A possible solution is to use the DNA ZAP solution, which I know many people used in adjacent labs and were happy with for cleaning their DNA free workbench. The product sheet states

  When 500 ng of template DNA is dried down in a PCR tube, it is rendered unamplifiable upon treatment with DNA ZAP solutions. Additional experiments demonstrate that the DNA is degraded down to free nucleotides.

Please note that I'm not promoting any specific product here and you can purchase any similar product/technology for your particular application. Obviously the best recommendation is to use new plates for each reaction but this/or a similar product can be an option too although the risk of DNA contamination in a PCR based reaction should be carefully balanced against simply using fresh plates considering the product itself is not free either.

The product sheet provides instruction for cleaning/treating PCR tubes hence I assume you use the same protocol for plates if you have the plate centrifuges available in your lab. You can get rid of the solutions by tapping the plates on a tissue to get the liquid out of the wells.


Can you measure plasma glucose with a regular glucose meter?

Excellent question... "Can you measure plasma glucose with a blood glucose meter?"

Absolutely Not! In my experience, if you try to measure plasma glucose with a whole blood glucose meter the results are highly variable for a number of reasons (mentioned below). Using blood glucose meters to measure plasma glucose is dangerous. The meters are calibrated for whole blood and not plasma, which is chemically different and will yield different results. Depending on the clinical situation (or experimental situation), the results can be significantly different and non-linear across a huge spectrum of concentrations.

Here is a nice link from the University of Virginia demonstrating the basics of how one type of these meters works.

There are a number of types of glucose meters commercially available to the public as well as healthcare facilities. Most of these meters use varying solid-state chemistry techniques to drive the production of an electrical current that can be measured by the glucose meter. In other words, when the blood is taken up by the strip in the meter the glucose takes part in a redox chemical reaction that creates a small "electrical current" that is detected by the meter. The amount of glucose in the sample is proportional to the electrical current produced. However, there are a number of assumptions that the meters make (which can differ between meters). One of the most clinically significant assumptions is that the meter assumes that the hematocrit (i.e. the percentage of blood volume that is erythrocytes) is normal or approximately 45%. If you use these types of meters on plasma (which has no erythrocytes in it), the chemistry is inaccurate because the meter "thinks" all the glucose that it is detecting is actually dispersed within a pool of erythrocytes in a hematocrit of 45%. There are a number of other issues and important points discussed in this review.

When the clinical trials (e.g. NICE-SUGAR) began showing that intensive glucose control was associated with improved mortality, clinical practices changed from keeping blood glucose concentrations in critically ill patients between 150 and 250 mg/dl to a much lower concentrations (i.e. 80-120 mg/dl). As these new guidelines began rolling out, there were a number of subsequent studies that showed that intensive glucose control was actually associated with more frequent hypoglycemia episodes. There were likely a number of issues to explain this, but one of those was that if your meters were not correcting for differences in hematocrit the blood glucose meters would read spuriously higher than what the true measurement was (thus, you could be treating someone with insulin to lower their glucose that was 160 mg/dl - when in true the value was much, much lower).


Are “Rings” in fish like rings in a tree?

It depends which structures you're talking about. However, several body parts of bony fish such as the scales and otoliths (earbones) generally contain a record of seasonal growth patterns. So in that sense yes, the process of ageing fish is similar to finding the age of a tree by counting rings in the wood. For different species of fish, different structures are used to determine ages.

https://www.nefsc.noaa.gov/fbp/basics.htm


What is this plant which closes its leaves when touched?

It is a Mimosa pudica, a wonderful plant. According to wikipedia you can find it in the following places:

  Mimosa pudica is native to South America and Central America. It has been introduced to many other regions and is regarded as an invasive species in Tanzania, South Asia and South East Asia and many Pacific Islands. It is regarded as invasive in parts of Australia and is a declared weed in the Northern Territory, and Western Australia although not naturalized there. Control is recommended in Queensland. It has also been introduced to Nigeria, Seychelles, Mauritius and East Asia but is not regarded as invasive in those places. In the United States of America, it grows in Florida, Hawaii, Virginia, Maryland, Puerto Rico, Texas, and the Virgin Islands.

If you think that's impressive, look at this video of Dionaea muscipula the venus fly trap:

https://www.youtube.com/watch?v=O7eQKSf0LmY


How are collagen fibers in skin aligned with respect to skin surface?

Collagen underneath the epidermis is not completely randomly oriented, in fact mostly they are directed along the muscle fibres beneath them.

This was first observed by Karl Langer and hence was given the name as langer's lines( of skin tension). This peculiar arrangement of collagen is responsible for maintaining integrity of skin at times of stretching force developed on them by the muscles. Had they perpendicular, then skin would tear easily.

This also has clinical relevance because during surgery if an incision is made along these lines the scar would be minimum.

Source: https://en.m.wikipedia.org/wiki/Langer%27s_lines


Using nanodrop for analysing biological samples other than nucleotides

The Nanodrop is a generic UV-visible spectrophotometer. According to the manufacturer, the latest model can measure absorbance from 190 to 850 nm. Its dynamic range is also very good: from about 0.1 to about 60 in absorbance. Therefore, as long as you don't use an incompatible solvent, you can measure anything that absorbs in this wavelength range. I use it very often for purified proteins. It also works well for turbid suspensions (like bacterial cultures; reading optical density at 600 nm gives an idea of turbidity).

It is easy to use, and of course the low volume requirement is a big advantage. One drawback is that it won't let you fine tune certain parameters like a "real" spectrophotometer would allow (bandwidth, gain, etc.). But you can definitely get decent spectra for characterization of mixtures and concentration estimation of pure samples.


Could silicon oil block Na+ ion channels in the membrane of an axon and prevent Na+ influx?

No, silicon oil couldn't block an ion channel. Oil is a nonpolar substance, just like the membrane lipids, so if you can get your oil to that cell, it will mix with the lipids within the membrane. The ion channel, which sits in the membrane, too, is rather closed to the membrane interior and opens to the inside and outside of the cell which, contrarily, is a polar solution of soluble molecules in water. So, to block one of the openings you better have a polar molecule that is water-soluble.

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

http://en.wikipedia.org/wiki/Polarity_%28chemistry%29


Why do people say that trans fatty acids are bad for your health?

Trans fatty acids are digestible, but they cause an increase in LDL and a decrease in HDL, which is the leading mechanism for atherosclerosis. So, they increase the risk of a cardiac infarct.

LDL means Low Density Lipoprotein, it's one of the 5 major lipoprotein groups. Lipoproteins carries the fatty acids and cholesterol which were absorbed from intestines (because lipids are hydrophobic and cannot be carried within the blood directly like glucose or proteins.)

So, LDL mainly carries cholesterol and fatty acids from intestines to tissues. (fatty acids and cholesterol are essential for cells.) But in excess levels, they tend to accumulate in vessel walls, which also starts and inflammatory response and makes the situation worse. (mainly includes macrophages and T cells) This is the main mechanism for atherosclerosis.

In the other hand, HDLs serve as a reverse cholesterol transport system, which carries the cholesterol back, mostly to the liver (for bile secretion) or steroidogenic organs such as adrenals, ovary, and testes by direct and indirect pathways. So a high HDL reduces the atherosclerotic process.


How does Celiac's Disease cause people to stop growing?

The "proper" term to use in a case of growth retardation in children is "failure to thrive", abbreviated as FTT.

Celiac disease is one of the most common Organic endogenous (genetically based) FTT syndromes.

The main cause of FTT in pediatric celiac patients is malabsorption. In a case of insufficient vitamins and nutrients absorption the child will (have) FTT.


How do you differentiate between SR protein and SR-like protein?

Im not 100% certain. If something is called an x-like protein, it usually means it is homologous and has some sequence and / or structural similarity to x. However, there may not be enough biochemical evidence to say definitively that it is in family x. I came across this paper where they are speaking about an SR-like protein. They said:

  While budding yeast lack alternative splicing, they do have three SR-like proteins: Npl3, Gbp2, and Hrb1. However, these have been best characterized for their roles in mRNA export, leaving their potential roles in splicing largely unexplored.

So in this case the protein has a serine/arginine binding domain and an RNA binding domain (just like SR proteins) but most of the biochemistry points to them being involved RNA export, not splicing (splicing, of course is what SR proteins are known for). So, they get the name SR-like. It will vary though. There is not a unified protein naming system


What is the field of view for the human eyes?

The general shape of the field of view has been answered in the related question "If human eyes watch an area, what's the shape of its capturing shape? Rectangular? Half spherical?"

Regarding the central view: yes, foveal view has a higher acuity than peripheral view.

Regarding the numerical dimensions of the monocular and binocular field of view: Monocular field of view  (measured from central fixation) is 160 deg (width w) x 175 deg (height h). The total binocular field of view is 200 deg (w) x 135 deg (h).

The region of binocular overlap is 120 deg (w) x 135 deg (h) (WebVision). The binocular foveal high-acuity part (central view) is about 6 degrees (5-15 degrees).


If a mother had a child with her own son, could a paternity test yield positive result for the son's father?

Let's approach some different methods of distinguishing parents:

1: The Y chromosome. These are passed down from father to son. Therefore, if the baby is male, its Y chromosome will be the same as John's and his father's - it will be indistinguishable who it's from.

2: The X chromosome. A male baby always has one of the mother's X chromosomes. A female baby always has its father's X and one of the mother's X. A male baby of John and Mrs B would always end up with one of Mrs B's X chromosomes, meaning that this can't distinguish the father. A female baby would have two X chromosomes from Mrs B (because John's own X came from her), proving that it is the product of incest.

3: Mitochondrial DNA. mtDNA is passed on from mothers to their children, never from the father. Therefore regardless of whether John or Mr A is the father, the baby would have Mrs B's mtDNA - not useful.

4: DNA fingerprint. This is primarily based on stretches of the human genome that contain repeats of short DNA sequences (so-called STR/short tandem repeats, or VNTR/variable number tandem repeats). In both cases, the sequence is the same in individuals, but the number of repeats is extremely variable and each human therefore has a (possibly) unique combination across the different repeat locations in the genome. Because children inherit 50% of their DNA sequences from the father and 50% from the mother, John himself will have his mother's characteristic lengths in 50% of repeat locations and his father's in the remaining 50% of locations (roughly). A child of John and Mrs B would have MrA's repeat lengths in 25% of locations and Mrs B's in 75%. The fractions "100% Mr A" vs. "50% Mr A" vs. "25% Mr A" can be distinguished by this method.


Why do you need you room dark for melatonin release?

The release of the hormone melatonin is responsible for the feeling of sleepiness. It is released by the pineal gland and production starts when the light fades, as it's production is inhibited by light stimulation of the retina, the onset of the production is called dim-light melatonin onset.

Read more about this at this previous answer.

This study on blind people will show you that the light entering the eyes is the (main at least) regulator of melatonin rhythms. They took blind people, 19 of whom could perceive light and 30 who could not, and showed that 14 of 19 light perceivers had normal melatonin rhythms while 23 of the light-blind people had abnormal or unclassifiable rhythms.


I found this question very interesting so I did some research. Here's a brief summary of what I've found:

Researchers have found that there are 11 different call types. Some of these include a "sharp alarm cry", "sociable clucking", chutter, whining, purring etc. Using body position and behaviour, researchers attempted to associate these vocalizations with behaviour. Some vocalizations had no apparent associated action including what researchers designated the "chirrup" ( I think this is similar to what your guinea pig might have emitted.)

For more information you can read the results section of this paper by Berryman. You can find a full description of each of the 11 calls and their assumed cause or purpose. Some involve social interaction, reproduction, and distress. Much of the research regarding Guinea pig vocalization involves communication and response between mothers and pups.

In short, it seems as though this chirping behaviour your Guinea pig is exhibiting is normal, but not of any known cause.


I agree with you that I can't see why Lamarck's hypothesis could not explain the presence of homologous structures.

The link you offer also claim that Larmarck's hypothesis would fail to explain "Biogeographical diversity patterns". While this expression is a little vague, I would fail to understand why Lamarck's hypothesis would fail to explain patterns of biogeographical diversity.

The phrasing of your scenarios (absence of the term allopatric speciation, usage of the term "develops" instead of "evolves" of just "adapts") suggests that you may take advantage of an intro course to evolutionary biology such as the short and good course by UC Berkeley called Understanding Evolution


How to predict a mRNA secondary structure with a large sequence?

Yes, the structure predicted by splitting up the sequence may not represent the actual structure of the full-length RNA. A simple hypothetical case would be that of an RNA whose 3' and 5' UTR interact to cause circularization.

I am afraid there is not clear rule for choosing the subsequences such that the assembly of the individual secondary structures is closest the the actual structure.

We may expect that, with better computational power, the limitation on the size of the sequence for secondary structure prediction, can be overcome.

However, there are experimental techniques using RNA-sequencing that can determine the actual secondary structure — SHAPE-seq (ver 2.0; Loughrey et al. 2014) and structure-seq (Ding et al. 2014). Structure-seq in-fact, tries to determine the RNA secondary structures in-vivo and hence may be a more powerful tool.

However, you said you are working with mRNAs. I guess for mRNAs you can predict the structures of UTRs and the CDS separately. Actually depends on what you are interested in. CDS usually does not harbour any structural motif and any secondary structure in the CDS is usually resolved by the helicase activity of eIF4A. However, secondary structures can slow down the translation elongation rate (Mao et al. 2010, Gorochowski et al. 2015).

Loughrey, D., Watters, K. E., Settle, A. H., & Lucks, J. B. (2014). SHAPE-Seq 2.0: systematic optimization and extension of high-throughput chemical probing of RNA secondary structure with next generation sequencing. Nucleic acids research, 42(21) e165.
Ding, Y., Tang, Y., Kwok, C. K., Zhang, Y., Bevilacqua, P. C., & Assmann, S. M. (2014). In vivo genome-wide profiling of RNA secondary structure reveals novel regulatory features. Nature, 505(7485), 696-700.
Mao, Y., Liu, H., Liu, Y., & Tao, S. (2014). Deciphering the rules by which dynamics of mRNA secondary structure affect translation efficiency in Saccharomyces cerevisiae. Nucleic acids research, 42(8), 4813-4822.
Gorochowski, T. E., Ignatova, Z., Bovenberg, R. A., & Roubos, J. A. (2015). Trade-offs between tRNA abundance and mRNA secondary structure support smoothing of translation elongation rate. Nucleic acids research, gkv199.


Well, for him the virus is already likely at minimum levels within his body. If he's recovered (pass the fever phase) then his immune system has already dealt with the majority of the viral bodies in his system, since the peak of the immune response comes after the peak of the viral infection density (ignore B):

How much of the virus was left in his system to actually spread is hard to guess. Sometimes infections never truly go away, but merely become undetectable by conventional testing. However, if we're to assume that there's at least some norovirus left to transfer to you then you should realize that the greatest chance for exposure has already come and gone.

The moment you were in the same room together, talking in close proximity, shaking hands (if you did), or generally being close is the most likely source of any infection you could have picked up. However, while most virii don't survive well outside of the body, the norovirus notably bucks that trend. The Hawaiian Department of Health (PDF) notes that the virus can definitely survive outside the body for several days on hard surfaces (though it will not grow), can survive being frozen, and that it only takes about 100 viral units to cause an infection (which could fit a few thousand times over on a grain of salt). Scientific American also notes that norovirus can survive for months or years in sources of drinking water.

What you've already done is pretty much what you should do to avoid infection. You've washed your hands, refraining from mucous membrane contact, etc.

Ultimately how long you should wait depends on where the norovirus currently resides. A week should be sufficient if all of the norovirus is contained on the book or on other surfaces that you're not making contact with. However, if it's already had contact with your skin or mucous membrane, then you're either already fighting it off or you're about to become ill. Unfortunately it's a lot easier to expose yourself than contain something you can't see, as the Mythbusters have done a good job of showing (Video).

In all likelihood if he was still infected enough to transmit the virus to other people by the time you two started handling the same equipment and you didn't use gloves, you've probably been exposed. However, exposure doesn't automatically mean you get sick. If you're not sick within a week afterwards, you've successfully fought it off. So, congratulations, perhaps!


Do we find protein not of cellular origin in nature?

On our planet, there is such an incredibly massive amount of protein creation by biological organisms (as well as smaller peptide constructs) that it would be essentially impossible to identify any that was created by a natural non-biological process.
Moreover, now that there is life, any location with the right conditions for non-biological creation of protein would likely also be a good place for modern microbes  to take advantage of those same resources to grow themselves, diverting the necessary inputs or quickly eating the outputs.
It is for this reason that we search for precursors of life in space, and have long ago found the basic building blocks. This is also why probes to other planets are carefully sterilized, because otherwise we will never know if life found on Mars is just hardy colonist organisms transplanted from Earth.
To the best of my knowledge, however, no non-Earth molecule has yet been found that has the full complexity of a protein, as opposed to just isolated amino acids.


Evolution of insects, spiders and jellyfish

Welcome to Biology.SE

Answering your question fully will require to write a whole book. Evolutionary Biology is a big field and I would recommend that your take some time to get an introduction (slightly more advanced than what you received in school). I am suggesting you take advantage of this free online resource.

I am briefly making comments and answering your question(s) below. They may be hard (or easy, I don't know) to understand but for more info you should really get to the above free online resource.

Species A evolved from species B

Evolution did not make mammals out of reptiles, mammals are reptiles. Evolution did not make birds out of reptiles, birds are reptiles as well (I am using here the phylogenetic definition of reptiles (Reptilia), more info there). It is wrong to think of any two extant species as one having evolved from the other one. But it is correct to understand how closely related are two extant species. It is also correct to make predictions about how the most recent common ancestor (MRCA) look like and it is true the the MRCA might look more like one of its descendents than like another.

We talk about clade as a lineage including many species. In these terms both any lizard species and any given bird species belong to the same clade, the Reptilia, they are both reptiles. They are also both vertebrates (Vertebrata) and animals (Metazoa) and eukaryotes (Eukaryota).

If the statements of the kind "mammals evolved from reptiles" are very misleading the statement "amphibians evolved from reptiles" is simply wrong. The MRCA of reptiles and amphibians was not a reptile (neither an amphibian), it was a tetrapoda (vertebrate).

I can roughly imagine that there are giant evolutionary gaps between an insect and a jellyfish but is there any common ancestor of all of them?

Any two species on earth have a common ancestor. The universal common ancestor, that is the common ancestor that any living thing (bacteria, plants, lizard, human, fungi, jellyfish, Archea, etc...) is called LUCA (Last Universal Common Ancestor). So yes, jellyfish and insects have a common ancestor. LUCA is one of them. Their MRCA is the same guy as the MRCA between jellyfish and you, as insects and primates are more closely related than are insects and jellyfish. This MRCA is an animal (a metazoa) and therefore is also a eukaryote (Eukaryota).

Do they also have some evolutionary table like vertebrates or was there evolution never that interesting to begin with?

Evolution occurs in every single living population. So yes, evolution occurs in jellyfish as it occurs in insects. The clade of jellyfish contains several thousands of species (most of them belong to the clade Hydrozoa). There are almost a million species of insects.

Here are just a few fun facts that come to my mind when I think about jellyfish:

Some species have tentacles, some don't.
Some species have alternance of generation (a given individual is either a sticking thing on the ground while its descendent is swimming).
Size of jellyfish vary wildly

And a few fun facts about insects:

Some have evolved 3 pairs of wings to fly (we think it evolved from gills but it might have evolved from the exoskeleton as well).
Some live in water, some not, some live in water in the larvea stage and not in their adult stage.
They have all sorts of diet
When flight evolved at first, they had 3 pairs of wings. All extant species (who are descendents of this species that evolved flight) have now lost at least one pair of wings, the one closest to the head.
Some species have lost flight.
Some species have lost a second pair of wings (diptera)
Some have evolved crazy mimetism and defense mechanism from the developmental pathway of the third pair of wings.
Eusociality (which is arguably one of the most mind boggling things in evolutionary biology) has evolved several times in insects.
Some species have sex that is determined the ploidy (number of sets of chromosomes) level (it is the case in many eusocial species).

1. What is the common ancestor between vertebrates, arthropods and molluscs?

You can explore the tree of life by yourself on tolweb.org. Arthropods and molluscs are more closely related than any of them are to vertebrates. The MRCA of vertebrates, arthropods and molluscs was a Bilateria (animal, eukaryote). You can see this bifurcation here on tolweb.org. I'd recommend to explore a bit this tree of life, it is pretty fun to do.

2. Is there an evolutionary tree for the last two like for the vertebrates?

Yes, see above.

BTW, I noticed that you talk about spiders in your title but not in your post. You'll find the spiders here on tolweb.org.


The main hypothesis is that all starts from RNA. "The RNA world". There was no DNA and no proteins. Both function was performed by RNA. Now there are no living organism that carrying information in RNA (only viruses...), but there is "enzymes" from RNA - ribozymes.
The evolution to DNA was later, according to this hypothesis.
There is really good article in wiki.
http://en.wikipedia.org/wiki/RNA_world_hypothesis
or if you want something more look here
http://www.ncbi.nlm.nih.gov/books/NBK26876/

Summary

  From our knowledge of present-day organisms and the molecules they contain, it seems likely that the development of the directly autocatalytic mechanisms fundamental to living systems began with the evolution of families of molecules that could catalyze their own replication. With time, a family of cooperating RNA catalysts probably developed the ability to direct synthesis of polypeptides. DNA is likely to have been a late addition: as the accumulation of additional protein catalysts allowed more efficient and complex cells to evolve, the DNA double helix replaced RNA as a more stable molecule for storing the increased amounts of genetic information required by such cells.


Rosette formation: in which order are leafs created

Spiral Phyllotaxis and the Golden Angle

The disposition of the leaves in your picture is not as simple as it seems. That's a spiral phyllotaxis, which can be very complicated.

The plant in your image is a houseleek, a plant from the Genus Sempervivum.
In those plants, according to Jeremy Burgess (Introduction to plant cell developmnent):

  ... leaf primordia are separated from each other in an angular arc that approaches 137°.

By the way, 137° is (almost) the golden angle (φ).

Here is an image explaining the phyllotaxis of Sempervivum (from Burgess, 1989):

Even more interesting is the pattern made by the 137.5° GA spiral of Aloe polyphylla:

Sometimes this can produce invisible spiral patterns, a phenomenon called parastichy:

Source: Burgess, J. (1989). An introduction to plant cell development. 1st ed. Cambridge [etc.]: Cambridge University Press.

PS: I know that this is off-topic, but I'd like to share this video from Cristóbal Vila, which deals with Fibonnaci sequence, golden ratio and golden angle in nature. Look at the flower disposition at 1:44 : https://www.youtube.com/watch?v=kkGeOWYOFoA


how to solve gap reactions in genome scale metabolic reconstruction

It is common that reactions in stoichiometric models cannot carry flux because there is a "dead end" metabolite somewhere. The problem may not be in the immediate reactants / products, but can be several steps away, and is not always easy to find.

If you have a network visualization tool, one option is to highlight all reactions that cannot carry flux; often this reveals an entire blocked pathway ending in the isolated metabolites.

A more systematic method is to examine the dual solution of the linear program for maximizing flux through a blocked reaction; this shows the active constraints, which are precisely the metabolites that are lacking for the blocked reaction to be able to run.


What is this large beetle from Shirpur, Maharastra (central India)?

Clearly not the best picture, but from the poor quality image it does appear you have a longhorn beetle (family Cerambycidae) in the subfamily Prioninae.

They are typically large (25–70 mm) and usually brown or black. The males of a few genera sport large mandibles that are used in fights with other males, similar to stag beetles. These beetles are commonly nocturnal and are attracted to light. The majority of the Prioninae whose biology is known are borers whose larvae feed on rotting wood or roots.

For example, your specimen looks a lot like Toxeutes macleayi from Australia.

 Source: England London - Natural History Museum
I'm not sure whether other closely related species live in India (none of the related Indian species that this site mentions look like your specimen), but I would guess if you look into it you might find a local bug guide that might help you find some other related species.
Based on your location in India, I'd say one place you could start looking is through species in the genus Prionus.

they're also large, generally brown or black, are nocturnal. Additionally,

All members of the genus Prionus have twelve or more strongly toothed or even flabellate antennomeres on their large antennae.

You'll obviously need to provide a better picture for us to examine that detail of your specimen.

I also recommend you examine the list of Indian Prioninae species listed here, including relatives of similarly sized/colored species with large mandibles such as Dorysthenes huegelii and Rhaphipodus fontanieri.
Again, your picture is too low of quality for an accurate ID, but these links should likely help you parse through similar species and hopefully find your answer.


How is adrenaline (also known as "epinephrine") a ligand?

The definition of "ligand" in the question, "a molecule or ion which donates a pair of electrons to a central transition metal ion in a complex" is clearly a more technical 'chemistry-type' of definition. Ligands in biology and medicine can be all sorts of molecules, though most of the time we think of them as molecules that bind to a particular receptor. Those receptors can be ion channels, enzymes, transmembrane receptors at the cell surface or within the cell in an organelle, nuclear proteins that control expression of genes in the cell nucleus (i.e. transcription factors), etc...the list could go on and on... In fact, more recently we have come to appreciate that compounds like bile acids - that were previously thought to be important only in fat absorption in the gastrointestinal/digestive tract - are also ligands for receptors that control gene transcription ("Farnesoid X Receptor") as well as increase energy expenditure in brown adipose tissue and skeletal muscle (through receptors like the "TGR5" receptor).

But... back to the question...

If a molecule binds to a receptor, then it's a ligand for that receptor. The ligand doesn't have to donate any electrons specifically to a transition metal. Most of the time in medicine/biology the binding of a specific ligand to its receptor is a reversible process that is dependent on the concentration of the ligand and the availability of the receptor (among other things). The specificity of ligand for the receptor is due to chemical factors like hydrogen bonding, electrostatic interactions (like positive charges attracting negative charges), as well as other chemical interactions beyond the scope of this question. As you can see from the picture below, the hydroxy groups (-OH) that are part of the serine residues on the receptor are hydrogen bonding with the hydroxy groups on the epinephrine molecule itself. Moreover, the carboxy group (-COOH) on the aspartate residue is binding to the positively charged amino (NH3+) on the epinephrine molecule.


You could’ve easily googled this, but anyway...

Placenta is a composite structure made of embryonic and maternal tissues.
The placenta is composed of: The chorion, which is the embryonic-derived portion of the placenta. Chorion contains the trophoblast cells (cells that make up the outer cell layer of the blastocyst). finger-like structures called chorionic villi are also present in the placenta. Lastly, the space in the placenta that surrounds the villi and the maternal blood is called the intervillous space.

Source: https://study.com/academy/lesson/the-placenta-and-the-fetus-structure-and-function.html


To characterise diameter of capillaries in organs

This question is dependent on the specific patient at hand.
I think in the normal situation the diameter of the capillaries is about the same in each organ.
Better question would be: how does the diameter changes in relation to the venous and arterial ends of the capillaries?
Then, think about how big portion of the capillaries are in the venous end in the organ.

I cannot say that 50% of capillaries are on the venous end of the organ and 50% on the arterial side.
This is again an open research question.


I've been able to narrow it down to 3 species in Musteloidea, the weasel superfamily, but I think you observed a Tanuki that was suffering from scabies.

1) Tanuki / Japanese raccoon dog - 'Tanuki' - (Nyctereutes procyonoides viverrinus).
Visually similar to what you observed. The feet and face in particular seems to fit with a tanuki. Tanuki are often observed in urban areas in Japan and have been increasing in recent years. There are frequent reports of tanuki with scabies that have missing fur and a similar appearance:
(Google search for "tanuki" and "scabies":
https://www.google.com/search?q=%E7%96%A5%E7%99%AC%E3%82%BF%E3%83%8C%E3%82%AD

2) Common raccoon - 'Araiguma' - (Procyon lotor)
Since they were introduced in 1962 as pets, there are some wild populations in Japan, including in Kanagawa prefecture where you observed the animal.

3) Japanese badger - 'Anaguma' - (Meles anakuma)
Another possibility but I think it does not fit your observation.

There are a few other species in this superfamily but I think it is safe to exclude them due to a lack of visual similarity.


I think Spread will be best for this work.

SPREAD: Spatial Phylogenetic Reconstruction of Evolutionary Dynamics

Authors: Filip Bielejec, Andrew Rambaut, Marc A. Suchard & Philippe Lemey

Homepage: http://www.phylogeography.org

License: LGPL


What is the most recent well-attested common ancestor of chimpanzees and humans?

Two reasonably close relatives of the most recent chimpanzee-human ancestor (CHA) are Sahelanthropus tchadensis and Orrorin tugenensis, but both are poorly attested.

One better candidate is Ardipithecus ramidus, which has a fairly-complete skeleton ("Ardi") among other fossils. It's a bit young (4.4 Ma), perhaps, to be a CHA but should be a close relative.

Another reasonable candidate is Oreopithecus bambolii. It is very well-attested. The trouble is that no one seems to know how it's related to humans; 'best guess' is that it's not actually an ancestor but a sister taxon.

(I'm not an evolutionary biologist, nor even a scientist, but I thought I'd leave what information I collected here as there is no better answer at this time.)


The question is rooted in a misunderstanding of what sexual reproduction is and is not.

Any good intro book to evolution has a chapter on the diversity of reproductive systems. Consider for example Evolution: Making Sense of Life. If you speak french, the book évolution biologique has a very chapter on the diversity of reproductive systems. If you want something more complete and more advanced, you can have a look at The Evolution of Sex Determination.

  It has always been said that sexual reproduction produces offsprings which are superior to their parents, due to the variations which they acquire causing them to survive better in their environment.

Who said that? The common simplistic idea and sex increases mean fitness because it increases genetic diversity is both wrong because sex does not necessarily increase genetic diversity and wrong because increase in genetic diversity does not necessarily result in increasing mean fitness.

You can have a look at the work of Nick Barton, Sally Otto and many others on the subject. The above misconception is well explained in the introduction of this talk from S. Otto's

  [..] But what when we talk about bisexual organisms, might they be plants, animals or any other life form?

I'm not sure what you meant here. You probably did not want to use the term bisexual. Maybe you meant dioceous.

Please note that sexual reproduction does not mean dioecy. Sexual reproduction does not even mean anisogamy and doe snot necessarily involved more than one individual (see selfing).

  Can't there be variations in their offsprings if they produce them asexually?

There is a whole range of reproduction mode and saying sexually vs asexually is making gross categories that make it sometimes hard to really answer the question. It is also hard to know what you mean by "variations" here. But shortly speaking:

Asexual reproduction does not necessarily mean total absence of recombination (see for example Narra and Ochman 2006) and definitely does not mean absence of mutations (see for example Sniegowski et al. 1997).

  It's like when they undergo gamete formation in different male and female structure present in that single parent, they'll surely undergo meiosis(if the parent is not haploid undoubtedly) forming the gametes which are dissimilar in their genetic makeup. When these fertilize, shouldn't they show variations?

If there is fusion, then there is sexual reproduction, even if it is selfing and even is they don't have genders (anisogamy).


A 10mm long creature in the California dust

I'm going to answer this question and close it. Based on the location, the environment, its appearance and behavior, I'm 90% sure that this creature was a Stiletto Fly (Therevid) larva. Most likely an Acrosathe sp., as those tend to be very common in the area. Thanks to all for your help in clarifying and narrowing it down for me.


What is most ancestral: isogamy or anisogamy?

As stated here the first sexual reproduction seems to be isogamy, which's purpose was likely to repair the DNA, as a damaged cell could repair its' (DNA) strands via recombination with a "healthy" one.

As for lineages, the only thing I could find was also in this book at the very beginning, but there doesn't seem to be a difference as for which is the most ancestral.


According to this source, gold is not a necessary trace element for living organisms.

Would have been cool, though...


Rate-determining steps in enzyme catalysed reactions

This is enzyme and substrate concentration specific, since the reaction rate depends on the reaction rate constant k that depends on the enzyme. However if there is a large amount of P present in the solution the EP -> E + P reaction slows down so this can be the rate determining step. On the other hand if you dynamically remove the P molecules from the system the ES->EP can be the rate determining step.


This is Mealworm beetle, Tenebrio molitor, a species of darkling beetle.

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

Thank you @terdon for help!


Image is of an 18% Tris-tricine small-peptide SDS-polyacrylamide gel stained with coomassie blue dye [source].

Your peptide is 1.6 kDa; it would not run off in 20% gel if you don't run it for a long time. Also, try to prevent heating up of the gel (you can run it in a cold room or in front of an A/C vent).  However, it is better to use other techniques such as chromatography. You can also try dialysis if other unwanted peptides are much larger.
Protocol for Tris-Tricine SDS-PAGE.


How exactly does alcohol solution kill or neutralize viruses?

Alcohols dissolve lipid bilayers

Many viruses have an outer lipid bilayer. Ethanol lyses cells, and in the same fashion damages membrane-bound viruses by rupturing the bilayer (which is made of ethanol-soluble lipids).

Alcohols misfold the protein coats of viruses

Additionally, alcohols denature proteins, which misfold in non-aqueous conditions. Some viral surface proteins are important for adhesion and attachment, and misfolding these renders the virus inactive. The total breakdown of viruses is essentially due to the misfolding of their protein coat (the capsid).

The same goes for bacteria

With the additional effect of dehydrating cells

Alcohols substitute the water contents of a tissue and have been as such used as fixatives. Common laboratory examples include methanol and ethanol.

Typically, 70% (140 proof) ethanol is used for bench wiping to kill or inactivate microbes. This includes viruses.

This is all standard, common, easily and readily accessible knowledge. Here's a bonus source.


Amplification technique for proteins similar to PCR for DNA?

There isn't any technique with one exception. PCR generates DNA from DNA so you can establish cycles. For protein synthesis, an mRNA is a template to produce proteins. Most likely proteins you are interested in would not synthesize mRNAs, so that you can not establish cycles.

The exception I said earlier is Protein Misfolding Cyclic Amplification (PMCA). Some disease associated misfold proteins can induce misfolding of the same polypeptide which is not misfolded. So you can establish cycles of misfolding reaction.

PS:

There are technique to synthesize proteins from DNAs or RNAs, but they are not chain reactions.
https://www.promega.com/products/protein-expression/eukaryotic-cell-free-protein-expression/
https://www.neb.com/products/e6800-purexpress-invitro-protein-synthesis-kit


How to synthesize and isolate single stranded cDNA from an RNA template?

Sure that will work, or gel purify the ss cDNA, or treat the rxn with alkali to degrade RNA.  The real questions in my mind are:

What will you use as a primer for the RT?
What are you going to do with this pure ss cDNA?

If you already have the target cloned (how else would you transcribe it in vitro?), then why not just do a linear PCR where you cut the plasmid to linearize it at the site of your choosing, and then throw it in a PCR machine with just one primer?

Why bother going through the T7 RNA pol and RT steps (if you don't need to)?


How do multiple replication forks function without 'colliding', and what is the benefit of this method?

To get to the exponentially increasing number of strands, the replication would have to be started on the already replicated strand, and not on the original strand. Replication in eukaryotes is tighly controlled and such an event is prevented by the regulation.

How can the cell prevent re-replication of the strand that is currently synthesized? By timing the steps of the replication in strict order and preventing any replication outside of that order.

Replication starts at defined origins of replication. In the G1 phase, pre replication complexes (pre-RCs) are assembled at the origins of replications. At these pre-RCs the replication can be initiated, but pre-RCs itself cannot be assembled in the later phases of the cell cycle. When the replication starts, the pre-RC is converted to a post-RC which can't initiate the replication anymore, preventing re-replication.

The benefit of multiple origins of replication is replication speed. Eukaryotic genomes can be much, much larger than those of simple bacteria. Replicating them using a single origin of replication would take a very long time.

Some further reading material:

Genomes, 2nd edition, chapter 13
Cell Cycle Regulation of DNA Replication


You breath it out, for the most part. Fat is "burned" to convert the carbons to CO2, which is breathed out. There's not very much fat-derived carbon in each breath, but you breath a lot, all day long.

At rest, an average 70 kg person consuming a mixed diet (respiratory quotient 0.8) exhales about 200 ml of CO2 in 12 breaths per minute. Each of those breaths therefore excretes 33 mg of CO2, of which 8.9 mg is carbon. In a day spent asleep, at rest, and performing light activities that double the resting metabolic rate, each for 8 hours, this person exhales 0.74 kg of CO2 so that 203 g of carbon are lost from the body. ... Replacing one hour of rest with exercise that raises the metabolic rate to seven times that of resting by, for example, jogging, removes an additional 39 g of carbon from the body, raising the total by about 20% to 240 g. ...
Our calculations show that the lungs are the primary excretory organ for fat.

--When somebody loses weight, where does the fat go? Ruben Meerman and Andrew Brown, BMJ 2014; 349


What is the specific role of the cerebellum when it comes to 'coordinating movement'?

The principal function of the cerebellum, which was detected years ago, is to calibrate detailed movements rather than initiating movements or deciding which movements to execute (Ghez et al, 1985). This was concluded by observing the changes which occurred after damaging cerebellum. Animals and humans with cerebellar dysfunction show, above all, problems with motor control, on the same side of the body as the damaged part of the cerebellum. They continue to be able to generate motor activity, but it loses precision, producing erratic, uncoordinated, or incorrectly timed movements. Thus, cerebellum helps in coordinating fine-tuned movements and inhibits involuntary movements. Apart from this, fMRI studies have indicated that more than half of the cerebellum is intertwined with association areas (Buckner et al, 2011). But since it is out-of-scope here, I'll leave it at that much.
See it like this:

For a more detailed mechanism and circuitry of the cerebellum, you can have a look at this interactive page from the University of Texas. @FilipeRocha have also come up with some fine details in their answer.

References:

Ghez C, Fahn S (1985). "The cerebellum". In Kandel ER, Schwartz JH. Principles of Neural Science, 2nd edition. New York: Elsevier. pp. 502–522.

Buckner RL, Krienen FM, Castellanos A, Diaz JC, Yeo BT (2011). "The organization of the human cerebellum estimated by intrinsic functional connectivity". J. Neurophysiol. 106 (5): 2322–2345. doi:10.1152/jn.00339.2011.


This is a bit hard to say exactly, since there is a number of possibilities. We can be pretty sure that these sample is from a Cypress, belonging to the family of Cupressaceae, but which subfamily or species this is exactly, can't be identified here. Therefore a wider image would be necessary, but since this is a potted plant, even this might not be enough, as a lot of these plants are used in gardening.


Confusion related to a term probe-by-background interaction

The "probe by background" interaction is the response of different probes as a function of background gene expression. For example, depending on which of the 6 backgrounds a probe is in, the drug response may go up or down. Probes as a function of background is probably easier to imagine than background as a function of probe (which is equally valid). For 39,115 probes and 6 background networks, there are 234,690 interactions.

In a technical sense, "probe by background" is the interaction term in the linear model that the authors fit for each drug. The details of the analysis are in the supplemental methods. The model they fit is

Drug_Response ~ Probe + Probe * Background + Background

which translates to "Drug response is modeled by Probe, the interaction of Probe and Background, and Background". The middle term (with the *) is the interaction term. Here is a page that helps to explain how to understand significant interaction terms in linear models.


The recurrent patterns of connections in a network are known as network motifs.

You can check this paper out. They have identified common network motifs in different types of real networks including neural networks (of C.elegans though).

Apart from feed forward loops, bi-fan is also a common network motif in neural networks.

Perhaps the connectome project has data for human brain which you can analyze for identifying network motifs. You would have to request for the data, though.


Does a specific blood group enhance the Plasmodium growth?

It is a well documented observation that Plasmodium (vivax and knowlesi) infection is dependent on the Duffy blood groups [1].

Individuals lacking the Duffy antigens (Fya and Fyb) have lower susceptibility to malaria. Plasmodium expressed Duffy Binding Proteins facilitate in establishing the initial contact between the merozoite and the RBCs.

However, Plasmodium has evolved to break this dependence on Duffy antigens [2, 3].

For, the ABO blood group system, it has been observed that the blood group-O is associated with lower severity of P.falciparum malaria in adults  [4, 5], which possibly happens because of reduced rosetting (binding of infected RBCs with uninfected RBCs) [5].

References:

Dean L. Blood Groups and Red Cell Antigens [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2005. Chapter 9, The Duffy blood group. Available from: http://www.ncbi.nlm.nih.gov/books/NBK2271/
Ménard, Didier, et al. "Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people." Proc Nat Acad Sci, USA 107.13 (2010): 5967-5971.
Mendes, Cristina, et al. "Duffy negative antigen is no longer a barrier to Plasmodium vivax–molecular evidences from the African West Coast (Angola and Equatorial Guinea)." PLoS Negl Trop Dis 5.6 (2011): e1192.
Cserti, Christine M., and Walter H. Dzik. "The ABO blood group system and Plasmodium falciparum malaria." Blood 110.7 (2007): 2250-2258.
Rowe, J. Alexandra, et al. "Blood group O protects against severe Plasmodium falciparum malaria through the mechanism of reduced rosetting." Proc Nat Acad Sci, USA 104.44 (2007): 17471-17476.


A fairly easy-to-understand example is that of the ABO blood group system. In this case, there is a single gene involved - ABO, which codes for an enzyme that modifies sugar groups on the surface of red blood cells. This ABO gene has three variants or alleles — i, IA, and IB. i (coding for Type O blood) is recessive, which means that its phenotype can only be observed if there are two copies of it – ii – one from the mother and one from the father. IA and IB are co-dominant, meaning that both can be expressed at the same time, and their phenotypes can be observed even if there is only one copy of that allele — for example, IAi would give Type A blood (as would IAIA), IAIB would give Type AB, and so on.

Major and minor alleles (at least in my mind) simply refer to the frequency with which an allele is found in a given population: a minor allele is one that is expressed less-often than a major one. The term minor allele frequency is sometimes used as a numerical representation of expression — a certain allele is only expressed in 3% of the population, for example.

These terms are all from classical genetics — talking about genes and variants without really knowing (or needing to know) what exactly the gene was made up of. Of course, we now know that genes are composed of sequences of DNA nucleotide base pairs (A, T, C, and G), which are then translated by 3bp-codons into proteins, where each codon corresponds to one of 20 amino acids, plus START and STOP sequences. It is in this context of DNA sequence analysis that terms like SNP or Single Nucleotide Polymorphism are used. If you were to compare two alleles, say IA and IB, any single-nucleotide difference between the two could be termed a SNP. Frequently, SNPs are often notated based on the changes the difference would bring to the translated protein sequence — for example, a AAG codon codes for the amino acid lysine, while GAG encodes glutamatic acid. In other cases, a SNP would make no difference to the protein sequence — for example, TTA, TTG, CTC, CTA, CTG, and CTT all encode leucine. You can find the DNA codon table here.

You should keep in mind that SNPs are not the only source of variation in genetic sequences — deletions, translocations, repetitions, inversions, frame shifts, and other mechanisms can all alter the DNA sequence at a particular locus or site. Taken together, all of these differences are often referred to as mutations, which simply means "changes."

I hope this was helpful, please let us know if you still have questions.


Can a human increase cold resistance through some practice?

The advanced Tibetan Buddhist meditational practice known as g Tum-mo (heat) yoga allows control of aspects of body temperature.

Physiological measurements on practitioners are described in the paper Benson et al. (1982) Body temperature changes during the practice of g Tum-mo yoga. Nature 295: 234-236

  Since meditative practices are associated with changes that are consistent with decreased activity of the sympathetic nervous system it is conceivable that measurable body temperature changes accompany advanced meditative states. With the help of H.H. the Dalai Lama, we have investigated such a possibility on three practitioners of the advanced Tibetan Buddhist meditational practice known as g Tum-mo (heat) yoga living in Upper Dharamsala, India. We report here that in a study performed there in February 1981, we found that these subjects exhibited the capacity to increase the temperature of their fingers and toes by as much as 8.3 °C.

In this paper the authors report measurements made on three subjects. The Figure shown below is the data for the third of these. The authors describe these results as follows:

  His finger temperature rose 3.15 °C while toe temperature  increased 8.3 °C (Fig. lc). There were no other large changes in skin temperature. Rectal temperature was unchanged…The most likely mechanism to account for the increase in finger and toe temperature is vasodilation.

If you wish to try this for yourself, here is a description of the practice as quoted in the paper:

  g Tum-mo yoga is a form of meditation which allegedly allows its practitioners to alter body temperature. Previously, only subjective descriptions of this phenomenon existed: "The neophytes sit on the ground, cross-legged and naked. Sheets are dipped in icy water, each man wraps himself in one of them and must dry it on his body. As soon as the sheet has become dry, it is again dipped in the water and placed on the novice's body to be dried as before. The operation goes on in that way until daybreak. Then he who has dried the largest number of sheets is declared the winner of the competition".


Statistical Analysis of Protein Folding Problem

One of the quickest ways to get oriented on what is going in the world of protein folding and modeling is to look at the proceedings of the Critical Assessment of Structure Prediction (CASP).  CASP is basically a contest, held every 2 years where anyone can use their algorithm to predict the 3D structure of a protein whose structure is known, but not publicly available.

Its been a few years since I reviewed them results much - it looks like this year was interesting, but a perennial winner has been Rosetta, which has turned into an edifice of many suites of software which each execute different tasks in protein folding and modeling.

Open source software is pretty hard to find in this field.  The software is complex.  It usually includes components of machine and statistical learning, molecular dynamics, specialized algorithms that build up the protein one residue at a time, others which manipulate blocks of the protein structure around in space, electrostatic calculations, you name it.  In addition, the software, once it gives some sort of result is quite valuable.  I don't think any of these suites has really been released.  I know that Rosetta is available to use as a web service, but you have to apply for access to the source.  I don't think its an easy thing to get.

Some of the most complicated components are available open source.  Molecular modeling and molecular dynamics open source software is quite sophisticated.  I think we need an open source protein folding suite open source.  I think David Shortle's algorithms might be a candidate for such a suite as its not so complicated and it works in some cases.

This field is pretty obscure and difficult to get around in.  There aren't any easy introductions that I know of.  Protein structures are computationally expensive and painful to work with in terms of writing software.  On the other hand protein folding that really works is a revolutionary breakthrough, at least equal to the impact of the development of computers as a technology.


How can I get the coding region from gene sequences?

Not all the exonic sequence is coding. The ends have 3' and 5' UTRs.

Can you find gtfs for your organism?  Those would be easier to work with.

Or, I'd do blastx against the protein, that should pull out just the sequence that codes for protein.


Would it be possible to eat things from another planet

Short Answer- No, chances are negligible.

Long Answer- Digestion is a chemical process which is mediated by enzymes. Enzymes are highly choosy molecules so that they only perform the work they're made for. In digestion, enzymes like proteases (for breaking down proteins), lipases (for breaking down lipids), amylases (for breaking down starch), DNAses (for breaking down DNA), etc. are involved. For example, amylase is specialized to break down polysaccharides (carbohydrate polymers) into mono/di/tri/oligo-saccharides. See this from wikipedia:

  The α-amylases are calcium metalloenzymes, completely unable to function in the absence of calcium. By acting at random locations along the starch chain, α-amylase breaks down long-chain carbohydrates, ultimately yielding maltotriose and maltose from amylose, or maltose, glucose and "limit dextrin" from amylopectin.

And this image from here:

Lets forget the "completely unable to function in absence of calcium" part as it is out of the scope of this question. But it is necessary to know how specialized enzymes are to answer your question. They are so specialized that amylase can break starch, but not cellulose. See this image:

Source

You must have noticed, in the diagram above, the minute difference between starch, cellulose and glycogen (BTW glycogen is another polysaccharide), but even that difference is enough for enzymes to tear apart one and pass on the other molecule.

The above explanation was necessary to tell why the answer is no. If we eat something, enzymes are needed to break it down. But if enzymes cannot recognize something, then they can simply not work on it. So, if you even want to eat space grass, forget about being able to digest it. Because even if we confirm that life on earth came from space through meteorites billions of years ago, then also during this time period of billions of years both that life of space and this life on earth would have evolved so much that they might not match, even chemically!

Hope this helps. Tell me if you want any more details :)


These are probably cockroach cases, or oothecae, that may contain up to 50 eggs, depending on species.

It looks like they are oothecaes of German cockroaches.

You can read more about baby cockroaches here.


Are the bacteria in the stomachs of unborn babies beneficial?

It's a fascinating topic! While most of the bacteria known to colonize babies comes from the vaginal tract during birth and then later, through breastfeeding, although there is evidence to suggest that microbial colonization may begin before birth.

Regarding what these bacteria are, our microbiomes are composed of probably hundreds of species of bacteria from at least four major phyla: actinobacteria, proteobacteria, firmicutes and bacteroidetes (see the review for more on them).

As for taking antibiotics, I find it highly unlikely that taking antibiotics would completely destroy any native gut flora species. I certainly can't find any evidence to suggest that that might be the case. In general, when we have to take antibiotics, the offending bacteria are a relatively small population, compared to our native species and are less well-adapted to our body environment. Antibiotics work with our own immune defenses to clear our system of pathogenic species. Antibiotics also hurt our native flora, but less so than the ones that make us sick.

As for your last question regarding health, I wouldn't exactly say that having a microbiome promotes better health, so much as that your microbiome is critical for survival and health. There are actually nutrients that we need for survival that we cannot digest without our microbiota and a wide number of diseases, from immune disorders to potentially depression, can arise from an unhealthy microbiome.

As a fun bit of trivia to ponder in parting, our bodies are composed of 90% bacterial cells by count. Sweet dreams...  :-)


That is a Franklin's Ground Squirrel

Winnipeg is part of its range:

Have a look at a gallery of such photos here: https://inaturalist.ca/taxa/179937-Poliocitellus-franklinii/browse_photos


What evolved to produce sweetness, plants or consumers?

None of the above.

Seeking sugar evolved long before animals, before multicellular organisms even.
Plant evolved a strategy to exploit it much much later with the evolution of fruit and nectar.

Animals evolved to like the taste of sugar since it is the primary fuel almost all life metabolizes to live in an easy to digest form, literally a simple carbohydrate. plants use sugar substances as lures becasue that's what animals already wanted and plants were already making it. Also a lure is not going to evolve before the seeking behavior that would actually make it a lure. fruit and nectar are new sugar is one of the oldest metabolic compounds in existence.

Metabolizing glucose is one of the shared characteristics between Eukaryotes and Bacteria and is present in nearly all life,source. Meaning it is was likely present in their common ancestor. This means plants and animals have been eating sugars since before they diverged into plants and animals. . Chemotaxis  of motile bacteria towards glucose is well understood, and likely predates the existence of eukaryotes. source

The production of sugar by photosynthetic bacteria predates the merging of Eukaryotic cells and chloroplast ancestors. It was present in the Cyanobacteria that gave rise to chloroplasts, meaning sugars were produced long before plants existed. source the attractive aspect was only exploited later with evolution of nectar and fruit.


Given an EC50 value, how do I reproduce the sigmoidal curve from which this was calculated?

Basic sigmoidal curve looks like that: zero at $-\inf$ and one at $+\inf$. All in between should look like an integral of gaussian distribution. Take a look on this wiki page for more information. Now, the question, why sigmoidal curve is integral of gaussian function, I will leave out for now. My understanding is that gaussian distribution tells you how much system response will increase (say, efficiency of treatment) if you increase stimulus by $dx$. E.g., how much response changes when you go from $5$ to $5+dx$ versus from $10$ to $10+dt$.

The problem, as you might realize, that gaussian distribution has two parameters: mean value and width of the function. When you construct your fit, frist one will be 19nM, but second, $\sigma$, is unknown from your question. What you don't know is how rapidly response changes when you increase concentration by little around your EC50. So all your sigmoidal plots will go through same point but with different slope, like that:

Without knowing second parameter, $\sigma$, it makes little sense to plot your sigmoidal curve. However, if you want to, this is MATLAB code. See that cumsum() function effectively integrates gaussian distribution rendering sigmoidal curve.

c = 0:100; % range of concentrations you test
sigma = 1; % unknown parameter
m = 19; % your EC50 19 nM
g = 1/(sigma*sqrt(2*pi))*exp(-((c - m).^2)/(2*sigma^2)); % gaussian
gs = cumsum(g);
plot(c, gs)

If you want, you can plot it with log-scale of X, using semilogx() instead of plot().

NB here I started with Gaussian function and its integral just as a wild guess. You real function might very well be something like $f(x)=\frac{1}{1+e^{-x}}$. "Sigmoid" function is just description of general shape, not mathematical definition.


Can Naegleria fowleri enter through the eyes ( example rinsing/splashing eyes with water)

In a 1987 article "Nonenteric Infections Acquired through Contact with Water", the author mentioned that "Infection of the ears, throat, respiratory tract, and cornea are also encountered" by virulent strains of Acanthamoeba and Naegleria fowleri. The only reference that implicates Naegleria fowleri is this one, but it doesn't mention modes of infection.

The long and the short of it is that Acanthamoeba infections can be acquired through contact with the cornea, but it's not clear whether Naegleria infections can also be acquired in this way.

n.b. The first link takes you to the JSTOR page.  In the event you do not have access, here is the PubMed page.


You can use the PCR purification kit for cleaning up the DNA.

You can use the primers that you used for RTPCR for sequencing. The universal primers would work only if the sequence complementary to it is there in the 3' end of your amplicon.


Where I can download the genome sequence of various species of Fusarium?

The standard source for open-access nucleotide sequences is GenBank. Searching for Fusarium in GenBank gives 440421 hits, but these are shorter reads, not full genomes. Depending on your purpose, they may be useful to you.

You may also be interested in assemblies, which are collections of aligned reads stitched together, often at the scale of whole chromosomes. Assemblies with 'Fusarium' in their keywords are available here.

Genomes may be found here, but it does not appear that GenBank holds a complete assembled genome for any Fusarium species yet.


Is a double-yolk egg capable of producing two viable chicks?

According to the discussion here they normally fail to hatch because the chicks cannot get enough leverage to break the shell.

Here is a video of an assisted hatching. It is claimed that these two survived.


The comment seems useful as your current definition of a gene list lacks context.

  How would you define a gene list?

There are many different kinds of gene list. Specifying gene lists from microarray and next-generation sequencing provides some context but both technologies are used to analyse many different kinds of DNA and RNA samples. Define the molecules that are being referenced by the gene lists.

Defining DNA or RNA isn't sufficient as each gene list is compiled to perform a research task. Genomic projects may provide lists of genes that were sequenced or mutated or contained single nucleotide polymorphisms. An RNA transcript project may create lists of genes where transcription was occurring in a tissue or whose RNA transcripts were influenced by experimental factors or whose splicing was altered. Most publications also include multiple gene lists and some of those will include rows that were removed following data evaluation. Define the kind of lists that you are collecting.

There's value in defining your search criteria well. It allows you to communicate your work to others and it can provide focus to your search efforts.

  What criteria did I use?

This was mostly answered above. I would also consider including some rules for the publications that you will search for gene lists.


What does entering of sex chromosomes to gametes mean during meiosis I?

I seem to now understand the sentence. I read the clause in other words:

  During meiosis I, the sex chromosomes of the gametogonia separate in
  anaphase I and II and become eventually different sperm or egg cells
  after cell differentiation and maturation: male spermiogenesis and
  female maturation into ovum.

Female thing does not seem to have a special name for the maturation thing.
Female does not seem to have differentiation part at the last part similarly as male, since only one ovum is formed after the sequence of events.
Sex chromosomes refer to your parents genotypes. [jg89]

Problem seems to be solved now.

I would not personally use the word "enter" in a such sequence. It is a shortcut. Better would be "enter eventually" or "enter after a sequence of events". I prefer explicity instead of implicity.


How does Australia fit into 'New World' / 'Old World' dichotomy?

First off - this is an answer without citations. I looked for them, but couldn't find any. The terminology is undoubtedly described in reputable sources, but it is unlikely a paper is dedicated solely to explain this terminology, making literature searches tricky. Having said that -

I discussed this question with an anthropologist and she agrees with my idea that the terminology Old and New World is a historic and Euro-centric one, dating back to the colonial times when Europe viewed itself as the center of the world.

The Americas were discovered relatively early, around 1492. It was designated the New World. Australia wasn't found until around 1606. By that time the New World was already a century old and very likely already solidly associated with the Americas.

The New World, in a biological context, is often used to describe groups of closely related species found in the Americas and not elsewhere, such as New World monkeys. In certain areas of expertise the terminology is baked in in the jargon, .e.g,  monkey and ape behavioral research areas. New World monkeys can be referred to by the Cebidae, as per the Linnaeus's classification. However, due to practical reasons geographical clustering of species can be more convenient.

The term New World means different things in a biological context or in the context of wines, for example (Americas versus Americas + Australia - admittedly Australian wines are pretty good).

In all, I think the terminology 'New and Old World' is confusing, rooted in historical considerations. Australia as well as Antarctica don't fit in this terminology.


Are humans more aggressive during a full moon?

This seems to be a piece of pseudoscience commonly seen these days. The truth is that this effect has never been statistically observed.

From the Skeptics Stack Exchange site:

  Ivan Kelly, James Rotton and Roger Culver (1996) examined over 100 studies on lunar effects and concluded that the studies have failed to show a reliable and significant correlation (i.e., one not likely due to chance) between the full moon, or any other phase of the moon, and each of the following: The homicide rate, traffic accidents, crisis calls to police or fire stations, domestic violence, assassinations, kidnappings, aggression by professional hockey players, violence in prisons, assaults, gunshot wounds, stabbings

... and many more seen here.


Finding targets of transcription factors

If you were interested in human targets, one easy way is GeneCards, which aggregates other resources, and combines computational and (some) experimental data:

In this case the inverse problem is particularly well accessible: e.g.: scroll down to section of Genomics (e.g.: for the gene called NOTCH http://www.genecards.org/cgi-bin/carddisp.pl?gene=NOTCH1&keywords=notch1 ).

If you you were interested in obtaining all genes of a given transcription factor, you could buy a license, costing around 150 USD per year, for the GeneALaCart service of the company that runs the free genecards ( https://genealacart.genecards.org ), upload a list of all human genes (which you could for instance obtain from ncbi's ftp server), and get a spreadsheet linking transcription factors to genes.


Is there a difference between NADH and NADH2?

They are often used interchangeably to indicate the reduced form of $\ce{NAD+}$.  The overall reaction when oxidizing some molecule $\ce{RH2}$ is: $\ce{RH2 + NAD+ -> NADH + H+ + R}$.  The proper reduced $\ce{NAD+}$ is $\ce{NADH}$ (it accepts two electrons and one proton), but sometimes $\ce{NADH2}$ is used to account for that second hydrogen that gets removed from the substrate being oxidized.  The notation $\ce{NADH2}$ doesn't really take into account the fact that the second hydrogen is charged, and not bound to the $\ce{NAD}$ in the same way that the first hydrogen is, so it is confusing.  The notation: "$\ce{NADH + H+}$" is more correct and is also sometimes used.


Typical here means representative of the whole.

from the google dictionary

  typ·i·cal ˈtipik(ə)l/Submit adjective having the distinctive qualities
  of a particular type of person or thing. "a typical day"
  synonyms: representative, classic, quintessential, archetypal, model,
  prototypical, stereotypical, paradigmatic;

There is such a variety of cells in the body no one is really typical.  Like a typical human.  Who would that be?  Me?  Chinese lady?  Indian kid?  There are many of us and a lot of variety.  Maybe you could say "typical older Scotsman" or "typical arrogant Stack Question answerer".  You could definitely say "typical liver cell"; narrowing down the zone limits the variety possible and lets you more accurately characterize a call as prototypical or representative.


How are cells of the cornea transparent?

Most cells are transparent, which is why we can see cells using bright-field microscopy, where the light travels through the cells before you see it. That's how we can see inside onion cells and see structures like onion cell nucleii, moss cells, human epithelial cells and animal mast cells.

The human cornea is made up of five layers, each of which have different structures allowing them to be transparent: the outer and inner epithelial layers are very thin and naturally pretty transparent, and the middle layers have collagen fibres; based on that Wikipedia article, it sounds like there are several hypotheses for why these layers are transparent, but it doesn't look like there's a definitive answer yet.


Adaptive radiation vs divergent evolution

They are similar, but distinct, concepts.
In divergent evolution, selective pressure causes differences within a single species to accumulate, eventually leading to speciation. Speciation can be caused by a variety of factors, such as geographical, reproductive, behavioral, or temporal isolation, etc.
In adaptive radiation, typically several niches are present in an ecosystem, leading to several species evolving from a single common ancestor. A niche is essentially an opportunity for a species in an ecosystem to evolve, to where there is little to no competition. Darwin's finches tend to be the prime example for adaptive radiation. Since there was little competition when the finches first arrived at the Galapagos islands, they speciated into multiple distinct species to specialize in consumption of seeds, fruits, insects, etc. Eventually, each species evolved to have distinct traits, such as in their behaviour and reproduction, making mating between species close to nill.


Merge several .ab1 sequence files into a single FASTA file?

In general you should use a base calling algorithm to generate the sequences from the chromatogram and not directly convert it to fasta (Courtesy: Sven [SEQanswers] ). As mentioned in the link, phred and TraceTuner are popular base calling software that can generate a fasta output.

The software mentioned by The Nightman can be used for converting .ab1 to fasta. You can also try this BioPython module called abifpy. You can easily read each .ab1 file, using a python script, and write the sequences in fasta format as a single file.

Combining multiple fasta is quite trivial. You can use cat as mentioned by others.


What part of food gives the blood red color?

The red colour of blood isn't actually to do with food at all.  The primary purpose of the blood is to carry oxygen to all the cells that require it to release energy.  Red Blood Cells are filled with an iron containing pigment called haemoglobin.  When it has oxygen bonded to it, haemoglobin  has a bright red colour - it is this that gives blood its red colour.

In terms of how food enters the bloodstream, it is first broken down into extremely small constituents.  This is done by mechanical action (i.e. chewing and the squeezing movement of your digestive system) and by chemical action through the use of enzymes.  Enzymes are proteins that are secreted by various glands in the mouth (and are therefore contained in saliva), stomach and both intestines.  These chemically break large food molecules down into small products such as glucose (sugar) and amino acids (protein-building blocks) amongst other things.  These then move across the wall of the intestines and into the bloodstream, which are separated by only one cell:

Unfortunately that's the best image I could find.  The intestine is everything outside of the pink layer (which is the wall of the intestine).  The small molecules are able to pass through the pink layer and straight into the blood stream.  The picture shows a fold in the wall of the gut, which increases its surface area so allows more molecules to diffuse across.


What is the reason behind the subphylum name "Urochordata" for tunicates?

In 1877, Lankester proposed in "Notes on the Embryology and Classification of the
Animal Kingdom" division of the group we now call Chordata into three parts:

Urochorda
Cephalochorda
Craniata

which is more or less the accepted division today, with Urochorda being called Urochordata now.

In this essay, Lankester says:

  The evidence of degeneration is admitted as conclusive in the case of the parasitic Crustacea and Cirrhipedes. It is equally incontestable in that very large and varied group of non-parasitic organisms, the Tunicata (Urochordate Vertebrata).2

(in the above 'Vertebrata' is what we call 'Chordata').  He adds this footnote:

  2The whole argument as to the Tunicates of course rests on the view- supported by many arguments, that the larval urochord, which many of
  them possess, is not a larval organ acquired by larval adaptation, but is hereditary and transmitted from adult ancestors.

The term 'urochord' seems to be established and used without comment there, and probably is taken as simple neo-Latin for 'tail chord', although that may be somewhat loose, perhaps meaning the notochord is present but does not extend into the head.  A 1913 Webster's Dictionary defines urochord as:

  (Zool.) The central axis or cord in the tail of larval ascidians and of certain adult tunicates.

In 1882, Lankester futher discussed the anatomy of the tunicates in the context of the division of the chordata in a paper called "The Vertebration of the Tail of Appendiculariæ".  This paper includes an illustration of a larval tunicate with the "notochord (urochord)" indicated.


Can a bacterium survive without GroEL protein?

In E. coli, GroEL/GroES is found to interact with about 10% of all soluble proteins (Kerner et al. Cell 2005) and is the only chaperone essential to the bacterium under all tested conditions (Horwich et al. Cell 1993).


Is far Infrared heaters in the market truly producing healthy far Infrared and is it practical to install them at home?

Far infrared is also known as thermal radiation. It is less harmful to the human body than red light and blue light. If you are under a cloudy sky and it is hot, say 30 degrees, that is how harmful thermal radiation is to the body.

The hight you climb up the electromagnetic spectrum, from radio waves to thermal waves to light waves to UV Xrays and Gamma rays, the more they can interfere with atoms and molecules, because they can disrupt bonds, ionize, and so forth.

So IR can only heat the body and can't ionize or disrupt the body.

Far infrared is the heat you feel when you are far away from a fire and the heat travels towards you without air transport. Near infrared is the heat you feel closer to the radiator, and that which causes convection nearest to the heat source, it gets absorbed faster by the air.

Insulation is most important for heating, as more than 50 percent of heating is lost through the ceiling. modern buildings in the west have high roof insulation standards.

oil heaters tend to absorb near infrared and reflect it back as far infrared better.

I think that the smaller and hotter the source, the nearer thermal wavs it produces, and the larger and less hot surfaces can make more far infrared.

It sounds like a lot of marketing terms.

Oil heaters are traditionally very efficient. I had one which i bought a bit rusty for 15 euros and it has lasted 5 years. the only issue with oil heaters is that they can eventually leak when very worn or less strongly welded.

microwaves are less HF than thermal, and they have not been associated with any health risks either even from phones used all day beside the ear.

You can think of far infrared as the warmth that is reflected from a hot wall heated by the sun. It is one of the least dangerous forms of radiation.

you may consider investing in a HPS lamp of 600 or 1000w because it produces 90 percent heat from that, and also vast amounts of light which are good for mental biology and good for growing tomatos and strawberries in the middle of winter. because they go in a ventilated area under a table in the house, the also radiate well. of all kinds of radiators, i prefer by far sitting under a hot lamp with a summer hat tending plants in the middle of winter, it's definitely hot. A 600W lamp can produce about 200 tomatos, 100 strawberries and 20 peppers and some melons/beans etc, in the winter months.


Is tunneling of a proton in our DNA a cause of mutations?

Keto-enol tautomerism involving proton transfer within a single DNA base can lead to mispairing and mutation during replication.  This is touched on in the previous citation provided by tsttst as well as this section from An Introduction to Genetic Analysis. 7th edition: https://www.ncbi.nlm.nih.gov/books/NBK21897/  I have not found a clear statement of whether the proton transfer is over sufficient distance to constitute "tunneling".


Why can blood vessel contraction be described as a second order system?

Many systems have this property. The plot you are looking at is the plot of the transfer function for blood vessel diameter vs time. A trick in mathematics or engineering is to understand a system is to sometimes look at at different system with the same properties that you do understand. For instance, a mass springer damper system is similar to a RLC circuit. That is, if we understand the mass spring damper system, we view the RLC circuit as the analog to the mechanical system and vice versa. In the case of blood pressure, we also have a driven force (the heart). Thus, an extremely simple model would be
$$
m\ddot{x} + c\dot{x} + kx = F(t)
$$
As we see below, the mass spring damper model produces the a similar plot of the transfer function. If you understand the mechanical system or RLC circuit, you can look at your plot parameters as an analog to one of these systems to understand the dynamics occurring in the body.

A more interesting question is can we use PID control to manage the overshoot, rise time, and settling time of the vessel diameter in the body?

The differential equation that models this process is probably related to a Bernoulli differential equation.

http://en.wikipedia.org/wiki/Bernoulli%27s_principle
page 15 http://www.physics.usyd.edu.au/~jbryant/Fluids/Fluidslect4.pdf
http://bme.ccny.cuny.edu/faculty/bfu/blood%20flow%20permeability%20in%20microvessels.pdf

A precise differential equation will need to account for pressure (Bernoulli), fluids (Navier-Stokes), and the elasticity of the vessel walls.


Why are female clones more often produced

They aren't, anymore.  It was a fair guess at the time, but first I think we should define what cloning in this context mean.

Our own cloning tag says:

  The process in nature or in the lab by which a new organism is created that is genetically identical to its predecessor.

For animals - I'm going to use Dolly as an example since you do as well - when we say "cloning" we usually mean somatic cell nuclear transfer.   This image from Wikipedia sums up the process:

Basically, you take the nucleus of your to-be-cloned animal and put it inside the egg cell from another animal.  Dolly was not produced by one animal but by two - a donor and and a surrogate.  She was made using mammary tissue (another good image here) from the donor, which is important to note.

Dolly was the only one out of 277 egg cells that made it.  This is a hard technique, and we still don't understand a lot of it.  With even less information at the time, some prevailing ideas were:

Maybe there's something special about reproductive-based tissue
Maybe there's something special about female tissues

Even when using a different technique (e.g. Cumulina), early cloning attempts hedged their bets with those same tissues. That's why Fibro, the first male cloned (from tail), was a big deal - he showed that any tissue could be used, and that reproductive or female tissue wasn't inherently special.  You still need an egg and a surrogate, but if you can get the nucleus right it's just as doable.


The "Description of the analyzed data set" section seems suspicious to me:

In a nutshell, young women between the ages of 14 and 17 years old
were identified and recruited by the project.
...
At each follow-up visit during the study period, enrolled participants
underwent STI testing and treatment. Also at each follow-up visit, the
participants received follow-up interviews, in which they were queried
about the number of unprotected coital events since previous visit.
Most of the participations did not visit the clinic every quarter and left the project before its completion.
For our analysis, we collected 1173 quarterly test results from the
first 200 participants who were never infected and have completed at
least two follow-up visits. Their average enrollment age was 15 years
with standard deviation of 1.1 years.

It means that data is biased as for some reason most of girls were not able to participate in the study.
And I'm not sure about the correctness of your interpretation. I'd interpret it as "females are 20x less likely get chlamydia infection after being treated and warned about STD" as there were relatively continuous followed-up 15-17 y/o females and no older females. And I guess it was one of the goals of this "Young Women’s Project".


What is the advantage of using plant-derived antibacterials rather than bacteria-derived antibacterials?

Bacterial isolates from ancient permafrost and isolated caves allow study of the resistome, or the collection of antibacterial resistance genes, in environments without exposure to modern antibiotics for medical and agricultural use. These samples have genes for resistance to antibiotics derived from a variety of sources, including fungal sources (penicillins, cephalosporins) and synthetic dyes (sulfonamides), as well as bacterial sources (macrolides, aminoglycosides, etc). This finding was surprising, but does help explain the rapid emergence of resistance in response to clinical use. The genes have been there all along.

The OP is correct that a great deal of our current armament of antibiotics were derived from bacterial products, but since fungal and wholly synthetic products don't solve the resistance problem, I don't believe plant products will either.


Identify this giant green moth(?) with great taste?

That appears to be an Oleander Hawk-moth a member of the Sphinx moth family.

I think the only other possibility for Taiwan is the quite similar Jade Hawk-moth, but that supposedly has a dark purplish colored head.

Image for comparison:

Source: Shantanu Kuveskar / CC BY-SA.


Summary
The apparent paradox is resolved by the fact that not all tissues possess receptors that cause them to respond to glucagon or, more generally, to the same hormone. Where different tissues do respond to the same hormone, the tissue response may differ because of differences between the pathways or particular enzymes within the different tissues. Tissues that use glucose in starvation generally do not have glucagon receptors. In the related situation of response to epinephrine, the glucose utilizing tissue, skeletal muscle, does not contain the particular enzyme isoform that is subject to cyclic AMP-dependent control in liver.
General principles of hormone action in the regulation of metabolism
Metabolism in simple, especially unicellular, organisms is regulated by supply and demand. The mechanisms underlying this are mass action and allosteric activation or inhibition of key enzymes. In more highly developed organisms with differentiated tissues serving specialized functions there are times when this intercellular control must be over-ridden to produce an integrated response to the overall benefit of the organism. This is the rationale for hormonal control.
An integrated response does not mean that each tissue responds in the same way. It means that each tissue responds in a manner that is appropriate for the organism as a whole, given the function of the tissue and its priority (e.g. for rationing of energy sources). A simplified example of how this is achieved is illustrated below.

Tissues 1 and 2 (e.g. liver and skeletal muscle) both contain pathway P1 (e.g. glycogen degradation), but only Tissue 1 responds to hormone H1 (e.g. glucagon) because Tissue 2 does not have the receptor R1, for H1. (SM is the second messenger involved in the signalling, e.g. cyclic AMP.)
Tissue 2 (e.g. adipose tissue) does have the receptor for hormone H1, but responds in a different way because it lacks pathways P1 and P2 of Tissue 1, but contains a tissue-specific pathway P3 (e.g. triglyceride breakdown).
Hormone H2 (e.g. epinephrine/adrenalin) affects Tissue 2 (e.g. skeletal muscle) as well as Tissue 1 (and 3), but the response is only partially similar in that although they share pathway P1, Tissue 2 lacks pathway P2 (e.g. gluconeogenesis).
Differential response to glucagon
Put simply, glucagon is a signal for starvation. Hence the appropriate integrated response is for those tissues (liver and adipose tissue) that can supply energy sources (glucose and fatty acids, respectively), and those tissues with greatest need for the scarcest resource (brain with its requirement for glucose) are supplied it, while those tissues that can manage with the alternative (fatty acid) are made to use it instead.
The brain has no receptors for glucagon (or insulin), so it can utilize the glucose made available by the liver. (Likewise the erythrocytes.)  The main factor preventing other tissues using glucose is that they have insulin-sensitive glucose transporters and the blood concentration of insulin drops in starvation. It is only liver where there is need to make sure that the glucose produced by gluconeogenesis is not glycolyzed.
But doesn’t the paradox remain if we consider epinephrine?
The function of epinephrine is to initiate the ‘fight or flight response’, which involves supplying energy metabolites for skeletal muscle contraction. This involves both the liver, which breaks down glycogen to supply glucose to the muscle through the blood, and the skeletal muscle itself, which breaks down its own stored glycogen. As epinephrine also acts through cyclic AMP, which inhibits glycolysis in liver, why is glycolysis not inhibited in skeletal muscle?
The answer to this is that cyclic AMP inhibits glycolysis by phosphorylating and activating the liver enzyme PFK2, which catalyses the formation of fructose 2,6-bisphosphate, an allosteric activator of phosphofructokinase. Skeletal muscle has a different form of FPK2 which is not affected by cyclic AMP, lacking the regulatory phosphorylation sites. (It is regulated by other metabolites.) Hence in liver, glycogen, through cyclic AMP, causes the concentration of fructose 2,6-bisphosphate to decline and, thus, the activity of phosphofructokinase (PFK) to be decreased, preventing glycolysis; whereas in muscle the concentration of fructose 2,6-bisphosphate does not change.

This regulation of phosphofructokinase by fructose 2,6-bisphosphate is described in sections 16.2.2 and 16.4 of Berg et al. (although they seem to have forgotten about skeletal muscle). However as the overall mechanism and details are somewhat complex, I have produced a simplified summary diagram of my own, above, in which the green lines indicate activation, and the red lines inhibition.


Hmmmm... the only one I can think of fitting at least in part your description would be the golden oriole (Oriolus oriolus).

I say partly because it definitely is not 2-3 times a blackbird, could be slightly bigger, but on average it is the same size. Also it sounds extremely unlikely that you have spotted it in early March in Zurich, as they should be in Southern Africa right now.

Image, from Wikipedia:

I could not find anything else fitting your description in my field guide (Mullarney & Svensson - Birds of Europe)


Lengthening muscles not good from evolutional perspective? Why do we do it with explicit stretching?

Muscles only ever work by shortening, as you say, but muscles in the human body tend to be found in antagonistic pairs.  These pairs of muscles act in opposite directions, one example being the biceps and triceps muscles - the biceps bends the arm (a flexor muscle) while the triceps straightens the arm (an extensor muscle), another example is the quadriceps-hamstring muscle pair in the upper leg.

If our muscles remained shortened, our mobility would be impaired.  If the biceps muscle remained too short, it would be impossible to extend our arms, for example.  Muscles do work by shortening, yes, but it's important for them to be able to stretch as well, and remain long enough for antagonistic muscles to have their full movement be possible as well.


How do the three mechanisms of the 1000X improved "new" vancomycin work together?

This is typically for a paper under embargo - it can be accessed by registered journalists so they can cover the original article when it is published. The paper is now published, so I changed the first answer.

Before I go into the details, it is necessary to have a short look at the working mechanism of Vancomycin and the way bacteria got around it (which took exceptionally long given that the drug is used since 1959 in the clinic):

Vancomycin works by inhibiting the proper crosslinking of the bacterial peptidoglycan in the cell wall. This is achieved by binding to the substrate for the peptido glycane synthesis, a D-alanyl-D-alanine end of a peptide. Cells then burst due to osmotic pressure.

Resistant cells have a D-alanyl-D-lactate ending of this peptide (all details can be found here or in the introduction of the paper) which lowers the effictivity of the drug by a factor of 1000. Interestingly, this resistance mechanism seems not to have evolved in pathogen bacteria itself, but has been "borrowed" from bacteria which produce Vancomycin and need this as a self-defense (for more, see reference 2).

Vancomycin forms a pocket around the d-Ala-d-Ala substrate, which is impaired in the resistant form. Overcoming the resistance means finding a variation of Vancomycin which effectively binds both of the variants and thus inhibits proper cell wall crosslinking.

To achieve this, Okano and his colleagues chemically modified the structure of Vancomycin with several different functional groups at different sites of the molecule, see this figure from the paper (figure 4 from reference 1):

Changing these residues changes the sensitivity against these modified Vancomycine quite a lot, as can be seen in the sensitivity table in the figure.

When they changed the molecule, they did not only change the binding pocket to allow binding to the different peptide substrates, they also introduced two other independent mechanisms against the bacteria. The most active compound (named 18 in the paper, seen above from figure 11) shows:

  Compound 18, which incorporates the redesigned pocket modification for
  dual d-Ala-d-Ala/d-Ala-d-Lac binding (blocks cell wall synthesis by
  ligand binding, including inhibition of transpeptidase-catalyzed
  cross-linking), the CBP disaccharide modification (blocks cell wall
  synthesis by direct transglycosylase inhibition without
  d-Ala-d-Ala/d-Ala-d-Lac binding), and the C1 quaternary ammonium salt
  C-terminal modification (induces membrane permeability), exhibited the
  most potent inhibition of cell wall synthesis in the assay of all
  compounds assessed.

Okano and colleagues also tested the different modifications one by one to see, which one has which effect and also tested the effectivity on resistant bacteria. The resulting table shows that the strongest effect is only achieved when all three modifications are present in the molecule.

Since these are independent mechanisms, it will also prolong the time until resistance against the new version of Vancomycin (given that is has a tolerable toxicity in humans and can be introduced into the clinic) will take a while to develop. Despite the optimism in parts of the paper this resistance will eventually develop, although it is quite complicated to overcome three different mechanisms.

References:

Peripheral modifications of [Ψ[CH2NH]Tpg4]vancomycin with added
synergistic mechanisms of action provide durable and potent
antibiotics
Glycopeptide antibiotic resistance genes in glycopeptide-producing
organisms.


Recording policies in functional magnetic resonance imaging

If I recall correctly, in BOLD fMRI an echo-planar imaging (EPI) sequence is typically used. In one example:

  44 slices were acquired, every 3 seconds, 96 times in a row, leading
  to a total number of 4,224 images acquired in 4 minutes and 48
  seconds.

— https://www.imagilys.com/functional-MRI-fMRI/

You can read more about EPI here. I think you will find the zig-zag pattern in this link interesting. See also this link for a description of EPI.

fMRI is slow and has a low temporal resolution, because the hemodynamic repsonse of the blood is around 6 second long. This is perhaps a limiting factor for fMRI, which is why there is a limit to optimizing the sequences. However, one real impact of faster sequences is to capture head movement artifacts more accurately. Other sequences are used in anatomical MR imaging, such as FLAIR.