How does the mechanism which controls blood pressure in the brain work? I know that pressure is sensed in the skin by mechanoreception mediated by skin receptors. Static pressure stimuli are mainly sensed by slow-adapting fibers connected to receptors like the Merkel discs. Vibratory stimuli are sensed by rapidly adapting receptors like the Pacinian corpuscle.

Blood pressure is also sensed by the body and the brain regulates blood pressure by influencing the peripheral nervous system that can increase or decrease the blood output of the heart.

How are blood pressure differences in the brain sensed and how do these receptors mediate cardiac activity? Are blood pressure differences in the brain sensed by rapidly adapting receptors akin to Pacinian corpuscles?

Blood pressure is sensed in blood vessels by baroreceptors. Baroreceptors are stretch-sensitive nerve fibers located primarily in the aortic arch and carotid sinuses. The baroreceptors send afferent fibers via the glossopharyngeal nerve to the nucleus tractus solitarii in the dorsal medulla in the brainstem. From there, efferent cardiovascular neurons send projections to the medulla and spinal cord. There are also stretch-sensitive receptors in the heart and pulmonary vessels, called cardiopulmonary receptors that use the same nerural connections as the baroreceptors.

The baroreflex loop results in activation of sympathetic or parasympathetic fibers to the heart, the smooth muscle of the peripheral blood vessels, and other organs such as the kidney to maintain arterial pressure at normal levels.

In a simplified scheme, increased pressure stimulates baroreceptors, which attenuates the sympathetic outflow to the peripheral vessels and the heart, restoring pressure to normal levels. The parasympathetic influence will dominate which is mediated by acetylcholine. Conversely, a decrease in pressure relieves the baroreceptors and increases sympathetic outflow. Sympathetic activation causes a release of noradrenaline that leads to vasoconstriction and increased cardiac output and hence an increased blood pressure (see Fig. 1).

Fig. 1. Control of blood pressure. Source: Human Physiology (2011).

Reference
- Cougias et al., Med Sci Monit (2010); 16(1): RA1–RA8

The control mechanism in the brain for blood pressure is a endocrine hormone named ADH.  This stands for AntiDiuretic Hormone.  This hormone is produced by special nerves in the hypothalamus and stored in the posterior pituitary gland.  ADH is stimulated by increased blood solute (particles like ions and other molecules) present or decreased blood volume level.  When you have adequate hydration, this hormone is actually inhibited.  On a very elementary level, it works by stimulating kidney tubule cells to reabsorb water rather than eliminate it.  Some drugs also interfere with ADH, most commonly ethanol (drinking alcohol).

Edit: Forgot to add that ADH is also known as Vasopressin, and is also responsible for constricting the blood vessels.


Why do men have a higher hematocrit (red blood cell count) than women? The hematocrit, also known as packed cell volume (PCV) or erythrocyte volume fraction (EVF), is the volume percentage (%) of red blood cells in blood. It is normally 45% for men and 40% for women.

so,Why do we have hematocrit for men?

First,I thought it might be caused by different hormones but I couldn't find adequate evidence to prove this Hypothesis.Therefore I decided to share it.

I found a nice article that has insights to this matter. As posted before me it is true that only adults, but not juvenile individuals show this difference. Direct and indirect effects of sex hormones on bone marrow erythropoiesis and renal erythropoietin production has been proven, but it works in both sexes the same way. Females are capable to elevate their haemoglobin / red blood cell levels to external stimuli, yet at same conditions (same altitude etc) the difference remains. Also:

  Men, premenopausal women and postmenopausal women have similar plasma erythropoietin levels, indicating that women do not attempt to compensate for their lower haemoglobin levels by increasing erythropoietic drive. These observations show that the prevailing lower haemoglobin level in females cannot be ascribed to a lack of bone marrow or renal erythropoietic capability: they indicate that adult females maintain their venous haemoglobin levels at a lower level than adult males as a physiological steady state — they do not try under physiological conditions to maintain the same levels as adult males.

This could be achieved by modulation of the juxtaglomerular apparatus signal (JGA) of the kidney. The JGA has important role in the regulation of the haemoglobin level - it is the main input for erythropoietic red blood cell production by regulating renal filtration and thus regulating the amount of oxygen that gets to the EPO producing peritubular cells.

It is noteworthy to say that similar difference exist in mammals and even there are examples among birds and reptiles.

It is described in the linked paper that both men and women achieve the same or very similar microcirculatory haematocrit level inspite the different mean venous haemoglobin levels.

This implies the very interesting theory / reasoning in the article:

  (...) that both sexes set their mean optimum level separately and to some degree independently.(...) the red cell mass is an enormous resource in animals — one third of the body's cells by number in adult humans, and demands enormous effort to establish and maintain.(...)This price must be paid for by increased fitness.(...)The excess red cells over the critical minimum that circulate in the large vessels (and slowly through in the spleen in some species) and that constitute half or more of the venous haemoglobin level probably provide a storage function for the reserve red cell mass for use when the need arises for increased work — fight, flight, food and reproduction. They may also act as reserves for heat exchange and iron storage. It is likely that the return in fitness from this reserve differs between the sexes, and therefore that the optimal size for maximal cost benefit also differs.

males have testosterone that increase thyroxin secretion.thyroxin is importnat for ATP production,then if there is more energy production more oxygen is needed that directly increase more epo production.


what kind of bonds join the okazaki fragments During DNA replication, the synthesized okazaki fragments adjacent to each other are joined up directly by DNA ligase-catalyzed phosphodiester bond formation. Can someone point out to me which part of this statement says it's false? All I know is that the fragments are joined together by DNA ligase, which can only mean the part about the phosphodiester bond is wrong, but arent the 2 nucleotides joined by a phosphodiester aka nucleotide bond?

I'm pretty sure the "phosphodiester bond" part is correct.

The only thing I can think of that might be questionable is the word "directly". If directly = immediately, then the sentence could be termed false, because they aren't joined immediately.

Even then, it seems like that's just grasping at straws, so I wouldn't worry too much about it. It sounds like you understand the concept, which is what matters.

Okazaki fragments do not attach to the lagging strand adjacent to one-another, but rather, attach randomly, some distance from one-another.


In marine DNA viral diversity studies, what would "paradigm of rampant mosaicism" refer to? The recent paper in Cell Marine DNA Viral Macro- and Microdiversity from Pole to Pole describes the (huge) new Global Ocean Viromes 2.0 (GOV 2.0) dataset.

In the Results and Discussion section, the subsection Validating Viral “Population” Boundaries begins with the paragraph:

  Defining species is controversial for eukaryotes and prokaryotes (Kunz, 2013, Cohan, 2002, Fraser et al., 2009) and even more so for viruses (Bobay and Ochman, 2018), largely because of the paradigm of rampant mosaicism stemming from rapidly evolving ssDNA and RNA viruses, whose evolutionary rates are much higher than dsDNA viruses (for review, see Duffy et al., 2008). The biological species concept, often referred to as the gold standard for defining species, defines species as interbreeding individuals that remain reproductively isolated from other such groups. To adapt this to prokaryotes and viruses, studies have explored patterns of gene flow to determine whether they might maintain discrete lineages as reproductive isolation does in eukaryotes. Indeed, gene flow and selection define clear boundaries between groups of bacteria, archaea, and viruses, although the required scale of data are only available for cyanophages and mycophages among viruses (Shapiro et al., 2012, Cadillo-Quiroz et al., 2012, Gregory et al., 2016, Bobay and Ochman, 2018).

I know what "rampant" means in the colloquial sense, and the colloquial form of "paradigm" is familliar as well. Mosaicism usually relates to genetic differences between groups of cells within an individual multicellular organism. I am not sure how it applies to virus populations.

Is it possible to explain the meaning of "paradigm of rampant mosaicism" in this particular context, and give it some background?

As I understand it from skimming the Cell paper and that by Bobay and Ochman, 2018, which it cites, the concern is the validity of the established method of defining viral species. Quoting from this latter paper:

  Members of a biological species are defined by their ability to exchange genetic material…

The problem would appear to be that ssDNA and RNA viruses evolve rapidly (rampant is probably meant to convey this idea), but most importantly, not just by acquiring point mutations or deletions, but by horizontal gene transfer from other viruses (and from bacteria).

The net result of this is that such viruses are made up of segments from different sources, some evolved by conventional mutation and others ‘hijacked wholesale’ (my own hyperbole) from other organisms. Another way of putting this is that their genome is a mosaic of genes from different organisms. An example of this is in the diagram below, taken from a paper by Juhala et al. entitled “Genomic Sequences of Bacteriophages HK97 and HK022: Pervasive Genetic Mosaicism in the Lambdoid Bacteriophages”.

For anyone unfamiliar with the word ‘mosaic’ (or its applicability in relation to genomes) I reproduce below a Roman mosaic from Pompeii. The idea is that what appears as an integrated organism is composed of disparate pieces with distinct boundaries.

(The protagonists in the mosaic are about to exchange blows, rather than genes. There are also mosaics at Pompeii depicting the latter type of exchange, but these are a little too ‘rampant’ to present here.)

The implications of ‘mosaicism’ for defining viral species is — I imagine — that viruses which could be regarded as distinct species from examining the sequences of the majority of their genes might still be able to exchange genetic material by crossing-over at genes they have acquired by horizontal transfer.

Oh, and what about paradigm? It would clearly be unfair of me to suggest that this is a fancy word that the authors have used to sound important. The Oxford Dictionary online defines it as:

  A typical example or pattern of something; a pattern or model.

I think that the authors mean that the viruses provide a good example of horizontal gene transfer.

I don't think this is an answer, but I have been told to write it as an answer by a mod:

it means
" ...the standard model of uncontrolled, widespread, pervasive mosaicism..."

Mosaicism mechanisms are probably for another topic, Wiki states that:
Genetic mosaicism can result from many different mechanisms including endoreplication, anaphase lag, and chromosome nondisjunction.


What sea animal is this? I am in a remote village and a young boy (second pic holding tail) says this thing is his friend. This creature is safe, we held it for pictures and released it after. None of us know what this is and we do not know who to contact. The young boy plays with it every day so it is safe but it still is strange.

These are salt water shores, not fresh water.

Someone mentioned a dugong but it is far too skinny I think. I didn't get pictures of the head as we didn't know if it had sharp teeth.
Image is taken in a remote village in Kavieng, Papua New Guinea.

The creature's head looked like this.

Link:
 polartrec.com/files/members/cara-pekarcik/images/dsc_0160.jpg

I'm no expert, but I don't believe seals are in Papua New Guinea, it's almost a hybrid of few things.

It's probably a dugong, based on the location, lack of a dorsal fin, split tail, lack of a blowhole, and narrowing of the snout.

The prominent vertebral column looks unusual, but that might come from the strange posture it is being held in or from malnutrition.

This publication from the Australian government shows necropsy of several dugongs (note, this PDF contains graphic necropsy photographs), including one that was malnourished (see page 53). This individual shows some of the characteristics of the OP, including pronounced vertebral column and a clearly visible neck. The text notes the presence of these features as well.

  Adult dugongs showing signs of malnutrition: a) with neck becoming visible
  and prominent backbone

Sadly, the other dugong pictures I found that look most like this specimen are also ones from news sources that are often dead or injured or needing some other human assistance. Some other examples:

Queensland couple come to rescue of beached dugong
Dugong dies from propeller wounds
Trang fishermen asked to help slow-moving male dugong
Rare Dugong saved in Maliangin Community Marine Sanctuary

Some pictures do show a prominent vertebral column near the tail in animals that seem otherwise healthy, but those images don't show the rest of the animal well (thanks to @theforestecologist):

http://www.oceanwideimages.com/images/11147/large/dugong-58M1444-20D.jpg
http://www.oceanwideimages.com/images/11144/large/dugong-58M1444-17D.jpg

As an extra piece of trivia, dugongs and their manatee cousins have been closely associated with mermaid legends.

Of course, a better picture of the animal's head, especially in profile, would make identification much more clear.

I think is blackchin guitarfish. Like that. But this picture not enought.


Why do some trees have a life span, while some don't? I have heard that there is no limit on the growth of trees, but then why do some trees, such as boxelders and poplars, tend to live shorter than redwoods, for example? Some advertisements for improved lombardy poplars state that their trees have an extended life span, up to 75 years? The trees with shorter life spans seem to weaken at a certain age, and then contract diseases more easily.

The answer to this could be that there are many factors contributing to the length of the life of tree species.

Climate: You can see that trees that have a reputation of becoming really old live in environments that have low moisture levels and much sunlight over the course of the year.

For example, you can see that the most long-lived trees in America are located in California, where the temperatures are relatively high, while moisture levels are low. If you have one without the other trees don't tend to live that long. Cold climates make growth
harder for each individual, yet hot and moist climates tend to help trees grow easier, but also die easier. Think of the amazon. It is one of the richest forests in the world, yet the growth of bacteria and high competition in the areas of the equator make life a lot harder for the longest living and slowest growing species.

As you can see, the vast majority of the longest-living trees are located in California, or other regions of the same latitude!
http://en.wikipedia.org/wiki/List_of_oldest_trees

Other species and the life around it/Its Ecosystem: Individual trees tend to be less likely to be destroyed by a fire, as they are less likely to catch fire. At some instances, forest trees or dried-out grass can catch fire and pass it on to other individuals.
Microbes and bugs found in some parts of the world are known to their abilities to destroy trees!

Current size of the tree: Larger trees are generally less likely to die of causes like drought or damage to their trunks, as they have greatly extensive nets of roots and thick trunks and thus are able to, even partly, recover these incidences.

If a rockfall for example causes damage to one side of the tree, some of the brunches will probably die, but the rest of them, that have their own network to the roots, will probably survive.

This means that luck is involved and if the tree is lucky enough to avoid dying for a certain amount of time, regular fluctuations in the environment do not kill it as they would kill a younger, less robust tree.

Biology of tree species: Debate is held as to whether tree cells have telomeres working the same way as they do in animals. Research published in 2001 suggests that telomeres don't work the same way, as plants developed without telomeres after six generations continue living and growing without problems. But even if they do use telomeres, they may use them in a different way. This is an area where research is still being conducted, though, and you may find controversies in the bibliography!
For example in the paper "Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva"
Barry E. Flanary & Gunther Kletetschka which can be found in the rep

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CCgQFjAB&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F7709949_Analysis_of_telomere_length_and_telomerase_activity_in_tree_species_of_various_life-spans_and_with_age_in_the_bristlecone_pine_Pinus_longaeva%2Ffile%2F9c96052bcf0a51be49.pdf&ei=zzrCU9OcMIjV0QXmt4CwCQ&usg=AFQjCNH7853fvZ8yneznSfIQQPsxtIDQag&sig2=-PELK5RCQlAGTvQODoyZ2A&bvm=bv.70810081,d.d2k

we can see that sometimes, short lived trees have longer telomeres than long lived ones!
(Look in the second paragraph of the section "Results"). This means that actually, nobody really knows!! It may be the telomeres, it may be something else, it may be a combination of factors.

http://www.madsci.org/posts/archives/2002-04/1019349924.Bt.r.html
(notice that this post has links to pages that are no longer available).

Distillation and the most important point: The way that the tree is adapted to its environment determines its longevity in it. Planting an olive tree in the amazon is a great way of making sure it will not survive! Some trees are better at surviving in a certain climate (even if it is at your own garden) simply because they have evolved to live there.

That means that the trees probably don't have a defined lifetime in general, but the life expectancy is defined in each environment, depending on the circumstances!

This means that species we currently think of as short-lived can reach get really old:
http://www.ncbi.nlm.nih.gov/pubmed/11295506

What some companies may have done is   try to combine characteristics of individuals through selective breeding - and yes, it works for trees as well!- to match the climate and terrain characteristics found in the certain country or region! Or they may have selected for resistance against the most common pests in your area!

I hope I answered you question adequately!

Although most plants can potentially reproduce sexually, there are some plants that effectively always reproduce by shedding off branches which, when they fall in the right conditions, grow into new 'clones' of the same tree, which the exact genetic material. In these cases, it is advantageous for the tree to be able to survive as long as possible. Plants that reproduce sexually by the cross of two different individuals have a recombined genetic material in every generation, and the survival of that plant with that new genome is usually shorter.


How can someone share 50% of their DNA with their parents yet all humans share 99.9%? I have heard that humans share 99.9% of their DNA with other humans. I have also heard that a child shares 50% of their DNA with their parents. How do I resolve this apparent contradiction? It has been really bothering me.

It will be clear with a simple analogy.

You are 50% related to any one of your parent

Let's say you don't have any biology books. You have two friends, Alice and Bob. They each give you a copy of the book Campbell Biology. You now have two Campbell Biology. You have received 50% of your Campbell biology books from Alice and 50% from Bob.

Similarly, you inherit 50% of your DNA from your mother and 50% from your father. You are related at 50% to any one of them.

Two randomly sampled individual are 99.9% identical

Now consider the list of all the copies of Campbell Biology in the world. As there exist different editions, all Campbell Biology won't exactly be the same.
Let's say you randomly sample two Campbell Biology from around the world and you align them letter by letter. What is the expected fraction of the letters that will be identical? If, for example you find the two sentences

  Selection is a fitness variance associated to a genetic variance among individuals in a population.

and

  Zelection is a fitnezz varianze azzociated to a genetic varianze among individualz in a populazion.

There are exactly 9 mismatches out of 99 characters, that is a 90% similitude.

Similarly, if you randomly sample two humans, align their DNA (a DNA sequence look like ATTTCGCTGTCGAATCGATCGGTA), you'll find that the fraction of mismatch is lower than 0.1%. Therefore, we all share 99.9% of our DNA.

Of course, alining DNA sequences (or normal sentences) is not quite that easy as some sequences (or sentence) can have more nucleotides (or letters) than others but I won't go into the details here.

How do these two measures relate?

Let's say that instead of giving you a book, Alice actually produced a copy of its book and gave it to you. The book you have received from Alice (that is 50% of all your Campbell Biology books) is 100% identical to Alice's book in term of mismatch.

Similarly, the 50% of your DNA that you inherit from your father (or mother) is 100% identical to the copy of the genome found in your mother.

Note however that

Your mother probably made between 10 and 100 mutations when copying her DNA so that the DNA you received from your mother is not exactly 100% identical to your mother's DNA

Similarly Alice could have miscopied her Campbell Biology book that she passes to you

Your mother actually recombined her two haplotypes

Similarly Alice actually had two different editions of Campbell Biology and she mixed them up a little bit before copying the resulting book!

The 99% and 50% refer to different senses of relatedness.

Humans share 99% of genes with other humans:  If you were to compare one human to another human with respect to every single one of their genes, you would find a 99% similarity.

A child shares 50% of his or her genes with his or her parents:  This 50% refers to a relatedness relative to the population rate of relatedness.  It actually refers to a gene within that 1% that is different (a polymorphism) between humans.  This is an approximation used in order to calculate what degree of prosociality an individual could be selected to impart to another individual, where the gene for prosociality would have some frequency between 0 and 1 (that is, there would be some difference between individuals at the locus where the gene is located).  Hamilton's (1964) rule is used for this calculation.  It is c < b*r, where c is the cost of the actor; b is the benefit to the recipient of the act; and r is the relatedness between the actor and recipient.  The r used in this rule between parent and offspring is 0.5.  The interpretation is that if a gene is responsible for a cost (c) to the holder of the gene (a parent) and a benefit to some other individual (an offspring), the relatedness (r) between the holder and the other individual must be greater than c/b because relatedness gives the likelihood that a copy of the gene responsible for the cost and benefit is also located in the benefiting individual and so the likelihood that the offspring shares a prosocial gene carried by a parent is half the difference between 1 and the background rate.  If the gene is at 70% frequency in the population and one parent has the gene, then the offspring's likelihood of having the gene is 85% (assuming the other parent has it with 70% likelihood).


Can the third sex be categorized as Male or Female? Hijra are people who have a penis (not sure if sexually active) but look much like a female (perhaps for some feminine biological property). Wikipedia says they are "physiological males who have feminine gender identity"

Also, I just came to know there are some more types of third gender people.

Now, is there really any BIOLOGICAL third gender which cannot be categorized as male or female? Or its always possible to categorize them to male or female?

When dealing with humans, there are only two Biological genders as defined by the presence or absence of the Y-Chromosome. If the Y-Chromosome is not present, or through some process gets totally deactivated, the human will appear and function as a Female.

XX = Female

XY = Male

XXY = Male (Klinefelter's Syndrome)

XYY = Male (Aneuploidy - Normal Functioning Males)

XXX = Female (Aneuploidy - Normal Functioning Females)

X = Female (Turner's Syndrome - Generally infertile, other issues)

Y = Fatal (The Y-Chromosome is drastically smaller than the X-Chromosome, which contains many necessary genes)

XXYY = Male

...

The list goes on, since there have been records of up to XXXXX.

If there is a Y-Chromosome present, the human born will be male.

However, that is not to say that a person cannot psychologically identify as something else. It's also worth noting that the majority of known species are asexual and do not have genders, and that those which do have genders do not always follow the same rules (Fruit Flies, for instance, use the ratio of genes to determine sex).

There is an actual third gender. That is true hermaphroditism. Some humans are true hermaphrodites. The most common cause of this? 2 eggs fusing, 1 male and 1 female before they start differentiation.

These have both male and female characteristics and so they can't be classified as either male or female.

Here is my source:

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


mRNA and Protein relation A and B are two different proteins:
1- can they have same mrna
2- is it possible that the gene types which encoding the synthase are same ?

my answer is yes to both .
because after protein synthased cell can remove aminoacids with  post-transcriptional modification etc.

1) Can two different proteins have the same mRNA?

This isn't clear enough to give you an answer:

Can two different proteins be made from the same mRNA molecule?

Yes, polycistronic mRNAs can encode several proteins which are translated separately (we can engineer this using internal ribosome entry sites, IRES).
Yes, different proteins can be translated from one open reading frame by failure of peptide bonding between two amino acids (we can engineer this using 2A peptide sites).
Yes, identical proteins can be translated from one mRNA and then modified differently after translation to yield different "final" proteins.
Yes, identical polypeptides can be translated from one mRNA and then incorporated in different protein complexes.

Can two different proteins be made from the same mRNA code?

No, not made in the sense of translated.
Yes, as above, identical proteins/polypeptides can be made and treated differently after translation.

2) Is it possible that the gene types which encode the synthase are the same?

Gene types? Do you mean genotype, i.e. allele? What synthase? Sounds like a homework question to me.

Answer is yes, by a logical approach, in superior organism where alternative splicing and post-transcriptional modification alter the protein structure.
In bacteria, this thing is not allowed. This scenario isn't common in functional protein, and start occurring by some alteration in the splicing process.

In real life, this is nearly impossible. A protein domain could be conserved, and so different protein can share parts of the amminoacidic sequence and, by that, the mRNA. But, as far as I know, there's no study confirming the evidence of same transcript and different proteins.


Is there any other function of DNA? We all know that DNA acts as a genetic molecule. Does DNA have any other function in the cell other than being a genetic material and carrier of information?

In eukaryotes DNA has a structural as well coding function. Parts of chromosomes called centromeres bind to proteins and form a scaffold which helps chromosomes attach to each other and correctly segregate during division. Technically this is still related to the transmission of genetic information though.

Since RNA can act as an enzyme (the so-called ribozymes), scientists have hypothesized that DNA can also have an enzymatic function, but no such function has been found in nature. Artificial DNA enzymes (deoxiribozymes) have been designed to cleave DNA, covalently modify proteins, ligate RNA molecules, and even catalyze reactions between small molecules. See this lab's website.

Yes, maintenance of the genome.  But not DNA specifically, but DNA and all of its associated proteins.


What type of fish is this and why is it so big? This is a screenshot from a youtube video that you can watch here:

https://www.youtube.com/watch?v=zcdJNPYkIE0

That is a Queensland Grouper (common name).


What is the purpose of co-translational transport? During intracellular proteins synthesis, all proteins are made by free ribosomes in the cytoplasm and some, but not all ribosomes (those which make membrane or secretory proteins) move to the endoplasmic reticulum (ER) and attach to it during translation (called co-translational transport).
Why are proteins that will be exported to the outer of cell are not made in the ER directly?
What is the function of ER in intracellular protein synthesis?
What is the purpose of co-translational transport?

Why are proteins that will be exported to the outer of cell are not made in the ER directly? What is the function of ER in intracellular protein synthesis? What is the purpose of co-translational transport?
This is a eukaryotic cell that we are talking about.Once the mRNA is synthesized , it has to move out from the nucleus to the cytoplasm.During its exit, SRP (Signal Recognition Particle) recognizes specific signal sequences in the mRNA and forms a complex with that mRNA.then SRP complex targets ER membrane proteins for cotranslational-transport.
If the secretory proteins are not moved into the ER , disulfide bonds would not be formed from cysteine residues . Because the necessary Enzymes required for this process are found only and only in the ER (namely PDI and ERO1).
Plus, these secretory proteins often have to be glycosylated to perform their action correctly.The Enzymes are located in the ER.
Moreover I believe that these secretory proteins will aggregate and degraded later if they are not transported into the ER.
I do not know WHY this process exists this way. That is Evolution and it is just about adaptation to the environment and not necessarily based on pure logical reasons.
Further readings : Molecular Cell Biology Lodish et al 8th ed at sections 13-1
and 13-3.
In addition see : Protein translocation across biological membranes , Targeting proteins to membranes: structure of the signal recognition particle   Post-translational translocation  Regarding to Ero1 and DPI
Formation and transfer of disulphide bonds in living cells

The secreted proteins are not made in the ER because ribosomes cannot get into the ER. Even individual ribosomal subunits are much larger (at least 10-fold greater in volume, if not hundreds of times greater) than a typical protein, so it is much easier to translocate the protein being produced by the ribosomes across the ER membrane than to translocate the ribosomes themselves. Even the protein being produced must be at least partially unfolded as it is being translocated.
That's not even taking into account that the mRNAs would need to be translocated as well if the ribosomes were to translate them while in the ER. The mRNA is again many times the mass of the protein (a nucleotide is ~3-4 amino acids "worth" of mass, and there are at least 3 nucleotides per amino acid encoded, more if you add the untranslated regions).


When did human ancestors learn to walk? Where does our ancestor learn to walk from? How do we control our legs whenever we take a step?  I confuse every time whenever I take one step.

In a sense, there's an easy answer to your question.  Humans became bipedal in Africa, since bipedality is well-established for the first species in the human lineage to leave Africa (Homo erectus/Homo ergaster).  This can be verified in many textbooks.  However if you ask the question when, in what species, or why, there's no easy answer to your question. The question comes down to (a) which fossils are specifically ancestral to humans (b) what fossils have evidence for bipedality, and (c) theories as to why those species became bipedal.

The narrow sense of humans, Homo sapiens, has been bipedal ancestrally.  Other closely related species were almost certainly bipedal (Homo neanderthalensis and Homo heidelbergensis for example).  In fact, the species or species complex from which humans likely arose, Homo erectus, was also likely bipedal (discussion below).  If we take the broadest sense of what "human" means, it could mean any species which split from the human lineage after the split with the extant great apes (specifically, post split with chimpanzees).  Here there's reasonable evidence for bipedality exists around the same time as this split, but not in all species.  Specifically, Orrorin tugenensis is a 6 million year old specimen with some (but not conclusive) evidence for bipedalism.

Question b, how do we know a fossil creature is bipedal, is a challenging question.  Homo sapiens, the only completely bipedal primate, have many adaptations which facilitate walking on two legs.  The shape of our pelvis facilitates the muscle attachments necessary for walking by flaring the ilium (the bone which forms the upper part of the pelvis).  This same flaring is found in Australopithecus afarensis (which includes the famous "Lucy" specimen), about 3 million years ago.  Australopithecus also has a fossil of footprints, which seems to indicate bipedal movement.  The human femur is bent inwards and the neck is thickened to support the weight of someone walking upright.  This same thickening is found in Orroin tugenensis and the angle in Homo erectus/Homo ergaster (these are two names which are either closely related species or the same species, depending on who you ask). The human big toe is also in line with the others in the foot, which likely allows us better motion on the ground.  This feature is also true of Ardipithecus ramidus, at about 4.5 million years ago.

The third part of your question, why humans became bipedal, is largely speculative.  Many theories exist for the process which lead to bipedalism.  A popular theory in the 1970s and 1980s was that humans became bipedal to enhance our abilities to see across tall grass, because many people thought Homo erectus/Homo ergaster was the first upright walking species, and grasslands dominated east Africa at the time.  However since earlier evidence for bipedality, many people have abandoned this hypothesis in favor of others.  These other hypotheses include that bipedalism arose after scaffolding on to arboreal (tree-living) adaptations.  If human ancestors lived in trees, they may have moved in a vertical posture, leading to many of the adaptations needed to move vertically on the ground.  Others include an increased reliance on meat, caught through endurance hunting, or even wading into tidal waters being the key feature (notably this is not the aquatic ape hypothesis, which is pseudoscience), and this reliance on key marine resources provided the essential stable food supply for brain enlargement.  The short answer is that there's a tremendous amount of speculation in this area, and few firm facts.

Whichever of these species you choose as the "first bipedal human," and how confident you want to be about that bipedality, they all evolved in Africa.

Africa. Humans evolved in Africa, and that's where our ancestors first became bipedal.

Most primates are arboreal forest dwellers. Ancestral hominids or humans are therefore seen as pioneers who ventured into savanna grasslands, similar to baboons. I'm not sure if there's a popular theory that explains exactly what motivated humans to walk upright, but there's obviously less opportunity for climbing in an open environment.


How does one find the corresponding SNPs in the pair of chromonosmes in a FASTA file? You might say I'm an amateur bioinformatician, or trying to become one.  I have a BAM file, from which I have succeeded, using UGENE , in extracting consensus data in FASTA format.  I now see a single series of nucleotides, and their complements, for each chromosome.  What I don't see is two corresponding sequences.  SNP data (e.g., SNPedia ) cites (if I understand it correctly) the SNP at the same site on each chromosome in the pair.  I don't know how to determine my variation, since I see only one nucleotide at any given site, not the pair.

Pretty sure I'm missing something fundamental here.  Thanks for any help navigating this jungle!

If you are looking for simple one off queries it might be better to load the BAM file and a relevant reference genome into a browser like IGV and simply navigate to that specific position.

For some data I had lying around a heterozygous SNP would look like the picture below, there has been an A to G SNP and a C to T:

For longer lists of queries I would take a look at BEDtools: https://bedtools.readthedocs.org/en/latest/content/bedtools-suite.html

If this does not help you, I recommend you ask your question on https://www.biostars.org/ There you will find help from true bioinformaticians.

I wouldn't necessarily expect regions of heterozygosity to be apparent from a consensus fasta.  I'd eyeball if you know some potential sites, or run your .bam through something that will call SNPs.


Why do seeds grow upwards? Why do seeds grow upwards?  Surely gravity would pull them towards the earth's core?  Can anyone shine any light on this? Do seeds that are planted deeper grow more quickly.

It is a reaction to gravity, it is called geotropism or gravitropism. The roots tend to grow in the direction of the gravity (positive geotropism) and the stem is going against gravity (negative geotropism).

The mechanism works with auxins, or plant growth hormones. They are pulled by gravity toward a side of the plant and will either stimulate or inhibited growth in that area.

Note added; Gravity is but one factor in a 'sea' of complex factors that have effected everything living in this thin blue line on Earth.  Atmospheric pressure, temperature, humidity, the medium's porosity, the Earth's spin counterbalances the gravity and a myriad of things I didn't list or was able to mention a myriad of things we humans just do not understand about life, gravity. I am trying to say that there is no ONE thing controlling the direction of the cotyledon nor the root growth.  Roots do not grow and grow towards the earth's core.  Roots stay within the top 4 to6" of topsoil for a reason and gravity has nothing to do with it other than gravity is part and parcel of all the systems that put pressure on an organism to make it adapt to its environment and file that information away in the seed of a plant, within every living cell. As DNA.  It is weird we share 99% of the DNA messages with all animals all plants all life.  What does that tell us?

Geotropism isn't quite right because it certainly is not the only factor plants have taken into consideration.  Again, roots grow horizontally to the force of gravity, not vertically.  The fact that gravity is a constant tells us that there has to be many forces that shaped the physiology plants display. We animals are able to run and jump against and with gravity forces.

This question is a very good one because it causes us to pause, step back to think about the larger picture, a picture we humans have just begun to imagine.Geotropism seems to be a pretty minuscule reason plants grow upwards and roots grow outwards.  No one thing could ever be pointed to as the reason a life form as evolved to survive with or against. If seeds are planted too deeply (more than 3X the widest diameter of the seed) that seed will more than likely damp off with fungus and decompose. Animals are the same, we sit still too long in one place and we start decomposing, grins!

I have a feeling that people think plants are dumb like rocks.  In fact, they were here first, before animals.  Lots more time to perfect their survival abilities.

If it was up to gravity, the roots would grow and grow and grow downwards.  That is not at all what happens.  95% of all plant roots are within the top 6" of soil. The reason is water doesn't infiltrate the subsoil well at all.  Plants 'know' this fact.  Roots grow where there is air and moisture and temperature stability. There is absolutely no reason to grow any deeper roots with the exception of a few plants that need find deep water sources, chemistry for photosynthesis and/or need support. AT the same time in the desert environment, cactus don't waste any energy on deep roots!  They instead, figured out how to store water.  They keep their roots very shallow and very small. Deep roots would be a waste of energy and resources. They can live to 150 years, 50 feet high but their root system is just enough to keep the 2 to 10 ton plant from falling over in a wind.

There are a few plants that are programmed to have tap roots that are for support and scouting that do grow very deep. 1000's of feet deep and 1000's of feet horizontally.  They don't have the ability to store water.

The cotyledons grow upward against gravity.  They don't even need light to be persuaded.  Plants have had more time than us animals to evolve.  Gravity is like a 'positive' stressor, makes plants and animals more 'sturdy'.  But gravity certainly isn't at all the main director of plant direction of growth.

It is said that animals share 99% of DNA with plants.  That number has qualifications but what does that tell us?  Other than plants were here first, DNA or the blueprint for life started earlier plants. Before that DNA was in virus and bacteria. Plants may be stationary but they are by no means dumb as rocks.  There is life in rocks that never sees light, O2 or any organic matter; bacterium and worms.  They eat rock.  They procreate once every 1000 years.

Dr. David Attenborough stated in a documentary called "The Earth's Core" that 50% of all life is below the surface of the soil, in the crust and mantel of the earth.  I have a hard time with that statement, but heck, David Attenborough? I filed that away to deal with later.  I am thinking 'numbers' of individual lives, not biomass?

Plant DNA guides them via experience of billions of years. As long as this planet hasn't stopped spinning, lost its oceans or heaven forbid is below 150 ppm atmospheric (manmade or not) CO2, or have temperatures too low for too long, plants will thrive.  Our current CO2 at 400 ppm is getting too low.  2000 ppm was dandy.

Plants even communicate.  Via chemistry.  Some amazing instances of plants getting together for survival, such as when an animal population gets too large?  Plants that evolved to handle some grazing by those animals as a mutually beneficial symbiosis, will become toxic to those same animals.  Herds have mysteriously died within days. Then it was discovered the plants had communicated and all switched their DNA to temporarily be toxic to the animals in their environment.

Plants are not at all dumb as rocks. They are just not as well understood as animals. Cotyledons grow upward in pure darkness.  When a light is turned on off to the side, that plant will grow towards the light.  If that light is turned off and another turned on that same plant will easily change directions.  Trying to get at light necessary for further growth and survival of that plant.

There are some incredible documentaries on the life of plants. If aliens show up they will be hard pressed to decide who is smarter; humans, other animals or the plant kingdom!

plants are smart

Also watch; "The Mind of Plants", a documentary I thought was excellent.

David Attenborough's documentary, "The Earth's Core" is a must.

Plants grow just fine in zero gravity


What is the evolutionary rationale for palm sweating? Sweaty palms seems to be a reaction to stress, anxiety, etc. For our forest-inhabiting primate ancestors sweaty palms could cause unwanted side-effects such as slipping off tree branches under stressful conditions, like when being chased by a predator.

Why did palm sweating became a reaction to fear, worry, anxiety etc in the course of human evolution? What is the benefit of sweaty palms?

As @Ben states, every theory of 'why' we evolve a trait is just a guess and never more than part of the story.   But there are theories.
The palms of our hands are a major source of heat transfer out of our body.  For bears it is the nose and pads of their feet, for dogs it is their toungue, for us a major portal for heat out of our body is the palms of the hands.

Black bears are extremely well-insulated animals, equipped with a heavy coat of fur and a thick layer of subcutaneous fat that help them maintain their body temperature as they hibernate through winter. But once spring arrives and temperatures rise, these same bears face a greater risk of overheating than of hypothermia. How do they dump heat without changing insulation layers?
Heller and Grahn discovered that bears and, in fact, nearly all mammals have built-in radiators: hairless areas of the body that feature extensive networks of veins very close to the surface of the skin.
Rabbits have them in their ears, rats have them in their tails, dogs have them in their tongues. Heat transfer with the environment overwhelmingly occurs on these relatively small patches of skin. When you look at a thermal scan of a bear, the animal is mostly indistinguishable from the background. But the pads of the bear's feet and the tip of the nose look like they're on fire.
These networks of veins, known as AVAs (arteriovenous anastomoses) seem exclusively devoted to rapid temperature management. They don't supply nutrition to the skin, and they have highly variable blood flow, ranging from negligible in cold weather to as much as 60 percent of total cardiac output during hot weather or exercise.

Given this, one could see how the palms of our hands are more likely to react to emotional situations where the heart rate elevates and sometimes we get hot under the collar.  The AVAs will
I am not physiologist, but the quote above comes from an article I stumbled upon a few months ago.  They use the AVAs to reduce the swelling associated with exercise and got some amazing results.  I guess that's another story though.

It was advantageous for our ancestor's grip while tree climbing millions of years ago, so the best current theory claims.


Any relevant knowledge/studies about voluntary goose bumps I'm not entirely sure how normal this is, but since I was a child, I've been able to produce myself voluntarily a "chill" sensation that seems to start on my head and traverse the rest of my body, being least intense in the feet. Looking around the internet and forums, looks like other people but not everybody also describe this ability. However, unlike other people's reports, I don't see "goose bumps" on my skin, at least there aren't any visibly; it's just the sensation.

Does anybody know if there are any relevant studies or knowledge out there about "voluntary goose bumps"? Is there even a proper name for that?

Recent studies prove that this involuntary phenomenon must be untrue. Obviously this is false, in order for research like this to take place people need to spend money. It would be interesting if we could create a crowd sourcing account maybe on kick starter to find ways to bring money into the research. I wish I had more information for you, I've been able to do it as long as. When you go to the dentist, just curious, you don't happen to have two bones underneath your tongue that is an anomaly as well? I've been trying to think of correlations for years. I can get the medical terms, if you like. Find me on Facebook Chris Azzy


What happens in the synapse when cocaine administration occurs in the human brain As far as i know when you accept cocaine in your blood some cocaine molecules reach some synapses in your brain and fill some Reuptake tunnels preventing the cell to simply "do not know that fired neurotransmitters have achieved their task" and doing so the cell fires neurotransmitters again becuase "it" simple do not know that "it" have achieved its task.
In this case cocaine molecules fill Reuptake tunnels in Dopamin Serotonin and Norepinephrine
orientated neurons.But since the firing occurs when an electrical signal occur how the neurotransmitters are fired again when such electrical signal does not exist?

If im mistaken in my physiology knowledge explained above please correct me!

You are correct that cocaine "fills the tunnel" (the pharmacology terminology is that it "blocks the transporter").  But it is not an autoreceptor, so the reuptake transporter does not send a stop signal, it just removed neurotransmitter from the cleft.  But once you've blocked it with cocaine, neurotransmitter is not being removed from the cleft so it has a much longer and stronger signaling effect on the post-synaptic neuron.

But cocaine can also block sodium channels, which assist in action potential propagation and that has more of a local anesthetic effect.

The effect you are thinking of would pertain to auto-receptors, not reuptake transporters.  Autoreceptors tend to be more like the post-synaptic targets of the neurotransmitter.

Cocaine is cardiotoxic. After chronic exposure to high doses I would assume that primary damage would attack the cardiovascular system before levels of dopamine would be able to cause damage. Cocaine intoxication deaths have mostly been caused by this cardiotoxicity. Primarily, myocardial infarction, arrhythmia, heart failure, and sudden cardiac death are a result of overdose. Cocaine is a vasoconstrictor, which may be a leading cause to myocardial infarctions.

http://www.ncbi.nlm.nih.gov/pubmed/19463023


In humans, are diseases inevitable during old age? Considering that dying "from old age" actually means that one dies from an illness related with aging, is it inevitable to eventually acquire diseases in old age?

There is a thought that aging itself should be considered a disease. In which case, death by disease is inevitable with our current level of medical technology.

  During the last 25 years, by targeting the underlying processes of aging biomedical scientists have been able to improve the health and lifespan of model organisms, from worms and flies, to rodents and fish. We can now consistently improve the lifespan of C. elegans by more than ten-fold (Ayyadevara et al., 2008), more than double the lifespan of flies and mice (Bartke et al., 2001; Sun et al., 2002), and improve the lifespan of rats and killifish by 30 and 59%, respectively (Valenzano et al., 2006; Zha et al., 2008) (see Figure Figure11 and Supplementary Table 1). Currently, our treatment options for the underlying processes of aging in humans are limited. However, with current progress in the development of geroprotective drugs, regenerative medicine, and precision medicine interventions, we will soon have the potential to slow down aging (Bulterijs, 2011, 2012).

"Old age" diseases are fundamentally malfunctions because stuff breaks. Some blame this on shortening telomeres, although an equally big part of the problem is that there are way too many important pieces that are unable to regenerate themselves.

Think of it as a machine where you can't normally get replacement parts. Stuff wears out, goes off warranty, and breaks.

Experimental regenerative medicine is working on fixing that with 3 fundamental approaches:

Adult pluripotent stem cells/regrowth. Researchers are looking for growth/regrowth/cell proliferation and differentiation mechanisms that already exist so they can be leveraged to regrow stuff that normally doesn't regrow. The advantage is that all the parts are grown from your own DNA or cells which means minimal problems with rejection or incompatibility. As an added bonus it could be considered "all natural". The main risk is cancer due to misconfigured cell growth/proliferation.
Lab-grown or 3D-printed replacement. Higher risk of rejection and other problems but simple and cheap compared to the others. Some research includes growing human-cell transplants in animals which raises various ethical and safety concerns.
Cybernetics or machine implants. Probably the most expensive and works out the best... when it works properly. "Robot" parts keep getting better and better, and have the bonus that they are more readily reprogrammable than DNA and biochemistry. A prominent research area includes brain/nerve interfaces with machine parts - expect pieces that either adapt to neural outputs or connect to nerves so you can "learn" how to use them.
The main drawbacks of this approach other than the cost include vulnerability to EMPs (a massive solar flare or EMP attack will fry all unprotected cybernetics/implants/robot parts), being dependent on both electricity and regular food, risk of getting hacked, and general lack of self-repairability short of replacing parts that break (again). Alternately you could argue that the risk of getting hacked through cybernetic implants and robot parts is a fair tradeoff considering they're immune to organic viruses and infections (except if someone invents bacteria that eat through solid metal or plastic pieces)


Why don’t humans have eyes at the back of their heads? How does evolution rule out the possibility of humans or others fragile herbivores from having 2 pairs of eyes, one at the front and the other at the back of their heads? Why didn’t that ever happen?

Vertebrates have ears which sense 360 degrees for a range of many meters, and they have social eyes, where they group many eyes and ears into one social group, it's easier to listen and live in groups, than grow eyes in the back of the head.

2 eyes exists in nearly all bilateral animals, arthropods, flatworms, sea-slugs, crabs, crickets, squids, flies. Arthropods have compound eyes and it would be easier for them to have 4 eyes, and only spiders and horseshoe crabs have more than 2.

It would be easier for a vertebrates to develop 4 nostrils and ears than 4 eyes because they are simpler than the orbs of the eye.

Same reason as 5 fingers has been the optimal numbers for all vertebrates since early lizards. in short, it's very easy to lose extra organs and to modify old ones, but it's very difficult to evolve new organs, and to relocate ones around the nerves and veins... centrally connected organs travel around the body and the circulation moves in front of them, i.e. if you did get 4 eyes and two of them moved to the back and sides, the nerves for your face expressions that are next to your ear would have to go in front, around, and through the moving eye pathways.

To simplify, we stopped evolving our symmetrical archetypes when we were related to starfish, ammonites and ediacaran fauna, and the fastest most versatile animals all had 2 sided symmetries, with entirely symmetrical nervous systems, and forwards moving at that point in time, using binocular compound vision, which did have 180, and that binocular compound vision afterwards became our 2 eyes. We share the kingdom Animalia with starfish, our common ancestor experimented with shape during the Ediacaran era.

To understand the difficulty of adding new eyes later, you should learn why nearly all vertebrates have 5 fingers, except some frogs which have 4. it

google: why do animals all have two eyes?


What is this worm-like creature? It is on my bed sheet. The hairy part the the rear end. The length is about the diameter of a US dime (~18mm).

The other answer is most certainly incorrect. Silverfish are silver/grey and (like all members of the Zygentoma order) have three distinct, tail-like caudal appendages from their posterior end -- really, two large cerci with a central long filament.
 [Sources: 1, 2, 3].

The OP's specimen resembles the larva of a dermestid carpet beetle of some type; specifically, the location and appearance make me think it might be a black carpet beetle (Attagenus spp) -- for example A. unicolor.

 Source: Univ of California Master Gardener Program of Contra Costa County Blog

Description:

Tell-tale characteristic: the tuft of numerous "hairs" on the posterior end:

  The larvae of the black carpet beetle, which may reach 12.7 mm in length, are very different from other carpet beetles’ larvae. They are elongate, carrot-shaped, golden to chocolate brown, and have a tuft of very long, curled, golden-brown hair at the tail end of their body.  [Source: Penn state Dept. of Entomology]

A description from IFAS suggests that larvae develop stiff, bristlelike tails when older.

See bugguide.net for more pictures, such as this one

Pest:

According to many of the sources I've linked to already, the larva is the damaging life stage of this beetle.

It's hard to tell from the image quality, but is it a silverfish? It has roughly the same body shape and size:

(source: umn.edu)


How statistically significant was the "sweaty T-shirt" experiment? An Overview of the Experiment.
In 1995 there was an experiment that involves young people smelling T-shirts worn by another gender and rating their preference. The researchers found that people preferred shirts belonging to people with a dissimilar Major Histocompatibility Complex (MHC). Another interesting finding was that this preference reversed for the women 'sniffers' that were using oral contraceptives.
Here is a link to the wikipedia entry.
These findings were reiterated by a study in 2005.
My Question.
I'm very ignorant in the subject of pheromones, particularly in humans. For those of us not 'in the know' a result like this seems like magic! I want to get a better grasp on how set in stone pheromone preferences like this are.
Unfortunately I do not have access to these articles at the moment. The actual statistical difference in populations isn't mentioned in the abstracts  (the cynical sceptic alarm bells are ringing!) other than the 2005 one stating that the total sample size was 58, which sounds low given that the total population is split into two.
Generally I'm looking for any supporting or opposing critiques of the study, specifically I want to know more about the statistics of the studies.
My question is:

What statistical validations and scores appear in these studies?

I also am willing to accept answers discussing validation in similar studies. I'm after a number or quantification for how consistent pheromone preferences are.

First, let's consider the original Wedekind et al (1995) study.

Sample sizes seem reasonable, if the effect is not very noisy:

  [...] 49 female students (average age: 25.2 years, s.d. = 4.0) and 44 male students (average age: 24.7 years, s.d. = 2.6) [...]

... and the statistical design accounts for individual differences in a fairly robust way:

  [...] women were asked to rate the odours of six T-shirts each, three of them worn by men who were dissimilar to the rating woman's MHC (average number of dissimilar HLA-antigens = 5.9, s.d. = 0.26), and three worn by men who were more similar to it (average number of dissimilar HLA-antigens = 2.7, s.d. = 0.74). We tried to present every T-shirt as often to MHC-dissimilar women as to MHC-similar women (average difference of presentations to thc two groups: -0.02, s.d. = 0.73). The presentation was random in every other respect [...]

Rather irritatingly, although the study design involved asking women to rate at least three attributes of the smells (sexiness, pleasantness, and intensity) the study performs a bait-and-switch in its results:

  The scores for sexiness are not shown in the figures as they were highly correlated with pleasantness (all scorings: r = 0.85, n =  294; for women who do not take the pill: r = 0.87, n = 186; for women who take the pill : r = 0.83, n = 108, p always << 0.001)

This is a bait-and-switch because even if A correlates with C, and B correlates with C, we do not know that A and B correlate with each other. Of the three measured attributes, 'sexiness' arguably has the most direct bearing on mate-choice. Because analysis for 'sexiness' is not presented, the paper ends up telling us much less than it could have about the relationship between MHC relatedness and mate choice.

The results for 'pleasantness' and 'intensity' look like this:

One further piece of analysis is presented: some number of the female subjects seem to have reported that particular smells reminded them of their partner or ex-partner; or reminded them of family members. Mentioning that a shirt smelled like a partner or ex-partner happened more frequently for MHC-dissimilar shirt smells (~17% vs ~9%; p = 0.038, two-tailed Fisher exact test). Oddly, no written response-collection is described in the methods, so I can only assume that these assessments were ad-hoc.

If this was all of the analysis that had been done on the topic, my assessment would be: this is amongst the many published research findings that are probably false. My main concerns would be that

Not all of the collected data are presented;
The most directly-informative contrast is not shown;
No adjustments for multiple comparisons are made on the statistical tests;
The data that are shown are very noisy, and sample sizes are not huge, raising concerns that the tests are underpowered;
The authors conduct tests based on data-collection which is not detailed in their methods, raising concerns about p-hacking.

And now, the 2005 paper!

Right off the bat, this paper cannot possibly replicate the findings of the Wedekind (1995) paper, because Wedekind et al found significant preferences for dissimilar MHC odours in women not taking the pill, and significant preferences for similar MHC odours in women taking the pill. In this study:

  [...] we did not distinguish between, in our statistical analysis, women who were taking oral contraceptives from women who were not.

  [...] Nine female participants (31.03% of female subjects) were taking oral contraceptives.

Sample sizes are smaller than Wedekind 1995 in terms of number of participants, but larger in terms of number of contrasts, because this experiment had two different sample types (sweat odour and urine), and had men smelling women as well as women smelling men. Within-individual effects are not modelled, so there is a potential for (e.g.) a small number of generically good-smelling individuals with rare MHC alleles at the population level to bias the analyses - whereas this potential bias was accounted for in Wedekind by performing within-individual correlations. The sample-sizes look like this:

The analysis was a series of Chi-squared tests, for data collected in four different sessions: one with men smelling female urine, one with men smelling female body odour, one with women smelling male urine, and one with women smelling male body odour. All chi-squared tests returned non-significant results with the exception of women smelling male body odour, for which the Chi-squared table looks like this:

So, this study didn't find the same result as the Wedekind study, but then, it couldn't find the same thing as the Wedekind study because of the way the analysis was performed, so that is no surprise. The authors claim that they found a significant effect of MHC relatedness on odour perception, but only in the proportions in the hard-to-interpret 'indifferent' response category. I am inclined to disagree. The authors presumably conducted 16 contrasts (a test of independence and three goodness-of-fit tests in each of four treatment types), and found one instance of p < 0.05. I would argue that the one 'significant' result is best explained as a failure to account for multiple comparisons.

Ending notes

If these two papers were the only things that had been published on MHC-directed mate preferences in humans, I would be far from convinced that the claimed effects were real.

however...

These are far from the only papers on the subject of MHC-driven mate-choice in humans. Wedekind and Füri (1997) conducted an analysis with very similar experimental design to Wedekind et al (1995), but arguably better statistical analysis, and found the same direction of association as Wedekind et al (1995), albeit still with a fairly high noise-to-signal ratio. Subjectively, this goes a reasonable distance towards making me think that the findings of Wedekind et al (1995) were not just a statistical fluke. I'm still not utterly convinced, but certainly more convinced than I would be if Wedekind's final paper on the topic had been the 1995 publication.

MHC-driven mate-choice has also been investigated using facial preferences and mate choice surveys. The combined evidence (across odour preference, facial preference, and mate choice surveys) is reviewed in Havlicek and Roberts (2009).

I have seen many studies on that matter, but I am far from convinced that MHC really effects mate choice. Reasons for this are the following:
 - iayork mentioned it already, the premise for the studies about mice mate choice has been disproved.
 - In population level, almost every one of the studies find no evidence to support MHC based mate choices in general population.
 - Perception studies done in the area have what I consider serious problems in replicating the results. For example, wedekind's both studies feature same smellers and t-shirt wearers, but their answers are not the same as in the first study.
 - The latest perception study cannot replicate wedekinds results and the methods are almost the same.

So we have a hypotese, which has lost its original premise (mice mhc based mate choices), first studies doesnt replicate the results with same individuals, there are only couple of population level studies that suggest disassortative mhc mate choices and the latest study cannot replicate the first two perception studies.

On an individual level, these studies are kind of silly. If the effect is true, how can you discriminate between partners who are dissimilar or similar, if you would score them 5/10 or 4/10. The same applies to the brazilian study: your probability of percepting your partner as indifferent or unpleasant changes based on your HLA-similarity from 50% to 60% in different scenarios. Your overall chance of being 2-3 HLA-similar with this sample is about 10%.

I am just worried about these studies as media picks them up. Some people may come up with anxiety over their partners smell, which is quite silly because with over 50% probability you may be completely dissimilar with your partner regarding HLA, but one still perceives his/her odour as indifferent or unpleasant.

bshane and iayork, do you have any comments of the subject at hand?


codon optimization / enzyme active site improvement Does one necessarily have to use de novo synthesis of DNA when attempting protein expression improvement by codon optimization? Or are there other ways?

e.g. Say the gene coding for the enzyme needed to synthesize a certain secondary metabolite is known & sequenced already. The standard cloning approach is to extract mRNA from (say) plant tissue, then construct a cDNA library & express it in E Coli using a suitable plasmid.

Now if the neucleotide sequence needs to be modified (to increase expression) does one have to start de novo or is there easier ways that can start from the mRNA / cDNA?

A variant of the same question is when I'd want to modify the gene because a protein docking study shows some ways to modify the active site of the enzyme by changing a residue or two in the amino acid sequence.

Kind of an old post, I'm surprised it doesn't have an answer yet.
There's no reason why you couldn't modify the RNA or cDNA directly, you just have to splice the gene correctly to make the changes you want. You're absolutely right that even a single amino acid change can have a huge difference if it's in the right spot.


DNA replication and combination "Each gamete is genetically unique because the DNA of the parent cell is shuffled before the cell divides. This helps ensure that the new organisms formed as a result of sexual reproduction are also unique."

Then why do we say that the DNA of the parent influences the characteristics of the child while the DNA of the child is formed as a combination of shuffled up nitrogenous and phosphate bases?

To explain it briefly:

Lets take a human as example, you are diploid and you have a pair of 23 chromosomes (= total 46) and the sex chromosomes which I will exclude for this explanation.

Your gamete is haploid and has therefore only one of the two paired chromosomes. So for every chromosome pair there are 2 possible chromosomes. So in total you have 223 possibilites to arrange chromosomes. The gamete from the sexual mating partner also has 223 possibilites to arrange chromosomes. So in total a new diploid organism has (223)x(223) possibilites. So unique.

However, it is always the chromosomes of the parents. So yes, parents influence the children because the genetic information of the children can be found in one of the two parents.

Furthermore you have recombination, but you already asked another question about this. So I will not expand this answer.

There are relevant articles in Wikipedia on genetic recombination and meiosis that I would recommend.

Parents influens children's characters because the shuffeling (crossing over)  changes only few genes present on the parent chromosome and also these changed gene peices are also parental so actually we recieve a non parental chromosome (generated by shuffling)but the genes present on it are still parental..  Hope this helps


Glycosidation and glycosylation I read somewhere that the function of Golgi bodies is glycosylation and glycosidation. What is the difference between the two? I searched google but it gives complex answers.

Glycosylation is a controlled process that involves a carbohydrate being attached to a hydroxyl or other functional group of another molecule. I think you meant to say glycation instead of glycosylation, and that is a random process that involves free sugars attaching to proteins.

https://www.neb.com/faqs/2015/04/10/what-is-the-difference-between-glycosylation-and-glycation


Can someone who cannot talk still whistle? Can someone who has a damaged larynx, which does not allow them to talk, still create a tune when they whistle?

I know that the larynx is what allows a person to manipulate their pitch and volume, but whistling sounds are just air making a noise as they are through the lips.

Would a person with a damaged larynx be able to whistle physically, but it would just be a toneless noise?

If this is so, is there any situation where a human would not be able to talk, but could still whistle with a tune and understand the speech of others perfectly? (i.e. having not suffered brain damage or are deaf)

Sounds such as certain phonemes are made merely with the use of air flow and movement of the lips or tongue, without the need for action of the vocal chords. Think of 'f', 's', 't', k in the English language. These are called unvoiced phonemes in phoniatrics (see the phonemic chart). Also, clicking sounds and whistling can be made without use of the vocal chords.

Yes, as long as the person is able to blow air and 'shape' it using their tongue+lips, a person can whistle; even if it means this person lacks the ability to create the vibrational patterns necessary to talk.


Biological key file format I am in the process of creating biological key software tool for use on android devices. I would like to know if there are any established file formats for storing biological key data.

Thanks

I searched a bit and could not find any such format, but I am not a specialist in taxonomy.

From what I understand, the structure you want is that of either a tree or a DAG (Directed Acyclic Graph). Both are straightforward to store in a variety of formats.

One possibility is to use a format similar to other biological data that has a similar data structure. For example, Gene Ontology is a widely used dataset that has the structure of a DAG and has a number of formats including XML listing the parents and additional data of each node in the graph. See here for their formats.

If you mean some thing like .doc .txt .rar or etc. I think there is no special bioinformatics file formats like that, for example NCBI, EMBL, Expasy and others use this common formats in transfering sequence data. BUT there is some thing called file format for introducing data to this data banks for example FASTA file format:

  >gi|5524211|gb|AAD44166.1| cytochrome b [Elephas maximus maximus]
  LCLYTHIGRNIYYGSYLYSETWNTGIMLLLITMATAFMGYVLPWGQMSFWGATVITNLFSAIPYIGTNLV
  EWIWGGFSVDKATLNRFFAFHFILPFTMVALAGVHLTFLHETGSNNPLGLTSDSDKIPFHPYYTIKDFLG
  LLILILLLLLLALLSPDMLGDPDNHMPADPLNTPLHIKPEWYFLFAYAILRSVPNKLGGVLALFLSIVIL
  GLMPFLHTSKHRSMMLRPLSQALFWTLTMDLLTLTWIGSQPVEYPYTIIGQMASILYFSIILAFLPIAGX
  IENY

As you see, a sequence in FASTA format begins with a single-line description, followed by lines of sequence data. The description line is distinguished from the sequence data by a greater-than (">") symbol in the first column. The word following the ">" symbol is the identifier of the sequence, and the rest of the line is the description (both are optional). There should be no space between the ">" and the first letter of the identifier. It is recommended that all lines of text be shorter than 80 characters. The sequence ends if another line starting with a ">" appears; this indicates the start of another sequence.
you can learn more things about these bioinformatical formats here and here.


What the name of this fish? Well saw this on a fish group on facebook. Noone can give a decent answer so I came to you guys hoping you can help us? The one who posted lives in the Philippines and he said he caught it in the river that is somewhat connected to sea.

This fish called neon velvet damsel fish (Neoglyphidodon oxyodon)

Check wikipedia


Is Chargaff's rule really applicable? Chargaff's rules states that DNA from any cell of all organisms should have a 1:1 ratio (base Pair Rule) of pyrimidine and purine bases and, more specifically, that the amount of guanine is equal to cytosine and the amount of adenine is equal to thymine.

As in the table $A \ne T$ and $C \ne G$.
So I was wondering if Chargaff's rule is really applicable?

In addition to Remi.b's answer, it should be noted that the phage Phi X 174 is the only organism in your list which significantly deviates from Chargaff's Rule (by more than 1-2 percentage points for the A-T pair). While sampling errors are indeed more likely in organisms with small genomes, there is in fact another factor in play here.

This is because Chargaff's Rule only applies to double-stranded DNA, due to the complementary base pairing that occurs between A-T and C-G. Since Phi X 174 is in fact a single-stranded + sense bacteriophage, Chargaff's Rule is inapplicable to it, since it does not obey the standard Watson-Crick base pairing that is the molecular basis of Chargaff's Rule. In fact, the Wikipedia article from which you obtained the chart states this as well:

  The following table is a representative sample of Erwin Chargaff's 1952 data, listing the base composition of DNA from various organisms and support both of Chargaff's rules. An organism such as φX174 with significant variation from A/T and G/C equal to one, is indicative of single stranded DNA.

March Ho's answer is correct. However the important thing to learn from this is that biology is not physics, and there are no rules — only observations and explanations. What Chargaff made was an observation for which he had no explanation. It was only when Crick and Watson postulated AT,GC base-pairing in double-stranded DNA that the observation was rationalized. More important, those DNAs that were exceptions to the 'rule' could be rationalized as differing from the Crick/Watson model. In the case of phiX 174 it was because it had a single-stranded genomic DNA, but one can envisage other (incorrect as it turns out) explanations in terms of modified bases that were not detected in the assay. Biology is a science of exceptions rather than rules.


Species identification - what kind of worm is this? I am finding these worms in my bathroom since summer arrived. I have been finding these on floor, walls and damp towel I left hung overnight in bathroom couple of times. When these worms are squished, a bang like sound is produced. Can you help me identifying this, is it something to be taken seriously & requires immediate action? Average length of these worms is ~ 1-1,5 inches.  Please find a closeup picture I managed to capture with mobile camera.

I moved into this house last winter so don't know previous summer history. Anyways I think I should get bathroom drain cleaned.

Edit: Just noticed it has very tiny hair thin, white/ transparent legs, many of them. These legs are barely seen with naked eye. May be they are just hair like things not legs (I don't know proper terminology).

Edit2: origin is Lahore, Pakistan. It's far from sea, open agricultural terrain. Climate is hot.

About movement, no they don't move like earth worms (shortening in length and then stretching). Neither it's snake like. It kinda straight. They also don't have legs as centipedes do, on their sides.

This is almost certainly not a millipede as it has no antennae and moves by compressing its body. My money is on insect larva, possibly a drain fly (which would make sense if you regularly see them in the bathroom).

It would be interesting if you could put one in a jar and see what it develops into.


Why has grey hair evolved? A vast majority of humans get at least some grey hair as they age. As far as I know this applies to both genders and all races. Presumably this means that at least some grey haired humans have noticeable reproductive advantage, or maybe they had it in the recent past.

Theoretically, because this feature is so prevalent, there must be a strong evolutionary pressure to keep it. Am I right? If so, what is it?

Presumably this means that at least some grey haired humans have
  noticeable reproductive advantage, or maybe they had it in the recent
  past.

No it doesn't.  Natural selection is not that strong, it doesn't optimize every single possible physical trait towards maximum reproducing.

And as others have mentioned, having lots of grey hair usually happens after reproduction is over.  Historically, lots of women did a lot of reproducing before they had any grey hair.

My theroy is that gray hair allowed a predator to pick out the weak one in the group and focus on it as a possible food source allowing the younger ones to escape and survive.

Gray hair is also a signal to a potential mate that you might not be providing young healthy genes.

Both of these could have allowed our species of human to succeed over others.


How much nucleoside triphosphate is required to form one peptide bond during protein synthesis? I'm trying to find out how many molecules of nucleoside triphosphates (ATP, GTP, UTP and/or CTP) it takes to release enough energy to link two amino acid monomers together with a peptide bond, specifically during the process of mRNA translation.

I've tried to do some research online, but I could not find a reputable source that will say definitely how much energy is consumed in the process. The best answer I could find is formulated based on 'Molecular Biology of the Cell' 4th edition by Alberts B, Johnson A, Lewis J, et al., which is that at least one molecule of ATP is consumed for every peptide linkage. Is this correct?

I've also read on a science forum that the amount of ATP consumed during translation is different for every amino acid, but I could not find a reliable source to back up that claim. Is this true?

Although the question shows considerable effort to achieve clarity, the way it is phrased as:

  How many molecules of nucleoside triphosphate… [does] it take to release enough energy

still allows ambiguity, as I would not really regard the NTPs involved in protein synthesis “releasing energy”. So let us consider two reformulations of the question, as the explanation of the answers is of more scientific interest than the actual answers.

1. How many molecules of NTP are hydrolysed in the reactions causing the formation of one peptide bond on the ribosome?

  Answer = 3

Formation of each peptide bond involves a cycle consisting of the introduction of a single new aminoacyl-tRNA to the A site of a ribosome carrying a growing polypeptide chain (or initiator tRNA for the first peptide bond), the peptidyl transferase reaction, and than translocation of the extended peptidyl-tRNA from A- to P-site. (See, e.g. Berg et al. online — Ch. 29)

1 ATP is hydrolysed in the aminoacylation reaction:

                Amino Acid + tRNA + ATP → Aminoacyl-tRNA + AMP + PPi

1 GTP is hydrolysed in the aatRNA binding reaction catalysed by EF-Tu/EF1.

1 GTP is hydrolysed in the translocation reaction catalysed by EF-G/EF2

No NTP is consumed directly in the peptidyl transferase reaction — the energy for bond formation comes from the ‘activated’ aminoacyl-tRNA.

2. What is the total energetic cost in molecules of ATP for the formation of one peptide bond?

Here one might argue that:

  Answer = 4+

The additional ATP occurs if one considers the total energetic cost of the aminoacylation reaction as 2 ATP, not 1 ATP. This arises from the fact that the ATP is hydrolysed to AMP (+PPi) and not ADP. Recycling of the AMP involves first the use of 1 molecule of ATP in the adenylate kinase reaction to produce ADP:

                                 ATP + AMP ⇄ 2ADP

followed by the energy (from membrane ATP synthase) to regenerate ATP from ADP:

                                 ADP + Pi ⇾ ATP

Why 4+? Certain amino acids (e.g. val and ile) are sufficiently similar to one another that the aminoacyl-tRNA synthetases have evolved a proof reading capacity, in which any incorrectly aminoacylated tRNA is hydrolysed. This only occurs for certain amino acids and at a rate that is difficult to determine, so the wastage of the ATP in this manner cannot be calculated precisely.

First, during the initiation of translation, a small ribosomal subunit binds to a molecule of mRNA. In a bacterial cell, the mRNA binding site on this subunit recognizes a specific nucleotide sequence on the mRNA just upstream of the start codon. An initiator tRNA, with the anticodon UAC, base-pairs with the start codon, AUG. This tRNA carries the amino acid methionine. And then, this process need one molecular GTP, and GTP--->GDP+Pi, which can provide energy for the assembly.
You can find more details in the book Campbell Biology, by Reece, Urry, et.al..


What is this Californian shrub? I spotted this shrub-like plant in California, USA.

Almost definitely not a CA native.

It looks like a coleus to me -- cultivars are pretty diverse but typically have variegated leaves with some amount of purple coloration.

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

It is Bouganvillia. If you have pets you don't want one even if your neighbors have pets. When the flowers drop they get all over the place and if they get into any food or water source for pets they will slowly die from the Poisonous oils that seep out of the flower. Other than that they are a very easy vine to grow and easy to train.


Why do people have antibodies against other blood types? The ABO blood type divides each blood type according to whether they have the "A" and "B" antigen(s) (AB has both, O has none). People also have antibodies against the antigens they don't have (AB has none, O has both), even before they have ever come in contact with those antigens.

Why do people have antibodies against these antigens they have never come in contact with? This isn't the normal situation for the immune system (e.g. for a virus or the blood type rhesus factor)

According to the Wikipedia entry for the ABO blood group system:

  Anti-A antibodies are hypothesized to originate from immune response towards influenza virus, whose epitopes are similar enough to the α-D-N-galactosamine on the A glycoprotein to be able to elicit a cross-reaction. Anti-B antibodies are hypothesized to originate from antibodies produced against Gram-negative bacteria, such as E. coli, cross-reacting with the α-D-galactose on the B glycoprotein.

The cited reference is Van Oss, CJ (2004) Letter to the Editor: "Natural versus Regular Antibodies The Protein Journal 23:357, available here. This source contains this statement:

  ..."we have known for more than four decades that these bloodgroup (antibodies) arise out of minor infections occurring very early in life..."

The cited references are:
Pettenkofer et al. Z. ImmunForsch. 119: 415-429
Springer, GF (1960) Klin. Wschr. 38: 513-514

Unfortunately I have access to neither of these articles, and besides they are presumably written in German.

I am posting so long after the initial question as I replied to a more recent similar question that was marked as a duplicate. On being redirected here I was surprised at the answers as the question (and certainly that of the supposed duplicate) did not give any indication that he was aware that the situation for non-compatible blood-group antigens was any different from any other foreign antigens. I think it appropriate, therefore, to append the following (@KennyPeanuts has also commented in this vein) for the benefit of those unfamiliar with the idea of clonal selection.

To put it simply, clonal theory of antibody selection assumes that the antigen-specificity of antibody-producing cells is random, so that all types of specificity will exist. On encountering an antigen a particular cell will be stimulated to divide and hence allow the production of a greater amount of antibody against the antigen.

Immune tolerance requires that cells producing antibody against self antigens be eliminated at some stage. Hence people of blood group O, lacking blood-group antigens A and B, will not have become tolerant to them, and will have antibody-producing cells capable of producing antibodies against them, should they encounter them in an incorrect blood transfusion.


How do plants get their O₂ for respiration during the night? If I am not mistaken the stomata are closed during the night. As a result I have a hard time to imagine how the plant can get the O2 it needs for respiration during the night. I thought the plant could produce the O2 internally through some chemical reaction. Such reaction might include splitting H2O absorbed through the roots in two. Or maybe the O2 diffuses well enough through the plant tissues.

How do plants get their O2 for respiration during the night?

Not all plants have their stomata closed during the night. A notable exception are Crassulacean acid metabolism(CAM) plants that keep their stomata closed during the day and open it during the night. This is a common evolutionary strategy with Xerophytes.

There are also 2 other types of metabolic pathways namely C3 and C4. As a consequence we get what is called a C3 and C4 plant, which aptly represent the predominant metabolic pathway it employs.

Additionally plant cells, like all life, can produce energy without oxygen by Glycolysis. Furthermore, when stomata is closed, oxygen respiration is restricted, not blocked entirely. Finally it might be important to note that plant metabolism is reduced during the night.

Full disclosure, I am not a botanist. Please let me know if there are any glaring errors.

Yes,each one of you are correct as there are many ways in which plant can get O2 as plants respire not only by leaves but also by stems and roots which help it to get oxygen present in soil and near surface,and other than that they have photolysis.


How is there no limit to a human lifespan again? It's probably just misconstrued pop science, but I thought a read an article recently that said there's no known limit on how long humans can live. I could have sworn though that there were a few automatic processes that took place though, like that the chromosomes all shorten in length every time they're copied (is there any limit to that? Also, why does that matter?), the retinas in the eyes harden, the metabolism slows down, the heart muscles wears out, etc.
So, how could it be true?

You're probably reading about the recently-published responses to a publication that argued there is a limit to human lifespan.

The original article is Evidence for a limit to human lifespan, and in the June 29 issue of Nature there are five responses to it:

Contesting the evidence for limited human lifespan
Many possible maximum lifespan trajectories
Is there evidence for a limit to human lifespan?
Questionable evidence for a limit to human lifespan
Maximum human lifespan may increase to 125 years

Each of these responses has, in turn, a reply from the original authors.

The arguments turn on fairly intricate details of statistical analysis and database interpretation, and I think it's fair to say that outside experts remain unconvinced either way -- neither the original article, nor any of the five responses, nor any of the five responses to the responses, presents a slam-dunk case for or against a limit to human lifespan.

There will be no "limit" to human lifespan, if for humans the "survival function" $l(x)$- the probability, for all subsequent ages $x$, that a newborn will still be alive at age $x$ - never hits $0$, but only asymptotes towards it. (The survival function is estimated by the fraction $l_x = \frac{N_x}{N_0}$, of a group of newborns, who in a cohort study are seen to still be alive at age $x$. For finite cohorts the fraction surviving of course will eventually hit $0$, when the last member dies, even if the idealized survival function does not.)

This is the case for "Gompertzian" survival functions, where $l(x)$ decreases super-exponentially, rapidly approaching but never hitting $0$.

(Gompertzian survival functions are more usually described in terms of their age-specific, instantaneous relative rate of decrease [the survival function's slope at age $x$, divided by its height at age $x$, times -1], which is also called the hazard rate or force of mortality $\mu_x = - \frac{{N'}_x}{N_x}$. For Gompertzian survival functions, the force of mortality grows exponentially with age.)

Human survival functions are roughly Gompertzian throughout most of adult life, although the force of mortality's growth may decelerate in very late life.


For how long can a person drink sea water? How long could a person of lets say 18 years be able to drink sea water without getting too much into trouble ? Or can a person drink it without noticing that it is a very bad idea ? I don't mean in just 1 drink session but like can one manage a day or two ? Can one drink it and go to sleep and be still healthy (although very thirsty) in the morning ?

(this is just a hypothetical question, I'm not a scientist at all, I'm not sure what tags to use actually)

Additional brainstorming:

kidney failure
any other organ failure
dying of thirst
...

(source: free.fr)

Alain Bombard

He is a french biologist who voluntarily tested how many days a man can survive drinking seawater and how?

Biologist point of view

Sea contains ~3.5% of salt$^1$. Our kidney separates the waste from water and excrete them in urine provided the salt content is less than ~2%.$^2$
So, it will take the water already present in the body. Causing excessive thirst and dehydration, eventually cause death.

Alain's Experiment

  Just one spoon of seawater at 20 minute intervals, drinking very
  slowly and letting the saliva in your mouth reduce the saline in the
  water you have swallowed.

Though he survived 65 days (From and including: Sunday, 19 October 1952
to Tuesday, 23 December 1952, ~4,400km) of his journey and lost 25 kg of weight, this result is never successfully reproduced.

Source:

http://oceanservice.noaa.gov/facts/whysalty.html
http://paradise.docastaway.com/drinking-sea-water

https://www.bbc.com/news/world-asia-45623130

This guy did it for 49 days involuntary .


Can you be immune to a coronavirus? Can one be immune to the new coronavirus?

Another question is what is the exact definition of "being immune". Does it mean that even when the virus enters my system, it cannot multiply?

It is hypothesized that exposure to and recovery from SARS-CoV-2 (as with other coronaviruses in humans) would generally result in short-term immunity to this strain, but we do not yet have data on this:

However, according to Dr Stephen Gluckman, an infectious diseases physician at Penn Medicine and the medical director of Penn Global Medicine, who spoke to the outlet, it seems likely that having the disease once results in immunity in most individuals - as is seen with other coronaviruses.
“Coronaviruses aren’t new, they’ve been around for a long, long time and many species - not just humans - get them,” he explained. “So we know a fair amount about coronaviruses in general. For the most part, the feeling is once you’ve had a specific coronavirus, you are immune. We don’t have enough data to say that with this coronavirus, but it is likely.”
This means that people who initially recovered are more likely to relapse rather than get reinfected with the virus.
According to one study, people with mild infections can test positive for the virus by throat swabs “for days and even weeks after their illness”.
But, that doesn’t mean it isn’t possible to contract the disease again, especially in those who are immunocompromised.
“The immune response to Covid-19 is not yet understood,” the Centers for Disease Control and Prevention (CDC) explains. “Patients with MERS-CoV infection are unlikely to be reinfected shortly after they recover, but it is not yet known whether similar immune protection will be observed for patients with Covid-19.”

Coronavirus: Can You Get Covid-19 Twice Or Does It Cause Immunity?

It is also hypothesized (in humans) that previous exposure to coronaviruses may enable immunity to certain other highly related strains:

These data indicate that challenge immunity to coronaviruses is strong, but highly virus strain-specific.

Virus strain specificity of challenge immunity to coronavirus., Archives of Virology (1989)

But these are all examples of adaptive immunity - not innate.

The CCR5-Δ32 mutation (2 deletions) which interferes with HIV might offer "immunity" to the virus causing the pandemic. -- This was the mechanism the experimental CCR5 antagonist Leronlimab (IgG4 mAb) may have accomplished with Covid-19 for several patients.


Do skin mites reproduce on human face during night? I've seen this circulating on social networks:

I was wondering to what extent is it true. Do skin mites really get on the skin surface to reproduce? Why is it so?

Yes, it is true that these mites exist on healthy human skin, on >98% of people, no matter the country or hygiene.

However, I'm sorry to say that this photograph is not the follicle mite Demodex folliculorum. This image has been widely circulated around the internet as Demodex, but it is actually the head of a silkworm, Bombyx mori. The above version has been modified slightly from the original, but you can see the original here: https://www.sciencephoto.com/media/720736/view/silkworm-head-sem

And here is a zoomed out version of a silkworm: https://macrocritters.wordpress.com/2012/11/26/photographing-down-the-food-web-silkworms-bombyx-mori/

You can find a real close-up of Demodex here: https://www.sciencesource.com/archive/Demodex-folliculorum-(SEM)-SS2367855.html

Not only do skin mites have sex on your face, but my suspicion is that -- quite often -- they're having INCEST on your face. (I.e., brothers inseminate their own sisters.) Admittedly, I'm not sure about the Demodex species that live on humans, but I know that among mites as a general group, there are various species that have evolved genetic mechanisms to make brother/sister mating less harmful than it would otherwise be.

And if you're a tiny, slow-moving creature that is unlikely to travel more than a few centimeters from the spot where you and your siblings hatched out, the odds of meeting an "unrelated" mite -- say, third cousin or farther -- are not very great. Most of your potential mates are likely to be genetically close kin; and sometimes, a sibling may be the only option. Beggars can't be choosers, any port in a storm, etc.