyma
Schlerenchyma

Vascular tissues

Xylem
Phloem

Source: Mauseth, J. (2012). Botany. Sudbury: Jones & Bartlett Learning.


Difference between imputing and typing in GWAS studies? In genome-wide association studies (GWAS), what is the difference between imputing and typing? Are they the same?

'Typing' is an SNV-typing. It is an explicit SNV detection using Affymetrix GeneChip arrays, Illumina BeadArray.

'Imputing' is an imputation. It is a statistical inferring from existing genotype data using haplotype estimation. It is useful because different genotyping arrays genotype a slightly different set of SNVs and they can't detect all variants as whole genome sequencing is still pricey.


Conjoined twins formation theory is it theoretically possible to take two fertilized mammalian eggs and push them together to make conjoined twins? How about forming non-identical conjoined twins?

The more generally accepted theory for conjoined twins is fission, in which the fertilized egg splits partially. So I don't think that what you said is possible. Not seen this happening before... even the conjoined twins share same placenta indicating they originate from same fertilized egg.


Which kind of mushroom is this? I'm in Western Arkansas, and these are red, hollow mushrooms with a brown slimy coating that popped up in our mulch, roughly a half an inch in diameter and they have grown several inches tall. Is there anything specific that I can/should do to these things? I have young kids and pets that I assume I don't want eating these things.

This looks like a type of stinkhorn fungus.  They commonly pop up in urban settings, including mulched areas, and can come in many different appearances.  The slime on these mushrooms is used to attract insects and flies which will disperse their spores. They are found in North America including in temperate and north-temperate climates.  According to MushroomExpert.Com these mushrooms will not hurt you, your children or pets.

Specifically, the stinkhorns in your photo look like Mutinus elegans to me.

Source: http://www.projectnoah.org/spottings/635556012


What kind melanin do fair or light skinned black or mixed people have, eumelanin of pheomelanin? I am doing a study on melanin and conductivity but I cannot find the answer to this question anywhere. Do light complected black or biracial people have eumelanin or pheomelanin? or both?

Pheomelanin is associated with paler skin, while eumelanin predomominates in people with darker skin — this is influenced by alleles of the MC1R gene Swope and Abdel-Malek, 2018, NIH article on MC1R.


What is the meaning of pygo and pagus in the word pygopagus? I know definition of the disease pygopagus but I want to know the meaning of separate parts of it, in fact what's the meaning of pygo- and -pagus in terminology?

According to Wiktionary.com:

pygo- means "rump" or "posterior" from Ancient Greek πυγή (pugḗ, “tail, rump”).

According to dictionary.com:

-pagus means "fixation" or "something fixed or solid" from Greek  págos.

So literally, pygopagus (or conjoined twins attached at the butt) means "fixed rumps".


Why haven't environmentally-reactive bodies developed as an evolutionary advantage? Regardless of region, earth's tilt results in yearly seasonal changes, which organisms deal with through processes like migration/hibernation. Both seem like attempts to avoid the extreme fluctuations... so why haven't certain organisms developed environmentally-reactive bodies, changing with the seasons throughout the year (based on measures like temperature- I.E., additional fur growth during the winter), and why hasn't this continued as an evolutionary advantage to allow organisms to thrive in longer
environmental ranges (like staying in place instead of migrating) or even go a step beyond and take advantage of the qualities specific to each season?

As Jamesqf pointed out, food supply was likely a big contributor. As a general expansion onto that, I believe a sufficiently reasonable answer could be that animals likely found solutions (I.e. migration and hibernation) to deal could with seasonal factors out of their control (like lack of resources) before natural selection leading to more defined adaption could/would've taken place. Their behavior dealt with the problem- which leads to another interesting idea that it could have been an early sign of organisms using their intelligence to survive and change the course of natural selection.


Why is Carbon Dioxide a Greenhouse Gas whereas Ammonia is not? Why are some gases Greenhouse gases while some are not?

I did search this on the net but didn't get any clearcut/credible answers.

What exactly is the property that is common among Ozone, Water Vapour, CFC and Methane?

This is better suited for the Chemistry site, but there are two reasons.  1) The gas allows visible light to pass, but blocks infrared.  (Which has to do with the nature of the bonds between atoms &c.) 2) It exists in the atmosphere in sufficient quantity to have an effect, which ammonia doesn't: https://www.livescience.com/57305-ammonia-detected-in-atmosphere.html  It's quite reactive, so ammonia that's released from e.g. fertilizers or urine doesn't stay around long.


Secretion in Gram negative bacteria Among the 6 secretion systems in bacteria, can these 6 ways be sorted out in the order of how harmful it is to the human host? Like say type 3 is highly virulent so that comes first, but I don't know about the rest of the systems. Being a computer science student, I have failed to understand the Wikipedia article to derive this order. Does a discrete order even exist? Can anyone answer this question?

I think you cannot find a better answer then the following review:

http://www.nature.com/nrmicro/journal/v13/n6/full/nrmicro3456.html

It was published in 2015, and it gives a good overview about the secretion systems. Anyway, T6SS can also be virulent. Vibrio cholerae can use an effector of this SS to cross-link actin in the host cell and modify its morphology and its cytoskeleton behaviour.
In general I think that there is not a general order of virulence, also because the T3SS was discovered long ago. Whereas, the T6SS just recently, so the amount of information about its function is still somehow limited.

Hope this helps.


Can DNA sequencing of food provide quantitatively the fraction of protein from chicken vs soy? There is some news about a report from Canada's CBC about fast-food chicken items containing as much as 50% soy protein, based on DNA testing. I won't do the report the service of linking to it directly, but you can search for the news "What's in your chicken sandwich? DNA test shows Subway sandwiches could contain just 50% chicken."

Isn't quantifying ratios of various DNA sequences fairly difficult, requiring rigorous sample preparation? Could results vary dramatically by varying cooking times, and the independent processing of the animal protein and the vegetable protein? Is there an reason to expect isolated DNA ratios to be a good indicator of protein ratios?

I'm also curious, is there a better way to at least try to do this study - perhaps search for key sequences of amino acids within the proteins to at least try to distinguish animal from vegetable proteins quantitatively?

edit: Here is a newer, more reliable, independent news item not written by the agency who paid for the testing.

The NPR news article DNA Tests Find Subway Chicken Only 50 Percent Meat, Canadian News Program Reports says:

  The tests were conducted by a DNA researcher at Trent University's Wildlife Forensic DNA Laboratory, for a CBC Marketplace episode dedicated to testing fast-food chicken dishes, and have not been independently confirmed.

Later in the same article a strong statement by one of the companies refuting the results has also been provided.

While this question falls somewhat between biology, chemistry, and food science, the use of quantitative DNA analysis as a proxy for estimation of relative protein fractions from two different species (in this case plant vs mammal) is probably on-topic here considering it is biologists who have invented, use, and interpret results of DNA amplification and sequencing analysis, and can best speak to their correct use and potential problems when used outside their accepted protocols.
I am not a trained biologist myself, so I can not state with authority that starting with a food product whose plant and animal components may have started from different places on Earth, been processed differently, then combined and further processed involving major excursions in heat (cooking) and in pH deviate substantially from accepted protocols for DNA quantitative analysis, but I have a strong hunch that this is probably so.
As @BryanKrause has noted in a comment, the laboratory in question's primary expertise is in animal identification - does a carcass or piece of meat or fish come from the species claimed or not, and this is a laudable service. But using relative fractions of DNA within a single sample of prepared food as proxy for relative contribution of protein is far outside that kind of service, and as far as I know, is not an accepted practice anywhere.
Ars Technica is a popular technical news source that generally does a excellent job of summarizing scientific topics when they do cover them, in my opinion at least. In an update to the article Subway releases data after scientists weigh in on 50% chicken test [Updated] they summarize released information from two independent laboratories using an "ELISA methodology designed for food products to quantify soy in the chicken." ELISA is a quantitative method that can be used to measure the presence of various proteins directly, and does not use DNA as a proxy.

Update, March 6: Subway has released the lab reports from both of its independent tests. Both Maxxam Analytics in Ontario, Canada and Elisa Technologies, Inc. in Florida used enzyme-linked immunosorbent assays (ELISA) designed for food products to quantify soy in the chicken. ELISA's are a standard type of assay that generally detect and quantify substances based on binding by an antibody. In the assay, antibody binding kicks off a detectable chemical reaction, commonly resulting in a color change. In the case of Elisa Technologies, the lab used an antibody that binds to soy flour proteins and the lab used known concentrations of those soy proteins for comparison to determine the quantity of soy protein in Subway's chicken samples.
In all samples, Elisa detected 3 parts-per-million or less of soy proteins, which is well below one percent of the chicken. Maxxam detected 5.3 ppm of soy protein in the chicken, which is still well below one percent. (emphasis added)


How DNA programs the first cell in womb into a human Sorry if you see me silly. I am just a programmer happens to be curious about biology...

So far I understand how DNA make protein, how cell divides, how one composed of cells->tissues-> organs.

But, still a piece is missing in my knowledge.. Given the sperm entering the egg creating the first cell, and the nutrients from the mother... how do that very first single  cell diversify , multiply, transform to a human of many different type of cells, tissue and organs ? Is this all the diversification and
specialization of cells directed just by the "child" DNA alone ?

Also, how does DNA (along with living condition ?) decide the course of my life  (making me 1m tall at 6 y.o , have my hair black, my life expectancy etc..)

The short answer is: "Nobody knows yet." The slightly longer answer is that different species use different mechanisms. In amphibians and insect the oocyte, or egg, produced by the mother, has a polarity such that some macromolecules are enriched in different regions of the egg. The best characterized examples are localized RNAs, but there could be other signals as well.  In nematodes the site of sperm entry at fertilization determines the polarity of the cells, which then leads to asymmetry, etc.

In mice, our closest approximation to humans, the early cells after fertilization all seem equivalent, but as the number of cells increases the cells on the inside of the ball and the cells on the outside start to choose different differentiation pathways. There can also be signals from the extraembryonic environment (i.e., the womb).