Difference between facilitated diffusion and secondary active transport in cells Specifically, what is the difference between facilitated diffusion carrier processes (passive transport) and secondary active transport co-transport processes (active transport)?

They seem to be the same thing - doesn't the passive process with the carrier transports substance $x$ against its gradient together with substance $y$ that is moving down its electrochemical gradient?

Similarly, in the active process, substance $x$ is transported against the gradient, and substance $y$ down its electrochemical gradient?

I don't see how energy differentiates the active transport in this case from the passive transport.

Short answer
Facilitated diffusion is a passive process in which membrane channels mediate the transport of polar, or big molecules that are not solvable in the cell membrane. Co-transport, on the other hand, is active transport, as it depends on the electrochemical gradient of ions across the cell's membrane, particularly Na+. Because ATP or other energetic compounds are not directly involved in co-transport, it is referred to as secondary active transport. The electrochemical ion gradient is mainly established by the Na+,K+-ATPase.

Background
As commented upon by others, your question is not entirely clear and the best way to approach this question is by defining the various terminologies and physiological mechanisms used in your question:

Active transport needs an energy source such as ATP. For example, the Na+,K+-ATPase is an enzyme that pumps Na+ and K+ ions against their concentration gradients into the cytosol (K+) or out of the cell (Na+). Note that both Na+ and K+ are transported against their chemical gradients (and Na+ also against its electrical gradient as the cell is negative). Therefore your statement that [...] in the active process, substance x is transported against the gradient, and substance y down its electrochemical gradient is untrue, and likely the cause of your confusion.
Passive transport is mediated by diffusion, which typically occurs through a concentration gradient. Only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates. Examples are gases (such as O2 and CO2) in the lungs, and small polar but uncharged molecules (such as H2O and ethanol) (Cooper, 2000).
Facilitated diffusion is an example of passive diffusion, but aided by membrane-spanning channel proteins that span the lipid bilayer. Therefore the particles (molecules or ions) do not have to dissolve in the cell membrane's hydrophobic lipid bilayer, allowing hydrophylic and larger molecules (carbohydrates, ions) to be transported into the cell. No external source of energy is needed and  travel across the membrane in the direction determined by their concentration gradients and, in the case of charged molecules, by the electric potential across the membrane (Cooper, 2000).
Co-transport is active transport, where the energetically unfavorable transport of a particle against its electrochemical gradient is facilitated by the co-transport of a favorable one down its gradient. In other words, multiple particles are transported so as to neutralize the sum of the transport. For example, sodium-dependent glucose tranporters transport glucose into the cell against the concentration gradient (unfavorable) and Na+ is transported along with it into the cell which is a favorable transport (Haraki & Inagaki, 2012). This is an example of a symporter. An example of an antiporter is the Na+/Ca2+ antiporter found in the heart to transport Ca2+ out of the cell against a steep concentration gradient and electrical gradient, while 3 Na+ is imported into the cell to balance the unfavorable Ca2+ transport. Note that all these mentioned co-transporters and many others are dependent on the Na,K-ATPase that ultimately generates the Na+ and K+ gradients by pumping Na+ out of the cell and K+ into the cell using ATP (Freeman, 2000). This generated membrane potential works like a battery being charged, and co-transporters discharge it by using the energy stored by importing Na+. Hence, it is referred to as secondary active transport, as no direct energy input from ATP is needed, but instead it utilizes the electrochemical gradient created by the Na+,K+-ATPase.

These considerations should clarify your issues and answer your question on what co-transport exactly is. Specifically, the glucose transporter mentioned, GLUT1 as you refer to, is a symporter that mediates secondary active transport.

References
- Cooper, The Cell, 2000
- Haraki & Inagaki, J Diabetes Invest 2012; 3: 352-3
- Molecular Cell Biology, 2000

The difference between the two definitions is not scientifically justified. Here is an example to clarify this point. A facilitated transport through a carrier A will dissipate the gradient of a substance a. This dissipation will consume energy indirectly if the gradient for that substance is maintained by an active (ATP-dependent) pump. Hence a voltage-gated sodium channel dissipates the sodium gradient maintained by the Na/K ATPase. We think of these sodium ion channel as facilitating the movement of Na down its gradient but in fact they also need the energy indirectly provided to maintain the Na gradient. Now let us consider a coupled transport, Na+/glu for instance. The favorable transport of Na down its gradient largely overcomes the energy cost of the transport of glu against its gradient. Our textbooks commonly justify that this type of transport is secondarily active because it needs the energy necessary to maintain the Na gradient. But isn't the same thing for the voltage-gated sodium channel? If there is no Na gradient, then the transport of glucose by the Na/glu cotransporter will not exist, same thing for the Nav sodium channel: there would be limited flux of sodium ions without the Na gradient (there will be a little due to the membrane potential).


Why do humans have digestive system present at front and kidneys back? Outlet of digestive system is present at back of the body but its digestive system at front.

Outlet of urinary system is present at front of the body but its system present at back.

Why do humans have digestive system present at front and kidneys back?

I don't claim to have the full answer to why these organs are located in the way they are, but I think these factors have an influence on the anatomy:

1- The urinary system's link with the reproductive system in male mammals: The male reproductive system outlet needs to be located as far to the front as possible in a 4 legged mammal to facilitate sexual function, forcing the urinary system to follow

2- The kidneys are very fragile and need to be protected by the thick back muscles and partly under the rib cage. They would be too vulnerable at the front

3- The urinary system is generally sterile of bacteria, and so is the reproductive system in males, and partially in females. The digestive system isn't sterile in both. The outlet of the digestive system can't be in the front of the genitals in a male as this will increase the risk of urinary infections overall and also genital infections after mating. It can't be in between the urinary and reproductive outlets for the same reason, so it has to be located behind both to cause the least interference with their functions


Cytoskeleton made of only actin? I am aware that the cytoskeleton has three structural components: actin, microtubules and intermediate filaments. I was wondering if any cell could possess a cytoskeleton made only of actin. Or made only of microtubules, for that matter. Is it possible for actin to perform the functions that microtubules ordinarily perform in a cell? Or vice versa?

1) Can cells survive without any of the different cytoskeletal components?

Yes, most certainly. At least for actin and microtubules (MTs) there are plenty of eukaryotic cell types that can survive without them. MTs can be disrupted by cold-shock (see for example here https://www.ncbi.nlm.nih.gov/pubmed/16505977). How well the cell survives depends on the type of cell, but the ability to survive without MTs can range from minutes to hours as far as I'm aware. Once the temperature goes back to normal, the MTs just grow back. Of course, the cells won't behave normally in the meantime, because many processes do depend on MTs. Actin can be disrupted using various drugs or genetic constructs, or they can be cut using femtosecond lasers (see for example https://www.ncbi.nlm.nih.gov/pubmed/28324605). Again, many processes are disrupted, particularly cell motility, but most cells can survive without actin for a while.

I'm not aware whether any eukaryotic cells exist that have no intermediate filaments or can survive at least for some time without them.

2) Could a cell function normally while lacking one type of cytoskeletal component?

First, to my awareness there is no eukaryotic cell without MTs or actin. We do commonly use actin and tubulin promoters for transgenes and assume that all cells will express them. So I'm taking this question hypothetically.

As with every hypothetical question, the answer then purely depends on the restrictions that you define. Can the cell possess arbitrary new proteins that currently don't exist? Then yes, definitely you could get eukaryotic cells with just MTs or just actin or just intermediate filaments. You just have to bend all the other things the cell does to fit with that filament type, and then enjoy arguing whether that's still a eukaryotic cell or not.

But I think actin would find it easier to take over the other filaments' jobs compared to the other way round.

MTs are large and rigid. They can't operate on scales below 25nm like actin can, and the individual tubulin dimers can't do anything useful until a tube of some minimal length has been formed out of many dimers. Intermediate filament monomers are pretty thin, but very long. Actin monomers are small and globular, and a supershort actin filament made of a handful of monomers can already function as a filament, branch out, form networks, pull on things etc. Actin-mediated endocytosis crucially depends on this (https://www.ncbi.nlm.nih.gov/pubmed/25675087 for example). It would be difficult to find workarounds for these small-scale functions of actin if MTs or IFs were to replace it. On the other hand, actin filaments can very easily be made into large, thick, rigid rods like microtubules. Many cell types do this constantly when they form filopodia. Actin meshworks can also provide similar mechanical support (both stable and flexible) as IF meshes. With minor shifts in the regulation of where, when and how to organise filaments, actin could probably take over the other cytoskeletons' functions. It would probably require a quite sophisticated regulatory system though to perform all the different functions at the same time in one cell.

I think sperm is only having microtubules (axoneme) in them as a part of the cytoskeleton. Different types of cytoskeletons evolved to perform the different function so generally they will not exchange their function but are precisely evolved to carry out their individual functions.

(From textbook Molecular Biology of the Cell. 4th edition https://www.ncbi.nlm.nih.gov/books/NBK26914/)In tail section of sperm, which is a long flagellum.The core of the flagellum is composed of a structure called an axoneme.The axoneme consists of two central singlet microtubules surrounded by nine evenly spaced microtubule doublets. These dense fibers are stiff and noncontractile, and it is not known what role they have in the active bending of the flagellum, which is caused by the sliding of adjacent microtubule doublets past one another. Flagellar movement is driven by dynein motor proteins, which use the energy of ATP hydrolysis to slide the microtubules.

But I would like to correct my answer, as sperm also contains actin for capacitation and acrosomal reaction.So I think sperm is a eukaryotic cell where you can only see 2 types of the cytoskeleton.Here is the link for the paper https://www.ncbi.nlm.nih.gov/pubmed/15749953


What will happen if a poisonous snake bites itself? I wonder if in general snakes are immune to their own venom. I would like to know studies or references about times snakes bit themselves and got sick or the contrary.

“The conventional wisdom is that they have circulating antibodies in
  their blood,” says Stephen Mackessy, Ph.D., a Professor of Biological
  Sciences at the University of Northern Colorado and an expert in
  venomous snakes. “This would protect them from their own venom, as
  well of venom from another snake in their own species.”

  Hypothetically, if a speckled rattlesnake bit another speckled
  rattlesnake, the immunity they’ve built from being exposed to low
  levels of their own venom—kept in glands behind their eyes and
  secreted when they bite—would protect them from a fatal wound. (Even
  though the glands are closed, they still contain blood vessels that
  allow the venom to circulate in their system, causing mild exposure,
  Mackessy says.) But a speckled rattlesnake that meets up with a cobra
  might have a different day entirely.

So in the case snake were to bite itself it wouldn't suffer as much from the poison compared to the actual bite it self-inflicted.


How to attract Cyanobacteria? I would like to attract cyanobacteria in one spot on an object (e.g. cloth,) instead of having it swim in the media. my current method is to pour it on the object in a beaker and wait for some of them to become attached (very pour attachment yield).
Now, I am thinking of making the object emit light. Do you think that the bacteria will swim all the way to the cloth because there are attracted to light?
is there a better method to help the bacteria get attached to the cloth?

It might work, many cyanobacteria are reported to be phototaxic. https://www.pnas.org/content/115/52/E12378


What is the difference between ferritin and hemoglobin? I have been reading that ferritin is the store of iron but hemoglobin is actually the amount of this in blood.

Does hemoglobin get sourced from ferritin? Is it possible for a person to be low on ferritin but normal on hemoglobin? Will he feel any symptoms of anaemia, if so?

Does hemoglobin get sourced from ferritin?

Yes, of course it is. Ferritin is the superior Group.

  Is it possible for a person to be low on ferritin but normal on
  hemoglobin?

Yes, since these things don't have something in common.

  Will he feel any symptoms of anaemia, if so?
  Why should he?? No, he won't get any crazy feelings from this.


Can ants survive a plane ride? I just came back home a few hours ago from the airport and my aunt had peaches in her car full of ants. This made me wonder if the ants had joined us from the plane?

This leads to the question can ants can survive at high altitude?

It depends on the altitude of the plane, species of ant, flight length, location in hold, and more, but generally yes, they should be able to survive. At such locations that a plane flies at, the temperatures range from 0 to -50 degrees Centigrade. At such extreme temperatures the ant's entire body system is brought to an almost complete stop, where their heart is barely beating, and nervous system barely functioning other than to tell the heart to beat, and other normal involuntary actions. This means they won't need to consume as much oxygen (because their slowed brain won't need as much) allowing them to survive with the minimal oxygen in the atmosphere.


What type of spider is this that just decided to stop my plans of sleeping This tiny little spider decided to stop my plans of sleep at 1am, since I have no plans of getting to sleep any time soon may someone tell me what type of spider could be this monsterous!

It is a male Steatoda, probably S. grossa (picture below).  These spiders are often called False Widows, since the females are generally a large purply black and look similar to their cousins the Black Widows. Steatodas are pretty harmless, though, although a couple of species (in the UK/Europe) are known to sometimes produce bite effects like a mild Widow bite.  Not at all dangerous, but a little disquieting if you're the one that gets bitten.  Presuming that you're in North America, though, you're fine.  Steatodas are Theridiid ("cobweb") spiders common in and around houses, and the harmless males are often encountered when they wander around looking for love as adults.

Bug guide has a good section on S. grossa, including lots of images of male spiders like this one.

https://bugguide.net/node/view/6932

Information on Steatoda envenomation is broadly available, but not in great detail.  The Wiki entry appended below covers the ground as well as any of them.

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

A spitting spider. Neat little spiders that I get in my house quite frequently. They're harmless and one of the few types of spiders that have six eyes instead of eight. Here's some more info.

https://imb.uq.edu.au/article/2017/11/spitting-spiders-natures-strangest-hunters

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


What evolutionary advantages does a longer muzzle have against a shorter muzzle and vice versa Basically I'm curious as to why when it comes to mammalian predators that some like say bears and canines tend to have longer muzzles than those like big cats.

aside from their ancestors/evolutionary line and such, what advantages or disadvantages do short muzzles and long muzzles have against each other and which is better?

Its mostly due to different forms of predation.

Longer jaws are deeper and can reach farther around a prey item, it also increases the chances of catching a moving target in the jaws becasue the area the jaw covers is larger, all things being equal it should always be favored but things are rarely equal, everything has a cost. It is common to see longer snouts in animals that hunt primarily with the jaws. There two ways to do this which depends on how big the pery to are after is, for predators going after relatively small prey they favor long thin snouts, is really noticable in aquatic predators like gharials, it makes for a very fast bite with a wide attack range. Alternatively if they are going after large prey they need to balance strength with speed so you see long, but not as long, more robust snouts. Think alligators, hyena, wolves. Whereas cats who attack with their forepaws can use a smaller head and jaw and favor a more precise bite, becasue they are moving with the prey becasue they have grabbed it, the arms are absorbing most of the stresses. Cats favor grabbing and strangulation for which a small short jaws works fine. Energy and material saved here can be used elsewhere. A longer snout would be weaker unless they add a lot more muscle to stabilize it. In terms of resources it is a lot of cost for little gain, whereas in wolves it is worth the cost becasue they need that strength anyway, becasue they jaw is where all the stress of the struggling prey is being transmitted.

You see the same thing in dinosaurs, predators that can attack with the claws have weaker bites/smaller heads. In the case of dinosaurs however snout length varies less because the small heads favor slashing bites, which favors a longer snout (thus a longer cutting row of teeth) there heads get narrower and weaker more than shorter.  Mammals can't use this strategy because they don't get replacement teeth, and they would quickly not have a tooth in their head, so instead you see strangulation favored instead.

Of course an animal can try to balance a range of strategies and there are all kinds of specialized forms like saber teeth, venoms, ect. Of course this is also simplified a lot of other things effect snout length as well, things like climate (long snouts cause less heat/water loss through breathing), sense of smell, or even vision.

https://www.cambridge.org/core/journals/paleobiology/article/dinosaurian-and-mammalian-predators-compared/BE3492DA7E0A103C6F6E77B9611D86A9

https://link.springer.com/chapter/10.1007/978-1-4615-0161-9_14

https://www.cambridge.org/core/journals/paleobiology/article/constraint-and-adaptation-in-the-evolution-of-carnivoran-skull-shape/77B1591461066F9D0E30F309F6C495C6

https://www.sciencedirect.com/science/article/pii/0034568770900757

This paper, The biomechanics of foraging determines face length among kangaroos and their relatives might provide some insight, but very likely misses a lot of factors that would apply, e.g., to wolves vs cougars.  In the case of carnivores or omnivores, hunting strategies, prey capture methods, and even tearing & chewing techniques are likely to interact synergistically with muzzle length via the Baldwin effect (Wikipedia). Another paper The Baldwin Effect and Genetic Assimilation compares the Baldwin Effect to the Waddington effect, which can have similar results.

Edit:
In response to the suggestion by @Willk and @tyersome, I've added the following explanation:

The Baldwin Effect is widely accepted among evolutionary biologists.  The Waddington Effect is not as widely accepted and is sometimes (incorrectly) interpreted as a form of Lamarckism.

In essence, the Baldwin Effect works like this:

a population is subjected to a new environmental challenge or opportunity
a few individuals learn a new strategy that overcomes the challenge or exploits the opportunity
natural genetic variation makes some individuals in the population more capable of learning the new strategy
Individuals whose genetic makeup makes them more capable of learning the new strategy have a fitness advantage and produce more descendants, so over time the proportion of individuals in the population who can are genetically equipped to learn and use the new strategy, increases.
Individuals whose genetic makeup gives them a physiological advantage in regard to using the new strategy will have a further fitness advantage, and will consequently produce more descendants than others in the population.

Let's say the environmental challenge for two different kinds of carnivore (let's call them Bogs and Dats) is to catch Mophers.  Both Bogs and Dats initially have the same medium-to-short muzzles.  Some Bog individuals figure out that they can dig  Mophers out of their burrows, and some Dat individuals figure out that they can catch Mophers at night when the Mophers leave their burrows.  Both strategies are successful.  Some Bogs happen to have longer muzzles than their cousins, and find it turns out that longer muzzles work synergistically with the digging strategy, allowing Bogs to stick their noses into the Mopher burrows to grab escaping Mophers.  The resulting fitness advantage results in an increase of the long-muzzle trait in further generations of Bogs.  Note that in this scenario it is the adaptive behavioral strategy that creates selective pressure that favors a particular genetic adaptation.

Dats on the other hand, because of their nocturnal hunting strategy, benefit from improved night vision; and long muzzles don't provide any fitness advantage to Dats because Dats don't dig Mophers from their burrows.  As long as Bogs and Dats don't hybridize, they will most likely end up with long and short muzzles respectively.

The Waddington effect, also called “Genetic Assimilation”, is somewhat more direct:

An environmental stress causes a proportion of a population to develop one or more abnormal traits, by interfering with embryological development.
If there is a selective pressure in the environment that favors some subset of those traits, individuals whose genetic makeup makes them more likely to develop that subset of traits, those individuals are likely to produce more descendants than other members of the population.
If being “more likely to develop” that subset of traits results from a weakening of genetically determined development controls that would otherwise prevent development of that subset of traits, then the subset of traits can eventually become the normal phenotype.

An explanation of how the Waddington effect might influence muzzle length requires a bit more hand-waving, largely because there is no evident environmental factor that would cause perturbations in the embryological development of, e.g., dogs.  However,  I'd assert that an abrupt release of a strong selective pressure can have a closely analogous result.  Wolves really have to look and act a lot like wolves in order to survive in the wild (partly because of their survival strategies), so they are subject to strong selective pressure.  Domestic dogs, on the other hand, are subject to much weaker selective pressure.  Moreover, when a variant shows up (a pug, for instance which has a very short muzzle), it is often considered “cute” and is bred separately to fix the trait in a subpopulation.  Although the "release of selective pressure" mechanism isn't quite what Waddington contemplated, the process is closely analogous.

Note that the Waddington effect and the Baldwin effect are not mutually exclusive.  Relaxation of selective pressure that reduces fitness of variants, and environmental factors that cause disturbances in embryonic development (a la Waddington) both produce a rich source of variants upon which the Baldwin effect depends.

However, It is very difficult to prove that any specific phenotypic trait in an existing species was caused by a particular selective pressure. At best we can only make plausibility arguments supported by models and rather sparse environmental & ecological data from the geological record, from analyzing genotypes, etc. In the case of canines vs felines (which split off from a common ancestor perhaps 42 million years ago), we can really only guess what the environmental challenges & opportunities might have been, and what behavioral strategies may have been adopted by different individuals and populations.


what is the name of this fish? ]2
fishes are of length 2 to 3 inches.

Looks like Jewel Fish, a cichlid that has been kept for a long time. Hemichromus bimaculatus , native to west Africa a bit different from "African Cichlids" which are from east Africa. Source : Exotic Aquarium Fishes by W. T. Innes ( the guy neon tetras are named after), 1937 ; But I don't think you can find it online .


Did toads evolve from frogs? I know frogs still exist but that doesn't mean there wasn't ever a frog population that evolved into toads. Did frogs evolve into toads because their available swamp slowly went away and toads could survive better without water? Did frogs and toads evolve independently from similar selection pressure for shape?

"Toads", as commonly used, are not a monophyletic grouping - that is, all toads do not descend from a single common ancestor which only produced other toads. Instead, it's a polyphyletic grouping of those frog species which show common morphological characteristics related to a primarily terrestrial lifestyle. As a polyphyletic group, the parsimonious assumption is that various species of toads evolved from frogs on multiple occasions.

There's several possibilities for similar morphological features in the different toad lineages. The first is convergent evolution - similar selection pressure in the shared terrestrial environment selected for novel generation of similar features. Another is that the common ancestor of frogs and toads had morphological aspects that were a blend between frogs and toads, and depending on environment "toad-like" or "frog-like" features become more prominent or recessive - that is, "toad" genes are sitting dormant in the DNA of most frog species, waiting for the right environment to be expressed. In all likelihood the true explanation probably will be a combination of the two.

By the way, most toad species still depend on bodies of water, particularly for breeding. For example, the common toad (Bufo bufo) will go to a pond to lay its eggs, where the young toads will spend time as aquatic tadpoles before they metamorphosize into the adult form. So when thinking about toad evolution, it's probably incorrect to view it strictly as frogs compensating for losing access to water (though that might have happened for some species), but rather toads evolving to take advantage of the opportunities presented by a terrestrial habitat that's coexisting alongside watery environments.

It is more important to understand the entire argument of evolutionary assumption. For instance, we have no solid observational, repeatable or testable evidence that the frog or toad evolved into one or the other.
We are assuming a lot in this instance. Convergent Evolution is totally crazy.

We hinge a lot of belief upon 'possibilities' and unobserved 'data' through computer generation, and uniformity.
The problem is no one considers that the genetic code will not and can not add information to the gene pool (such as teeth to no teeth, hard skin, or wet skin,) some mutations and adaptations can improve a kind of life form but it has its limits in the DNA.

The truth is, we cannot say that frogs and toads evolved into anything because we have not observed this ever.
We have observed species varying among kinds. However, the toad and the frog are different kinds of reptiles just as the lizard differs from the tortoise.
Always go by fact question assumption.


Giant insects growing question During the dinosaurs time 100-200 million years ago there were giant insects like 1 meter long. An example is here. One of the theories why they could grow this big is that oxygen level was much higher than now. Now we have like 20% oxygen in the air and that time it was 30 or 40.
The question:
If I make a tank/aquarium with 40% oxygen and all the equipment to make this oxygen concentration constant. I put there modern insects, dragon fly, worms, slugs, etc. Will they grow to much bigger size than normal from the 1-2 generations, or I will need to have 100 or 1000 generations before they will be bigger?

that sounds like a fun experiment!  But unfortunately you are right, the size difference is shaped by genetics as well as an environmental condition that might be hard to pin down.
For the genetics, It would indeed take millions of years (or at least 100,000s) for the genetic adaptation to kick in to create that change.
As for the environmental conditions, another source of gigantism is being on an island.  As the small number of species expand to fill out all the niches in the tank, they may get larger simply because the environment allows it with no predators.
The tank would have to be enormous to get those niches I think. This paper describes an archipelago of islands and shows that you tend to get smaller animals more easily with smaller islands, and larger species need larger islands.  Large here is millions of square meters.
Both of these processes take many generations. This is not my field but this paper studied 200 generations of plants and showed only migration and lifespan changes.  Size adaptations that come with changing ecological roles might have to take 1000s of generations. We'd have to freeze ourselves to see the giant slugs.  I'm sure there's a better answer out there, but this is what i found so far.


Sequence analysis software suites I have used DNAStar laser gene and VectorNTI in the past for cloning, primer design, sequence alignments, etc but no longer have access to these. Are there any comparable replacement suites or what stand alone packages would you now recommend?

I would strongly recommend benchling https://benchling.com

This is an awesome web based tool for cloning, primer design, multiple sequence alignments and everything else you are used to doing with the other tools. It is very user friendly, and most importantly you can share designs with your collaborators. Also, the graphics are very beautiful. I recently started using it and I am really impressed with the technical support they offer: you can chat with them and they would reply within minutes. Also, if there is a feature you would like to have implemented they would definitely consider it. Benchling is free, open source and you might be even able to code up some features yourself.

Geneious is probably the strongest standalone package, but real bionformaticians rarely deal with GUI driven programs.


Why do humpback whales sing songs? Scientists have documented that it seems to only be male humpback whales who sing structured songs, but do we know what purpose their songs play?

There are four hypotheses with varying levels of supporting evidence for why humpback whales sing.

Yes, only males have been shown to sing. It used to be thought that the songs only occurred on breeding grounds and therefore served a reproductive purpose. However, songs have since been recorded on migration routes and feeding grounds, though not as prolifically.

The hypotheses are:

"Mate Attraction" whereby males sing and females approach them to mate. No evidence has ever shown a female humpback whale approach a singing male. Rather, a group of males will swim after a female, vying for position, until she is receptive to mating. Then the closest whale (the primary escort) will be best poised for success. In my opinion, this is the least plausible hypothesis.
"Lekking" whereby a group of males sing to stimulate the females to begin estrus and advertise their body size and health for female mate choice. https://en.wikipedia.org/wiki/Lek_mating This may allow for female selection of choosing a mate later while being pursued as part of competitive group. I am unaware of which articles support this hypothesis and provide evidence. Birds and land mammals are much easier to observe in a lekking behavior than any underwater animal is.
"Territory establishment" whereby males sing to mark their territorial bubble of water. If a male has a larger territory, then it is more likely a female will pass through that larger territory so that the male can respond by pursing her. This could be supported by proving that male humpback whales respect each other's territories and space themselves consistently across their watery world. Refer to http://dx.doi.org/10.1121/1.4962217
"Orientation by echolocation" has recently been put forward by Edward Mercado that song reflects on a broad scale around the whale's environment to provide feedback for navigating the general area. Many researchers argue the plausibility of such low frequencies echoing effectively.

New studies into cultural transmission of parts of songs across ocean basins may suggest the song is not just for reproduction but to fulfill wider communication needs or generate a form of social creativity. See work by Ellen Garland.

Mainly done by male whales during mating season, the songs serve to attract females (possible flirt with them), escort them from place to place and as a means of definining territory to other competing male whales.


What does DNA taste like? I've seen plenty of speculation online, but does anyone know of a scientific study or have a definitive argument?

I'm thinking probably not sweet, because the deoxyribose sugar is bound in the structure of the helix. Salty, due to group I counterions? Bitter due to the alkaline phosphate groups? I'm guessing not sour, because despite the name nucleic acids are in their conjugate base form at physiological pH. I've read some nucleotides can activate the umami/savory taste, would this be significant?

I am aware essentially everything we eat contains DNA, but I'm interested in the taste of DNA itself, pure/isolated if necessary you like.

Youtube chemist NileRed chemically extracted DNA from strawberries in this video, he also tastes it if I remember correctly: https://www.youtube.com/watch?v=araeHtN_3Lk

TL;DW: He gets the DNA from the strawberries and says it has a slimy texture as it isn't soluble, and it tastes salty more than anything. Note though that this could be from leftover reactants from the reaction, so take this with a grain of salt.

According to DNA Vineyards:

  Flavors of ripe Santa Rosa plums with hints of new French oak


Why proximal muscle weakness is seen earlier than distal muscle weakness in Dermatomyositis? It is said that in dermatomyositis(DM) , proximal muscle weakness is seen earlier than distal muscle weakness. It is also said that , DM is due to damage to small blood vessels contributing to muscle injury.( from Robbin's textbook of pathology pg.no: 1238-1239, 10e)

Shouldn't the distal group of muscles being smaller show weakness earlier? Why inclusion body myositis does not follow the pattern as in DM?

Usefull links:
https://www.mda.org/disease/dermatomyositis/causes-inheritance
https://emedicine.medscape.com/article/332783-overview#a1

My hypothesis are

1) Since skin, is commonly involved in sunexposed areas, may be enviornmental factors do play a major role. So, Proximal Muscles are more used in day to day work, so are more favourable site for drugs, autoantibodies to act upon.

2)May be, in case of due to drugs or vaccines, proximal muscles may be are preferrential site of action of these, making these group of muscle more suceptible.

By the way correct answer would be: Its under research.


How does UV light damage the DNA when the chromosomes are deep inside the cell? When UV light falls on the skin it has to go through the cell membrane and the nuclear membrane to reach the chromosomes. So it looks like that the DNA is protected but it probably isn't. Won't membranes be damaged first and the so that the cell dies before the DNA is affected and is replicating wrongly (if it is damaged too)? Or is DNA just really much more vulnerable than cell membrane?

UV Rays kill the cells by damaging the DNA. UV lights do not disrupt the cell membrane. If a cell is exposed to UV light, it creates THYMINE dimers (bond). Thymine dimers are the actual disruption in the kinks of DNA. UV exposure to skin is proportional to the cell damage.

P53 is a gene product which takes care of fixing cell damage. However it has a tolerance. If the damage is less, P53 sends damage repair machinery. If it's non-fixable, then P53 directs the cell to programmed death.

More UV exposure, more thymine dimers causing more cells to die (cell death). If the damage is not extensive, then that may cause cancerous cells (Result of cell damage).

When UV light is on your skin it has to go through the cell membrane
  and to the membrane of the core. So it looks like that the DNA is
  protected.

I don't understand what you mean by membrane of the core (perhaps nuclear membrane) but yes there is cell membrane and other cytosolic components. You should, however note that not all cells are spherical; some cells like skin cells are flat and along the thickness axis the DNA is much "less buried".

However, UV light does get attenuated by different cellular components. Melanin (which gives the skin a tan), for instance, absorbs UV and protects the DNA.

In spite of all this UV can reach the DNA. Furthermore, DNA (basically the bases) can absorb UV because of the nature of their chemical structure. After absorbing UV they reach an excited state and can become reactive. Reactions such as pyrimidine dimerization happens because of UV absorption. Note that this kind of an effect is elicited only by high energy UV (200–300 nm) (Durbeej and Eriksson, 2002; Svobodová et al., 2012).

Low energy UV (UVA) does not damage the DNA directly but can do that indirectly by generating free radicals. These free radicals are generated when other cellular components absorb UV and become reactive. Lipids are also affected by UVA and UVB; lipid peroxidation happens in the presence of UV and these peroxides are a source of free radicals (Morliere et al., 1995). So, the membrane is indeed "damaged".

It is also interesting to note that UVA is the most available to the skin cells because UVC and UVB are filtered to a great extent by the ozone layer and also scattered/absorbed by skin components (What is the relationship between UV wavelength and penetration depth into human skin?).

To summarize, DNA is more vulnerable to certain UV ranges but the damage frequently happens indirectly by other free radicals generated in the cytosol.


How are T cells transported? T cells are formed in bone marrow and mature in Thymus. How are they transported from bone marrow to thymus ? Through the lymph vessels ?

The progenitor cells of T-cells (they do not develop into T-cells and show their characteristics before reaching the thymus) are mobilized into the bloodstream and enter the thymus from it by crossing the endothelial barrier. The figure shows schematically the development of the precursor cells from hematopoietic stem cells (HSC) and the migration of the precursor cells (it is from the paper linked below):

See this review for the details (if you have problems accessing the article, let me know):

The long road to the thymus: the generation, mobilization, and
circulation of T-cell progenitors in mouse and man.

prothymocytes are attracted to the thymus from the Bone Marrow by a chemotaxis , thymotaxin, a factor from thymic epithelial cells.
then it enters into the thymic cortex where Thy-1  and terminal deoxynucleotidyl transferase (TdT) is expressed. During TCR gene rearrangement, TdT increases TCR diversity by inserting nucleotides at the D and J junction sites. IL-2 and IL-2R are expressed leading to autocrine proliferation of T cells.
now the  pre-T cell  rearranges TCR genes (gamma/delta, alpha/beta). At this stage the pre-T cells are CD3+CD4-CD8- or "double-negative" cells. Double-negative cells that productively rearrange gamma and delta chain gene segments develop into CD3+CD4-CD8- gamma/delta T cells that are exported to the periphery in small numbers. Successful rearrangement of a set of TCR genes suppresses further rearrangement of TCR genes on the sister chromatid , thus each cell only expresses TCR with a single specificity.
The majority of double-negative cells will go on to rearrange alpha and beta chain gene segments. The beta chain genes are rearranged and expressed first with a pre-T alpha chain to form the pre-TCR . Once the pre-TCR recognizes some intrathymic ligand , a signal is transmitted through CD3 which:
halts further beta chain gene rearrangement (allelic exclusion)enhances alpha chain gene rearrangement causes CD4 and CD8 to be expressed
The alpha beta T cells now become CD4+CD8+ or "double-positive" cells. T cells which fail to productively rearrange TCR genes die by apoptosis.

At this point the T cells are in the deep cortex which contains epithelial cells expressing both class I and class II MHC molecules. T cells with alpha beta TCR which are capable of binding self-MHC on epithelial cells continue to proliferate and differentiate into CD4+CD8- or CD4-CD8+ T cells. Nonreactive (not self-MHC restricted) T cells die by apoptosis. Thus, T cells are positively selected for self-MHC restriction in the thymus.

T cells that survive positive selection traverse the junction between the cortex and medulla. Some of these T cells have low affinity TCR for self-MHC alone or combined with self-peptide while others have high affinity TCR. The medulla is rich in BM-derived dendritic cells and macrophages which express high levels of class I and class II MHC. T cells with high affinity TCR for self-MHC alone or combined with self-peptide interact with these dendritic cells and macrophages, and are eliminated by apoptosis. Thus, negative selection eliminates self-reactive T cells  in the thymus.


Do we see protocells forming in nature today? I understand that the current theory of chemical evolution (aka origin-of-life, abiogenesis) involves lipid-based protocells that enclosed RNA and perhaps some other compounds as a first steps to life.

I'm wondering if we see them forming today in nature, and if not, why not?

Are there successful experiments creating them in the lab?  If so, what are the required conditions?

we don't think so, some parts are easy. liposomes form all the time, and can be created in lab quite easily. They quite readily encapsulate any material present when they form, including DNA. So once you have the right stuff (likely RNA) it is very easy to enclose it in a lipid bilayer.

RNA has been formed from scratch in a lab it is even easier than we thought it would be. It may form in nature today but is unlikely , the current atmosphere is very oxygen rich and bacteria are not just willing to eat RNA but also basically all the chemical building blocks as well so it is difficult to build up a concentration of the precursors in nature today.

Worse evidence of it forming today would be ridiculously difficult to demonstrate because there is a constant contamination of biologically produced RNA from decaying organisms. There is basically no place on earth today with liquid water that does not have life in it.

Here and here is a review of our current models for the origin of life, Be warned the first link is a file.There are many steps involved to get a cell but it all starts with the first molecule capable of making copies of itself.

Forming self catalysis strands in a lab would be the best evidence but has one major problems, Money. Earth had an ocean sized laboratory and millions of years to stumble one of the strands with one of the right codes through random chance (remember a self-replicating code only has to happen once) which likely could only be duplicated by doing millions or even billions of identical laboratory experiments.

Finally while the Urey-miller experiment was historically important it is by no means the best nor most modern experiment you can find much more information about the variety of experiments at this question.

Basically the closest we've come to a living organism from scratch is an autocatylitic RNA set. Look it up.

But we haven't actually made any self contained life yet, although this video is VERY interesting.

Life can't form anymore. We have oxygen, which like Abdul said, smashes delicate primordial molecules. Also, we have an ozone layer, which stops the UV rays from hitting the earth, which as demonstrated in variants of the miller Urey experiment, were probably instrumental in the formation of life.


Does evolution select against genetic diversity? Only the best genotype in a species will win. So it sounds like evolution selects against genetic diversity.

TL;DR

In a population, directional selection reduces genetic diversity.

Simple scenario

In a population, directional selection reduces genetic variance (at the loci that are under selection and other linked loci). Selection selects for variants that are associated with the highest fitness. Hence, selection reduces the number of variants (or at least the frequency of the variants that are associated with a lower fitness).

Note that, by reducing genetic variance, selection also reduces heritability (see this post for definition) for the selected trait.

Note that, for a correct terminology, you should not say that selection "selects for" low genetic diversity. Selection "selects for" variants associated with high fitness which causes a reduction in genetic diversity. Selection indeed does not "select for" any population-wide statistic but only for specific variants in the population which affect those population-wide statistics.

Selection vs evolution

You say

  Does evolution select against genetic diversity?

Please do not confound "evolution" with "selection". There are a number of "drivers" of evolution other than selection (e.g. genetic drift, mutation, migration). Both selection and drift reduce genetic diversity, however, mutation and incoming migration will typically increase it.

Balancing selection

Note also that there are types of selection that maintain genetic variance such as negative frequency-dependent selection, or heterozygous advantage for examples. Those types of selection that maintain genetic diversity are called balancing selection.

Multiple populations

Imagine a scenario where two populations are present in two different environments. If there is directional selection going into opposite direction in each environment (aka local selection), then selection will still reduce within-population genetic diversity but will increase the among-population genetic diversity.

Definitions of genetic diversity

Genetic diversity is a concept used in population and evolutionary genetics. The term genetic diversity is typically defined as the probability of non-identity by state of two alleles. In a single population, this is identical as the definition of expected heterozygosity. Let $p$ be the allele frequency in a population, the genetic diversity $\pi$ at this locus in this population is defined as $\pi = 2p(1-p)$.

More info about these definitions and their relationship to $F_{ST}$ (a widely used statistics of population divergence) in Nei (1973) and Charlesworth (1998).

Definitions of genetic variance

Genetic variance is typically a term used in quantitative genetics. One could say that genetic variance is defined by the phenotypic consequences of genetic diversity. See this post for the definition

For simplicity, above, I used the terms genetic diversity and genetic variance correctly but without highlighting that they take different definitions.

Intro to evolutionary genetics

Your question is a very introductory question in evolutionary genetics. You might be interested in some intro books (have a look at the post Books on population or evolutionary genetics).

Heterozygote advantage, multiple population, balancing selection etc merely delay the problem or break it down into smaller pieces. There is no way to get around the fact that the best genotype in a population will win for the vast majority of traits.

The practical consequence is

https://www.natureworldnews.com/amp/articles/16388/20150907/endangered-species-genetic-diversity-explains-decline.htm

  Some species may face extinction when they are not able to adapt as easily to changing environments or defend against new diseases. To better identify or rank threatened and engendered species, researchers from Purdue University suggest using the animals' rate of genetic diversity loss.

Of course this is attributed to more proximate causes and not evolution.


Does the Plasma Membrane have a hydrophilic interior/exterior/contain vesicles? I am very new to the study of biology, and have been unable to find information in other sources which could tell me whether the plasma membrane has the following traits:

has a hydrophilic interior
has a hydrophobic exterior
contains vesicles

Thank you!

The plasma membrane is a lipid bilayer. Plasma membrane lipids have a hydrophilic head group and hydrophobic tail groups. Since cells are usually in an aqueous environment (and are filled with aqueous cytoplasm), the hydrophilic head groups is face both the exterior and interior of the cell. Between these head groups facing the interior and exterior, the hydrophobic tail groups of opposing lipids associate with each other to create a hydrophobic core within the membrane.

Vesicles are also made of lipid bilayers. Vesicles can exist within cells or be released by cells.

The plasma membrane typically refers to the double lipid bilayer, which has a hydrophillic exterior and a hydrophobic interior.  In your case, the only thing I can think of is a layer/mixture of inverted micelles, which would fulfill your three criterion.

Image is from "Lecithin-based nanostructured gels for skin delivery: An update on state of art and recent applications"


Is this aquatic plant duckweed or something else? This plant has been growing in my pond for quite a time now. It multiplies in large numbers rapidly.
 Some told me it is duckweed or is it something else?

That looks very much like a duckweed.

The multiple roots rule out most genera within this group and so this is probably a Spirodela.

The apparently relatively large size and red undersides are consistent with this being Spirodela polyrhiza.

Picture by Christian Fischer available under Creative Commons Attribution-Share Alike 3.0 Unported.

Not duck weed. It is Salvinia species very easy to grow ( invasive). I believe it is illegal to introduce in some US states. Koi /carp will eat duck weed.There are a few similar species of salvinia , unfortunately references will give the same name for different plants. My book ( Aquarium Plants ; Barry Jones, Tetra press) calls it auriculata which I believe is wrong. Auriculata is also called giant salvinia and looks different ( see comments @ tyersome ). I have grown Auriculata but not the salvinia that you have.


How is the timing of gene expression controlled in developing embryo? I understand how cell differentiation works in general (gradients of homeobox proteins etc), but how is timing controlled? Why do some genes switch on at a very specific moment of development and then switch off.
I imagine that the timing could be enabled by the same homeobox proteins (genes are switched on as soon as the proteins diffuse far enough, and switched off as soon as the homeobox is used up), but perhaps there's some special mechanism of gene expression timing?

How can gene expression timing affect the formation of a developing embryo?

We should know that genetic imprinting is passed down. The formation of an embryo is not. Some takes on form when provoked, it is much like when oocytes are stimulated with a prod duplication
Happens automatically. The embryo is affected by the proximity of cells. Clusters, spread out, far apart. All make the cells behave automatically. But it's the first ignition of development that sets off growth. The cells have been through many phases and timing is not controlled by either proteins or genes.


Can I figure out the identity of my grandparent from this information? I know all my family up to my grandparents, with the exception of the grandfather on my mother's side. At the time my mother was conceived, my grandmother was having an affair so no one in my family knows for sure who the grandfather was.

In high school we learnt that blue eyes are a recessive trait and brown eyes are a dominant trait, as such I should be able to figure out who my grandfather is, but I only studied up to that level and I want to check with someone more knowledgeable than myself if it is correct.

So here's my reasoning:
I have blue eyes, meaning I have two blue eyed genes and got one from my father and one from my mother.
My mother has brown eyes, meaning that she has one brown eyed gene and one blue eyed gene to pass it on to me.
My grandmother has blue eyes, so she passed one on to my mother.
One of my potential grandfathers had blue eyes, so if it had been him my mother would have received two blue eyes genes and have blue eyes. But she has brown eyes so it must be the other potential grandfather (who's eyes I don't know the colour of).
Can someone tell me if this is correct, and if not, why not?

One of my potential grandfathers had blue eyes, so if it had been him my mother would have received two blue eyes genes and have blue eyes.

No, this does not necessarily follow, because eye color genetics are more complicated than just one dominant-recessive gene. See, for example this article from a someone at  Stanford University on How Blue Eyed Parents Can Have Brown Eyed Children. It isn't common, but apparently it does happen.

Solving your inheritance just based on eye color with 100 percent certainty is not possible.

On a high-school level you are right. Still, the answer to your question is no.

As you may have already noticed, nothing in reality is as simple as schools tell us. Eye colour is generally determined by one gene, but there are other genes which can modify the effect. Think about this question: if there were just two alleles, blue and brown, where would green-eyed and grey-eyed people come from?

If you want to investigate your who is your biologic father, you can ask them both to take a genetic test. If they decline or cannot comply, try comparing many traits, not just one. Ask for photographs of you mother and both possible fathers when they were your age and make a list. What is everybody's hair colour? What is their height? What is the shape of their faces? the proportions of bodies? the skin colour? shape of mouth, nose, eyes? Do you know everybody's blood type? Maybe you just look a lot like one of the men, then you can assume he's your father. Maybe you look a lot like your mother and there are only subtle differences which point to one of the men? Remember that this comparing does not give you certainty, only clues.


Probably a moth larvae but better to confirm What I know,
It reacts to light
the red seems to be blood but can't say for sure
1 to 10 mm
it has a casing of something soft fabric possibly
it grabs to walls

This is probably a larvae of Tinea pellionella, the case-bearing clothes moth.
T. pellionella is a species of tineoid moth in the family Tineidae (i.e. the fungus moths).


What is meant by "a codon codes for an amino acid"? What is meant by "a codon codes for an amino acid"? Does it mean in order to build that amino acid you must combine those three nucleotides?

Does it mean anything more than provides the instructions for manufacturing that amino acid.

It does not means "provides instructions for manufacturing an amino acid".  How could three little letters encode so much?

A codon is a three nucleotide sequence that matches the anti-codon of a t-RNA molecule capable of carrying one kind of amino acid.  The GGG codon, for instance, binds the t-RNA that binds to glyceine.  So the codon GGG in an mRNA ends up amounting to "put a glyceine here in the amino acid chain"


What decides whether a lysogenic cycle or a lytic cycle will take place? A virus can either participate in a lysogenic cycle or a lytic cycle. What decides that?

It depends on a few factors, such as how many phages infected the cell, whether or not the cell is in good growth conditions, and so on. If the cell is in stress or has low amounts of nutrients, the lysogenic pathway is typically activated.

The underlying mechanism has to do with a protein cascade involving either the cro or cI protein that is encoded by the virus. The cI protein is a repressor, and it will prevent the lytic genes from being transcribed. By default the virus will transcribe the lytic genes, so they must be repressed for lysogeny to occur. Similarly, cro is also a transcriptional repressor. The two proteins work in opposition to each other. cro binds to an operator, oR3, that is involved in repressing cI, which may prevent cI from being expressed and thus preventing it from repressing lytic genes (however the importance of this is debatable because if you replace oR3, the cell can apparently still lyse).

There are numerous other proteins, such as N and Q, that are involved. The N protein has to be transcribed by the polymerase ‘anti-terminating’, or reading through a termination signal. This will happen more frequently when the protein RNase III is present at high concentrations. The N protein is a lytic regulator. Thus, when there are high amounts of RNase III there will be more N expressed which leads to the lytic cycle. RNase III is not a viral protein. It is a host protein and the host expresses more of it when nutrients are abundant. This is how the virus is able to ‘sense’ if nutrients are high enough to enter the lytic cycle.

The whole system is way more complicated but this is it in a nutshell.

http://www.annualreviews.org/doi/full/10.1146/annurev.genet.39.073003.113656

The term “lysogenic” implies that prophages are capable of giving rise to active phages that lyse their host cells.  This occurs when the viral genome exits the bacterial chromosome and initiates the lytic cycle.  The triggers for this switch-over are usually environmental factors such as mutagens (e.g. radiation and presence of certain chemicals)


Do homing pigeons fly straight home or follow certain "highways"? Homing pigeons (Columba livia) have been prized for their navigational abilities for thousands of years. They’ve served as messengers during war, as a means of long-distance communication, and as prized athletes in international races. (Source)

Do all homing pigeons just pick a direction, and fly "straight" home, or do they all follow certain "tunnels" or "roads" to get closer to their home area, before heading home? (similar to cars getting on a highway between two regions)

Does any information about that exist? I'd be interested to know if pigeons released in the same area (with different target locations in one common direction) tend to do follow the same paths, or if it's just a chaotic crisscross.

They have mental maps of landmarks, which they use as well as "compass" cues:

  ... experienced birds can accurately complete their memorized routes by using landmarks alone. Nevertheless, we also find that route following is often consistently offset in the expected compass direction, faithfully reproducing the shape of the track, but in parallel.

--Pigeons combine compass and landmark guidance in familiar route navigation

Landmarks are more important than compass cues in general, and pigeons develop their own landmark maps:

  we show that homing pigeons (Columba livia) not only come to rely on highly stereotyped yet surprisingly inefficient routes within the local area but are attracted directly back to their individually preferred routes even when released from novel sites off-route. This precise route loyalty demonstrates a reliance on familiar landmarks throughout the flight, which was unexpected under current models of avian navigation.

--Familiar route loyalty implies visual pilotage in the homing pigeon

That means that different birds do use different routes:

  Here, we demonstrate that birds develop highly stereotyped yet individually distinctive routes over the landscape, which remain substantially inefficient.

--Homing pigeons develop local route stereotypy

In fact the same bird might use different routes over time as it learns new landmarks:

  a wide intraindividual variability was observed in repeated tosses at the same site; some pigeons remained faithful to the first route, whereas other birds tried successive new routes which, in most cases, were significantly shorter than previous ones. This result indicates that pigeons try, and are actually able, to improve their performance in subsequent releases from the same site.

--Pigeon homing: The influence of topographical features in successive releases at the same site

I study sharks and I have found that several things have electroreceptors like cockroaches, bees, platypus and even pigeons. On top of that. Mammals have what is known as magnetite crystals in the brain. A compass works because it is a weaker magnet than that of the earths magnetic field and aligns with the stronger field. I have a feeling that pigeons use a combination of all of this as well as memory of landmarks and such but I am unsure. I study sharks

https://en.m.wikipedia.org/wiki/Magnetoreception#In_homing_pigeons
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC49775/


Theranos blood test's Specificity and Accuracy? I am studying the limitations of Theranos device.
They have 238 documents in Google Patents Search (Inassignee as Theranos), here.
Which patents are relevant for their device?
They have 70 tests which are not necessary to consider now.
Just the basics of the device.

My intuition says that it uses PCR to multiply the microliter of blood for the analysis.
What are limiations of multiplying so little blood?
I think this is where their engineering work applies.
What components do you need to multiply?
I think all is not necessary.
Otherwise, the specificity and accuracy can be difficult to hold.

How can Theranos blood test's be specific and accurate compared to conventional full blood test?
I suspect if you can do the conventional full blood test with Theranos device with the same accuracy and specificity as the conventional one.

Which patents are relevant for their device?

They currently only have about 27 issued patents (US)
Of those patents about 10 of them are related to network/internet/health record/algorithm (so not really about their device)
The remaining patents focus on a few areas: sample acquisition (getting the blood drop and handling of it), Patch based technology (before they pivoted), sample quality analysis (this is key to making sure the small sample is good quality), microfluidics/modular device (these are the patents relating to the actual testing and device)

What are the limitations of multiplying so little blood?

From a molecular standpoint (PCR) the smaller sample you start with, the less of the original nucleic acid template you have to start with.  Lower end PCR testing uses 10uL of sample.  This is ok when you are trying to bring molecular diagnostics to the point of care or developing markets, but the best PCR tests use 50uL of sample (more than a drop of blood which is traditionally 25uL or so),  regardless of how good your device is, at some point you start amplifying junk. The better the primers and other reagents the less junk you amplify, but at the end of the day you want more sample to be more sensitive.
From a NON-molecular standpoint (chemistries, cellular analysis, coag, etc.), they aren't/can't multiply the analyte of interest.  In these tests, they rely more on dilution or small volumes to perform detection.  This is where their ability to reliably dilute and correct for the dilution comes into play. Although there is certain limits to this.  Coagulation tests would not be representative if you diluted the sample so in this case they will have to rely on working with a small volume.  Cellular analysis can only be diluted so much as you get to a point where you miss important but less common cell types.  Take eosinophils (a type of WBC) while they can get to 15 or 20 percent of all WBC cell types, in general they only make up a couple percent.  Assume that 2% of all your WBCs are eosinophils.  If you only have 3500 WBCs per 1uL of blood (which is on the lower end of normal), you have approximately only 70 of these cells in that same volume.  If you dilute the sample so that way there is more of it available for other tests like electrolytes, but you still analyze 1uL, The number of those cells is even less.  If you had perfect detection you might be ok, but you generally want to analyze more blood so that statistics work in your favor and your performance goes up. Most of the other chemistries, proteins, and as mentioned earlier, electrolytes will probably be ok for dilution and detection and in fact this is why there are plenty of small devices already out there that use a drop of blood and perform the same tests.
Their issue in diluting or amplifying analytes of interest is that biology still is governed by the laws of physics and even though technology may allow you to analyze samples down to 10nL, that just isn't use full in biology, and limits their their capability to perform the supposed menu of tests from one microtainer of blood.  They don't publicize that they may need to draw a venous sample (needle in your arm) for some tests and depending on what tests you order, you may need a separate finger prick for each test.

How can Theranos blood test's be specific and accurate compared to conventional full blood test?

If they reliably control dilution of the small sample, they maybe able to provide high quality results for some tests.
Finger pricks actually can be easily skewed via technique.  Theranos has specially trained people to draw these samples, but it is time consuming >5 mins and until it is fully automated this is one variable that no matter how good sensors are, you can't correct for variation pre-analytically when you have that small sample.  Finger pricks also skew certain tests even when technique is good such as platelet and WBC values in the CBC.
I discussed the sample volume issue above regarding PCR amplification and how good tests use up to 50uL.  So if they compare to a 10uL test, they may be able to compete, but not full lab quality.
A lot of the future techniques they have regarding small techniques (in their applications) like their coagulation tests work great in an academic setting, but they fail to be able to handle the full range of blood samples they will see, so it will be interesting to see how that plays out.

Takeaway

Theranos is working on modular micofluidic devices/cartridges that will use small sample
There are certain biological limitations that stand in the way of them performing all the tests in their catalog with only a drop of blood
The FDA will eventually be requiring them to submit their tests for approval as they are currently doing tests that are available on commercially and FDA approved devices already (this makes sense because LDTs were never ment to be used in place of standard tests and equipment and since there is NO published data on their performance it can be worrisome to providers and payer)
Their true business plan has yet to be elucidated, but if they really did have a box that did all this, they would be selling them to physicians and clincs where those results could actually be used in diagnosis rather than 4 hours later.
I hope they succeed, but there is just way too much hype to buy in on it yet.

I am sorry I don't have sources, most of this is from intimate knowledge of the space and from the little info available on them so I could definitely be wrong on some of this.  I hope this helps!

I haven't seen their device and I won't want to see it, I want to first understand the concept better independently. I am not an expert in biology but I have feeling how such device could be done.
Noname covers sensitivity and new concept "amplification" raising a new puzzle: is amplification done by analog methods (op-apms), digital methods, dilution or/and some other methods?

Summarising the Noname to sensitivity, amplification and background

(I added bolding)

"Theranos is working on modular micofluidic devices/cartridges"

"regardless of how good your device is, at some point you start amplifying junk. The better the primers and other reagents the less junk you amplify, but at the end of the day you want more sample to be more sensitive."

"they aren't/can't multiply the analyte of interest. In these tests, they rely more on dilution or small volumes to perform detection. This is where their ability to reliably dilute and correct for the dilution comes into play. -- if you had perfect detection you might be ok, but you generally want to analyze more blood so that statistics work in your favor and your performance goes up. Most of the other chemistries, proteins, and as mentioned earlier, electrolytes will probably be ok for dilution and detection and in fact this is why there are plenty of small devices already out there that use a drop of blood and perform the same tests."

"They don't publicize that they may need to draw a venous sample (needle in your arm) for some tests and depending on what tests you order, you may need a separate finger prick for each test."

where by (2) more sensitivity can actually be a good thing; by (3) same tests already done by other devices in small size: what is so special with Theranos device? and by (4) one drop of blood not enough for all tests.
"What are limiations of multiplying so little blood?"

Decision Analysis (DA) and Compositional Blood Analysis (CBA): I see such a device as a Decision Analysis (DA) device where you need to do compositional blood analysis (CBA). You get a lot of vague information on which you do sensitivity analysis. Conventional full blood tests can be seen as devices where the sensitivity is very very low to other factors. It is not surprising that development has lasted about 10 years, sensitivity analysis is very low research project. For example, Chevron's DA model started 1990 and continuing, implementation takes time. For example, scale hydration level to some level in all samples. When you have low-quality information, you need to use ad hoc models (often based on high-quality samples) such as supposed correlations between things to improve prediction accuracy.

1.1. What are Decision factors?

1.1.1. Rheology of blood? Dry or liquid phase samples?
1.1.2. Correlation of red/white shells: I don't use the word "approximation" because the number of red shells correlated with the number of white shells
1.1.3. Density (~1.05 kg/l)
1.1.4. Colour of blood
1.1.5. Hydration level
1.1.6. other factors?

"How can Theranos blood test's be specific and accurate compared to conventional full blood test?"

I think this question mis-framed. It is better to ask "How much extra value does such a device can offer?"
Smaller size and less blood mean convenience. It may be useful with athletes, new markets. More convenient to patients/users even though suffering from some abnormalities due to its intrinsic limitations related to its small-volume measurement method.

What components do you need to multiply?

I think this is an important insight: is it possible to multiply blood somehow ensuring its quality for testing? This would make blood tests less painful for patients. Perhaps this is related to stem-cell research? Perhaps not, the Noname covers this in terms of dilution more closely.


Which of the three is true for insulin receptors? I have seen the following question in a Cell Biology exam:
Which of the following is true"

Insulin has an hydrophobic Signal Peptide and the insulin receptor does not have an hydrophobic Signal Peptide

The insulin is coded by two genes, the insulin receptor has an hydrophobic sequence in the middle of the protein.

Receptors in the ER bound the SRP that is bounded to the insulin receptor, SRP is made of RNA and proteins.

I think that (1) is the right answer. However, people I talked with thought (3) is the right one.
I think 1 is right because I have never seen anywhere that insulin receptor has a signal peptide so I assumed it does not have.
I also think that SRP is a part of the insulin receptor, which is located on the ER (and not bounded to the ER by receptors), this is why I thought (3) is not the right answer.
Am I right, or did I miss anything?

Signal recognition particle (SRP) receptor, also called docking protein, is a dimer composed of 2 different subunits that are associated exclusively with the rough ER in mammalian cells. The surface of the rough endoplasmic reticulum (often abbreviated RER or Rough ER) (also called granular endoplasmic reticulum) is studded with protein-manufacturing ribosomes giving it a "rough" appearance. so i don't think (3) is the right statement.
the insulin receptors is made up of two hormones, insulin and glucagon, are at the center of this signaling system. there is no such things as hydrophobic sequence in the middle of the protein i believe.
also, Insulin is a peptide hormone produced by beta cells of the pancreatic islets and and insulin receptors doesn't have an hydrophobic signal peptide. so i think (1) is the correct answer.
Edit :
https://en.wikipedia.org/wiki/Signal_recognition_particle_receptor
https://www.healthline.com/health/type-2-diabetes/insulin#Function1
www.news-medical.net/health/What-is-Insulin.aspx


Division of proteins This textbook states

Proteins determined by a single gene may divide to form different proteins with various physiological actions.

First how do proteins divide? Second if it's just fragmentation then what is this process called? Third since my textbook doesn't explain it could anyone explain with an example of how different parts of original protein( considering that protein has divided by fragmentation) perform different physiological actions?

This is not a very helpful passage, I agree.  Some proteins are cleaved by other proteins (a protein that cuts another protein is called a protease).  Other proteins cleave themselves.  Otherwise, proteins are quite stable and don't just fragment wily-nily.

In the case of the first group (proteases acting on other proteins) the coagulation cascade may be a good place to start for you.  Precursor proteins in this pathway are converted to active enzymes by a chain reaction of protein 'division' and other protein modification.  This page has other interesting cases of this process, such as in food digestion, which may be what you're looking for.

Some of the second group are self-cleaving such that an intervening sequence is removed, and the ends are pasted back together.  (This is analogous to how introns are spliced from messenger RNA and the exons are spliced together.)  Such intervening protein sequences are called 'inteins'; the removal of one intein can generate one functional protein, so this isn't protein division.    However, some viruses encode self-cleaving regions that will split the mother protein into two or more pieces.  A famous example of this process, now used widely in biotechnology, is the 2A peptide, which is used to 'split' a single transgenenically-expressed protein into 2 (For instance if you want to express a protein and a marker such as GFP simultaneously, you could employ the 2A peptide to link these together.)

The first group may be of more interest to you because of the known role of these proteases in human health.  Also, in your question it sounds like you also may be referring to random 'fragmentation' of proteins, which is not currently known to be an important contributor to protein breakdown in the human body, even in the stomach.  Enzymes such as pepsin are responsible for digesting proteins.

I don't have access to the textbook, but my first thought is that the author is talking about gene duplication during evolution. If a gene duplicates, the two copies may end up diverging, creating two similar but slightly specialized proteins that fulfill different functions.Wikipedia

I agree that the sentence is not well written, whatever the intended meaning. Some context may be helpful.


Can scientists "see" thought? Touching an object activates a nerve - something that can be observed by scientists.
Scientists can also trace the resulting "signal" through your nerves to your brain. They may know which portion of the brain is activated.
The next step is to think about the thing you just touched.
Does this process generate something physical that scientists can detect? Or is though, so far, "invisible"?
To put it another way, do scientists know what "thought" is made of?

Depending on the technique used, the short answer is yes.  For those of us who have been in the field for a long time, questions like this bring up memories of articles or seminars we have seen, but we really have to sift through a lot of non-digitized articles to find it. Although I will have to do some searching  to find it, there is a beautiful article using voltage clamping in very skilled fighter pilots where the author suggested (accurately IMO) a graphic representation of the formation of a thought. (I realize that without references, it is still hearsay, but perhaps someone else will recognize the details & be able to fill in the gaps more quickly.) But I will try to find the article and post the details.


Why do dogs come in all shapes, but cats are generally all the same? Minus hair and fur, cats (the domestic kind) seem to be just scaled versions of the same thing.  Dogs on the other hand can have long necks, short necks, long bodies, short legs, long ears, short ears.....

Until recently, cats were not extensively selectively bred, but were allowed to roam freely and therefore interbred randomly.  Darwin pointed this out, contrasting cats to species that were routinely "enclosed":

  On the other hand, cats, from their nocturnal rambling habits, can not be easily matched, and, although so much valued by women and children, we rarely see a distinct breed long kept up; such breeds as we do sometimes see are almost always imported from some other country.

In contrast, dogs and some other species were selectively bred for certain characteristics "each good for man in different ways":

  The key is man's power of accumulative selection: nature gives successive variations; man adds them up in certain directions useful to him. In this sense he may be said to have made for himself useful breeds.

Why were cats not selectively bred, while dogs were? This gets to be somewhat speculative, but it's clear from looking at dog breeds that many of the different breed functions need to have a larger animal than a cat, as well as one with different personality: Herding sheep, hunting foxes or badgers, fighting bulls, etc.  Cats' function for humans has traditionally been to hunt mice and rats, a role for which they're already beautifully adapted.

(There are a number of small dog breeds, of course, but these parallel cat breeds in that many are ornamental, or else originated as rat-hunters.)

Cats are small size for hunting closer on the ground for small rodents

dog were born with longer legs for travel linger distance because of great stamina

cats dont have stamina like dogs but they are great sprinters to run 30mph for short burst


Find the concentration of free receptors in a solution of 90% free ligand and 10% receptor-ligand complex, knowing only the value of kD I could use some guidance on how to utilise the equation for the disassociation constant kD to find the concentration of free receptors [R] in a solution containing 90% free ligand [L], and 10% bound [RL] complex.

The Kd of the receptor-ligand interaction = 10^-8 mol l-1

Where Kd =  ([R][L])/([RL])

I assume as a percentage I could state, [L] = 0.9 and [RL] = 0.1, but am not sure if I'm taking the right approach.

Any clarification on this would be appreciated.

One big thing you're missing is units: Concentrations here must have concentration units - they can't be dimensionless numbers or percentages.

So one of the things you need to figure out is how to convert the percentages into concentration units. In this case, it's difficult to do directly, but we can apply a bit of algebra to figure it out. We're talking about 90% and 10% of the ligand in different forms, but we don't know anything about the total amount of ligand - that's alright, we'll just represent the total concentration of the ligand as $\ce{x mol \cdot l^{-1}}$. Therefore, we can now state that:

$$ \ce{ [L] = (0.9x) mol \cdot l^{-1}}$$
$$ \ce{ [RL] = (0.1x) mol \cdot l^{-1}}$$

Now the other bit of information we have is the equation for Kd:

$$\ce{ K_d = \frac{[R][L]}{[RL]} }$$

So we're looking for $\ce{[R]}$ (with associated concentration units!), and we know $\ce{ K_d }$, $\ce{[L]}$ and $\ce{[RL]}$ - or at least up to the unknown of $\ce{x}$. But, if you substitute the values you do know (including the factor of $\ce{x}$) into the equation and do some algebraic manipulation, I believe you'll find it doesn't actually matter what the value of $\ce{x}$ is - it should cancel out.

Note: If the value of $\ce{x}$ doesn't matter, why did I bother with the whole rigmarole of including it? Why didn't I just substitute 0.9 and 0.1 directly?

Well, the answer to that is my lead sentence - the concentrations in the equation should have (compatible) concentration units. If you don't have concentrations, you're using the equations incorrectly. (Look into the concept of dimensional analysis for a valuable way to help make sure you're doing many (but not all) calculations like this correctly.)

While for this specific problem things worked out nicely if you substitute the fractions/percentages directly, that's not a general solution. Depending on the exact setup of the problem, the $\ce{x}$s may or may not cancel cleanly. You may have to use some other equation/knowledge to put additional constraints on the value of $\ce{x}$. The only way to know that is to properly account for them from the start.

According to the information you have provided isn't the starting equation:

1 x 10EE-8 = (0.9 x [R]) / 0.1

So you can solve for [R]?

[R] = (1 x 10EE-8 x 0.1) / 0.9

I am not saying this is correct, but by substituting the values you provided isn't this how one would algebraically solve for an unknown? Maybe I am missing something(?)

You state you wish to know the concentration of free receptor. Wouldn't you need to know the total number of moles of receptor present in the equilibrium binding reaction, and wouldn't you need to know the final volume of the reaction?


Why is it so important to avoid infection of lacerations to the scalp? There is supposedly something unique with regards to infections of the scalp, although I cannot remember, perhaps it was to do with the CSF and its build up? I have scoured the internet for hours but have not found an answer.

Deep lacerations of the scalp that penetrate the fourth layer (area of loose connective tissue) have an increased risk of infection. This is because pus and blood spread easily within it. This can easily pass into the cranial cavity along the emissary veins Therefore, infection can spread from the scalp to the meninges and could lead to meningitis.


If Evolution Is In Progress, Why Fight Extinction? Natural selection is a central tenet of evolution. However, most biologists seem determined to prevent the extinction of the species that have been selected against. Why is this? Preservation of genetic diversity?

I thought evolution was supposed to create diversity not destroy it. What am I missing?

First, a shorthand definition of Evolution is heritable change and not 'progress' (which is a rather loaded word). Also, evolution is not 'supposed' to do anything, and can lead to both an increase or a decrease in diversity, since (local) diversity is simply the net result of speciation rate and extinction rate (if we exclude colonization of new species from other areas). Therefore, I think the question is framed in the wrong way.

Second, there are many reasons why biologists might want to halt species extinctions, as hinted in the other comments and answers. Most obviously, conservation biologists want to prevent man-made extinctions which are due to how we have influenced/modified/destroyed the natural environments. I don't think conservation biologists in general are determined to halt all 'natural' extinction. However, most of the time it is really hard to pinpoint what would be a 'natural' extinction. Either way, the current rates of extinction, which have been estimated to lie 100-1000 times (IUCN, 2007) above background rates (some say it's closer to 10000 times higher), indicate that most extinctions are man-made.

The rationales people use for preserving biodiversity can however differ. Three distinct categories are:

1) For human survival and/or economy, e.g. through ecosystem services or resources we rely on.

2) For human welfare, e.g. recreation or esthetical reasons.

3) Ethical considerations, e.g. inherent value of species or to preserve the unique evolutionary history of the system.

Another way to structure these is to label 1) & 2) as instrumental values and 3) as inherent values. The instrumental values can then be subcategorized as services, goods/resources, information (e.g. genetic to be used in medical research), and esthetical/spiritual values.

Since the direct value of individual species are often (usually) uncertain (irrespectivly of the direct rationales used) the precautionary principle is often invoked to justify species conservation. Also, numerous examples exist of how aspects of biodiversity are related to human values (some recent examples are Garibaldi et al. 2013 and Gamfeldt et al. 2013), such as production or services, which can also be used to justify both conserving biodiversity or individual species. However, other aspects of biodiversity are functional diversity, which focus on preserving functional groups of species, or phylogenetic diversity, focusing on taxonomic coverage and uniqueness (evolutionary history), instead of 'overall' biodiversity (see e.g. Flynn et al, 2011 for a discussion of these concepts). Under these perspectives less focus is placed on individual species.

Simply put, evolution through natural selection is a process which occurs naturally. It will occur to any self-duplicating organism with: variations, hereditary traits and threats to propagation (e.g. all life forms we are familiar with). Evolutionary biologists study this, the same way astrophysicists study space, and studying black holes or life forms doesn't indicate anything other then knowing how it works.

Actually, considering that most people in a certain field take interest in it (because logic), it is to be expected that biologists as a whole would rather see life doesn't go extinct then it does - again saying nothing about whether extinctions have or have not happened in the past.


Why do I want to urinate when I touch water? I've noticed that whenever I come in contact with running water (especially when I do my dishes), I have a desire to urinate. A quick Google search (link,link) gave me few different hypotheses:

Cold diuresis. Being in contact with cold water reduces temperature on the skin, which then constricts blood vessel to reduce heat loss, thereby increasing blood pressure and prompting the bladder to release excessive fluid.
Afferent innervation. I wasn't able to comprehend all the details of the process, but it seemed like this hypothesis is pertaining to the nervous system than circulatory system, hence different from first hypothesis.
Learnt psychological response. Second article linked above argues that this is a conditioned reaction, where even the sound of tap water triggers the desire to urinate. While it did not mentioned specific details of how this happens, I'm also assuming that this hypothesis is different from aforementioned hypotheses, because this hypothesis sounds more like a psychological response than biological reaction.

Which one of these hypotheses accounts for the desire to urinate when in contact with water? How exactly does it happen? If there is any other reason, feel free to add in the answer.

FIRST PART:
I am writing this answer with an analogy.I have analogised your question to a childhood habit developed by our mothers-when she would want us to urinate all she had to do was to take us to the toilet and make a "siiii" "siii" sound to mimic the sound of running water(more or less)
Since I have analogised in that way I think the third hypothesis (referred in your question)is more apt.
SECOND PART:
What fascinated me more about your  question was your comment-"I'll also be interested to see why the people will learn to have desire to urinate at the sound of tap water. Is there any reason that for that? – Hosea Jul 14 "
Indeed there is because we still have our mirror neurons
[SOURCE]
What I wanted to understand is if mirror neurons contributed to Pavlovian reflexes.The answer was yes
Furthur I could find out from sources that the micturition process has centres in the brain stem which are controlled by higher centres in the brain.One of them was the "medial frontal cortex".
Read the following article:

The Pontine micturition center (PMC, also known as Barrington's nucleus) is a collection of neuronal cell bodies located in the rostral pons in the brainstem involved in the supraspinal regulation of micturition. When activated, the PMC relaxes the urethral sphincter allowing for micturition to occur. The PMC coordinates with other brain centers, including the medialfrontal cortex, insular cortex,hypothalamus and periaqueductal gray(PAG). The PAG acts as a relay station for ascending bladder information from the spinal cord and incoming signals from higher brain areas.[source]

From the outline in the following lines I could conclude that there are mirror neurons in this region which 'may' be involved in the micturition control:

Yoshida et al. [26] recently recorded from neurons in the medial frontal cortex, some of which selectively responded to self or observed actions within a social context
[source]

Although research has confirmed that mirror neurons contribute to Pavlovian reflexes no such pathway has yet been discovered which can directly help us to confirm  and understand its relation to urination urge in contact with water.

I asked my doctor about this issue. I had noticed the effect after age 65 and I remember my mother putting my younger siblings when they were just a year or two old, on her insteps as she sat down, and imitated the sound of running water - like a half whistle - soothing sound. And pee came. Now when I do dishes, I immediately feel to pee although I did not really want to before. I know this happens to most older folks. My doctor said maybe it is nerve anticipation that activates the urethral muscles, and too, maybe the instinct of a baby in the womb of the mother surfaces again. I did not quite get that part. I think it is a psychological thing where we respond to brain-nerve-urethra instinctive coupling, something we have no control over. I have started to empty my bladder before going to do dishes. When you shower, it is natural to pee when the water hits you, even if you had no urge to pee before. This is no fancy explanation but I just thought it might contribute.


Any latest edition or successor of "Invertebrate zoology" by Ruppert & Barnes 2003? I have the 6th edition of the textbook "Invertebrate Zoology" by Ruppert and Barnes from 1993. I know there is a 7th edition from 2003, but is there and will there ever be a 8th edition? Assuming they should come every 10 years, shouldn't there have been one in 2013? So if Ruppert & Barnes retired, is there any more recent successor or alternative?

A worthy successor to this book series is "Invertebrates" by Richard C. Brusca et al. The latest edition being from 2016, so exactly what I was looking for.

https://www.amazon.com/gp/product/1605353752/ref=pe_353720_261047730_em_sp_C_1p_1_ti


Why is offspring of identical twins not identical? When identical twins marry identical twins, the children of the couples will be full genetic siblings but why are they not genetically identical?

They are not identical for the same reason full siblings are not identical.

A simplistic Mendelian setup would be the following:

X1/X2 = Mothers
X3/Y = Fathers

That means the children could be:

X1/X3
X1/Y
X2/X3
X2/Y

So children born to two married couples composed of identical twins only have a 50/50 shot at being the same gender, much less have the exact same set of genes and express them in the same way.

Now, the simplistic view above only concerns 4 alleles - but the human genome is composed of thousands. By the end, the chances of genetically identical offspring from a set of identical twins is still very, very low.

And you haven't even began to include epigenetic variations, which often arise as a response to the environment! One cousin might be shorter due to their diet as an infant, one might have allergies the other does not depending on if they played outside as a child, and for non-Mendelian traits (incomplete dominance, co-dominance, phenotypes that rely on more than one allele [especially hair, eye, and skin color]) there's even more opportunity to introduce differences!

There was actually a 1960s TV sitcom based on the notion of identical cousins. It was called the Patty Duke show. In reality the only way to have cousins that look alike would be through a quaternary marriage. That is when twins marry other twins. The children from the two marriages would technically be 1st cousins yet genetically they would be siblings as well. In other words, it would be impossible to figure out who the biological parents are based on the DNA alone since the parents (being identical twins) would share the exact same genetic material. The truth is the Patty Duke show scenario is highly unlikely. Patty and Cathy could not be identical cousins because the only way we get identical offspring is when a fertilised egg splits into two cells. Those identical cells grow into identical twins. So there would be a strong resemblance between Patty and Cathy but the odds of them looking like identical cousins is unlikely. More likely they would look like fraternal twins. Patty would indeed look like Cathy but you could tell the difference between them just as you could between any pair of sisters. The cousins wouldn’t look identical but they wouldn’t look like cousins. They would look like sisters.


What cell types comprise the median eminence and the tuber cinereum? I have tried pretty hard to get a detailed description of what exactly the median eminence and the tuber cinereum are but to no avail. I am very familiar with their anatomical relationships (spatially) with the hypothalamus, 3rd ventricle, mammillary bodies, etc; however, I still do not quite understand what they are or what cell types comprise them.

Are they areas of grey matter? Are they some sort of modified ependymal cell layer of the 3rd ventricle floor?

Or are they areas of connective tissue that merely "house" white matter projections from the hypothalamus to the pituitary? So, to repeat the inquiry from above:

What cell types comprise the median eminence and the tuber cinereum?

And, moreover, what's the actual function of the cell types that comprise them?

The tuber cinereum is the "swelling" at the ventral surface of the hypothalamus (Subarachnoid space surface) at the base of the infundibular stalk. The median eminence (a circumventricular organ) is an elevation on the ventricular surface of the infundibular recess of the 3rd ventricle.


Can pheromones be received other than by odor? I'm trying to understand how deodorants affect pheromones in humans.

Wiki states:

Axilla

  In humans, the formation of body odor happens mostly in the axillary
  region. These odorant substances serve as pheromones which play a role
  related to mating.

Deodorant

  A deodorant is a substance applied to the body to prevent body odor caused by the bacterial breakdown of perspiration in armpits, feet, and other areas of the body.

Can the opposite sex receive pheromones if a person uses crystal deodorant (doesn't have a fragrance; doesn't block sweating; prevents body odor by creating an invisible, protective barrier against odor-causing bacteria)?

We have only 5 senses, a 6th sense has been controversial, and some 6th senses are sometimes reported in new research in newspapers, but none have been conclusively been added to the clearly known 5. There is a second olfactory organ that deals with social signals in other animals, that we possess, the vomeronasal organ.

Pheromones are only olfactory molecules, so you can't get them other than by catching molecules and analysing them, i.e. smelling.

Humans react very strongly by attraction to some perfumes other than pheremones, and you arent supposed to block all your smells, only make them containable, a bit is probably a good thing.

Scientists did publish a study claiming that people can tell if they make a good immune response / metabolic genetic combo with a partner from smelling a potential partner's t-shirt.