Looking for source: Biologic reactions of people saying "no" Searching for this topic is incredibly tedious because the word "no" is the main point of interest and I always end up on sites saying how "saying no is good for your health" but I am looking for the medical evidence of this claim.
I remember very faintly hearing about measurable physical effects on a person in a situation where this person says the word "no" to something.
There was an experiment where scientists (I suppose neuro-scientists?) were able to measure the effect of saying "no". Colloquially speaking the body was "closing" in a sense that the person went in some unconscious defence mode, stress levels were rising, change in muscle tone were measurable etc.
When I also remember correctly these effects were measurable even without exposing the person to a specific situation. Just saying "no" wholeheartedly triggered those effects.
Did someone hear about this one? I am looking for any clue to get more information on that.
Edit: I add to the excellent hint from Vadim: I am indeed looking for a credible source where experiments were conducted in a controlled manner and not someone sticking electrodes on people in the mall :D. And I also think this experiment would be hard to do right in the first place since you basically would have to deprive the people from any external stimuli which by itself would probably also already cause side effects.

Most of the claims that "saying no is good for one's health" are grounded in psychology. In other words, they are  not experimentally verifiable. Likewise, health here refers not only literally to physical health, but also to psychological health, which in itself is something hard to define.
Surely, in situations of high stress saying "no" can actually result in some measurable responses, in which case it can be studied within the context physiology and neuroscience. However, this would address only a small part of the situationd covered by the original claim - discarding any effects on psychological health as well as long-lasting effects on the physical health.
To summarize: for a scientific study the claim needs to be made more specific, i.e., apply to well-defined situations and responses.
Disclaimer
I feel that a clarification is needed, lest what I wrote above is interpreted as a negative view of psychology.
I am not claiming that all of the psychology is outside of the scientific method, but a big part of it is - at least outside of being possible to study in a laboratory setting. And this is by no means unimportant part, in terms of the role it plays in our society. While words not scientific often carry negative connotation, in practice any scientist should recognize that scientific method has its limitations - many phenomena (psychological, social, economic, etc.) are not sufficiently reproducible and controllable to study experimentally, yet too important to dismiss.


Can humans live without their right atrium? The right atrium  is one of four chambers (two atria and two ventricles) in the hearts of mammals (including humans) and archosaurs (which include birds and crocodilians). It receives deoxygenated blood from the superior and inferior venae cavae, the coronary sinus, and the anterior and smallest cardiac veins, and pumps it into the right ventricle through the tricuspid valve.

Can humans survive without right atrium? In this condition blood would fill the right ventricle directly, comparable to some animals like  frogs, toads, snakes and lizards. What advantages does the normal human heart have to this anatomy ? If we had this anatomy, where would the best place for pacemakers be, like the sinus node?

This is an interesting theoretical question, but several things would need to be clarified:

Does removing the R atrium relocate the SA node to the R ventricle or remove it completely from the picture?
Does the remaining R ventricle have a tricuspid valve?

Technically, the R atrium is the home of the sino-atrial node, which provides natural pacing of the human heart between 60-80 beats/min. Without this natural pacing, our hearts would rely on back-up pacer systems such as atrioventricular node, His-Purkinje systems or the intrinsic but ectopic pacing of individual atrial or ventricular cells.

1

It is possible for humans to survive without the SA node because of these back-up systems. However, our heart rates would be lower, or bradycardic. Although there are many individuals who survive with bradycardia ranging from top athletes to the elderly, this condition could lead to negative symptoms including fatigue, dizziness, lightheadedness, syncope, and even cardiac arrest [2]. Ideally, the SA node would be located at or near the area of blood entry into a chamber (or, put another way, opposite from the side where blood exits the chamber), so that blood is pushed synchronously out of the chamber rather than against a wall or the entry, causing turbulence.

The R atrium also provides a chamber through which venous blood can sit before it is pumped into the R ventricle to be pumped again into the pulmonary vasculature to be oxygenated. This function allows blood to enter the pumping ventricle quickly, a physiologic benefit [3]. In a heart without a R atrium, if the R ventricle still had valves to be able to keep blood from backing up into the vena cava system, then this function of filling and pumping would still be preserved, although it would not be as efficient as if there was a preceding atrium.

In nature, there are three-chamber hearts found in certain amphibians and reptiles. However, usually it is made of 2 atria and one ventricle, rather than 1 atrium and 2 ventricles. In this model, deoxygenated blood and oxygenated blood are mixed (to different degrees, based on the animal), which is not ideal. However, these animals usually have other modes of oxygenation such as through the skin.

In summary, the short answer is- yes, probably, humans can survive without the R atria but it would not be without serious consequences in quality of life.


How Does NADPH Reduce 1,3-BPG? If NADPH returns to being NADP+, then that means one proton and two electrons have been incorporated into 1,3-BPG. If only one proton and one electron were attached to the carbon in 1,3-BPG (removing phosphate), I’d understand, since there’s a single covalent bond between carbon and hydrogen which establishes stable octets. But there’s another electron hanging around. What happens to this one? Or am I totally mistaken about the whole process?

This is the chemical formula for G3P:

The Lewis diagram below shows the top part:

As stated, NADPH gave off 2 electrons, yet only one is needed to bond with carbon (orange). Where did the other electron disappear to?

Single covalent bond is a shared pair of electrons. For stable bond there should be 2 atoms with unfilled higher orbitals and at least a pair of electrons that is "distributed" among those slots.

UC Davis have hilarious page on that.


Is cell membrane living We say cell wall is dead but nobody says cell membrane is dead.

Is cell membrane living or dead ? If it is not dead then why is it not included in protoplasm :

  Protoplasm is the living contents of a cell that is surrounded by a
  plasma membrane.

(Source : Wikipedia)

It is neither living nor dead. It is simply not alive the way that any other collection of chemicals is not alive. Is salt alive or dead?

A cell's membrane consists of a collection of chemicals (mainly lipids and proteins). Individual chemicals can never be considered living or dead, any more than rocks or water can be living or dead. While the actual definition of life is tricky, everyone agrees that in order to be alive you need to (at the very least)

Somehow interact with your environment
Be able to make more copies of yourself

Therefore, the cells themselves are alive but the individual parts of the cells are not since they cannot make copies of themselves (this gets complicated when considering some organelles but never mind that here). Similarly, you are alive but your teeth are not. While you can make more of you (you can have children) your teeth cannot make more teeth.


Do the light and dark reactions happen at the thylakoid? My professor said that light reactions and dark reactions happen at the thylakoid. He did not choose the answer that "both reactions happen at chloroplast".

Isn't the thylakoid a part of the chloroplast?

The light dependent reactions involve an electron transport chain with enzymes embedded in the thylakoid membrane. NADPH and ATP are generated in the stroma and water is oxidized in the thylakoid lumen.

I'm not sure if it's correct to say that the light independent reactions occur "at the thylakoid" since, in plants, they could really occur anywhere in the stroma (not necessarily "at" the thylakoid, and certainly not within it). It's possible that the enzymes involved in the light independent reactions are somehow localised at the the stromal side of the thylakoid membrane for efficient use of substrates, but I have no idea if that is actually the case and I don't have time to review any literature.

In plants, all of these processes occur in the chloroplast. However, photosynthetic bacteria don't have chloroplasts so you can't categorically say that the photosynthetic reactions occur only within chloroplasts. Cyanobacteria do have thylakoids where the light dependent reactions occur.


If re-boiling does not curdle the milk, can that be taken as an indicator that the milk hasn't developed the bacteria (and their toxins)? Usually when left in hot temperature, the milk curdles (which I know when I boil it and it starts separating).

If the re boiling does not curdle the milk, can that be taken as an indicator that the milk hasn't developed the bacteria (and their toxins)?

This is the milk that I use.
http://www.amul.com/products/amul-taaza-info.php

Fresh milk does not separate when boiled. I use it in sauces and pan gravies and it always boils and never separates.

My suspicion is that you are separating it on purpose, for example to make cheese. In that case you have to add acid or rennet to separate it. If you then re-boil it to separate it again, you get very little solids. I have made cheese at home then tried to 'ricotta' the left over whey and all I get is a tiny bit of solids.


Diabetes Mellitus and renal failure? I have studied that Diabetes Mellitus leads to kidney failure and that this is because of the damage to the blood vessels (especially the blood vessels in the kidney) due to high levels of blood glucose?

How do high levels of blood glucose damage blood vessels?

I am putting here the main points from the link given by @WYSIWYG (i.e. this):

  High glucose levels reduce the levels of the powerful vasodilator nitric oxide in blood vessels, a shortfall that increases the risk of high blood pressure and eventually narrows down the vessels...increased modification of proteins by a glucose-derived molecule is a player in vascular problems associated with hypertension, stroke and obesity as well...the researchers found that there was an increased activity by O-GlcNAc in the blood vessels, which competes with another mechanism for modifying proteins called phosphorylation. In blood vessels, phosphorylation modifies the enzyme that produces nitric oxide, called nitric oxide synthase, so that it makes more of the blood vessel dilator. O-GlcNAc seems to beat phosphorylation to the punch so there is the opposite result.

Here, O-GlcNAc refers to O-linked β-N-acetyl glucosamine.


What could cause a forest of bent trees? While hiking on the northern Idaho-Montana border, I encountered a large area where virtually every tree is bent at the base in the downhill direction.  Only the very largest and very smallest trees are straight.  What could cause this?

The phenomenon in question is probably related to geotropism.

If the hill soil is "on the move" it will cause the bend on the trees -

  If the soil in a slope is moving downward, the trees on this slope
  will tip downward.  As the tree continues to try to grow upward, the
  trunk will show a curve. The degree of bending could indicate the rate
  or amount of movement of the soil.

source


Possible complications due to gene-therapy? Edward Lanphier, CEO of Sangamo BioSciences mentions here(https://youtu.be/dJ1B8XnyEnM?t=1215) that scientists can now specifically target cells, change the genome within a cell. Say you want to cure a type of disease, which can be linked to your genome. You have successfully removed the faulty gene in your genome (GenomeA), replaced it with a correct gene resulting in a improved genome (GenomeB) in a single cell. The next step will probably be to put it back into the human body. However, as I understand it every human cell contains your faulty human genome (GenomeA).

Question:

Even if you put a few cells with the correct genome sequence (GenomeB) into your human body, it is probably going to be overwhelmed by the other cells that contain your faulty genome (GenomeA). Cells containing the correct genome (GenomeB) will divide and multiply but so will cells containing the faulty genome (GenomeA). In this “genomic war” will the fewer cells containing the correct Genome (genomeB) ever win? Or will you need period infusions of cells with the correct genome "forever"?

How would you guys think about this?

Optional questions:

Even if it wins, it will probably take a very long time to completely replace all the cells with the faulty genomes. How much time is required before you can completely replace all the cells with the incorrect genomeA, with cells containing the correct genomeB?
Say you realize that you have a faulty genome (GenomeA), and you attempt to replace your genome with a correct genome (GenomeB). After 2 years, you have another disease and realize that you have to again correct your genome with GenomeC. However, 2 years is not enough to replace all your cells with the incorrect GenomeA, with the correct GenomeB. If you attempt to undergo genetherapy, now you will have to introduce another group of cells with GenomeC. Now you have cells with multiple different types of genomes floating around: genomeA, genomeB and genomeC. Are there any complications that happen due to the presence of multiple types of cells with different genomes in your body?

Your question is too broad. It is better to take some specific example.
Not all cell's in the body divide. If you take cell out of the body and want to return it back, it must divide. So we probably could talk about stem cells for example. The stem cells don not really sit in one place. And it almost impossible now to get such cells from the place that they sit in it, and then return in back. It is possible with bone marrow for example.

If we take some example, like ALS - some percent of the disease is thought to be genetic. But the mutation is in all the body cells. Mostly it's affects astrocytes, microglia and motor neurons. You cant take them out of the body, fix and return back. The only chance to fix is to work inside the body. For example by using some sort of virus (AAV for ex.) And CRISPR.

However, if we follow your story and we insert cells with genomB, they will live together with cells with genomA, if there is not some bigger mortality of the original cells.


Why is western blotting used to confirm positive ELISA HIV tests? I know that when an ELISA test indicates a positive result for HIV, a western blot is done to confirm. When I search online for the reason why, all that I see is that western blotting is "more specific" than ELISA. If they both use antibodies, shouldn't these procedures have similarly accurate results?

My only guess would be that the combination of Ab-Ag binding in addition to expecting your antigen to be a certain size is sort of a "double yes" and thus western blot results would possibly be taken as more accurate.

One reason a Western blot is more specific than an ELISA - even one using the same set of antibodies - is background.

Antibody-linked colorimetric reactions aren't completely on/off. There's always some background reaction. The antibodies are a little bit cross reactive, or non-specifically sticky, or the colorimetric coupling enzymes aren't completely washed away, etc. There's a number of reasons you'll get a small amount of signal even in the abscence of the desired reagent.

So imagine how this non-specificity looks in an ELISA assay. You're only getting a single readout. Any non-specificity/background in the assay adds noise to your output level. Hopefully for any decent assay the noise is normally well below the threshold for crossing over into a "positive" readout, but if the noise is Normally distributed, there's always a small chance that the noise will exceed that threshold. (There's also those non-normal failure modes, where you mess up a wash step, or you get a bad tube of antibody, etc. Negative controls help, but only so much.)

In contrast, think about how non-specificity/background looks in a Western blot. If you get non-protein linked background, the presence of this background will be across the entirety of the blot. It's very obvious that something went wrong with the assay in those cases. Even if you get random spots and not overall background, the chance you'll get a random spot at just the correct molecular weight is very, very unlikely.

An additional benefit is that Western blots first separate the proteins prior to doing antibody-linked detection. This means if there's some protein in the sample which cross-reacts with the antibody, it's very likely it will migrate at a different molecular weight and not be counted as a false positive. (As opposed to ELISAs, where every signal counts toward the total.)

These effects mean that if you're looking for low false positives (as you would with an HIV test) a well-done Western blot is likely to give a more confident signal than a well-done ELISA would. (At the cost of time and effort.)

A final issue is that combining the two will give you more confidence in a positive result than either one alone, especially if you use different antibodies for each. The final confidence in a positive result is not just the confidence from the Western blot, but the confidence that both the Western and the ELISA report positive results, so there's a benefit of doing both, even if they were equally specific.


Why do bats huddle during late fall? In the late fall, bats hibernate in clusters with many bats pressed together and holding on to one another. Which of the following supposed advantages of huddling behavior is, in reality, not true?

Any heat generated by any bat is shared by other bats.
Less surface area is exposed to the environment.
Huddling behavior decreases the amount of food needed for bats to stay warm.
In this configuration, less heat is needed for each bat and, therefore, each bat requires less food.
Huddling behavior helps bats stay warm while they feed.

This is basically a trick question and a bit of a cheap shot. All of the reasons cited boil down to "bats huddle to conserve heat", they are basically the same, single, reason.

In order for bats to feed, they need to move, fly out of their cave or wherever they happen to sleep and go forth and look for food. Therefore, they will not be able to huddle while feeding because they will be flying around trying to find fruit or donkeys or whatever each species feeds on. Unless they can figure out a way to huddle while flying, they will not be able to huddle while feeding and so number 5 is wrong.


Confusion related to the DAVID tool I am trying to use the DAVID tool to do some gene analysis. I have some probe set intensities for some cancer cell lines. I found this link in the DAVID tool http://david.abcc.ncifcrf.gov/tools.jsp. I am a bit confused with the terminology introduced here. It says gene list for the probe sets why is it so? I mean in the example you can see the probe sets like

1007_s_at
1053_at
117_at
121_at
1255_g_at
1294_at
1316_at
1320_at
1405_i_at
1431_at
1438_at
1487_at
1494_f_at
1598_g_at

Buy why are they called gene list not probe sets. Why?

Its a bit confusing, but DAVID uses the term Gene List as a generic term.

Looking at Step 2, you can submit many kinds of lists to DAVID, including actual gene symbols, Ensembl or RefSeq Accessions, etc... actually nearly 30 kinds of terms including 'not sure' which probably looks at your list and tries to guess.

Affymetrix or Illumina probe set IDs are each designed to measure a gene, ideally, though its not precisely a one Probe Set to one Gene relationship.  This is because when the array is designed there may be a partial transcript RNA records which turn out later to be parts of a single gene.  There are also probe sets which may turn out to hybridize to similar sequences in more than one gene.

Its messy, but its also true that often more than one gene symbol will appear for the same gene because of historical naming conventions...


Why is the Pentose Phosphate Pathway so active in erythrocytes? Is it because glyceraldehyde -3-phosphate (a molecule which when enter glycolysis help produce ATP through substrate level phosphorylation) can be prepared without losing an ATP through this process?

No. Your supposition is incorrect — the phosphate in glyceraldehyde 3-phosphate has to come from somewhere, and it comes from glucose 6-phosphate. The reason a second ATP is required before you get to the triose phosphate stage in glycolysis is that you are generating two molecules of triose phosphate. In the pentose phosphate pathway (energy-producing non-oxidative branch) you are not generating two molecules of triose-P from one hexose-P, you are generating two hexose-P and one trisose-P from three hexose-P, as shown in my Diagrams 2 and 3 below. (The other three carbon atoms are lost as CO2.)

A good way of approaching this question is to ask “What can be produced by the pentose phosphate pathway that cannot be produced by glycolysis?”.

Glycolysis may be summarized in this context as:

  Glucose + NAD+ ➝ Pyruvate + NADH + 2ATP

But to allow glycolysis to continue the NADH is reoxidized to NAD+:

  Pyruvate + NADH ➝ Lactate + NAD+

So the sole product of glycolysis for the erythrocyte is ATP (primarily for active cation transport to maintain cell shape) lactate passes into the blood for recycling.

The Pentose Phosphate Pathway (the oxidative stage) is shown in Diagram 1, above, and may be summarized in the way done for glycolysis as:

  Glucose + ATP + 2NADP+ ➝ Ribulose 5-P + CO2 + 2NADPH

Ribulose 5-P has two possible fates, but only one differs from glycolysis, so the two distinguishing products of the pathway are ribose and NADPH.

Ribose is important for nucleic acid synthesis, particularly in dividing cells, explaining the increased activity of the pentose phosphate pathway in those cells. This cannot be the reason for the high activity of the pathway in erythrocytes as they have no nuclei and do not divide. In fact the ribulose 5-P is fed back into glycolysis for generation of ATP as shown in diagrams 2 and 3.

NADPH, then, is the answer in this case. It is the reducing agent used in the cytoplasm for synthetic processes (unlike NADH used particularly for ATP generation in the mitochondria), and so the pentose phosphate pathway is found in cells such as adipose, mammary gland and liver, that synthesize fatty acids, and cells that synthesize steroids. However that is not there is no fatty acid or steroid synthesis in the erythrocyte.

NADPH is important in erythrocytes as it is the specific source of reducing power required to keep the molecule glutathione in a reduced state. This has an important protective role in reducing cellular molecules that have become oxidized by molecular oxygen, a problem that is more acute in erythrocytes than in perhaps any other cells as they are the carriers of molecular oxygen. The cell membrane is particularly prone to oxidative damage. You can read about this online in this chapter in Berg et al.


What insect is this? (Black body two orange lines in its back and six legs) I found this today in the library while studying. I am very curious to know whether this particular insect has a name that I can look up and find more information about:

Full length is almost one centimeter. It doesn't bite or anything. It has lots of small hairs in its back (similar to cockroaches and ants) and has a tail that a white sticky substance comes out from.

It's a larvae from a ladybird (or ladybug).  Judging by the stripe pattern it is a Common Spotted Ladybird (wiki: Harmonia conformis) and from the body shape & size I'd also say 3rd instar.

The one you have photographed, and the one on flickr, are larval forms of the ladybug, just like when a catepillar becomes a butterfly, the ladybugs also have a larval stage in their life cycle which crawl around and look very different to the adult form.


What Ultimately Controls DNA Transcription? Transcription of DNA and further splicing of mRNA is regulated by various transcription factors, small nuclear RNAs and so on; similarly such related mechanisms as transposition of transposons.

All such factors and mechanisms, including those linked to inter-cellular signalling mediated by peptides and various so-called epigenetic enzymatic processes, require and are dependent upon transcription itself, in the first place of DNA codons.

What mechanism then is supposed ultimately to control the expression, eventually as peptides translated from mRNA, of information encoded in DNA; if it is not peptides thus encoded? That is, since transcription depends on transcription factors which themselves require transcription requiring further transcription factors, does this mean that in the entirety of its function, DNA controls itself?

How then can DNA and its transcription be conceived as a such a self-controlling function?

Transcription of DNA is ultimately controlled by "various transcription factors, small nuclear RNAs and so on" in the cell.

The molecules which make up the "various transcription factors", etc. are already present in the cell when a new transcription begins.  As you note, most all of these molecules are themselves dependent on the transcription of DNA, but also of the availability of component molecules (e.g. nucleotides, amino acids) and of processing mechanisms such as ribosomes.

So, a new instance of transcription requires a working cellular environment, and that environment was created and maintained as directed by DNA molecules at an earlier time.  Usually those DNA molecules were exactly the same as the ones from which the transcription is proceeding. Occasionally, those DNA molecules would have been physically different, but adequately compatible, such as the source chromosomes which were copied during mitosis to create the current DNA molecule.


Acrosomal enzymes and the female reproductive tract My textbook wrote that the reason why acrosomal enzymes are so securely contained within the sperm (thus needing capacitation to facilitate their release) is to prevent any premature release in the male reproductive tract. If they were released, they would start digesting the male organs. However, wouldn’t this apply in the female reproductive tract too, once capacitation has occurred? Does the female reproductive tract have some sort of protection against this? (I’m assuming that the sperm has been capacitated but has not fertilized the egg yet.)

The acrosome reaction does not take place till the sperm reaches the zone pellucida of the ovum, which causes the acrosome to rupture. Thus the female reproductive tract does not get exposed to the enzymes.

Links:
https://en.wikipedia.org/wiki/Acrosome_reaction


Cloning Ice Age Lion Cubs It was just on the news that scientists discovered "Two cubs in Russia's Sakha Republic last August in a near-perfect state".  And the South Koreans and Russians are attempting to clone these extinct Ice Age lion cubs. (Link to one such news coverage)

According to this answer, we seem to be able to sequence its genome but cloning may be difficult.  However, is this find likely to be the rare large chunk of well-preserved material that makes cloning possible?

The answer that you link to provides a pretty good overview of what it might take to clone an extinct organism from preserved tissue and what some of the challenges are. I won't repeat that answer, but in a nutshell, two big obstacles are incomplete sequences and a host womb.

To get at your question of whether this preserved "chunk" of flesh will lead to the cloning & revival of extinct species...you're a little late to the game. :-)

In 2003, researchers used preserved DNA to revive the Pyrinean Ibex, a goat native to the Iberian Peninsula, that had recently gone extinct. The results were mixed. The experiment worked, in the sense that the scientists were able to successfully bring a recently extinct animal to term, but unfortunately, the revived goat only lived for a few brief minutes, due to developmental abnormalities. It's important to note that this was achieved using DNA that was even better preserved than that of the cave lions in the Mirror article.

So, will the DNA found in the cave lion cells lead to successful cave lion revival? If such a revival occurs, I'm betting that it will be due to advances in how the ancient DNA is integrated with reference DNA and in how fertilization and implantation are carried out, more than on the quality of the found DNA.


Where I can download the genome sequence of various species of Fusarium? I'm looking for genome sequence of various species of Fusarium (a kind of fungus!) on net, but I found no suitable information. Could you please help me out for this purpose?
Thanks in advance

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.


Aren't antibiotic resistant probiotics dangerous? Multidrug resistant probiotics are often recommended by doctors in various cases. But since bacteriae can easily exchange genes by conjugation or other means they could promote the drug resistance of other dangerous bacteriae residing in the bowels. (Which could be just "visitors" otherwise causing infections somewhere else)
Or there is something that withholds this transfer? I think not and so my former genetics professor.

Usually, resistance genes are located on plasmids---additional DNA rings in the bacterium that are part of the genome. These plasmids cause their own exchange with other bacteria, even from other species.

B. clausii, the probiotics organism in question here, appears to be special, though, in that it has no plasmids. His resistance genes come with the primary ring-shaped genome and should not be transferred via plasmid exchange to other bacteria. This doesn't rule out other means of gene transfer like phages or conjugation, however. In one study, it was unsuccessfully tried to transfer a macrolide resistance gene to other bacteria. They conclude

  A potential hazard is transfer of resistance to microorganisms
  pathogenic for humans. The risk that this event will occur and the
  consequences in terms of morbidity and mortality have not been
  evaluated. Parameters required for risk assessment include studies on
  the nature and mobility of the resistance genes of probiotics.

The only other paper on a B.clausii resistance gene didn't look at its transferability. That clearly shows we don't know enough.

B. Bozdogan, S. Galopin, R. Leclercq: Characterization of a new erm-related macrolide resistance gene present in probiotic strains of Bacillus clausii. In: Applied and environmental microbiology. Band 70, Nummer 1, Januar 2004, S. 280–284, {{ISSN|0099-2240}}. PMID 14711653. PMC 321311.


Can any organism possibly have the capability to create a new species every time it reproduces? There are lots of different kinds of living organism in our planet. So i was wondering if such an organism could possibly exist?

Can any organism possibly exist, that would have the capability to acquire some genetic information of the organism it consumes, and pass that along with its own genetic information, forming a new species every single time it reproduces.

Concept of species

First have a look at How could humans have interbred with Neanderthals if we're a different species? to better understand the concept of species.

I will assume that you are using the "biological species definition" which is based on reproductive isolation.

  Can any organism possibly have the capability to create a new species every time it reproduces?

The question is mainly non-sense. In short, if it is true that all offspring are a new species, it means that by definition the lineage is asexual and then the concept of species is typically considered to be of little interest. Let's consider both asexual and sexual lineages separately to maybe clarify what I mean.

Asexual lineages

For exclusively asexually reproducing lineages, either we decide the question makes no sense because the concept of species does not apply to them. Or we decide the concept of species applies and then every individual is necessarily a new species. So, yes, by definition there is no exclusively asexually reproducing lineages where a new species isn't created at every reproductive event.

Sexual lineages

For sexual lineages, the question would make no sense either as if it was the case that every individual was it's own species, then the lineage would be asexual!


How do prokaryotes perform cellular respiration without membrane-bound organelles? In order to survive, prokaryotes such as bacteria need to produce energy from food such as glucose. In eukaryotic cells, respiration is performed by mitochondria, but prokaryotic cells do not have membrane-enclosed organelles. How do prokaryotic cells respirate without mitochondria?

Mitochondria are very similar to bacteria and are thought to have originated from bacteria. This points you to the answer: bacteria produce ATPs the same way mitochondria do, with the oxidation machinery place in their plasma membrane (analogous to the mitochondrial membrane).


Why do mammals produce more carbon dioxide than insects? I understand that mammals produce more carbon dioxide than insects on a gram per gram basis, but why is that? I'm thinking it might be because mammals are warm-blooded, which require more energy consumption. Could it also be due to the fact that insects are less active than mammals? AKA they do less work?

As you said, endothermic animals such as mammmals or birds consume more energy and therefore expelmore CO2 not only because of a higher betabolic rate or to keep warm, but also because they are more active. Even taking all that into account you are missing the biggest difference between them: size. The consumption of energy is not directly related to the size, in fact, the energy requirements drop exponentially with the reduction of size. The same phenomenon explains why they are far stronger, fall-resisting...


Help identifying spider found in central Indiana US I noticed this spider outside my garage tonight, and I'm curious if anyone can help identify what type it is.

A few details to help:

I live in central Indiana, United States.
I saw it for the first time at night.
It's body was roughly 3/4 inches (might be slightly bigger).
Each brick in the picture is about 2 1/8 inches.
It seems to have a black velvet like texture.
It was sitting on a gas pipe that leads into my house.
It was under a bush.

Sorry the pictures aren't great. Being under a bush and trying to use a flashlight made it a bit harder.

More photographs

This looks like a black lace-weaver, or Amaurobius ferox. Based on the size you described it seems as though this one is an adult female. These spiders avoid bright spaces and if they feel cornered they might bite you.

For pictures of it you can look here https://www.arkive.org/black-lace-weaver/amaurobius-ferox/ and for more information you can look here https://en.wikipedia.org/wiki/Amaurobius_ferox


What makes tones sufficiently useful that it would lead to the evolution of tonal processing? I will define a "tone" as  a steady periodic sound. As an example, I consider a sinusoidal wave to be a tone. By "tonal processing", I mean ratio relationships between the notes. For instance, if I play 220Hz sine wave then a 440Hz wave will be perceived as an octave higher.

I don't understand why humans have the ability to perceive frequency relationships between tones. I have read several evolutionary anthropology books like The Singing Neanderthal and Finding Our Tongues and, between these two books, they suggest that the obvious evolutionary purpose of music is for communication. Each author takes a slightly different approach but the basic underlying point remains that tonal processing exists because it gives us advantageous communication abilities. But even accepting this hypothesis, it doesn't explain why humans have a tonal processing mechanism that is specific enough to perceive ratio differences between notes. The tonotopic organization of both the basilar membrane and the precortical auditory pathways might partially account for the machinery used for tonal processing and why the advanced forms in music could have developed. But this still leaves us with the question as to why would such information be useful?

I remember reading somewhere one person hypothesized that the purpose of perceiving these differences was to identify "relative pitch", i.e. the ability to identify or re-create a given musical note by comparing it to a reference note and identifying the interval between those two notes. But this hypothesis doesn't really make complete sense to me because it doesn't explain why the brin can have such specificity when identifying the ratio between two notes.

Another phenomena that seems pertinent is the idea of a "drifting reference point" which Glimcher discusses in Foundations of Neuroeconomic  Analysis. In Chapter 12, he explains how our perception of color isn't fixed but depends on context and in this sense drifts. IIRC, there is a literature that discusses possible neural mechanisms for this. Perhaps something similar would be relevant here for explaining why humans can process tones so precisely.

My Question:

What are the accepted arguments for why would ratios between tones would be be useful information for social communication?

Just to clarify, I am expecting the answer to this question to involve a discussion of the physical properties of tones and why a hominid brain would find this useful information for communication purposes.

I think the whole issue is that you put all your focus into music. The ability to tell apart different tones hasn't evolved with the culture of music playing. It is much older.

Ability to distinguish different tones in non-human animals

Humans are of course not the only animals that are able to recognize tones. Mice for example can as well accurately tell the difference between two close tones (ref.).

Perceiving its environment

So why is the ability to tell different tones apart important. It is important because it allows one organism to better perceive the elements in its surrounding. For example, consider being in the savanna and you can't tell the difference between a lion roaring and a water fall. It seems to be a pretty important handicap.

Tones recognition in social contexts

A very large part of animal's communication is based on tons. Very primitive forms of language are mostly based on tones. Courtship display for example is often based on the tone of the other gender (the tone is correlated with the size of the organ producing the tone). A very large part of human's communication is based on tone as well. You might want to have a look at Albert Mehrabian.

If you have more questions about the importance of non-verbal communication you will need to ask your questions to psychologists (on CognitiveScience.SE) and not to biologists. Note btw, that the condition of being unable of recognizing different tones is called tone deafness.


Can species be paraphyletic? I thought that according to cladistics, only monophyletic groups were valid as species or any other taxa. But extinct species, like say H Erectus must be paraphyletic, as the common ancestor of H Erectus is also the common ancestor of modern man. So if species are frequently paraphyletic, how can cladistics be tenable?

Edit. Also, I'm new to this forum. The people responding here, I'm assuming are actually biologists with a specific knowledge of cladistics, right? I'm a post-grad (philosophy of biology rather than biology per se) so I'm not really looking for links which explain what cladistics is, and certainly not wikipedia. I can access most journals if there is a paper on this subject. I can't find anyone in our dept who can give me a steer on this. I realise thhis is a slightly unorthodox research method, but I'm at a bit of a dead end here!

You say that "only monophyletic groups are valid as species"... That is according to a certain interpretation of evolution that is not necessarily mainstream, (you wouldn't be taught that definition of species in Oxford or Yale) and which idealizes cladistics into simple trees, which don't reflect reality of hybridizing species like orchids and hominids, where simple tree like branching has been proven to not exist. Inflexible definitions of phylogeny should be taken with a pinch of salt, because pollen and other reproductive systems cause many species to be flexible. It's unwise to state that definition of species without being well aware of the mainstream one: Ernst Mayr definition.

Strict interpretations of species lead to problems, because
Darwin wrote:
No one definition of species has satisfied all naturalists; yet every naturalist knows vaguely what he means when he speaks of a species. Generally the term includes the unknown element of a distinct act of creation.

If you check the Wiki page on species, they state 11 contrasted definitions of species which are not necessarily cross compatible.   https://en.wikipedia.org/wiki/Species#Standard_definition:_Mayr.27s_Biological_Species_Concept

The definition of species that i was taught had nothing to do with the parental mechanisms that shaped the species differentiation from other species, and that it is a practical concensus to effectively group animals methodically, which doesnt actually reflect natures unmethodical reality.

Seeing as humans interbred with neanderthal and denisovan species, and orchids interbreed very commonly, the following image refers to an idealized phylogenetic model which is not applicable to all reproductive systems, and it isn't applicable to humans.


Why it is so difficult to treat leukemia? I want to ask what is the reason that T315I type CML leukemia is currently untreatable. I have read quite a few papers in this subject. Why the current genetic oriented engineering drugs failed to stop the leukemia stem cell's expansion but can only slow the secondary leukemia stem cell's expansion? I found it to be utterly hopeless for a patient to be in such a position, as chemical therapy does not work well and radiation therapy can only target specific area. There are experimental drugs in the developmental stage but from what I know they are mostly unreliable.

The T315l mutation of BCR/ABL gene produce the complete resistance of CML leukemia to all currently available BCR/ABL inhibitors.

There is a idea that is not yet tested for such patients - allogenic hematopoietic transplatation.

More information:
http://www.ncbi.nlm.nih.gov/pubmed/20657522
http://www.ingentaconnect.com/content/maney/hem/pre-prints/1607845412Y.0000000050


Why Is The Toughness Of Skin Different On Different Parts Of The Body? My cat was licking my arm with his sandpaper like tongue. It hurt and the area he was licking was slightly smarting afterwards. However, when he licks the palm of my hand the feeling is rather ticklish and results in no pain during or after.

We can pick up sharp, prickly, abrasive objects with our hands (palms/fingers) and even rub against them and have little to no damage incurred. However, if we do the same with say the back of our hand we are more likely to be injured.

I thought maybe the skin is thicker in our palms and that is resulting in our palms being more resilient. But, our palms are so sensitive to touch that it makes me think the skin is thinner to allow the nerves closer access to our environment.

Why is there such a stark difference in different areas of skin on our body when it comes to feeling pain and being susceptible to injury from scrapes, bruises, cuts, etc?

As dd3 said the density of mechanoreceptors dictates skin sensitivity to touch (also look at penfield map. It is a nice illustration of how different senses are mapped to the brain and to what extent each region is sensitive to stimulus). Skin thickness is also different in different regions. This article says that Dikkopf1 (a Wnt pathway antagonist) controls skin thickness.


Sequence evolution simulation tool I'm looking for a tool to simulate sequence evolution given a specific mutation model and birth-death model. I'm aware of tools and packages like INDELible, Seq-Gen and PhyloSim, but they simulate evolution along phylogenetic trees. What I want is to give a sequence and ask the tool to simulate the evolution of this sequence through N generations. The output should be a big bunch of descendant sequences. I've been thinking about writing such a tool myself, but it's always better to look for something already coded.

There exists a bunch of population genetics forward and backward (coalescence) simulation platforms. Here is a non-exhaustive list. They all differ and you'll have to go through their manual to see what is more adapted to your needs.

List of softwares

Here is a long list of such platforms. The list might arguably be a little bit outdated today though and many of these softwares might be slow or abandoned by their authors.

Most common softwares to my experience

Some are more known than others. Personally, I already saw uses of the following platforms in publication: SimCoal, Nemo, Slim and SFS_Code.

SimBit

Of course, I must indicate my own simulation platform SimBit. To my experience, SimBit is typically faster than Nemo. It is slower than SFS_Code and SLim for very small simulations but become much much faster than SFS_Code and SLim when you need simulations with a descent amount of genetic diversity.

Most important point about these softwares

You should compare softwares based on

Availability of the author to advice and bring new features

I won't talk about my personal experience here by respect for the authors!

Speed / RAM usage

I think SimBit is typically faster (and use less RAM) than Nemo. SFS_code and SLim are very fast for simulations with low genetic diversity but very slow for simulations with high genetic diversity.

Flexibility

Nemo, SLim and SimBit are very flexible (but they do different things) but SFS_code is not really.

User interface

I find Nemo error report pretty poor. I like SimBit error report. SLim interface is very nice (using eidos) and it even comes with a GUI (I have never used the GUI myself).

Free of Bugs

Several people have found important bugs in SFS_code (personal communication and experience).

Slightly more detailed comparison between Nemo, SLim, SFS_code and SimBit

I have personally used NEMO, SFS_CODE and SLim in the past (I now use SimBit only). So I can only talk about these 4 below.

All four models are well updated and maintained by their authors and of course everyone has a access to the source code.

SFS_code and SLim are very fast for small simulations. The issue of SFS_code and SLim is that the RAM usage and run time are exponential function of the genetic diversity. This means that some simulations can quickly become totally unmanageable. But it is a great tool if you expect little genetic diversity.

SimBit is typically faster than Nemo, at least for large genomes. This difference becomes particularly obvious for large genomes. One might think "Oh I am fine to wait a few extra days to get my results" but the difference in speed between two softwares can also be a difference in whether you have to wait a week or 20 years to get your results, so do not neglect the importance of running time and RAM usage without estimating your needs.

Nemo is very flexible when it comes to the order of life-cycle events (is migration before or after selection for example) and the newest version allows for simulating age structured population. SimBit is very flexible, very fast and allow for simulating multi-species and their ecological interactions. SFS_code is less flexible.

  My only concerns about NEMO are that each individual dies after reproduction and that there can't be more than 256 alleles at the same time.

SFS_code limits the number of alleles to 4. Nemo limits the number of alleles to 256 (but you can also use phenotype and have a float number at each locus). SimBit uses either bi-allelic loci, a block in which the number of mutations are counted (max: 256 mutations; this is different than 256 alleles per say) or continuous float number at each locus for the phenotype. Do you really need more alleles? Why can't you just use several loci to represent a sequence with multiple alleles? Real biology can only have 4 alleles in its smallest locus! SimBit uses a bit-per-bit system. If you need, say 50,000 alleles, then you just need to ask for a sequence of 16 bits (2 bytes) and you can get $2^{16} = 65,536$ alleles.

If you need more alleles in a single block (which is a little surprising to me a priori), you can probably just ask the author and he might accept to helping you if you convince him it is of interest to add this feature (he might also be more willing to help in exchange of authorship if you need more support).

Hope that helps. Good luck!


Can Hepatitis be caused by Bacteria? There are many information about viral hepatitis. But it is interesting for me, can bacteria cause the hepatitis too?

Hepatitis is a condition of the liver where the cells of the liver organ are inflamed. Most often it is caused by a viral infection, hepatitis A, B and C are all viral forms of the disease.

Bacteria (and Fungi) can cause hepatitis of the liver, and two examples would be the Staphylococcal and Streptococcal bacteria. These can directly infect the liver, and are also responsible for some inflammations in other tissues of the skin and heart and elsewhere.

Prolonged alcohol abuse is another cause of hepatitis (as well as cirrhosis) and is not associated with bacteria virus or fungi, but instead from a damaging effect on the liver.


Micelles Sticking Together I have a quick question regarding micelles. I have tried googling the answer but can't seem to find the answer. The question is, during digestion lipids are emulsified into micelles in order to increase their surface area for digestion but my question is, why don't the micelles stick together and form a clump which would decrease it's surface area?

Thank you.

Micelles have a hydrophobic core and a polar, hydrophilic surface. This surface will preferentially associate with water molecules and become solvated, rather than sticking to lipids.

Negative charge on phospholipids at the micelle surface mediate electrostatic repulsion to other micelles, keeping them from sticking together.


Why cancer mutations do accumulate sequentially? According to Knudson hypothesis, cancer mutations accumulate in order. Statistics says, that cancer probability increases as sixth order of age, which may mean six consequential steps to cancer.

But, mutations are random in nature. There is no apparent cause, why mutations ABCDEF can't occur in reverse order, i.e. FEDCBA and any other possible orders.

If unordered, any number of required mutations should cause flat age dependency.

Hence, something is ordering these mutations, i.e. making mutation B impossible until A occurs and so on.

What is it?

UPDATE

Cancer incidence dependency on age:

The graph is not linear, which means that mutations are not independent.

UPDATE 2

Let's regard some cancer, which requires 6 mutations. It's incidence distribution should be like shown above.

Now suppose we knew the distribution of all precancer stages, i.e. the distribution of people with 1, 2, 3 and so on mutations. These distributions should look similar to final distribution

Now let's regard only one (first) mutation.

Why is it's incidence age dependent?

Mutations are random. They should not depend on age. If they do depend on age, then they are not random. If "they" are not random, then "they" are not mutations.

Or, in other words, the cause of progression is not a mutation itself.

Isn't it true?

TL;DR:

A sixth order probability curve of cancer does not mean six steps. The order of the curve has nothing to do with the number or sequence of mutations.
Causes why ABCD could be more likely than DABC exist and have been extensively studied
Repair and control ("defence") mechanisms are what does the 'ordering' of steps by selecting for mutations which can circumvent them

The sigmoidal shape of the curve thus reflects the slow accumulation of "defence"-damaging mutations, which increase their own probability and thus the slope of the curve. I don't know if the slight decrease in slope towards the end reflects a real limit to the incidence of cancers, or if it's an issue related to the data, its availability or the way it is gathered (but has no basis in substance i.e. there isn't actually a limit).

To elaborate:

There are many biological factors which play into helping you understand the problem you are wondering about, and the fact that different cancers work differently does not make it easier. I would highly recommend that you check out Hallmarks of Cancer, the Wikipedia article also cites the interesting original publication. Basically, certain principles underly all cancers, but different cancers have different tendencies to develop certain hallmarks in a particular order.

Randomness of mutations:

Mutations are not random. The nature of DNA sequences affects their susceptibility to DNA lesions, i.e. damage caused by chemical processes such as a nucleotide losing its base, dimerisation of thymidine, single or double strand breaks and so on. Lesions occur all the time, so there are mechanisms in place to fix all types of DNA lesions. Occasionally however, the circumstances will permit e.g. two lesions to coincide or the repair process itself to make an error, which then leads to a permanent change of the DNA sequence that cannot be fixed anymore because the original sequence has been lost. This is a mutation, and mutations are also not random because the nature of DNA sequences affects the chancefor them to incur lesions that cannot be repaired.

Hence, one reason why certain mutations occur more frequently than others is because they are actually more likely to occur. But this isn't the main reason.

Cell self-control

There are higher levels of control than DNA repair. Various mechanisms in the cell exist to detect malfunctioning proteins (due to mutations in their gene) and degrade them - though sometimes malfunctioning proteins can still escape these mechanisms. Even in this case, there is an additional safety layer created by various mechanisms which lead a cell to kill itself (apoptosis). These are triggered for example if excessive DNA damage is detected, or if the cell-internal signals for and against proliferation are conflicting.

Sequential accumulation of mutations

The result of repair and control mechanisms (which I will now call "defence mechanisms") is on the one hand that we are far more resistant to mutations than we would be without them. On the other hand however, they create selection for mutations which are not affected by them.

This is where multi-hit models of cancer come from. A "first hit", "enabling mutation" or whatever you want to call it would be a mutation which itself is not affected by defence mechanisms - and simultaneously impairs the defence against other mutation(s). The "second hit", "initiating mutation",... would be a mutation which causes cancerous cell behaviour, but would be eliminated by a defence mechanism without the first hit.

This means that mutations do not always occur in the same sequence but rather, they occur in all sequences and sequences other than those that we find in cancer cells are eliminated.

Note that not all cancers have several mutations or a sequence. For example, chronic myeloid leukaemia (CML, a blood cancer) in the vast majority of cases is caused by a translocation from chromosome 19 to chromosome 22 which results in the famous Philadelphia chromosome and produces the BCR-ABL fusion gene. This single mutation is sufficient to cause CML.

Age-dependency of mutations:

Mutations can affect all parts of a cell's machinery, including the lesion repair mechanisms. This means that throughout its life time, a cell can (and will) accumulate mutations which increase the likelihood of further mutations. Mature cells usually have short life spans and mutations to their DNA repair machinery die with them relatively soon (days or weeks). However, pluripotent stem cells (PSC) in the tissues are just as likely to develop these mutations as mature cells - and PSCs are the ones which renew the tissue throughout life by differentiating into mature cells.

Thus, a mutation in a PSC remains for life, and the longer you live, the higher the chance that one mutation will affect the chance for gaining further mutations. This is why for all cancer types, the risk to develop them increases with age (though there are a few which are most likely at young age!)


Cockroach brain functional anatomy In insects like the cockroach the brain is distributed, i.e. some parts lie in the head and some in the abdominal cavity. Which part is responsible for controlling locomotion?

Technically speaking, locomotion is actually not produced by the brain in cockroaches; there are neurological controllers in the legs themselves which produce locomotion even when contact with centralized nervous system is severed.

I include this for reference, because it was not explicitly stated in your question.  However, I believe it was intended to be implied by the phrase "responsible for controlling."  In other words, from my understanding, you're more interested in what section of the brain actually controls those actions in a normal cockroach.

From Central Nervous Control of Cockroach Walking by Charles R. Froutner, you can see even just in the abstract that the movements became spontaneous when the connection with the segmental ganglion was broken, showing that this is very likely where the control is exerted.  (The segmental ganglion, for reference, is a part of the dorsal "brain" you made reference to.)


Why do cells have an average 'life span' I've heard of Henrietta Lacks. As a result of a genetic mutation, her cells never died. I've heard/read that overtime, our cells stop multiplying as much, (as an effect of aging). Why? Why do we age? Why do cells eventually die? What causes our bodies to degenerate? It is encoded for in our genes? If we treated our bodies in the highest regard, accounted for accurate diet and sleep, with the introduction of genetic engineering, could everlasting life be possible?

We refer to the number of times the cells of an organism can possibly divide as the Hayflick limit for that organism. The Hayflick limit serves as a theoretical life span, because telomeres (on the ends of chromosomes) get slightly shorter with each round of division, until they are gone completely. Telomeres are put on the ends of chromosomes by the enzyme telomerase, which is abundant in infants (who are growing and undergoing rapid mitotic divisions) but bodily abundance of the enzyme quickly diminishes with age. Without telomeres, our actual chromosomes would shorten in length during each round of division -- essentially, this is what happens after the telomeres are eroded away at in the later years of life. The Hayflick limit for humans is given to be 120 years -- with perfect self-care, 120 years of life is possible.


How long the homologous arms of the "repair" sequence must be to do homologous recombination? I am trying to figure out the details of the homolougous recombination in order to be able to insert a certain piece of DNA in the host genome after double strand break.. Does anybody know how long the homology arms of the repair template must be ? Can the left arm be longer than the right one? I have read several papers which have different sizes 90 bp vs kb..
In my case, i am not so much preoccupied by off target but the insertion should occur also on the desired site possibly at high frequency and as fast as possible.
Thank you,
Paola

As little as 14bp of homology can work. See this reference.

I would recommend at least a length of 90bp but 1kb is probably overkilled. Yes both arms can have different length (staying in the same order of magnitude).


Magnetic-activated cell sorting vs. FACS When sorting cell populations it is possible to use either magnetic-activated cell sorting or fluorescence-activated cell-sorting (FACS). I am wondering when you would choose either technique and what the pro's and con's of each technique are.

As FACS sorts cells one by one, I can imagine magnetic-activated cell sorting is a faster process. So I guess if time is an important factor this could be used to base your decision on. Also by sorting cells one at a time I assume FACS is a lot more precise, and will lead to less 'contamination'.

So, are there other factors at play here that can influence the choice of magnetic-activated cell sorting over FACS, and what are the pro's and con's of these techniques respectively?

Magnetic-activated cell sorting (PDF download), or MACS, is a procedure developed by Miltenyi Biotec to separate cells from complex mixtures using antibody-coated magnetic nanoparticles. The antibodies are specific for certain cell surface markers, either expressed on your population of interest (positive selection), or expressed on undesired cell types (negative selection). After adding the antibody-coated beads to the cell mixture and incubating, the suspension is added to a special single-use separation column affixed to a magnet, to which the beads stick, while unlabeled cells flow through. If performing a negative selection, the flow-through is your population of interest and the bound beads and cells are discarded. If your cells of interest are bound to the beads (positive selection), the column is washed several times to make sure unbound or weakly-bound cells are washed through, then the column is removed from the magnet and the cell-bead complexes are eluted.

In fluorescence-activated cell sorting or FACS, the initial complex cell mixture is first labeled with one or more cell surface marker-specific antibodies that have been conjugated to fluorescent dyes. Cells can also be analyzed that express one or more recombinant fluorescent proteins in conjunction with a gene of interest, allowing for selection of cells without using antibodies. After incubation and wash steps, red blood cells are lysed, if analyzing whole blood. The reason for RBC lysis is shown below:

Without lysis, the RBCs overwhelm the cytometer, as they make up around 95% of the cells in human whole blood. White blood cells (leukocytes), on the other hand, only make up 0.1-0.2% of cells, and lymphocytes between about 15 to 50% of leukocytes.

The cell mixture is then analyzed on a cell sorter such as a BD FACSAria.

From: https://commons.wikimedia.org/wiki/File:Fluorescence_Assisted_Cell_Sorting_%28FACS%29_B.jpg

The cells pass in single file past one or more laser beams, which excite the dyes and cause them to fluoresce at a certain wavelength. The user can then use gating to select the combination and intensity of colors they are interested in, and when a cell meets the criteria, it is given an electrical charge, and electro magnets direct it into a collection container.

So what are the pros and cons of each technology? MACS separation generally is quicker than FACS staining, and a greater number of cells can be processed at one time (sometimes orders of magnitude more, depending on instrument and protocol). If you are, for example, looking to purify large numbers of CD4+ T cells from whole blood, MACS may be the better choice of the two (although I prefer the RosetteSep system for that particular requirement). MACS doesn't require a rather expensive dedicated instrument, although automatic platforms are available if needed. On the downside, most MACS-qualified beads are mostly only available from Miltenyi, so if they do not have beads with your particular marker of interest available, you will need to do the conjugation yourself, at the expense of time and possibly precious antibody while you optimize conditions. Fluorescent-conjugated antibodies are extremely common, and available from practically innumerable companies, so unless you are working with a self-generated antibody it's much more likely that you'll be able to find one for FACS quite easily. There are MACS beads that contain antibodies directed at certain fluorophores, so you can use flow antibodies for MACS, although optimization is likely still necessary. Finally, MACS separation is only an option for cells that have your marker of interest expressed on the cell surface.

One of the major advantages of FACS is multicolor staining (depending on the instrument you're using). This makes it much more straightforward to purify potentially rare populations that are only differentiated by their combined expression of a number of surface markers, necessitating multiple gating steps. If this were to be accomplished by MACS, you would need to go through multiple rounds of purification, something that could take longer than FACS, and not necessarily be feasible, as a certain number of cells are required for each MACS run. With FACS, these rare populations (which may only be tens or hundreds of cells per million) can be collected just as easily as more common ones. Also, as mentioned above, there are more antibodies available for flow/FACS than for direct MACS. Additionally, FACS allows for sorting of cells expressing GFP and relatives, letting you collect populations based on internal markers.


Spider with brown zig zags on abdomen and black head Found this spider roaming around my room the other day.. can someone tell me the species?

Location: Central KY, USA

Also, here's a video of him moving around in a glass candle lid, where you can get a really good look.

As far as I know you've found a male steatoda triangulosa or triangulate cobweb (weaver) spider

More info:
https://en.m.wikipedia.org/wiki/Triangulate_cobweb_spider
http://lancaster.unl.edu/pest/resources/triangulatespider.shtml


How were the first genes isolated from genomic or cDNA libraries without already knowing a hybridization probe? Let us go back in time to around 1975. It is my understanding that at that point (or at least by the end of the decade), both genomic and cDNA libraries had been created for a few organisms, e.g. rabbits. I'm interested in the logic of techniques that first used these libraries to isolate genes encoding for particular proteins. Note: I'm not interested in how we'd isolate a gene today; I want to understand the history.

First, consider the following thought experiment. Say it's around 1975. The one assignment for my Cal Tech biology class is a doozy: it goes as follows. The instructor (Tom Maniastis?) hands me a protein along with the cells from which the protein was isolated as well as genomic and cDNA libraries of the organism that makes the protein; the challenge is to isolate the gene encoding for the protein. I do not know anything about the protein except that the product I've been given is pure.

Of course, the basic idea is simple: isolate the gene by screening the libraries with a radioactive nucleic acid probe and using a hybridization assay. But alas, I do not have a complementary probe: all I have is the protein! What do I do?

Here is one solution I can imagine. (I don't know whether it was possible around 1975, much less whether it actually happened.) I could try to isolate the mRNA that codes for my protein (but how to do that?), then radiolabel it and use the radiolabelled mRNA as a probe in a hybridization assay on the cDNA library (not the genomic library, since the unprocessed DNA could have noncoding regions).

Would this have worked?
Did anyone actually do this?
If yes to either (1) or (2), how could one figure out which mRNA coded for the protein?

The question, in essence, is how to get to DNA, given only a protein, circa 1975.

The following is based on a chapter on Cloning DNA in the 10th edition of The Biochemistry of the Nucleic Acids (RLP Adams et al.) published by Chapman & Hall in 1986. (This is probably more pertinent than the 11th and final edition, which was published in 1992 and had a more contemporary treatment.) Apologies for the fact that it will be difficult to find.  It should be available from some university libraries and through inter-library loan systems in certain countries. Section A.7.3 gives a taste of the methodology used at that time.

Protein properties that could be used as the basis of a cloning strategy

In attempting to clone DNA for a particular protein for which there were no pre-existing clones to use as hybridization probes, one had to consider the properties of the protein one is able to exploit. These might include:

Amino acid sequence
Antibodies to the protein
Biological activity
Particular physical properties, such as size

(Clearly if one had no such ‘handle’ to the protein one was not in a position to try to clone its cDNA or gene.)

Three general approaches

There seemed to be three general approaches:

No expression
Indirect expression
Direct expression

The approach that one might take was also governed by whether the protein is particularly abundant in a specific tissue, when one might expect less sophisticated more labour-intensive approaches to stand a chance of success.

Another point to emphasize is that, at least with eukaryotes, one would look for a cDNA clone first, and only try for a genomic clone after one had this to employ as a hybridization probe.

1. ‘No expression’ approaches

In the no expression approaches one relied on the amino acid sequence to identify the cloned DNA. One such approach was to use hybridization probes against stretches of amino acids, the codons of which had limited redundancy (Met and Trp have a single codon, and some other amino acids only two) using low stringency hybridization conditions. This required luck. Alternatively one could sequence random clones and hope to find one that correlated with the amino acid sequence. At that time DNA sequencing was slow and labour intensive, so that this was only applicable to proteins that were relatively abundant in the tissue from which the libarary was prepared.

2. Direct expression approaches

Direct expression generally entailed using a bacterial expression vector which produced a fusion of a bacterial protein with a part of the eukaryotic protein. (Statistically only one in six of clones would have the correct reading frame in a fusion protein.). This approach was favoured if one had an antibody, which did not require a complete protein.

3. Indirect expression approaches

By indirect expression was meant using immobilized cloned cDNA to select corresponding mRNAs (‘hybrid selection’) which could be expressed in a cell-free system. This was appropriate if the distinguishing characteristic required a full-length protein, as in the case of biological activity or size.


Energy released during the production of ATP? When glucose is used during aerobic and anaerobic exercise, how much energy is expended or required?

During aerobic exercise:

$C_6H_{12}O_6 + 6 O_2 \to ATP + H_2O + 6 CO_2$ + energy

During anaerobic exercise:

$C_6H_{12}O_6 + 6 O_2 \to 2 C_3H_6O_3 + 2 ATP$ + energy

For each of the reactions above what is the value of the '+ energy' part?

This is difficult to answer exactly since the thermodynamics of cellular metabolism are not well understood.
These are spontaneous reactions, so there is certainly a loss of Gibbs' energy $\Delta G < 0$; this energy corresponds to your "energy" term on the product side of the reactions. For the anaerobic case (glycolysis) a balanced reaction formula is

Glucose + 2 ADP + 2 Pi $\rightarrow$ 2 Lactate + 2 ATP + 2 H2O

Details like phosphate (Pi) and water is important here. Now, if we know the free energies $G$ of each substrate and product, we can calculate the $\Delta G$ as the sum of the products' energies minus the sum of the reactants. Unfortunately, this energy $G$ is hard to get at. It depends on a number of things, like the molecule structure, concentration, temperature and the pH and ion strength of the solution. These things are not exactly known, so the answer will be uncertain. This is actually an active area of research, and sophisticated methods have been developed for calculating $G$. One of the best are from a groyp at the Weizmann institute in Israel, and is available at http://equilibrator.weizmann.ac.il

If we assume all concentrations to be 1mM, this method gives $\Delta G = -118.7$ for the glycolytic reaction above. This is the energy lost (mainly as heat) in the reaction. For comparison with energy captures by ATP, we can break up the reaction into two parts and calculate

Glucose $\rightarrow$ 2 Lactate $\quad\quad\quad\quad\quad \Delta G = -206.7$

2 ADP + 2 Pi $\rightarrow$ 2 ATP + 2 H2O $\quad\quad\Delta G = 87.0$

which sums to -118.7, as expected. This tells us the fraction of the Gibb's energy captured as ATP is 87/206.7 = 42%, while 58% is lost as "heat". So glycolysis has an efficiency of 42%. (For comparison, a combustion engine is somewhere at 15--20%.)

The aerobic case is more difficult, because the stoichiometry is not even fixed: the number of ATP molecules actually obtained from 1 molecule of glucose depends on the efficiency of the respiratory chain, on cytosolic NADH oxidation, and otherthings. But let's say we get 30 ATP. Then

Glucose + 30 ADP + 30 Pi + 6 O2 $\rightarrow$ 6 CO2 + 30 ATP + 36 H2O

has $\Delta G = -1608$, which can be broken up into

Glucose + 6 O2 $\rightarrow$ 6 CO2 + 6 H2O $\quad\quad\Delta G = -2913$

30 ADP + 30 Pi$\rightarrow$  30 ATP + 30 H2O $\quad\quad\Delta G = 1305$

So here 1305/2913 = 45% of the energy is captured. So in this sense, glycolysis and respiration are similar in efficiency. Varying the number of ATP changes this value; try it! Of course, glycolysis can only partially oxidize glucose (into lactate), while respiration achieves complete oxidation to CO2, extracting much more energy.

Again, these values depends heavily on concentrations of metabolites inside cells, which are not well known. Try changing them at the equilibrator web site and note the effects! Unfortunately, many biochemistry textbooks present values of $\Delta G$ assuming reactants at 1M (!) which is completely irrelevant to actual conditions in living cells.


Lotka-Voltera predator prey model isocline? In lotka voltera predator prey model, why do we get a straight isocline with variable prey/predator population for single value of corresponding predator/prey?

I understand that we get the prey isocline by the equation

N1=prey population ; n2=predator population

What I don't understand is why we are getting variable prey population on isocline for same value of predator population. Shouldn't the prey population be also constant?

PS: I picked the graph image from the internet so the symbols are different. Sorry.

I think your issue is mainly with the interpretation of the isoclines.

If you assume this standard predator-prey model:

$$\frac{dN_1}{dt} = rN_1-pN_1N_2$$
$$\frac{dN_2}{dt} = apN_1N_2-mN_2$$

you get the isoclines:
$$ N_2 = \frac{r}{p} $$
$$ N_1 = \frac{m}{ap}$$

with the first isocline referring to prey and the second to predators. These isoclines mean that the population growth rate of prey and predators (respectively) will be zero exactly at these isoclines (as well as at the point N1=N2=0). Since the isoclines, for this partuicular model, are fixed values and not functions of N1 and/or N2 they will be strait lines. Also, in a sense, you should view the isoclines as the borderline case where population growth rate shifts between a positive and a negative value (ie a growing or a decreasing population). The isoclines are not giving you the population size of the prey at a certain predator population size (which you seem to be implying with "...why we are getting variable prey population on isocline for same value of predator population"), but the locations in the plane where the population growth rate (for either prey or predators) is zero.

A graphical view of only the prey isocline (with some color coding) can be:

This means that the prey population (blue) is growing (arrows to the right) below the blue prey isocline, so there if a "flow" to the right there, while it is declining at predator population sizes above the isocline (arrows to the left). So basically, for all predator population sizes (N2) below isocline the prey population will grow, and for all N2 above the isocline the prey population will decline. In reality the rate of increase/decrease differs depending on how far from the isocline you are (so arrows should be of different lenghts), but to simplify the issue and to show the general principle I'm just showing the direction of flow here.

The same picture for the predator population is:

Here the predator population (orange) is declining to the left of the orange predator isocline (arrows down) because there is too little prey to sustain the population, and increasing to the right of the isocline (arrows up).

If you combine these you get this, with the black arrows showing the overall direction of the combined population trajectories:

I hope this clarifies the issue a bit. Otherwise, please comment and hightlight what parts you find unclear.

Also, the dynamics of this Lotka-Volterra model also means that populations that start exactly at the intersection of the isoclines (i.e. both N1 and N2 will lie at that point) will stay there, since that is an (unstable) equilibrium point. Populations that are started anywhere else in this plane (except for cases where N1 and/or N2 is zero), will follow an oscillating population trajectory, that will not change if there isn't any external pertubations (environmental changes, input/output through immigration/emmigration etc). Therefore, the combined trajectories of N1 and N2 will form an ellipse in the plane, until they are perturbed (by something outside the current model), when they will then settle at a new ellipsis. For examples of the ellipses, see this phase-plane graph from Wikipedia, with initial values as points:

However, also note that changing the model, i.e. to include a logistic component to the prey population, will completely change the population dynamics.


What would be the scientific name of this worm I saw this pic while crawling online and it was a bit different for me to predict which worm is this.

Source: http://www.seafishingtackle4u.com/softbaits/ragworms-latex-lures/

It appears somewhat different form other annelids as parapodia or setae are somewhat transparent and very attractive too.

What worm is this?

If you would have read the text from the source of that image (which by the way you didn't mention, I did a Google Image search and edited your question to include it), you would have known that what is seen in the picture is not a living thing, it is a latex fishing lure:

  Product Description: Sandworm/Ragworm 8″ size, sure fire fish catching lures. Costing less than live worms, but lasting much longer, never be without worms again.

Source: http://www.seafishingtackle4u.com/softbaits/ragworms-latex-lures/


How is membrane capacitance related to the increased speed of saltatory conduction? Here is the original question which inspired my question. As explained by the answers there, the reason saltatory conduction in myelinated neurons is faster than non-myelinated conduction is because the capacitance of the membrane is lowered by reducing the number of channels (Channel density) or equivalently, increasing the spacing between channels. I also did a preliminary study of membrane electrodynamic modelling here and here.

From what I gathered from the linked question, the decreased capacitance overcompensates the effect of absence of channels reinforcing the sodium current, and on the whole, increases the speed of conduction by allowing the depolarizing potential to travel to the adjacent node faster than in case of an unmyelinated fibre. In view of this, I have a question:-

  Why does lower capacitance increase "the effectiveness of nearby
  nodes" or allow the depolarizing voltage to "travel not by ion
  diffusion, but as an electric field"? I am comfortable with capacitors
  and related physics, but why would lower capacitance allow propagation
  of the changing voltage as an electric field, is still unclear to me?
  (The links I have placed also help quantify the problem
  mathematically. This allows us to say that $\lambda$, or the rate of spatial
  decay of potential, increases, decreasing the effective
  length of the neuron. Why should its decrease help faster conduction?)

  And another question is, how would reduced density of sodium voltage
  gated channels cause a decreased capacitance?

Very nice question! I'll go through your three questions sequentially.

Q1: Why does lower capacitance increase "the effectiveness of nearby nodes" or allow the depolarizing voltage to "travel not by ion diffusion, but as an electric field"?

A: Capacitance basically results in sequestering of charge of opposite polarities along the cell membrane, which basically results in a neutralization of charge differences. The effect of this is explained on the website of Amrita and I quote:

  [...] a higher capacitance results in a lower potential difference. In a cellular sense, increased capacitance requires a greater ion concentration difference across the membrane.

What myelin does is insulating the neuron, thereby decreasing its capacitance. You could say that by increasing the thickness of the membrane, the negative insides of the cell do not attract positive charge outside the cell. It's a bit simplified, yet it effectively describes what myelin does (see cambridge web page on capacitance).

So in a myelinated axon, when Na+ enters the cell in a node of Ranvier, the positive charge entering the cell is not counterbalanced by outside negative charge and hence, the charge is not or at least less counterbalanced. This allows for the depolarizing potential to be transmitted by electric charge. If there were no myelin, the depolarizing potential would fade out pretty quickly along the axon by neutralizing charges outside the cell. Without myelin the opening of more sodium channels in the direct vicinity are necessary not only to transmit the action potential across the axon, but it is also necessary to amplify the signal to prevent it from dying out. In a myelinated axon, hence, the depolarizing potential reaches much farther and in answer to your next question:

Q2:This allows us to say that λ, or the rate of spatial decay of potential, increases, decreasing the effective length of the neuron. Why should its decrease help faster conduction?)

One could say that myelination effectively decreases the length of the axon (the lamba parameter) as the depolaring potential reaches further along the axon.

The fact that the depolarizing potential reaches further means that voltage-operated sodium channels can be activated at larger distances from a certain depolaring potential. Hence, adjacent nodes of Ranvier can be spaced by as much as 1.5 mm. Due to the fact that the next node is activated by passive spread of an electric field, which is pretty much instant, it skips the intervening distance with about light speed, greatly enhancing conduction velocity.

Q3: And another question is, how would reduced density of sodium voltage gated channels cause a decreased capacitance?

Basically there are no ion channels below a myelin sheath as they are totally useless there. It is the myelin that decreases capacitance and there happen to be no channels underneath.


Telomere elongation methods? What sort of telomere elongation methods are there currently?

Would this stop aging? (edit: No, probably)

I couldn't turn up anything good on google. I was thinking that maybe you could sequence the telomeres, trim them all at a certain point, and then engineer a polymerase molecule to extend from that same point. Is this how it's done?

It would be simpler to simply activate telomerase genes or insert them using some vector virus. However, telomerase is a key component in the process of tumoral transformation. Basically, if you don't let cells die they will stack mutations until they become tumoral.


Fraction of channels open at equilibrium I found the formula for the fraction of channels open at equilibrium for a three-state mechanism (Colquhoun's paper in the microelectrode book http://www.utdallas.edu/~tres/microelectrode/me.html)

k1 and beta are forward rate constants. k-1 and alpha are backward rate constants.

p1(equilibrium) = (Xa/Ka)(beta/alpha) / (1+ ((Xa/Ka)(1+beta/alpha)))

Can someone show me how to arrive at this by derivation. I tried and I got it wrong (obviously!!!).

Xa is the concentration of the agonist and Ka is the equilibrium constant k1/k-1

The mechanism given by the OP is renowned in the world of pharmacology and drug-receptor interactions, and is due to Castillo and Katz (1957). A very readable review of the history and importance of this mechanism may be found in Colquhoun (2006), published in Trends in Pharmacological Sciences. (For more great papers from the Colquhoun lab, see here)

If A is the agonist, R the vacant receptor, AR an occupied but closed form of the receptor, and AR* the occupied but open form of the receptor, the situation where an agonist must bind before the channel can open may be represented as a three state receptor model (unoccupied, occupied-closed and occupied-open) as follows:

$$\ce{A + R <=>[$k$_1][$k$_{-1}] AR <=>[\beta][\alpha] AR{*} \tag{1}}$$

We need to be more specific here, and define exactly what is meant.  Let $A$ be the concentration of free agonist (ie agonist not bound to receptor), let $AR$ be the concentration of occupied closed receptor, and let  ${AR^*}$ be the concentration of open occupied receptor.  In addition, let $k_1$ be the second-order rate constant for the association of agonist with unoccupied receptor, and let $k_{-1}$ be the first-order rate constant for the dissociation of agonist from the occupied, closed receptor. Finally, let $\beta$ and $\alpha$ be first-order rate constants for the inter-conversion of the occupied receptor between closed and open states, respectively. Rate constants may be thought of simply as constants of proportionality arising from the law of mass action (see below).

The OP asks for a derivation of the following equation,

$$p_1^{(equil)} = \frac{({\chi}_a/{K_a})(\beta/\alpha)}{1 + ({\chi}_a/{K_a})(1+ \beta/\alpha)}\tag{2}$$

where $p_1^{equil}$ is the fraction of channels open at equilibrium, ${\chi}_a$ is the total agonist concentration, ${K_a}$ is the dissociation constant (not the association constant) for the binding of agonist to the closed receptor.

The situation is very nicely illustrated in the following diagram, taken from Colquhoun & Hawkes (1995)

Derivation

Although Eqn(2) looks daunting at first sight, the derivation is surprising simple.

Let $R_t$ be the total receptor concentration. An expression for $p_1^{equil}$ (the fraction of receptor channels open at equilibrium) may now be written as follows:

$$p_1^{(equil)} = \frac{AR^*}{R_t}\tag{3}$$

As

$$R_t = R + AR + AR^*$$

Eqn (3) may be rewritten as follows:

$$p_1^{equil} = \frac{AR^*}{R + AR + AR^*}\tag{4}$$

The problem with Eqn (3) & Eqn (4), of course, is that they are pretty close to useless. The total concentration of receptor is unlikely to be known, and obtaining reliable estimates for $AR$, $R$ and $AR^*$ present almost insurmountable experimental difficulties.

By the law of mass action, which holds that states that the rate of any reaction is proportional to the product of the reactant concentrations (and where rate constants may be considered constants of proportionality), the following may be written assuming the system described by Eqn. (1) is at  equilibrium.

$$ {k_1}. A. R = k_{-1}. AR \tag{5}$$

$$ {\beta}. AR = {\alpha}AR^* \tag{6}$$

Let  ${K_a}$ be the dissociation constant for the binding of agonist to the closed receptor. From Eqn (5), the following may be written.

$$ \frac{A. R}{AR} = \frac{k_{-1}}{k_1} = {K_a} \tag{7}$$

Therefore:

$$ R  = \frac{{K_a} AR}{A} \tag{8}$$

An equation for the total concentration of agonist, ${\chi}_a$, may be written as follows:

$$ {\chi}_a  = A + AR + AR^* \tag{9}$$

The problem with using Eqn (9) to obtain an expression for $A$ (the concentration of free agonist) is that it makes the resulting equations very difficult to solve. As regards the algebra, the situation is make a lot simpler by assuming that the total agonist concentration is equal to the free
agonist concentration, ie by assuming that Eqn (9) may be written as follows:

$$ {\chi}_a  \approx A  \tag{10}$$

When the concentration of agonist is very much greater than that of the receptor, this approximation is justified.

Eqn (8) may be re-written as follows:

$$ R  = \frac{{K_a} AR}{{\chi}_a} \tag{11}$$

From Eqn (6), an expression for $AR^*$ may be obtained.

$$ AR^* = \frac{{\beta}. AR}{{\alpha}}  \tag{12}$$

By substitution for $R$ (using Eqn 11) and  $AR^*$ (using Eqn 12) in Eqn (6), followed by cancellation of the common term ($AR$), the following expression may be obtained:

$$p_1^{(equil)} = \frac{\beta/\alpha}{1 + {\beta/\alpha} + K_a/{\chi_a}}\tag{13}$$

Multiplying Eqn (13) 'above-and-below' by ${\chi_a}/K_a$ gives Eqn (2), the equation requested by the OP.

Comment

Note that when $K_a$  = $\chi_a$ and $\beta/\alpha$ >> 1, almost all of the receptors are open as $p_1^{(equil)}$ is close to 1.  When $K_a$  = $\chi_a$ and $\beta/\alpha$ << 1, almost all of the receptors are closed, as $p_1^{(equil)}$ is very much less than 1.

Note also that $K_a$ is a dissociation constant and is the ratio of a first-order rate constant and a second-order rate constant, and will have dimensions of concentration.

Addendum

It may be of interest that Colquhoun's great book, Lectures on Biostatistics, is (legally) available free of charge (as a pdf) from here

DC's Improbable Science

A great site


Can ants sense food from a long distance? I recently had ants find and then swarm to a food container that I put down on a desk. I'm curious as to whether an ant would have needed to get lucky (i.e., discovering the food after crawling up the desk) or ants have the ability to sense food from a distance.

I'm skeptical of believing that ants simply scout around until finding food; I'll use this case as an example:

My room has had no food or drink in it for weeks, so the area wouldn't be a "hotspot" for ants to be interested in.
I put the mostly empty food container down on my clean desk and turned my lamp off to work on the computer. No more than 2 hours later did I turn my light back on to discover a trail of ants swarming to the container I put down. It happened pretty quickly.
The desk is high, standing on four thin legs. I find it difficult to believe that an ant would crawl up the desk as often as a 2 hour time frame to scout for food, for the message to be passed to the colony so quickly.

I've been curious about this scenario for a long time. So my question:

Can ants sense food from a long distance? If so, how does it work? If not, how is the phenomena (ants locating food quickly in unlikely places) explained?

Ants follow odor cues in the wind.  A study by Wolf and Wehner (2000) manipulated ant antennae and wind direction to show that ants followed odor plumes on the wind. A more recent study by Buehlmann et al. (2014) showed that desert ants of the genus Cataglyphis cued in on linoleic acid, a so-called necromone (death scent) released by dying insects. Here's a popular article that summarizes the latter study.  Chances are good the ants are followed the odor plumes coming from your mostly empty food container.

Literature Cited

Buelhman, C. et al. 2014. Desert ants locate food by combining high sensitivitty to food odors with extensive crosswind runs. Current Biology 24: 960-964.

Wolf, H. and R. Wehner. 2000. Pinpointing food sources: Olfactory and anemotactic orientation in desert ants, Cataglyphis fortis.  Journal of Experimental Biology 203: 857-868.


Does any one know which species of insect is this one? I found this insect, in multiple zones of Imbabura - Ecuador. https://en.wikipedia.org/wiki/Imbabura_Province

Sorry for not having something to scale with, but it's about 15 cm long.

Another picture here:

That is a male dobsonfly. I know this is a male because it has long mandibles which are used in mating. Female dobsonflies have short mandibles. larval dobsonflies are called hellgramites,and it really hurts a lot when they bite you.Look here https://en.wikipedia.org/wiki/Dobsonfly or here entnemdept.ufl.edu/creatures/misc/eastern_dobsonfly.htm


Univocal identifying of a plant cell We yesterday got our biology-exams back and there's one exercise where I don't agree with my teacher. However, since he is the expert and not me, I need the support of external sources, i.e. experts in order to justify my statement.

  Now in the exercise, we first had to identify the parts of a cell (which was shown in form of an image) and then in part b) reason whether it was an animal or plant cell.

I had identified a chloroplast and a vacuole and stated that the only cell with this organelles was the plant cell. My teacher answered that I had missed the fact, that the cell had also a cell wall (which is indeed a difference between plant and animal cells).

My question is

  Is the fact that the cell had a cell wall necessary in my argumentation, i.e. are there other cells having chloroplasts and a vacuole without being a plant cell?

Could you provide a source which supports, or doesn't support my statement so that I can show it to my teacher?

Thanks in advance

Your teacher is right, chloroplasts and vacuoles are not sufficient to define a plant cell.

Amoeba have both chloroplasts (McFadden et al, PNAS, 1994) and vacuoles (Day, J. Morphology, 1927) but they are not plants - and they do not have a cell wall.

Sea slugs eat algae and can "steal" their plastids and keep them working for weeks/months, effectively becoming photosynthetic animals for a while. This is called kleptoplastidy (Pillet, Mob. Genet. Elements, 2013).


about the direct intervention of a child's gender Can we determine the gender of a child now,I mean,not randomly?
There are equal amount of sperms with X chromosome and Y chromosome.
Can these two kinds of sperms be distinguished easily?
If yes,we can choose the kind of sperm to meet the ovum,then the gender of the child can be determined.

Sperms can and are sorted using flow cytometry to attempt to separate sub-populations carrying X or Y chromosomes. The technique isn't perfect but it is undergoing "clinical trials" in the USA.