Had there been a non-flying pterosaur? Since there are non-flying birds and secondary non-flying insects, it is reasonable to assume there were also non-flying pterosaurs.

Well, according to this source there are no flightless bats, so it isn't an absolute that all flying clades have flightless members:

https://pterosaurheresies.wordpress.com/2011/07/21/meet-the-first-flightless-pterosaur-sos-2428/

  Everyone knows about the various flightless birds: the penguin, the dodo, the ostrich… the list goes on. There are no flightless bats. And no one has ever discovered a flightless pterosaur… until now.

But the short answer to your question is: no confirmed flightless pterosaur fossil seems to have been discovered so far.

The longer answer is: from what I can tell no pterosaur has been found that was clearly flightless, but pterosaur flight isn't well-understood in the first place so there is debate as to how and whether some specimens could have flown. It seems to be the consensus so far that they did fly however (based on the lack of mention of flightlessness on the Wikipedia page, and the last paper I link to in this answer is fairly convincing).

As far as not finding flightless specimen, the above link claims to have found one but the source is not reputable and I found no confirmation of it elsewhere (Wikipedia confirms, and I'm usually all about Wikipedia but here the page has all the hallmarks of having been written by the same person who wrote the blog). The same author argues a large pterosaur is flightless here, but their arguments are quite poor compared to others made in the field and they seem again to be the only ones making them.

Here is a post from Tetrapod Zoology in 2008 imagining what a flightless pterosaur might be like, and also claiming none have been found:

  Long-time readers will know that I am an unashamed fan of both speculative zoology, and of Dougal Dixon’s hypothetical ‘alternative’ animals. Inspired by a comment made here in August by Jenny Islander, I have been having a re-think about the possible evolution of flightless pterosaurs: the fossil record gives no indication that such animals ever existed, and maybe they didn’t, but that hasn’t stopped people from speculating.

A similar quote from the 2004 book "Posture, Locomotion, and Paleoecology of Pterosaurs":

  So far, there is no example of flightless pterosaurs.

The Wikipedia page for pterosaurs makes it clear how hard it is to figure out how pterosaurs flew.

Here is one of the main arguments that the largest pterosaur Quetzalcoatlus northropi was flightless

  The estimated mass for the largest pterosaur known, Quetzalcoatlus northropi, exceeds the previous highest estimates by more than 100%, and it is argued that this extremely large pterosaur is better interpreted as a secondarily flightless form.

And an argument that the largest pterosaurs would have been flightless based on a comparison to modern oceangoing birds:

  Our result therefore casts doubt on the flying ability of large, extinct pterosaurs. The largest extant soarer, the wandering albatross, weighs about 12 kg, which might be a pragmatic limit to maintain a safety margin for sustainable flight and to survive in a variable environment.

This paper summarizes the debates and argues against those assessments (the whole paper is worth reading actually):

  While the conclusions on giant pterosaur flight by Chatterjee and Templin [19], Sato et al. [17], Henderson [25] and other workers using avian analogues for pterosaurs are not without merit, we find that they leave themselves open to criticism by not considering alternative data sources when making inferences about the palaeobiology of extinct animals. Giant pterosaur anatomy, functional morphology and, in the case of Pteranodon at least, sedimentary context all indicate that they were flighted animals and, likewise, clear anatomical distinctions between birds and pterosaurs indicate that only basic mechanical details can be treated interchangeably.

Two more flightless pterosaurs have been discovered.

Alcione is a flightless nycotosaur.
http://reptileevolution.com/nyctosaurusUNSM.htm

PIN 2585/4 a flightless unnamed anurognathid
http://reptileevolution.com/jeholopterus-CAG.htm


Do animals get Post Traumatic Stress Disorder after escaping from a life threatening situation out in the wild? Can animals come down with PTSD in the wild by themselves? For example, would a gazelle that nearly pulls away from a cheetah at the last second and heard the cheetah's jaws clamping down at air right behind it's tail, show symptoms of stress and anxiety after the event?

And if not, why can we as humans succumb to these kinds of disorders, and not animals in the wild?

Peter Levine speaks to this in his book, "Waking the Tiger:  Healing Trauma".  Most animals in the wild which experience a trauma through natural species interactions will go through a sequence of recovery stages.

First, when the trauma or death is considered inevitable, the animal will "faint", losing sensory awareness and consciousness. If the trauma or death is averted, the animal will then partially waken out of that faint, and "shake off" the trauma.

This "shaking off" looks remarkably like an epileptic fit, but when the movements are analyzed, they are a muscle-twitch repeat of the sequence of movements that animal took from the time it realized its hazard to the time it fainted. It is this same muscle-twitch capacity which allows human athletes to practice their skills both mentally and physically, without moving from one spot.

Once the "shaking off" is complete, the animal is able to rise and continue its life activities without any longer-term impacts such as PTSD.

Neurologist Dr. Robert Scaer has an explanation for this lack of PTSD.  Lasting trauma is only taken on when the "victim" experiences repeated episodes of the same kind of helplessness and hopelessness.  We humans are very good at giving ourselves and other species repeated episodes of helplessness and hopelessness, and animals which interact with us often pay a price in PTSD.

In short, yes. It is not the same disorder we as humans suffer from, as our brains are much more advanced and more of our brain is affected. Species of animals such as elephants and chimpanzees, found to have many social and neurobiological similarities with humans, have been found to suffer from this disorder.

PTSD describes anxiety based responses from witnessing life threatening responses. Animals are used quite often when it comes to studying the effects of certain events on a human's life, and many experiments have proved that they do, indeed, suffer from this disorder.

According to this, experiments have been undertaken to replicate torture, loss of a family member, and incarceration humans are exposed to during wartime.

Most elephants in these experiments have suffered from not just PTSD, but from many different stress disorders in captivity. They have been wrenched from their natural environment in which the communities that made up their lives previously are not there to comfort them.

It may be that wild animals can suffer from PTSD for a while, but most likely not for their full lives. Lone animals may suffer from this a little bit more than, say, an elephant in a herd will, so it is entirely possible that they can experience it.


Current along an axon When an action potential is induced on a neuron, the local transmembrane potential jumps from $E_{\mbox{rest}}$, the resting potential of the neuron, to $E_{\mbox{eq}}$, the equilibrium potential of an ion or group of ions in the vicinty. Current thus travels in and out of a part of the neuron's cell membrane as ions are exchanged during an action potential. This effect repeats itself as the neighboring regions of the membrane are depolarized, causing the action potential to propagate along the neuron's axon.

Take $\Delta Q$ to be the total charge exchanged locally during an action potential, $C$ to be the membrane capacitance, and $\Delta t$ to be the duration of the action potential. While we can approximate the local average current through an neuron's membrane by taking $$I = \frac{\Delta Q}{\Delta t} = C\frac{\Delta V}{\Delta t} = C\frac{E_{\mbox{eq}} - E_{\mbox{rest}}}{\Delta t}$$ Is there a way to approximate current traveling along the axon of the neuron? Is there even such a thing?

As far as I was able to find there exists two models of the action potential by using RC circuits. Do note that there is no flow of electrons per se across a tube, but rather a migration of potential. See this.

The Hodgkins Huxley model :

  The Hodgkin–Huxley model, or conductance-based model, is a mathematical model that describes how action potentials in neurons are initiated and propagated. It is a set of nonlinear differential equations that approximates the electrical characteristics of excitable cells such as neurons and cardiac myocytes, and hence it is a continuous time model

http://en.wikipedia.org/wiki/Hodgkin%E2%80%93Huxley_model

The Fitzhugh-Nagumo model:

  The FitzHugh–Nagumo model is a simplified version of the Hodgkin–Huxley model which models in a detailed manner activation and deactivation dynamics of a spiking neuron. In the original papers of FitzHugh, this model was called Bonhoeffer–van der Pol oscillator...

http://en.wikipedia.org/wiki/FitzHugh%E2%80%93Nagumo_model

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

Hodgkin, Allan L., and Andrew F. Huxley. "Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo." The Journal of physiology 116.4 (1952): 449-472.

Now, I have not dealt with differential equations in quite a while, and hence may not be the best source for explaining the model itself, but I'll try and update the post with what (if anything) I understand.

The electrical impulse through the axon is a transverse wave of ions moving in and out. There is no net change in charge to the axon itself.  It isn't an electric current at all; it is a transverse chemical wave powered by electric charges.


Why aren't plants' roots as diverse as leaves? I have been doing some gardening recently and I suddenly realised that all plants have superficially identical non-woody roots of the same size from gigantic trees to small fruiting plants and vegetables. They are all white, no more than 1 mm across, long and flexible with no distinguishing marks. Only when the root start to become woody do they become different in appearance.

Leaves are very diverse even when they have just started to grow, i.e. before they have reached their full size. I can recognise many different plants from their smallest leaves alone but I wouldn't be able to differentiate plants by looking at their roots. So why aren't roots anywhere near as diverse as leaves?

To answer this type of question, we should start by defining 2 concepts: the functions of the root and the external condition that brought to a specific evolution.
Evolution is a necessary process to all organisms, which evolve to optimize a specific function and to better adapt to the external conditions.

There are 3 main and common functions between all land plant's roots: fix plants to the soil; absorb water and minerals; establish specific relationships with other organisms, principally fungi and bacteria. The external conditions of roots (soil) are quite stable, even though, the different "physical" composition of soil, that is the quantity of sand, clay and rocks, change the physical appearance of size and proportion between the main and the lateral roots.Therefore it is plausible to say that it is not necessary to have a great variety in root's structure; since all roots must carry out same functions, all plant's root underwent a similar evolution.

For the leaves it is a bit different. Leaves must also carry out specific and common functions, as: exchange gas (CO2 and O2); contain photoreceptors to "absorb" light for photosynthesis. However, the external conditions of leaves are shortly and continuously changing and highly different (consider the vary regions of the world, as desert and rainforest) with reference to roots. Therefore each plants underwent evolution depending on these types of external conditions, so as to, of course, optimize their functions but at the same time protect themselves as much as possible. Consider, for example, the intensity of sun's radiation, which, if too strong, can destroy cellular structures, the quantity of CO2 in the air, or the high biodiversity of insects, which can carry diseases, ecc...

Interesting book about evolution is: J.C. Harmon, S. Freeman, "Evolutionary analysis", where it is given an idea of the type of evolution, different species, could undergo.
(hope my english is not too bad)

I originally listed two reasons for the relative lack of diversity among roots - the substrate and roots' primary function, transporting water and nutrients. After giving it more thought, I've expanded the list to four reasons.

1. SUBSTRATE - Burrowing animals are far less diverse than animals that live aboveground; note the remarkable similarity between moles, golden moles and marsupial moles - all unrelated. The obvious reason is that they're adapted to living in soil. Roots are similarly constrained by their environment. It's hard to imagine a giant palm leaf growing underground.

2. UNIFORM ENVIRONMENT - Leaves experience light and dark, daily temperature fluctuations and even greater seasonal fluctuations. They may be pummeled by high winds, hail and fire. These variables may influence leaf evolution in many different ways. In contrast, roots grow in an environment that is always dark, relatively protected from wind, hail and fire and relatively stable temperature wise.

3. FUNCTION - Aside from anchoring plants, roots' primary function is transporting water and nutrients. The optimum shape for this is round, similar to the veins in our bodies and the plumbing in people's homes. Rectangular roots or roots shaped like maple leaves make no sense.

4. PREDATORS - A wide variety of animals feed on leaves, which may evolve defenses against predation. For example, a cactus' spines are modified leaves that are widely believed to serve as defenses against animals in search of a juicy cactus. In contrast, relatively few animals feed on roots. There are a few species that dig for roots, and some burrowing animals feed on roots, but virtually no wild primates or ungulates feed on roots.

In summary, leaves grow in an environment where they are less constrained and less protected by the surrounding substrate and are exposed to a far greater variety of environmental variables and predators.

As far as color goes, I don't see much difference; most roots are whitish or brownish, while most leaves are green. Of course, leaves of some species do change colors in the fall, when temperatures begin to decrease. But, once again, roots are relatively insulated from the cold, especially if the ground is covered with a blanket of snow.


Why does replication require primers while transcription does not? In transcription, there is no need for any primer. I guess the basic mechanism of DNA polymerase & RNA polymerase is the same. So why does replication have the need for a primer?

I'm no expert at transcription but from what I can figure out here and here transcription requires a promoter region acting as a template-directed mechanism for allowing transcription, which presumably bear a certain sequence recognised by the RNA polymerase and associated complexes. However DNA polymerase requires primers to guide it to the correct location on DNA.

EDIT: In light of comments below, according to here and here, RNA polymerase is capable of de novo synthesis meaning it is capable of initiating synthesis of RNA without primers and this is done by RNA polymerase binding to two nucleotides rather than nascent RNA polymer and a single nucleotide. Initiating nucleotide hold RNA polymerase rigidly in place, facilitating chemical attack on the incoming nucleotide. For bacteriophage T7 RNA polymerase, transcription begins with a marked preference for GTP at the + 1 and + 2 positions. DNA polymerase cannot add primers, and therefore, needs primase to add the primer de novo.

In replication you have 2 strands made.
In transcription you have 1 strand made.

Transcription uses ONLY the 3' → 5' DNA strand.
This eliminates the need for the Okazaki fragments seen in DNA replication (on the lagging strand).

And it removes the need for a RNA primer to initiate RNA synthesis, as is the case in DNA replication.

Edit; instead RNA Polymerase binds to Promoter region to initiate transcription, in replication (leading strand) DNA uses 1 Primer to initiate. And as AMR comment, RNA Polymerase dont need to add nucleotides to existing part.


What characteristics do living organisms (like humans or plants) have that viruses don't? I am not too sure if viruses are considered living organisms.

I learned that living organism:

-Change their size
-Reproduce
-Heal themselves
-Need energy (by eating)
-React to the environment
-Have a lifespan
-Made of at least 1 cell (some exceptions)

Which features that are listed are not in viruses?

If I need to be more clear, please tell me as I'm not very good at explaining.

Linving organisms have intricate metabolic pathways that viruses donot have viruses stay in equilibrium till they infect host meaning that they they donot exachange matter and energy with surronding when they are outside the body but is a property shown by humans and living organisms.


Which mushroom species is this? Which type of mushroom is this? Hope the image has enough quality to allow answering the question.

Following community rules...

Images: please find below
Location: West-Northern Germany
Size - about 7 cm height, 5 width
Prior research: very hard to undestand which species is this, therefore asking here. Maybe this could be a Gymnopus peronatus - but here the stem is darker.
Specific characteristic: hollow stem

You are probably right that it is a Gymnopus, It's difficult to know which one. There's also Gymnopus Fusipes. For a difficult ID, it's best to have a cross section, a description of the scent, compare the color under the youngest specimens, as the gills often change from very light to very dark with age.

It has characteristics of a Chantrelle ; I would start there to identify it. Chantrelles are usually more orange or yellow but I have mushrooms in my yard that look very similar to the picture and after checking several references I believe it is a Chantrelle .


Is it common to have multiple recessive traits in humans? I just started thinking about my phenotype and realized I got multiple recessive traits. I have attached ear lobes, my blood type is O-, I got green eyes (I think eye color in polygenic but still somewhat recessive), a few years back I was in the control group of a study that was looking for a link between an allelic variant and the development of diabetes mellitus in patiences with another disease I forgot which, I was the only homozygous among all control patients! so you get the point. I am just wondering if anyone has any notion of how often humans present multiple recessive traits, maybe in terms of allelic frequency or something like that, or where can I find information about it. And maybe if there is something health related that may be worth knowing. I mean apart from a minor allergy I'm a really healthy person, but I may have predisposition to something.

It depends on how long a population in your dominant heritage was genetically isolated, how common certain recessive traits are.

However, you might reconsider about the "green eyes".  Iridologists claim that there are only blue eyes, and light brown eyes.  All other colours are indicative of bioaccumulation of various substances (evidenced by a return to blue or light brown when the body is supported in excreting these substances), and health issues in certain tissues.

While there is argument about how scientific a technique iridology is, all medicine begins as observation of patterns, and development of models based on those patterns.  Models in medicine are constantly undergoing upgrading and replacement, as old models no longer explain new and well-observed patterns.


What material is permeable for plant roots, but "impermeable" for fungi & bacteria? I'm designing an experiment where the roots of the plant will grow in a sterile environment while the shoot will grow in a non-sterile grow room. For this reason the environments of the shoot and the root should have some form of physical separation.
Is there any material that allows roots to grow through it but will stop fungi and bacteria?

I might have found a solution! Kuijken et al. (2015) first germinate seeds in a sterile eppendorf filled with agar and nutrients. They then cut off the bottom of the eppendorf and stick it through the lid of a sterile plastic jar and pad it with sterile cotton. So I guess they are using the agar as a material that is permeable to the roots and "impermeable" to bacteria and fungi.
Kuijken, R. C., Snel, J. F., Heddes, M. M., Bouwmeester, H. J., & Marcelis, L. F. (2015). The importance of a sterile rhizosphere when phenotyping for root exudation. Plant and Soil, 387(1-2), 131-142.

I suggest using an inorganic substrate (soil) and drip irrigation with a solution of 300 to 1000 ppm hydrogen peroxide. Peroxide is a well-known antiseptic and in these concentrations are not likely to damage root tissues. I do use peroxide in these concentrations for control of fungus in my garden and immerse roots in it when repotting bonsai and other potted plants. Furthermore there is a commercial broad spectrum fungicide preparation sold under the brand name Zerotol. However, all these applications, the existence of the peroxide solution on plant tissues is temporary/transient. I have not, however, used the peroxide solution as the sole source of plant water as I am suggesting, nor do I know of any studies of its use in this way.
I grow trees in Turface MVP, a high-fired montmorillonite clay and use only inorganic fertilizers, yet indigenous mycorrhiza spontaneously appears in my pots. Pumice is commonly used as a bonsai substrate used in association with organic fertilizers that are utilized only through bacterial action. This is to say that I don't think there is a solid growth substrate that is inherently antiseptic.


Is there a biological urge to have children in women? Searching information about this subject often leads to personal stories from women making the choice to live childfree and women stating they either always wanted to have children or experienced a sudden 'baby fever'. Often this baby fever is understood to be a biological urge.

In this article a link between hormones and the need for own offspring is made a couple of times, but also contradicted.

  In  the  context  of  evolutionary adaptedness, all women were exposed
  to babies and infants, and the ‘default’ setting for the female  body
  is  to  have  experienced  both nurturing  and  pregnancies  by  the
  early  twenties. Rotkirch therefore suggests that longing for a baby
  develops out of hormonal changes evolved to prepare women for
  motherhood. These might be triggered by falling in love; the ‘nesting’
  behaviour associated with settling down; exposure to infants or the
  aging process. Conversely, however, Kravdal has found evidence in
  Norway of a demographically significant cohort for whom reproduction
  and finding a long-term partner and ‘settling’ down’ are quite
  exclusive (Kravdal 1997).

In the same article, the effects of hormones on human intercourse and attractiveness between men and women is briefly explained. However, to me it seems that the urge to have sex is something different from the urge to have babies or to become a parent. I would like to know if there are hormones or other biological changes in women that cause something like 'baby fever' or if it is rather more of a more psychological or social environment phenomenon.

Other relevant articles are often not accessible to me or prove too difficult to understand with basic biology knowledge.

The biological urge to find a mate means that an innate desire for children is unnecessary. Having sex with a partner pretty much guaranteed children before contraception was available.

It's hard to imagine why an urge to have children would exist, but that's not the same as saying it doesn't -- but I also can't imagine how you'd be able to pull apart biological vs social pressures in such a complex and core part of being human.


Why does Helium make your voice change? When we breathe in helium and then speak, our voice changes drastically. Does it happen only due to helium or can happen if we use other gas? What factors of the gas does our voice depend on (like density, temperatue etc.)

Helium is not as dense as air, and when your vocal cord vibrate with the helium, it vibrates at a higher frequency, making your voice higher. sulfur hexafluoride Is Denser than air, making your voice deeper.


Why is human vision restricted to 400-700 nm? Across the electromagnetic spectrum, 400-700 nm is a narrow spectrum of frequencies and focused in the region of short wavelengths. For example, radio waves cover a large range of frequencies unexploited by the visual system. So what biological reason is there that evolved us to use such a small frequency bandwidth for vision?

Short answer
The visible spectrum has the highest energy in sunlight at the earth's surface, explaining the gross location of the visible spectrum in life on earth. The specific frequency range varies across species and can be explained by species-specific survival strategies.

Background
When you look at the solar light spectrum at the earth's surface the visible spectrum has the highest intensity (fig. 1).

Solar irradiation. Source: University of California.

So it makes sense to use the range of frequencies that is represented most in sunlight as a starting point.

Then the question becomes, why do humans utilize approximately 400 to 700 nm, and not infrared or UV? That can be explained because we do not need it. Our range has been hypothesized to be related to foraging behaviors and our visual system is particularly sensitive in the frequency range of the coloring of (ripe) fruits, which is thought to have been of great benefit to our hominid ancestors (Osorio & Vorobyev, 1996).

Why then do animals extend their vision into UV? Many fish, amphibian, reptilian, avian, and some mammalian species use UV vision. Many birds can identify UV-reflected nectar and berries, and UV-reflecting plumages in birds, and scales in fishes are used for recognition (Shi & Yokoyama, 2003). Moreover, some arthropod species are know to use UV vision to reduce light-reflection distortions under water, such as in the mantis shrimp that features 12 photoreceptor types (as opposed to four in humans) (Thoen et al., 2014).

Why then do animals extend their dynamic range into the infrared? A notable beneficial effect of perceiving infrared is the detection of body heat. The generation of heat is accompanied by the generation of infrared light. The detection of this emitted light is highly useful for nocturnal predators, like the rattle snake (Hartline & Newman, 1982).

References
- Hartline & Newman, Sci Am (1982); 246(3): 116-27
- Osorio & Vorobyev, Proc Roc Soc B (1996); 263(1370)
- Shi & Yokoyama, PNAS (2003); 100(142003): 8308-13
- Thoen et al., Science (2014); 343(6169): 411-3

Further Reading
1. Is our color vision calibrated to sky, vegetation, and blood?
2. Is there a physical reason for colors to be located in a very narrow band of the EM spectrum?

These wavelengths happen to satisfy two conditions.

First, shorter wavelength photons (EM radiation) tend to be dangerous for biology. Even UV light (<350nm) is already can damage DNA. That is due to the fact that bond energies in biological molecules tend to have values close to energy of short-wavelength EM radiation. These is why high-energy particles called ionizing radiation. For reference, see this paper. ionization energy for DNA estimated in 4-5eV range, which is 300-250nm.

Secondly, on low-energy hand of spectrum, water absorbs a lot of IR radiation:

So, as you can see, what we see aka visible spectrum is sitting nicely in valley of water absorption but does not extend to area of harsh UV light that will damage chemicals of your body.

Now, why is that so? Because atoms have these masses and electrons around them have these energies. So bonds and molecular interactions have these values.

(In radio range of frequencies you, opposite to UV, have not enough energy to elicit any significant molecular changes, which is why you can't perceive WiFi)


Do beneficial viruses exist? If so, what examples are there? Typically, people call viruses some kind of organic compounds that cannot reproduce autonomously and which lower the fitness of their hosts. Even the word "virus" means "venom" in Latin.

But from the perspective of natural selection, one would expect those organic compounds that cannot reproduce autonomously, but which would increase the fitness of their hosts, to be more widespread. One can see an analogy with bacteria: people are more aware of harmful bacteria and even such words as "microbe" are perceived as somewhat harmful (among non-biologists for sure). But we know that an animal body contains many more useful bacteria than harmful ones, and animals have their own microflora, which are necessary for survival.

The same must be true for viruses: those viruses which were useful (or at least unharmful) to their hosts would be passed more easily to other organisms since their hosts would have a selective advantage.

So, do such beneficial for their direct hosts viruses exist? If so, what are they called? What are the examples?

Do they exist? Yes

What are they called? Marilyn Roossinck calls them viral mutualistic symbiotes. She has an excellent review here.

What are some examples?

My personal favorite is GB-Virus C, or Hepatitis G, which appears to slow the progression of HIV using a number of different mechanisms:

  Box 1. Summary of the effects of GBV-C infection in HIV-positive individuals

  GBV-C infection downregulates HIV entry co-receptors CCR5 and CXCR4, and increases secretion of their ligands RANTES, MIP-1α, MIP-1β and SDF-1.
  In vitro GBV-C NS5A and E2 proteins inhibit X4- and R5-tropic HIV replication, and NS5A protein downregulates CD4 and CXCR4 gene expression.
  HIV-infected individuals positive for GBV-C E2 antibodies have survival benefit over HIV-infected individuals with neither GBV-C viremia nor E2 antibodies; in vitro GBV-C E2 antibodies immunoprecipitate HIV particles and inhibit X4- and R5-tropic HIV replication.
  GBV-C induces activation of interferon-related genes and pDCs.
  GBV-C promotes Th1 polarization and the NS5A protein contributes to this effect.
  GBV-C infection reduces surface expression of activation markers on T lymphocytes, suggesting its role in T cell activation signaling pathways.
  GBV-C protects the T cell from Fas-mediated apoptosis and as a result of its effect on immune activation may also play a role in protecting lymphocytes from activation-induced cell death.
  GBV-C viremia reduces IL-2-mediated T cell proliferation suggesting a significant interaction between GBV-C, IL-2 and IL-2 signaling pathways.

Endogenous retroviruses

As @mbrig recalls in the comments, there are a number of retroviruses that have inserted themselves into the germ line. Those are called endogenous retroviruses, and they interact with the host genome in a number of ways. Some are even translated:

  Proteins produced from ERV env genes have also been demonstrated to function as restriction factors against exogenous retroviral infection

Biologically, all viruses by themselves are bad.  More accurately, they have a negative effect.  They work by injecting a strand of DNA into one of the host's cells, which makes the cell produce viruses instead of more cells.  However, some viruses negative effect when paired with another virus can produce a double negative.  Unfortunately, it never quite cancels out.

To sum it up, if you have a virus, there is definitely something bad happening in your system.


Plasmid addiction system in high-copy number plasmids Are there high-copy number plasmids that utilize a plasmid-addiction system?

According to the review by Kroll J, Klinter S, Schneider C, Voß I, Steinbüchel A. Plasmid addiction systems: perspectives and applications in biotechnology. Microbial biotechnology. 2010;3(6):634-657. doi:10.1111/j.1751-7915.2010.00170.x., there are high-copy-number Plasmid Addiction Systems (PAS), "specifically the addiction system depending on plasmid‐borne ORT utilizing the lac repressor."

  The lac repressor protein (LacI) binds to the lac operator (lacO) and therefore represses the expression of the kanamycin resistance gene. When IPTG is available as an inducer, LacI is titrated by lacO, and the E. coli cells were able to grow in media containing kanamycin due to expression of the corresponding resistance gene. The same result was obtained when high‐copy‐number plasmids harbouring lacO were used for ORT. In this case the plasmid was stably maintained over 72 generations (Williams et al., 1998).

ORT = operator repressor titration

ORT is one of the three main groups of PAS.

The other answer is a good one, and I just wanted to add a quick note for anyone wondering what a plasmid addiction system is, and to add some more context to the question. This is from my Molecular Genetics of Bacteria Snyder, L. et al. book which is sitting right next to me.

"There is good rationale for plasmid addiction systems, in that they prevent cells cured of the plasmid from accumulating, and thus help ensure survival of the plasmid"[...]"therefor, it was a surprise to discover that similar toxin-antitoxin systems also occur in the chromosome. Some of these are on exchangeable DNA elements, such as genetic islands nd super integrons, and may play a role similar to that of the addiction systems of plasmids."

The example in the book is the P1 phage-encoded Phd-Doc system


Why does the seed of the coconut tree have a liquid in it? What is the purpose of water in the coconut seed?  The reason I ask this is that I was reading about coconut water and all the benefits it has for us Humans.  But why does the tree put a liquid in the seed?  I read a lot more and learned that the liquid becomes a solid and is called endosperm, which is food for the coconut tree.  I'm still not happy with that answer because all seeds are food for the plant they become.  They are also a lot more.

I have come up with a very good explanation for the existence of coconut water and I want see if anyone else has any ideas.  Remember, I am not trying to find out why there is food in the shell.  That's obvious.

It is a transitory state.

During coconut development the "milk" actually starts as a spongy solid a multinucleate endosperm. As the coconut develops it absorbs this tissue. Because of a coconuts hard structure this leaves a cavity since the coconut cannot change shape as the tissue density changes, some fluids including oils are left behind as hte tissue is broken down and reabsorbed. But this fluid will be reabsorbed as the the developing cotyledon fills in the cavity. The fluid is a by product of the cavity but the the cavity is needed due to the unusual development of the coconut.

As a side note most comercial coconut milk is actually squeezed out of the solid endosperm.

Here are two things that I have not see anywhere else in my research on the subject.

First, I will explain why coconut trees at the edge of the beach seem to "reach" toward the sea, but usually go straight up when planted away from the beach.  Then I will get to why the coconut tree puts a liquid in its seed.

The main purpose of many seeds is to to take themselves away from the parent to start a new life somewhere else (hopefully better).  Just like us humans the coconut tree wants it's offspring to migrate.  It uses the sea as the medium on which it travels.   The coconut is too heavy to move toward the sea using wind or animals. It's also too tough for most animals to be able to get the nutrition locked inside it.  So the tree, which in nature would most likely find itself on a beach, contorts itself so that it's "head" is above the sea and then it drops is seed in the ocean to travel and find a new place to grow and propagate.  That would be my reasoning for explaining the commonly seen phenomenon of coconut trees leaning over the ocean.

So now that the coconut has started it's travels into the unknown, it needs to find a place to grow.  The seed bobs up and down on the ocean until it lands somewhere.  It could land on the same island or travel thousands of kilometers and land on another island or coral atoll or a sandbar.  This is where the liquid comes in to play.  The liquid which has been moving inside the coconut suddenly stops.  After a certain amount of time the next step in it's growth is triggered because of the still liquid.  Also, the cavity in the coconut keeps it from drowning.

That's it.  The "water" is a "level" that tells the coconut when to "drop a root and send a shoot"

Let me know what you think.


What is the medical definition of death? What is the medical definition of death? And how do medical examiners determine whether a person has really deceased, as opposed to for example a condition like brain death?

Ok. So when a doctor declares a person dead, it is when their heart or brain is totally not working, and won't start working no matter what they do.

This is legal death.

If your heart stops cold, you are clinically dead. This is reversible, if you are lucky. This definition basically only exists so people can say they "died". It has no real biological significance, except for the fact that your heart is not pumping blood and providing you with oxygen. This will cause...

Biological death:
Within 5-10 minutes at room temp you have reached the event horizon of biological death. Biological death is real death.

Once this time threshold is crossed, there is almost always no going back.
This is because Cells in the brain are destroyed by oncosis, and other mechanisms and forces far beyond me.


What evolutionary reason is there for having the urinary duct and reproductive organs so close together? As the old joke goes, "God must have been a civil engineer. Who else would put a waste facility straight through a recreational area?"

But maybe it wasn't God. Is there any evolutionary reason (or background for) having the urinary duct and reproductive organs right next to each other (in both humans and many other vertebrates)?

To be clear, I'm not asking why isn't it elsewhere. I'm asking where the original "design" came from that spread everywhere.

The reason lies within our wormy chordate ancestors - an orifice used to eliminate waste can also function as an orifice to eject eggs. My vertebrate zoology is a little bit rusty so I would suggest picking up any first-course book on the subject, most of them cover the evolution of urinary/reproductive organs extensively.

Human body has three channels for excretion of substances, one for each of the three physical phases of matter: lungs for gaseous substances, such as CO2, anus for solid substances such as feces and urinal channel for liquid substances.

It turned out that sperm is liquid, so it uses the same channel as liquid urine.


Why doesn't the herbicide 2,4-D damage lawn grass? I sometimes use 2,4-Dichlorophenoxyacetic acid to control broadleaved weeds in lawns. It is selective, and quickly kills the dicot weeds, while other plants are unharmed.

2,4-D is a synthetic auxin, a class of plant hormones. It is gets taken in through the stomata on the leaves, and is transported to the meristems of the plant. This causes uncontrolled, unsustainable growth, and the plant wilts, and dies.

Why doesn't this affect most monocotyledons?

According to this link from Purdue, the seed of the answer is this:

  The herbicide is used to kill broadleaf weeds, which are dicots, while monocot grasses, such as sorghum and corn, are more resistant. That's because grasses inactivate 2,4-D inside the plant, while broadleaf dicots do not.

But on the other hand, Song 2014 has this to say about 2,4-D:

  However, the underlying molecular mechanism of how auxinic herbicides selectively kill
  dicots and spare monocots is not
  understood yet (Grossmann 2000; Kelley
  and Riechers 2007; McSteen 2010). The mechanisms of auxin biosynthesis, transport,
  and signal transduction
  are conserved in monocots and dicots make this question more complex (McSteen 2010). Early research has
  proposed that the selectivity of auxinic herbicide is because of
  either limited translocation or rapid degradation
  of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots (Monaco et al. 2002;
  Kelley and Riechers 2007). Auxin transport is influenced by plant vascular
  systems (Mattsson et al. 1999;
  Scarpella et al. 2006). The difference in vascular tissue structure between dicots
  and monocots may contribute
  to the selectivity of auxinic herbicides. In monocot
  stems, the vascular tissues (the phloem and xylem) are
  scattered in bundles, and lack a vascular
  cambium; in dicot stems, the vascular tissues are form
  ed in rings and
  possess a cambium.

So in other words, we don't know yet. It seems to be very strongly tied to auxin transport, but we do not have the full mechanism of action; since auxin is such an important plant hormone, and the pathway is therefore highly conserved (that is, the genes tend to be nearly identical on the parts of the sequence that affect the phenotype), the general conclusion is that the pathway itself is not affected, but an accessory pathway clears up auxin in levels excess of any normal amount in monocots.

Edit: Whoops, got the author's first/last names mixed up.

The specificity of 2,4 D may be due to either limited translocation or rapid degradation ,altered vascular anatomy or altered perception of auxin in monocot


Mutated cell proliferation Reading Jennifer Doudna's fascinating book on CRISPR. So she describes rare cases where a mutation in a single cell removes the gene responsible for a genetic disease. The cell proliferates and the disease is cured. What I don't understand is--aren't all the aberrant cells also still dividing and passing on the harmful mutation to their progeny? How does the single healthy cell edge out all the other cells to "cure" the patient.

There are some diseases in which a minority population of normal cells can rescue the organism, even in the presence of a majority of mutant cells.  Sort of like a group vacation to Kazakhstan with one friend who can speak Kazakh.  Very different experience from a vacation where none of you speak Kazakh.

Take for example hemophilia A.  Cells have a mutant gene for factor 8.  Without factor 8 blood does not clot properly and people have bleeding trouble.  You do not need much factor 8.  Just a little bit can prevent spontaneous bleeds.  People who are heterozygotes for hemophilia A (carriers) are fine at 50% normal.  So if you edited mutant liver cells such that they could produce factor 8, even if they were only 10% of the total cell population of the liver, having some factor 8 would sidestep the full hemophilia phenotype.

Likewise metabolic mutants - some children are born unable to handle certain substances.  Phenylketonuria is the one you read about every time you drink a diet coke.  If a minority population of cells could be produced that were able to handle phenylalanine, those would rescue these kids even if most of the cells still could not.

Are you talking about people?

Because in bacteria, a mutated bacterium with a beneficial mutation will definitely edge out the competition, or if it is in a "good mood" (cell humor lol) it will share its DNA with the other bacteria.

You're absolutely right about people, though. One cured cell won't cure the patient.


Is evolution a fact? Richard Dawkins in one of his videos says that Evolution is a fact and not just a theory.

He goes on to say that man and chimpanzees both evolve from apes.
Is this correct (Is evolution a fact and did humans & chimps evolve from apes)?

A tiny bit of terminology

Fact

In popular culture, the term fact means "something that is true". I would consider a theory as being the closest concept in science to what is called a fact in the population culture.
In natural sciences, the term fact is rarely used but would have the same meaning than the one in popular culture. The reason we are not often using this concept is that in science (nor in any other field of knowledge) one can never definitely know the truth. We can only have evidence that are congruent with a hypothesis or body of statements. In such case we talk about theory (see below).

Theory

In popular culture, "theory" is used to mean what the natural sciences call a "hypothesis."
In the natural sciences, a theory is a body of thoughts/statements that is very well supported by loads of evidence. In science, a theory is not a hypothesis. For example: Theory of evolution, Theory of general relativity, transition state theory, etc. Note by the way that various definitions of theory are in use (ref.). The below answer respects the definition that I gave above.

The scientific terminology presented above is actually a matter of philosophy and not science. If you need more information about the definitions of "theory", "fact" and other related terms, you may want to ask on Philosophy.SE. Stephen Jay Gould summarized the concepts of theory and facts nicely when saying

  [..] facts and theories are different things, not rungs in a hierarchy of increasing certainty. Facts are the world's data. Theories are structures of ideas that explain and interpret facts.

In the answer below, I am using the scientific terminology.

Your questions

  Is evolution true?

Evolution is what is called a theory in natural science (The Theory of Evolution a.k.a. modern evolutionary synthesis), and it is extremely well-supported. Evolution is NOT a hypothesis. In other words, we have a lot of supporting evidence that living beings have evolved and are evolving.

  Did both humans and chimpanzees evolve from apes?

Humans and chimpanzees are apes (great apes to be more accurate). Both humans and chimpanzees evolved (and are still evolving) from a common ancestor who already was a great ape. We have a lot of evidence to support this common ancestry.

What does the theory of evolution say?

Understanding Evolution (by UC Berkeley) is a short and introductory course to evolutionary biology. Of course, there exist other good sources of information online such as Evolution and the tree of life by Khan Academy.

We have a number of posts providing book recommendations for

General biology (Books for beginners and Introductory biology text for an outsider)
Intro to evolutionary biology (Text Book Recommendation: Organic Evolution and Introductory books about evolution)
Intro to evolutionary genetics (Books on population or evolutionary genetics?)

You will also find a lot of introductory posts on biology.SE such as for examples:

Why do some bad traits evolve, and good ones don't?
Is there a biological mechanism for evolution encoded into our DNA?
Does it make sense to classify all humans in a single species?
Why is a heritability coefficient not an index of how “genetic” something is?
How could humans have interbred with Neanderthals if we're a different species?
If dinosaurs could have feathers, would they still be reptiles?
Why does evolution not make our life longer?
Why don't mammals have more than 4 limbs?
How to define “evolution”?
How did some humans evolve to be white?
Who are humans' closest relatives, after primates?
Did cats evolve from monkeys ? or vice versa?
Why do the ancestors of birds still exist?
How does Natural Selection shape Genetic Variation?

What are the evidence?

Demonstrable and repeatable examples of evolution lists sources that list evidence. There are probably thousands of pieces of evidence listed in total, all explained in lay terms with links to the original article. Of course, this is just a small sample of the evidence we have.

The post Is there any biological evidence that is not suggestive of or seems to disprove evolution? might be of interest too.

Thanks to @CortAmmon's comment for correcting a very poorly phrased sentence.

Evolution is most real. Have a look at this Wicked Cool Phylogenetic Tree from wikipedia:

What it implies is that there is one common ancestor.

EDIT:

I remember my professor telling me that phylogenetic trees work like a cot mobile. During our lectures on phylogenetics he would on occasion pick up the chalk and make crude drawings of three fish of dissimilar sizes on the blackboard. Always three fish. He would then tell us about how the bigger fish eat the smaller fish. The way I interpreted this is that natural selection played a role in what we observe today as protein to protein or gene to gene similarities. That is what this phylogenetic tree represents. I think my professor made the analogy to mobiles not because they go in circles but rather because phylogenetic grouping can be monophyletic where an ancestor with all it's descendants are considered a group, paraphyletic where an ancestor but not all it's descendants are considered a group, or polypheltic where the common ancestor is not taken into account. I pasted this phylogenetic tree with a monophyletic view on the matter.


Why don't Australian magpies in Tasmania swoop at people? I'm currently living in Tasmania (Australia) and I have noticed that Magpies don't swoop at you here, yet they do in other parts of the country.

Just wondering: does anyone know why?

I cannot give you a proved explanation of why magpies don't swoop in Tasmania. Nevertheless, my goal here is corroborating your impression with some data, and indicating a possible cause.

Aussie Magpies and swooping

Australian magpies are not the same species of European magpies (Pica pica). Actually, they are not even corvids. They belong to the Family Artamidae, and their scientific name is Gymnorhina tibicen (synonym: Cracticus tibicen). Here is a male magpie (you can tell he's a male by the white colour in his back):

Australian magpie in Victoria

Magpies are territorial birds and in the breeding season (which is right now, as I write this, in September) a small percentage of the males become quite aggressive towards people approaching the nest.

According to the Wikipedia link above:

  These magpies may engage in an escalating series of behaviours to drive off intruders. Least threatening are alarm calls and distant swoops, where birds fly within several metres from behind and perch nearby. Next in intensity are close swoops, where a magpie will swoop in from behind or the side and audibly "snap" their beaks or even peck or bite at the face, neck, ears or eyes. More rarely, a bird may dive-bomb and strike the intruder's (usually a cyclist's) head with its chest.

Cyclists are well known targets:

As a personal and anecdotal note, I have to say that I bike during the breeding season and I was never attacked by a magpie, nor I've ever seen a magpie swooping.

No swooping in Tasmania

Your claim sounded quite incorrect to me when I first read your question. After all, the magpies in Tassie (short for Tasmania) and the magpies in the mainland belong to the same species (G. tibicen).

However, after some research, your claim seems to be correct: there is very few, if any, report of magpies swooping in Tassie.

For instance, this is a chart from the Magpie Alert website:

As you can see, there is no registered attacks in Tassie (TAS) from 2013 to 2017.

And here is a map of the attacks (the online version is here):

Most of the attacks happen in Victoria and New South Wales. However, besides Tasmania, you can see both in the chart and in the map that there is no attack registered in Northern Territory (NT) and New Zealand (NZ) as well.

That data doesn't prove that there is no swooping in Tasmania, but it does show that, somehow, Tasmanian magpies behave differently. Maybe they are more shy, or maybe the males over there perform other behaviours to drive off intruders before swooping. It's also possible that the explanation is completely different: maybe people in Tasmania don't like to go online and complain about magpies.

A possible cause

The Tasmanian magpie (G. tibicen hypoleuca) is the smallest magpies of all in Australia. Besides that, it is the magpie that forms the largest groups (Kaplan, 2004), with as many as 15 individuals.

Tasmanian magpie, also a male

Coincidentally, magpies form smallest groups exactly in the areas of higher incidence of swooping, like Victoria and New South Wales. The possible correlation among those variables (swooping rate, body size and group size) is something that is still to be investigated.

Conclusion

However, regardless the actual explanation, the fact is that the number of registered attacks in Tassie is, indeed, smaller than in the mainland. After doing a lot of research, the explanation for this remains unknown to me. Let's wait for more answers.

PS: as I said in my comment, magpies are not that aggressive: they are very nice birds and very intelligent ones as well. So, one way to avoid attacks from the magpies in your area is becoming friends with them: magpies have a good memory and they can recognise a face after years. So, if you become friends with your local magpies, they probably won't attack you if you get closer to the nest. By the way, the best way to making new friends is with food (that works with humans too).

Source: Kaplan, G. (2004). Australian Magpie: Biology and Behaviour of an Unusual Songbird (Australian natural history series). CSIRO Publishing.

A little late with this response but here goes. My home in Tasmania is a semi rural bush block that is also home to a primary magpie family (3 to 5), and also home to an ever changing peripheral group (upwards of 20) of older juvenile magpies. Although the magpie family make it clear the patch belongs to them, they show their superiority more with irritation, the odd sneaky peck or two, than outright aggression. As long as the other magpies defer to them when they're all in the same vicinity peace reigns.

My theory is the family, who I have a close relationship with, know I wouldn't be happy if they attacked other magpies, so they keep their disdain fairly low key.

They proved this recently when next door's free range chooks were causing a problem. I only had to chase them away for a single day before the 'family' took over and chased them away for me. But, even then, non contact swooping was applied.

Tasmania is filled with low key people who have time to take the time...just a guess, but perhaps this friendship factor is the key to the lack of magpie swooping in the state. Or, more likely, Tasmanian magpies have simply evolved to be a less aggressive breed.


What kind of microorganism is this? It moves like a worm pretty much. I found it in a pretty big pond with brackish water. The water temperature was around 10 celsius.

Here's a video of it moving

Now  I cannot really tell the name of it without knowing more of its properties and characteristic features, e.g. size. (I am afraid I am not very good with faces, especially of microorganism :D)

But I am 90% sure it might be an
Oligochaete


Please help identify insect found indoor in Malaysia, south east Asia Found this insect in my home. About half an inch long. Would appreciate it if any of you could help me identify it. Thanks.

In the USA we call these insects crickets. Because they make a noise that sounds like the pronunciation of their name. This one looks like a male with two cerci.


Why we can't feel the different parts of ear during hearing which is mentioned in all biology books? We can't feel our outer ear, middle ear and inner ear during hearing something. Why is that such a complex phenomenon is happening all the time but still we don't have any clue regarding that in our practical life?  We just get the sensation of hearing something and get no sensation/feeling how  different parts of our ear work all together .why all these happening within our ear and we never conscious about them ? In fact , we can know them only after studying biology.

Going to be productive instead of posting unhelpful snarky comments and downvoting.

You can only perceive what you have nerves for. Considering humans are unaware of all the rattling going on between the eardrum and inner ear, the only logical explanation is that there are no nerves in the region made to perceive said rattling.


Difference between autonomic and paratonic movements in plants I can't understand the difference be because both involvery the main cause that is an external stimuli, so how do they differ(

its about the gene that is involved in autonomic movements. while, there is no gene involved in plants for paratonic movements.furthermore, autonomic movements are presents in plants by birth, and paratonic movements are induced in plants by an external stimuli only and not present in plants by birth.


How are fingerprints formed? I know what influences the fingerprints to be unique always. But what actually process is taken to make these as we grow?

Fingerprints are called epidermal ridges in Biology. These are formed between the 3rd and 4th month of the fetus. The epidermal layer looses its strength, becomes like a cloth from a piece-board and falls on the underlying layer of skin cells, the dermal papillae. Now, you must realize that not all tissues are as smooth as the skin for evolutionary reasons. This tissue, although a part of the skin, is irregular and some its cells get little more swelled up. After falling, the epidermis begins to harden up and thus takes its shape.
This phenomenon has probably evolved from providing friction for traction and increase in surface area for sweat to come out.
Read more at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1013024/


How do antibiotics combined with a non-Western diet affect weight loss? Wikipedia describes a Western diet as:

  ... higher intakes of red and processed meat, butter, high-fat dairy products, eggs, refined grains, white potatoes, french fries, and high-sugar drinks.

In the following article there is information about research done that suggests mice eating a high-fat diet while taking antibiotics become obese:

Scientific America: How Gut Bacteria Help Make Us Fat and Thin

I was wondering whether there has been any similar study to see what happens to obese mice or humans that take antibiotics while eating a non-western diet such as the Mediterranean diet, which this Guardian article suggests does not cause weight gain?:

The Guardian: High-fat Mediterranean diet does not cause weight gain

I don't believe elevated polyunsatured fatty acid consumption falls under the tendencies of the western diet, and may be more reminiscent of the Mediterranean diet, so hopefully this answers your question. This study took mice with elevated blood and tissue omega-3 levels, and were used to identify if high levels of omega-3's could prevent the deleterious effects of excessive antibiotic use on gut microbiota. Regarding microbiota diversity, antibiotics are known to create an imbalance between bacteroidetes (decreased) and firmucutes (increased) - this study evidenced that the omega-3 mice were able to rapidly recover their bacteroidetes composition and reduce the amount of firmucutes present in comparison to the control, which in short is good news, as this also prevented later-life obesity in the omega-3 mice in contrast to the obese controls.

For skeptics of microbiota-influenced weight loss (and I know there's many), there is quite a bit of literature out there describing the relationship between gut microbiota diversity and energy expenditure. The short description is that elevated bacteroidetes (in proportion to firmucutes) is associated with lean phenotypes, that diet is very much capable of modulating gut microbiota over short periods of time, and transplanting microbiota compositions into obese individuals has definitively shown an effect on metabolism. The only problem to a gung ho microbiota therapy is, no one knows the gold standard for microbiota composition.

There is no reason to think that taking antibotics is going to tweak your gut flora in a way that will make you lose weight for good.


Is a species lifespan affected by meat consumption? I read a review-like article about the hypothesis of Caleb E. Finch  in a science magazine. The article of interest engages with the idea of Finch

  "[arguing] that immune functions and nutrition have been of major importance in the evolution of aging and longevity."

According to this, humans started to regularly consume meat. Meat itself, carrion or injuries during hunting have chances of getting infected and thereby causing death to humans. A strong defensive system against infections lets you survive and its coming into existence may be accompanied by an elongation of our lifespan.
I find myself now asking two questions:
(1) Because the whole article is only about the primate branch, I wonder, whether there are other omnivores that drifted apart concerning their eating habits and if now there is a more carnivorous, longer-living genus?
(2) Do carnivores, in general, have a long lifespan (or is their lifespan highly dependent on a healthy predator–prey equation)? I tried googling, but could not find a relevant scientific resource on this topic.

I don't think that the theory is very reasonable, because animals drink from stagnant ponds (i.e. savanna wells , forest puddles) and have lots of vectors of infection other than rotten meat: cuts and grazes, tract infections, parasites like mosquitoes and nematodes.

The olfactory sense is also very sharp in many carnivores and they can gage the decomposition state of meats. Even humans have a very strong sense of the age of meat using smell, although I can't find  research on it.

The fun thing is to see the age of other animals, i.e. birds and bears. The oldest zoo birds:

Flamingoes, seagulls, vultures, 50-70
parrots 90-120 years.

the oldest panda: 37
the oldest grizzly and polar bear: 40 and 42

Oldest reptiles:
lizards crocodiles and tortoises: 50-100 years
giant tortoise: 150-250 years.

Other herbivores with slow senescence: donkey 60, bison 50, gorilla 60...

research papers don't include any evidence to correlate carnivory and lifespan. It's mostly body mass and ecology, i.e. predation rate.

Carnivores have must stronger stomach acid also which mitigates some of the risk.

Study by Loma Linda showed that 1) a very low meat intake was associated with a significant decrease in risk of death in 4 studies, a nonsignificant decrease in risk of death in the fifth study, and virtually no association in the sixth study; 2) 2 of the studies in which a low meat intake significantly decreased mortality risk also indicated that a longer duration (>/= 2 decades) of adherence to this diet contributed to a significant decrease in mortality risk and a significant 3.6-y (95% CI: 1.4, 5.8 y) increase in life expectancy; and 3) the protective effect of a very low meat intake seems to attenuate after the ninth decade. Some of the variation in the survival advantage in vegetarians may have been due to marked differences between studies in adjustment for confounders, the definition of vegetarian, measurement error, age distribution, the healthy volunteer effect, and intake of specific plant foods by the vegetarians.

CONCLUSION:
Current prospective cohort data from adults in North America and Europe raise the possibility that a lifestyle pattern that includes a very low meat intake is associated with greater longevity.

This study can be read at https://www.ncbi.nlm.nih.gov/pubmed/12936945.


Is there in vivo evidence of Amyloid beta toxicity? Amyloid beta is thought to be toxic, however from a brief search, this is based on (1) in vitro (2) measurements of some proxies of toxicity (e.g. Ultrasensitive Measurement of Ca2+ Influx into Lipid Vesicles Induced by Protein Aggregates referenced in Wikipedia).

My impression is that we do not have any high-quality evidence that amyloid beta is toxic in vivo and that there is significant circumstantial evidence against it being toxic (links below). Is this correct?

"30% of elderly people have #Alzheimers pathology (plaques &/or tangles) but no disease"
There's an elderly woman with large amounts of amyloid plaques but no symptoms of Alzheimer's
According to Derek Lowe "all of those amyloid-antibody trials have ended in grievous, expensive failures"

From a quick search, it seems that there is plenty of solid evidence for in vivo toxic effects. A couple of papers here and here.


Does a severed limb/finger experience pain after its separated? If a person ends up with a severed finger will that finger, after falling off, experience any pain and start writhing? Can a limb kind of have a mind of its own for a few more seconds after separating from the body like for instance the tail of a lizard?

Pain is a signal emitted from a nervous pain receptor cell (called a nociceptor) to the central nervous system (CNS, i.e. the brain). If I hurt myself causing a small cut in my finger, nociceptors around the cut will send the pain signal to the CNS, which in turn processes it and causes the physical feeling of pain in that region.

If a finger is severed, nociceptors just above the cut will be extremely active, interacting with the CNS and causing a lot of pain. On the other hand, nociceptors in the finger itself have nowhere to "push" the pain signal to, so in this sense they cannot measure any pain - there's not a CNS connected to the finger anymore that is able to process the signal emitted by any nociceptors in the finger.


Which modern methods of antibiotic production are there? For my seminar paper in the field of biology, I have to collect modern methods of antibiotic production. The topic is a little overwhelming, but the work should also be quite extensive (approx. 18 pages).
I've already done some research, but most of the results don't help me. I would be very grateful for a few web links and keywords that I could research for in order to break down the topic.
I will visit the university library in the next few days. It would help me a lot if someone could recommend a few good books references.

For Penicillin production try from page 165 of:
Industrial Microbiology: An Introduction
by
Michael J. Waites
Neil L. Morgan
John S. Rockey
Gary Higton
There is also a table in that chapter listing the other antibiotics and which organisms are used to produce the basic form.
I found it very readable.


Why were dinosaur skeletons so light compared to mammal skeletons? I was watching a presentation by Dr. Jessica Theodor [1] who discusses (at 38:10), among other things, the skeletal structure of dinosaurs vs. mammals. "Dinosaurs have way lighter skeletons, which means that for the amount of material they can be bigger. If we start to look at sauropods, they have this really interesting set of structures, these big holes in their vertabrae...
it allows you to build a lighter, stronger skeleton. Mammals can't do that. It's not how we build our bones."

Why don't mammals do this? Are there fundamental trade-offs that make our (apparently) weaker, heavier bones better, or is it just chance that we haven't matched this development?

(Of course I'm open to the possibility that I misunderstood the talk, or that it was simplified to the point of inaccuracy on this point.)

[1] Jessica Theodor, Being Giant: Why are mammals not as big as dinosaurs? (2015)

I have also heard the claim that dinosaur bones were lighter than mammal bones of equivalent  size, and at the moment I do not believe it.  I will not believe it until somebody explains it to me how that is possible.

If you have a structure that you want to add more weight to, to support that weight, you want to ADD structural elements, not subtract them.  If the structure could support itself before adding more weight, then adding structural elements will make it stronger (unless it's already at the absolute limit).  Otherwise, the structure does not stand at all.

If you google about the weight of bird bones, you can find recent research saying that bird bones are actually not lighter than mammal bones.  Their weight is just distributed differently (more densely on the outside of the bone, as opposed to more evenly spread throughout the bone as in mammals) to resist bending and twisting better at the cost of being weaker to impacts.  Birds arguably have a much stronger reason to lose weight than dinosaurs, but their bones are still just as heavy as ours.  Since birds are dinosaurs, I find it very unlikely that ancient terrestrial dinosaurs had magic bones lighter than both mammals and birds.

Also, I'm aware that the internal structure of our bones is very efficient.  As I understand it, the bone on the inside of a bone grows thicker where it is more stressed.  If you train a computer to calculate the ideal lattice structure to support the stresses of a given bone shape, the computer calculates pretty much the exact same lattice as what actually exists in our bones.  So, if the internal structure of our bones adapts to better handle the stresses we experience in life, and if the bones of vertebrates can evolve into any external shape whatever, I cannot imagine how dinosaur bones could be stronger than ours unless they were made of a different material.  I am not aware that this is the case.


The fundamental importance of R.E.M. Sleep. (Rapid Eye Movement) Question:
I know that experiments have been conducted to determine the importance of R.E.M. sleep in our sleep cycle. It is particularly important for learning, information synthesis, and recovery from distress. Why else is R.E.M. sleep important? What experiments have been done/observations been made to determine the neurological mechanisms underlying R.E.M. sleep? I know that we exhibit high frequency $\alpha$ waves, similar to the waves we experience during wakefulness.
Wiki:
During REM sleep, high levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the neocortex, and lower levels of acetylcholine and norepinephrine in the neocortex encourage the spread of associational activity within neocortical areas without control from the hippocampus. This is in contrast to waking consciousness, where higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing "neocortical structures to reorganise associative hierarchies, in which information from the hippocampus would be reinterpreted in relation to previous semantic representations or nodes.
Do these reorganized neocortical hierarchies remain this way?
Just HOW integral is R.E.M. sleep to our brain development?

REM sleep stimulates the brain regions used in learning. This may be
  important for normal brain development during infancy, which would
  explain why infants spend much more time in REM sleep than adults (see
  Sleep: A Dynamic Activity ). Like deep sleep, REM sleep is associated
  with increased production of proteins. One study found that REM sleep
  affects learning of certain mental skills. People taught a skill and
  then deprived of non-REM sleep could recall what they had learned
  after sleeping, while people deprived of REM sleep could not.

  Some scientists believe dreams are the cortex's attempt to find
  meaning in the random signals that it receives during REM sleep. The
  cortex is the part of the brain that interprets and organizes
  information from the environment during consciousness. It may be that,
  given random signals from the pons during REM sleep, the cortex tries
  to interpret these signals as well, creating a "story" out of
  fragmented brain activity.

Source: link


sodium chloride and amylase activity So, I did an experiment on the effect of sodium chloride on amylase. and I found out the higher the concentration, the slower the activity.

Therefore, is it valid to make the assumption that when we consume food with starch and high salt concentration, it can affect our digestion of starch? like slower break down of starch?

I highly suggest you actually look at studies that analyze this and there should be a good number since amylase is a well defined enzyme. (Bailey K, Hopkins RH, Dolby DE)

Not only that but applying this type of logic to any problem results in bad conclusions and therefore is bad science. (Berkeley)

The process of proving something scientifically is something that follows a somewhat predictable route. I only say that because not everything follows this exact path.

There is usually a nicer looking picture though I cannot seem to find it.

(Source)

So to answer bluntly, no. You cannot make that conclusion with any stretch of the imagination.

Being that amylases are so well studied you may have your answer after a few google searches, but the case remains that it took many years of research to reliably say so.

I found that the higher the concentration of NaCl, the higher the rate of reaction
Why is this different to yours?


Can a human smell through the ears? The title does, prima facie, appear absurd.

Performing a swallowing action whilst pinching the nostrils shut gives the impression of listening through a bucket filled with water around the head; audible sound levels are perceptibly reduced. Some humans may encounter a similar sensation blowing their nose - hard.

This makes sense give the ears connect to the mouth/nose through the eustachian tubes. Can an odour make its way to the olfactory sensors through the ears?

A quick diagram to point out to people who may not know what Eustachian tubes are (#2).

In order for the aromatic molecule to reach the olfactory bulb, it would first have to get through the Tympanic Membrane (#22) [a.k.a. - Eardrum]. The Tympanic Membrane is water/airtight unless pierced.

So, while it's plausible that an aromatic molecule could travel through the Eustachian tubes and enter the pharynx areas, there isn't any way to get into the middle-ear in the first place unless the Tympanic Membrane has been compromised.

In a healthy and intact individual, the answer should be No.

Modified 6 Dec 2012: One approach to this question is to perform a sequence similarity search for genes encoding genes with a functioning in sensing external stimuli, be they
olfactory receptor, taste receptor or other such genes that are expressed in cDNAs or RNA-Seq data from library preparations of the appropriate ear tissue. While there is not likely at this point in time to be much data available in RNA-Seq format, one might find cDNA libraries from cochlea or neighboring tissue.

A "hit," meaning there is evidence that, for example, an olfactory receptor gene is expressed in cochlea, eg, only means that there is potential to smell through the ears. Taste receptors are expressed throughout the alimentary canal in humans, but tasting the contents - food or other - is not readily perceived as de facto taste outside the oral cavity. Nonetheless, there is no reason not to expect such sensors are expressed to relay information to the brain as to what is or is not present. "Smelling" in/by the ear for the purpose of detecting the presence of a given entity or molecule could serve a similar function.


What species is most prolific? What species represents the largest biomass on earth, ie, how much does the entire population weigh? Also, what species has the most members?

This article covers your desires. Briefly, the single species that weights the most is the cow (520 million tonnes in 2011, now probably way more). About the most members, it looks like that the prize could go to the Antarctic krill (7.8 x 10^14 according to Wikipedia. [

This BBC article, instead, argues that collembola might be the most numerous group on Earth, being present in the number of 10000 per square meter (I leave the calculation to the reader). Collembola, however, are made up of ~6000 species. The same goes for ants and termites.

Regarding bacteria, the same article mentions
cyanobacteria, and more interestingly Wolbachia, an intracytoplasmic parasite that can bend the sex of the progeny of its host to spread more effectively.

The discovery of this giant Armillaria ostoyae in 1998 heralded a new record holder for the title of the world's largest known organism, believed by most to be the 110-foot- (33.5-meter-) long, 200-ton blue whale. Based on its current growth rate, the fungus is estimated to be 2,400 years old but could be as ancient as 8,650 years, which would earn it a place among the oldest living organisms as well.
And in 2003 Catherine Parks of the USFS in Oregon and her colleagues published their discovery of the current behemoth 2,384-acre Armillaria ostoyae

No weight is given.
https://www.scientificamerican.com/article/strange-but-true-largest-organism-is-fungus/


Is Thyroxine a hormone? I have read the phrase 'T3 is three to four times more potent than T4' several times both in books and websites. But isn't T4 a prohormone of T3? Why do then these sources talk about its potency as a hormone(I suppose)?

It is necessary to distinguish between classical and non-classical actions of thyroid hormones.

Classical action involves nuclear THR (or TR) receptors (TR alpha1, TR beta1, TR beta2). They are activated by T3, 3,5-T2, TRIAC and 3,5-DIAC, and blocked by rT3 and rTRIAC. T4 and TETRAC hardly have an effect on nuclear thyroid hormone receptors, but they are converted in the periphery and in target tissues by deiodinases to T3 and 3,5-T2, and TRIAC and 3,5-DIAC, respectively. From the classical perspective, T4 and TETRAC are therefore prohormones and not hormones in the narrower sense.

Non-classical action denotes binding of thyroid hormones to integrin receptors on the cell membrane. The resulting non-genomic actions may be directly mediated by T4 and TETRAC and don't require deiodination. From the non-classical perspective T4 and TETRAC are hormones sensu stricto.

Figure from Hoermann et al. 2015 (CC BY license)

References

Hoermann R, Midgley JE, Larisch R, Dietrich JW. Homeostatic Control of the
Thyroid-Pituitary Axis: Perspectives for Diagnosis and Treatment. Front
Endocrinol (Lausanne). 2015 Nov 20;6:177. doi: 10.3389/fendo.2015.00177.
eCollection 2015. Review. PMID 26635726
Davis PJ, Goglia F, Leonard JL. Nongenomic actions of thyroid hormone. Nat Rev Endocrinol. 2016 Feb;12(2):111-21. doi: 10.1038/nrendo.2015.205. PMID 26668118.

I don’t know, but I suspect that T4 was characterized first and fulfils the classic definition of a hormone being secreted by a gland and carried in the blood to its target.

Potency is the measure of some biological or biochemical assay of the effect of these agents in the target tissue, so that you can talk about potency regardless of other attributes of a molecule.

Even when it was established later (I presume) that T4 is converted to T3 in the target tissue, and T3 is very active, the possibility would have existed that this conversion might only be partial (there will presumably always be some T4 present there) and the question arises whether both of these molecules have biological activity and function. The results of measurements of ‘potency’ are part of the argument or consideration as to whether T4 is just a precursor or also an agent in its own right.

I think the thing to bear in mind is although you might read nice clear-cut statements in text books and the like, the observations on which they are based are often not so clear-cut, so authors are being both prudent and scientific in presenting the data to the reader.

Finally, there is the question of semantics. Even if T4 is completely converted to T3 in the target tissue, you could still say that it is a hormone because it is secreted by an endocrine gland, passes in the blood to a target tissue where it has an effect. The fact that its effect requires it to be modified in the tissue doesn’t invalidate its description as a molecule that has an effect on a target tissue. So on that basis you can justify calling it a hormone (as well as a prohormone). I also suspect there may be historical reasons for retaining the description.


Why is thymine rather than uracil used in DNA? What is the advantage gained by the substitution of thymine for uracil in DNA?  I have read previously that it is due to thymine being "better protected" and therefore more suited to the storage role of DNA, which seems fine in theory, but why does the addition of a simple methyl group make the base more well protected?

One major problem with using uracil as a base is that cytosine can be deaminated, which converts it into uracil. This is not a rare reaction; it happens around 100 times per cell, per day. This is no major problem when using thymine, as the cell can easily recognize that the uracil doesn't belong there and can repair it by substituting it by a cytosine again.

There is an enzyme, uracil DNA glycosylase, that does exactly that; it excises uracil bases from double-stranded DNA. It can safely do that as uracil is not supposed to be present in the DNA and has to be the result of a base modification.

Now, if we would use uracil in DNA it would not be so easy to decide how to repair that error. It would prevent the usage of this important repair pathway.

The inability to repair such damage doesn't matter for RNA as the mRNA is comparatively short-lived and any potential errors don't lead to any lasting damage. It matters a lot for DNA as the errors are continued through every replication. Now, this explains why there is an advantage to using thymine in DNA, it doesn't explain why RNA uses uracil. I'd guess it just evolved that way and there was no significant drawback that could be selected against, but there might be a better reason (more difficult biosynthesis of thymine, maybe?).

You'll find a bit more information on that in "Molecular Biology of the Cell" from Bruce Alberts et al. in the chapter about DNA repair (from page 267 on in the 4th edition).

Thymine has a greater resistance to photochemical mutation, making the genetic message more stable. This offers a rough explanation of why thymine is more protected then uracil.

However, the real question is: Why does thymine replace uracil in DNA? The important thing to notice is that while uracil exists as both uridine (U) and deoxy-uridine (dU), thymine only exists as deoxy-thymidine (dT). So the question becomes: Why do cells go to the trouble of methylating uracil to thymine before it can be used in DNA? and the easy answer is: methylation protects the DNA.

Besides using dT instead of dU, most organisms also use various enzymes to modify DNA after it has been synthesized. Two such enzymes, dam and dcm methylate adenines and cytosines, respectively, along the entire DNA strand. This methylation makes the DNA unrecognizable to many nucleases (enzymes which break down DNA and RNA), so that it cannot be easily attacked by invaders, like viruses or certain bacteria. Obviously, methylating the nucleotides before they are incorporated ensures that the entire strand of DNA is protected.

Thymine also protects the DNA in another way. If you look at the components of nucleic acids, phosphates, sugars, and bases, you see that they are all very hydrophilic (water soluble). Obviously, adding a hydrophobic (water insoluble) methyl group to part of the DNA is going to change the characteristics of the molecule. The major effect is that the methyl group will be repelled by the rest of the DNA, moving it to a fixed position in the major groove of the helix. This solves an important problem with uracil - though it prefers adenine, uracil can base-pair with almost any other base, including itself, depending on how it situates itself in the helix. By tacking it down to a single conformation, the methyl group restricts uracil (thymine) to pairing only with adenine. This greatly improves the efficiency of DNA replication, by reducing the rate of mismatches, and thus mutations.


What makes a gene dominant or recessive We all carry two copies of each gene (outside of male sex chromosomes).  If the two differ from each other often one is dominant and one recessive.  How does this mechanism work on a molecular level?  What mechanism determines which gene gets expressed?

On the molecular level, genes most often encode proteins which perform some function for the cell: For example, they could be enzymes and catalyze chemical reactions. They could also have some structural function, such as make up the "muscle" part of your muscle cells... You get the idea.

In the most simple case, the dominant allele encodes a protein that can perform its function. For example, the dominant allele for the CFTR gene encodes a channel that can let chloride into and out of the cells. The recessive allele, on the other hand encodes a protein that cannot do its job correctly (this also called a loss-of-function mutation). So if you inherit a functional copy from one parent and a non-functional copy from the other parent, you will still have one copy of the protein that can do its job. Only if you get a nonfunctional copy from both parents will you have a recessive condition called cystic fybrosis.

On the molecular level a gene can also encode a dominant-negative variant of a protein. In this case the protein cannot do its job and also prevents the functional version of the protein to do its job too.

A third way this could work is by a gain-of-function mutation. In this case, the gene encoding a protein acquires a mutation that gives a new function to the protein. For example, in Huntington's disease, the mutant Huntingtin protein acquires the ability to clump together in large plaques, which are poisonous to some neurons in the brain. Since it takes only one copy of the protein to perform the new function, the gain-of-function allele is a dominant one.

These are only a few examples that deal with simple dominant and recessive inheritance. Most often there are more complex mechanisms of inheritance at play.

Generally if one of the genes' biochemical functions becomes knocked out completely, the other copy will fill in for it, making the trait recessive - requiring both copies being knocked out.

An example of such a recessive trait is Albinism - if both copies of the enzyme participating in melanin biosynthesis are ineffective, the result is someone with no pigment.

Dominant genes are often variant genes which convey a new ability (phenotype) and as such the trait can show up with just one copy has this variant. Phenylthiocarbamide tasting is an example of this dominance. If both copies of the gene were the variant, the original ability might disappear - making the original trait dominant as well. On the molecular level, genes most often encode proteins which perform some function for the cell: For example, they could be enzymes and catalyze chemical reactions. They could also have some structural function, such as make up the "muscle" part of your muscle cells... You get the idea.

In the most simple case, the dominant allele encodes a protein that can perform its function. For example, the dominant allele for the CFTR gene encodes a channel that can let chloride into and out of the cells. The recessive allele, on the other hand encodes a protein that cannot do its job correctly (this also called a loss-of-function mutation). So if you inherit a functional copy from one parent and a non-functional copy from the other parent, you will still have one copy of the protein that can do its job. Only if you get a nonfunctional copy from both parents will you have a recessive condition called cystic fybrosis.


Why would a human female have a sexual display despite male biased operational sex ratio? why would a human female have a sexual display despite male-biased operational sex ratio?

In human society there is a male-biased sex ratio, due to female child rearing, which results from anisogamy. Human females sometimes expend great amounts of energy and resources performing display acts and doing things to attempt to improve their apparent quality to males. Human males tend to be eager, despite a certain level of socially imposed monogamy, and many males will mate with a low quality female. Why do human women do sexual display behaviors, when there are so many eager males to choose from?

Sexual arms race.

There is a fine and internally consistent theory that this strategy by females evolved to oppose the strategy of infanticide by males.  Males of many species including primates and possibly humans can increase their own genetic fitness by killing infants that are not their own.  This frees up attention and physical resources of the female to instead have the baby of the infanticidal male.  Lions are famous for this.  But this is in opposition to the genetic fitness interest of the female, who just invested a bunch of efforts gestating and rearing an infant who was then killed.

My favorite writer on this is Sarah Hrdy.  From the Wikipedia article on this\

  This is where the idea of sexual counter-strategies comes into play.
  Hrdy theorized that by mating with as many males as possible,
  particularly males who are not part of the colony, mothers are able to
  successfully protect their young, as males were unlikely to kill an
  infant if there was the slightest chance that it might be their own.

This explains why women have the sexual displays referred to in the OP.  Other aspects of female human biology match.  Humans keep big breasts so they always look like they are lactating (compared to other animals) - to keep males guessing.  There is no external sign to indicate when a human is ovulating.  Females of other species are receptive and mate when they are ovulating - humans can mate any time.

A strategy of keep the guys guessing.  If one time he had sex with a given female, probably he shouldn't kill the kid.  Maybe it is his?

An interesting (& extremely arguable!) corollary to this is the premise that human culture in its entirety is the male countermeasure to this prehistoric female defense against infanticide: that male dominated culture is a method to ensure paternity.

Based on what is currently known, I would say that while females might find sperm readily available, it is common for human males to not only provide sperm but also help rear the offspring (e.g., provide care, financial support, food, transportation).  So, they might provide sperm to a woman they're not impressed by (by "impressed," I mean convinced the woman has whatever characteristic the sexual display is supposed to exhibit), but they only offer rearing investment to offspring of a woman they are impressed by.  So, basically, the woman is making a demonstration in order to garner investment from the male.  I think there's more to it than that, but this answer is based on what is currently known and robustly supported in the literature.


Surrogacy Post Fertilization The wikipedia page on surrogacy highlights two main forms of surrogacy: Traditional Surrogacy and Gestational Surrogacy. Traditional surrogacy inseminates the surrogate mother with sperm, while gestational surrogacy uses in vitro fertilization to form an embryo from egg and sperm, which is then transferred into the surrogate mother.

It does not discuss whether surrogacy is possible after a natural fertilization has already taken place, such as if a woman becomes pregnant and then wishes, for whatever reason, to have a surrogate take the baby to term. Is this biologically possible? If it is possible, what is the mechanism? Also, if possible, is heightened risk a major reason it is not more common?

No, it is not possible. The problem is the fertilization which takes place near the ovary. It takes the new forming blastocyst about 4-5 days to wander through the fallopian tube to reach the uterus and 8-9 days in total to implant itself into the uterine wall. See the picture below (from the Wikipedia article on fertilization):

You would have to get the blastocyst out of the right fallopian tube, make sure it survives the procedure and then implant it into the uterus of a woman which is about in the same phase of their period (otherwise the uterus is not ready to allow implantation).
It is already hard enough to do in vitro fertilization where you can control the environment.

There are different types of surrogacy, but as you said the most common one are traditional and gestational surrogacy.

Traditional surrogacy normally involves intrauterine insemination (IUI), so the eggs of the surrogate are used in the surrogacy process. Once the fertilization takes places it's not possible to extract the embryo.

On the other hand, in gestational surrogacy the creation of the embryos is done via an IVF process, and once they are created they are transferred to the surrogate. So in this process, the fertilization process take place out of the surrogate body.

So, in summary, while gestational surrogacy uses a IVF technique to create an embryo that afterwards is transferred to the surrogate, traditional surrogacy uses IUI to artificially inseminate the gestational carrier. IUI is less complicated than IVF, and this process can be repeated several times until a pregnancy is achieved. However, it's not possible to make the fertilization in one woman and afterwards transfer the embryos to the surrogate, that would be extremely complicated.

Here you can get more info about the different forms of surrogacy.


How can binaural beats change mental state? Can anyone tell me how binaural beats of 10 Hz can cause a person to calm down and one of 40 Hz to cause someone to heighten their attention. All I know is that they work on the principal of Brainwave Entrainment. I am confused as to how can a 10-Hz difference in 2 sounds cause the brain to change its state of mind! A detailed but simple explanation would be great.

It is thought that binaural beats entrain the brain in the frequency of the binaural beat. These beat frequencies show up in the EEG.

The EEG in turn represents synchronous activity in the cerebral cortex (Fig. 1).

Fig. 1. EEG frequency bands and their associate mental states. source: Conor Russomanno

Now if you look at where 10 Hz EEG waves show up it is in the alpha frequency band associated with a relaxed mental state. The 40 Hz band on the other hand is associated with beta activity associated with an alert state.

Indeed, presentation of beta-frequency binaural beats have shown to improve the performance on psychophysical tasks and performances were better than when binaural beats were presented in the theta-delta range (Lane et al., 1998).

Reference
- Lane et al., Physiol Behav (1998); 63(2): 249–52

I will put here a link that I think explained this phenomenon more fully by looking at a huge number of different scientific studies done on the matter...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428073/#!po=11.3861

If you find the article too long, read the last paragraphs to find their conclusions.