text:
Subtracting shared DNA with half-sibling
I want to note that I am not a biologist. I've been on a nearly 20-year search for the identity of the parents of my 4th great grandfather (not an easy task.)
I'm using ancestry.com DNA, GEDmatch, and family trees of my matches in hopes of using DNA triangulation to find my ancestors. In addition, I have a half-sibling who also had his DNA tested which allows me to find common ancestors on this side of the family.
I read the article "Relatedness" on the topic of inherited parental dna with two half-siblings and I'm not sure I understand what the writer means when she says:

In other words, you and your half-brother should be able to figure
out what part of your DNA came from your mom.  And if you subtract out
that shared DNA, what is left must have come from your dad!

My first thought was that a person and their half-sibling wouldn't inherit exactly the same DNA from their mother, could they? For example, the mother has two different alleles for some trait. Her son could get a copy of one and the daughter could get a copy of the other. Therefore, in the author's example, how could subtracting out the shared DNA with the brother give the girl the ability to identify exactly which DNA must have come from her dad?
I read on and the author addresses this by saying:

One brother inherited the green version of the mother’s chromosome 2, while the other brother inherited the blue version.  This means that none of the chromosomes match!  So testing wouldn’t tell the brothers which version of chromosome 2 came from which parent.
It turns out, though, that it’s really unlikely that siblings would
have two totally different versions of a chromosome.  This is because
of something called recombination.

She's talking on entire chromosomes here which is different, but it doesn't seem to address fully why the girl should be able to 100% identify what DNA came from her dad by subtracting the shared DNA with her brother. I read that half-siblings share 25% of the DNA, but the mother here surely contributed more than 25% to each of her children.
In practice, my half-sibling shows a genetic relationship to people on our shared parent's side that I do not (and likewise, I have genetic relationships to people on our shared parent's side that he does not.) Therefore, I'm positing that my brother and I each inherited some different DNA from our shared parent.
I would take the writer's word for it, but I'm confused. Where am I going wrong? (Sorry about the bad biology background.)

The website is just wrong when it says for DNA tests on a person and their half-sibling:

In other words, you and your half-brother should be able to figure out what part of your DNA came from your mom.  And if you subtract out that shared DNA, what is left must have come from your dad!

Consumer autosomal DNA tests do not identify which of the two chromosomes present in the sample a detected variant can be assigned to.  The tests show only the two variant values detected at each location tested, and not which chromosome they come from.
Using this data from two tests, comparisons can show stretches of chromosomes which have matching patterns of variants which indicate with good probability that the corresponding pieces of chromosome have the same origin.  The tests do not tell you about the source of the pieces outside these stretches.
Each of two half-siblings do get half of their autosomal DNA from their common parent.  On average, half of the DNA each gets from that parent will also be inherited by the other half-sibling, and so will show up as matching stretches when the tests are compared.  Thus half-siblings will show around 25% shared DNA (around half of the 50% that comes from the shared parent).
Given a matching stretch of DNA results, one can determine the DNA variants that came from the other, non-shared, parent for the locations within that stretch of chromosome.  However, the locations outside the set of matching stretches cannot be identified with a particular parent (without testing of the parents).
There are two spots on that web page that do get this right.  One is in this diagram:

In the above, the bracketed area does identify the associated parents, but the unbracketed areas cannot be so identified.  (The colors shown are not reported by the DNA tests, so you can't just "follow the color" to identify matching chromosome areas outside the brackets.)
The other spot the web page gets it right is in this paragraph:

By finding the shared DNA, the brothers can find the pieces of the 23 chromosomes that came from their shared parent, just like we did for chromosome 1.  Any genetic information from the DNA on the corresponding sites on the other 23 chromosomes will tell the brothers about their fathers.

Outside of these two places the web page seems to mislead one into thinking that all the DNA can be associated with the correct parent, which is not the case without the parents being tested.

Oh, that's really disappointing given it appears to be a Stanford public education outreach type of program in charge of the website's Q&A. Thank you!


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Do non-pathogenic organism not have PAMPs? Are there any research paper which proves that a certain microbe is non-pathogenic?
According to this

PAMPs are delivered along with additional information that can be
  used by the host to distinguish pathogenic from nonpathogenic
  microbes and thereby guide the ensuing innate immune
  response.

Does this statement mean that non-pathogenic bacteria do not have PAMPs? If yes, then how would the host body differentiate between a pathogenic and a non-pathogenic microbe? Is there any well-known source containing a list of non-pathogenic microbes? Are there any research paper which proves that a certain microbe is non-pathogenic?

https://en.wikipedia.org/wiki/Pathogen-associated_molecular_pattern#MAMP

source: Stack Exchange

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sort: votes


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How to identify Ag nanoparticles in a solution?
Doing an experiment involving the production of Silver nanoparticles using bacterial extracts. The issue is proving that they've been formed.
AgNO3 is added to the solution, and the reduction environment of the bacteria reduces into silver nanoparticles of various size, depending on many factors.
Color change can be seen, and a change in the UV-vis spec also, but beyond that, is there anything else that can be done?
The papers I'm basing this project off of have access to electron microscopes, I don't.
Is there any sort of biological assays that react to metallic silver? or maybe to Ag NPs?
Or anyone have any experience involving biologically producing nanoparticles?
I'll be asking in Chemistry as well for a possible chemical reaction of identify metallic silver.

This paper says that silver nanoparticles enhance the enzymatic reaction that happens in a normal ELISA assay. You should be able to observe a significative shift in UV absorbance comparing your bacteria to a control.
Otherwise, I'd think simply of lysing the bacteria and centrifugating the lysate. I'd expect the pellet to contain nanoparticles and to be somehow different (in color?) from a control pellet.

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Catching a cold outside in winter?
We have all heard the typical “Put a jacket on youre going to catch a cold.” Usually stated by an older person typically a grandmother. Excuse the stereotype. Is there any evidence that colder weather makes one more prone to catching the flu or cold or is this simply a myth and misconception.

@Remi.b - That answer covers only seasonal flu, not colds.

This is a pretty old old-wives tale, taking many forms: don't go out into the cold while it's raining, or without a hat, with wet hair, without a warm coat or scarf, without boots, etc., "or you'll catch your death of cold."
The old wive's tale was immortalized by Jane Austin in her book, Pride and Prejudice, when the heroine's sister Jane falls ill after getting a soaking in the rain.
This has been studied extensively. A New York Times article describes one such uncomfortable-sounding study:

In the 1950's, Chicago researchers repeated the experiment on a larger scale with several hundred volunteers sitting in their socks and underwear in a 60-degree room before being inoculated with infectious mucus. Others, in coats, hats and gloves, spent two hours in a large freezer. The conclusion: all 253 chilled volunteers caught cold at exactly the same rate as 175 members of a warm control group.

In other words, being cold had no effect on catching a cold.

A survey of the medical literature shows that for more than a century, scientists have invested an extraordinary amount of time and energy in debunking this old saw, with the aid of a small army of shivering, sneezing volunteers. But despite their efforts, the link between colds and the weather still lingers and continues to inspire yet more research.

A 1968 experiment studied the effect of (among other methods of chilling) a cold water bath at several stages during and after inoculation with rhinovirus (one of the many viruses responsible for the common cold). No effect.
Yet the studies continue, because anything shown to decrease the incidence of the common cold would be beneficial to the sufferers, as in the US alone, 75 to 100 million physician visits are due to the common cold, and millions of days are lost from school and work.
But what has never been proven is that getting chilled in any way causes one to come down with a cold.
There are a lot of studies that fail to show a corellation. However...
there are a handful of small studies that show that having cold and dry nasal mucosae increases the susceptibility of infection when inoculated with rhinovirus, though. So, if these studies are accurate, then being in the cold when exposed does increase the chance of becoming symptomatic.
'You'll Catch Your Death!' An Old Wives' Tale? Well...
Exposure to Cold Environment and Rhinovirus Common Cold — Failure to Demonstrate Effect
Acute cooling of the body surface and the common cold

That 1950's study seems odd in that 60°F is not very cold at all.

Agree that 60° is balmy. Freezers less so.

How stupid of me to miss the freezer part…


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Mechanism behind Philadelphia chromosome translocation?
I was reading up on causative factors of leukemia on medicinenet and I came across the following statement:

...an exchange between chromosomes 9 and 22 leads to what is known as the Philadelphia chromosome.

What is the mechanism behind this? Is it purely mechanical? Would the locations on both chromosome’s be equidistance from the end (for lack of biology vocabulary.) In other words, would each segment involved in the swap have to be similarly sized?

Hi, in this paper you might find some details: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1762911/
In brief: 1) the mechansims can be several, I wouldn't say "purely mechanical" but it is related to the physical/chemical properties of the region of chromosome involved (some regions have sequences that for partly unknown reasons are more prone to be translocated than others). 2) It is not necessary that the two regions have similar size, and actually unbalanced translocations (in the exchange is not reciprocal) exist.

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Does octopus eye presents the equivalent of fovea in primates?
I'm working on a simple computational model of Primate eye:  as we know, it presents a central part, the fovea, that is very rich of receptors in comparison with eye periphery. I'm wondering if other species eye, like octopus, present a similar structure: a central fovea.
Thanks

Yes, they do have an area of densely packed receptors, although not point-like as the human fovea.
Talbot and Marshall (2011) performed a retinal topography analysis in three species of cephalopods: a cuttlefish, a squid and an octopus.
According to the authors:

It was found that all species possessed an increase in photoreceptor density in a horizontal streak approximately placed at the position of a potential horizon in the habitat.

Here is an image from the same paper:

The retinal topography of each of the three species in this study: (a) S. plangon and (b) O. cyanea show a prominent, horizontally orientated band of increased photoreceptor density across the horizontal equator of the retina; (c) S. lessoniana shows a more centrally positioned area of increased photoreceptor density.

Source: Talbot, C. and Marshall, J. (2011). The retinal topography of three species of coleoid cephalopod: significance for perception of polarized light. Philosophical Transactions of the Royal Society B: Biological Sciences, 366(1565), pp.724-733.


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What is the active site (not metal binding site) of tyrosinase and other monooxygenase/oxidoreductases?
On https://www.uniprot.org/uniprot/P07524, tyrosinase is shown as a monophenol monooxygenase. However, the UniProt database only shows a metal (copper) binding site, when there is presumed to be an actual active site that performs the reactions, other than the metal binding site. Are there any clues to find the actual reaction active site for a monooxygenase? Please include the sources, if there are.

Your question is a bit low on information. Is this the exact protein you're working on? The uniprot website states that all the information is inferred from homology, did you check homologous proteins? Did you check if more information is available for closely related proteins?

Tyrosinase uses two copper ions as cofactors. The copper binding site is the enzyme active site.

The active site of the crystal structure of tyrosinase from Streptomyces sp. (PDB code: 3AWT) is shown below. Note the two copper ions (coordinated by active site histidine amino acid residues) and an oxygen atom (of a water molecule) bound to the copper ions:

Matoba et al. (2011) J Biol Chem 34: 30219-30231.

The Cu(II)-soaked crystal structure of tyrosinase ... possesses two
  copper ions at its catalytic center.


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Do all living humans literally descend from one ape?
In the opening chapter of Sapiens, Harari writes:

Just 6 million years ago, a single female ape had two daughters. One became the ancestor of all chimpanzees, the other is our own grandmother.

Is there evidence that this is literally true? There seem to be two ways in which it could fail:
(a) Weak version---there is an individual last universal common ancestor, but it's not an ape: that is, all humans (and chimps) share a single individual creature as an ancestor, but that creature was not an ape. It was some earlier ancestor whose descendants would go on to be apes.
(b) Strong version---there is no individual last universal common ancestor: if tracing the entire history of life on Earth and assuming some "stopping point" where we saw life emerge as (e.g.) from a volcanic vent primordial soup, we would find distinct creatures emerging simultaneously in a population, with similar but distinct genetic code, from one of whom some species (such as humans) evolved, and from another of whom others evolved.
Is there evidence that neither is the case? First, (1) that there is an individual creature, rather than a population of creatures, from whom all life descended. If that is true, then it follows that all humans have an individual as a common ancestor, since you can at worst follow the line of descent back to the primordial individual. And, next, (2) that the last common ancestor of all humans (and chimps) was also an ape, rather than say some other animal.

Did you read about Mitochondrial Eve and Y chromosomal Adam: https://en.wikipedia.org/wiki/Mitochondrial_Eve

As the answers describe, this quote is true, but the wording is a bit misleading. A better quote would state "One became an ancestor of all chimpanzees," because there were other apes in that population that are also ancestors to chimps and/or humans. But, the quote is accurate in that there was one female ape with two daughters, one of whom is the mitochondrial ancestor of all humans, the other is the mitochondrial ancestor of all chimps. The mother in the quote is the human/chimp mitochondrial most recent common ancestor. These apes likely greatly predate the human/ape speciation event.

Just 6 million years ago, a single female ape had two daughters. One became the ancestor of all chimpanzees, the other is our own grandmother.

Short answer
Whether or not the claim is true actually depends upon the specific DNA sequence you are considering. The claim is true for sequences without recombination (such as mtDNA and most of the Y chromosome). The claim does not hold true for most of the genome and it is therefore misleading.
Long answer
Basic knowledge required
First, if you don't know the concepts of

allele
haplotype
ploidy
selection
genetic drift
segregation
recombination and crossover

, then you might want to have a look at a short introduction of evolutionary biology such as Evo101 for example. The below answer will make more sense to you with some a priori knowledge.
Coalescence
Imagine there is today a population of $N$ individuals. We are going to look at this population backward in time (which is a little bit unintuitive). For simplicity, we will assume asexual reproduction, no recombination, absence of selection (only drift) and constant population size of $N$ individuals. The assumption of no recombination is key here. The other assumptions are details just to make my job at explaining coalescent theory easier.
We start at time t=0 and are going backward in time. If two individuals are siblings at $t=0$, then, it means that in the previous generation, they share the same parent. Therefore, if we connect individual from generation $t=0$ to their respective parents at generation $t=-1$, we see that some group of individuals (the siblings) "coalesce" to fewer individuals (their parents). Individuals at generation $t=-1$ that are not connected to individuals at generation $t=0$ are those who did not reproduce (or who did not leave offspring that have survived until adulthood).
You can keep iterating over generation $-2$, $-3$, $-4$, etc... At each generation, the number of individuals that are connected (that our ancestors) to present day individuals is diminishing as more and more coalescence happen. After a sufficient number of generations, eventually, only one parent will remain. This single individual will be the ancestor of all present individuals.
If you enjoy math, then note that such process is actually a simple a branching process for which it is relatively easy to calculate the expected time (and the whole PDF) to the next coalescent event and the expected time (and the whole PDF) until all individuals in the population coalesce.
So, assuming no recombination, if you consider individuals in a modern population, then you can be sure that all individuals share a common ancestor who is a single individual, at some point in the past.
Incomplete lineage sorting
The process of all individuals coalescing into a single ancestor takes a little bit of time. For recently diverged species (say species A and species B), it is possible that this common ancestor is older than the time of divergence between species. If this is the case, it is then incorrect to think of a mother who gave birth to two individuals, one becoming the ancestor of all individuals of species A and one becoming the ancestor of all individuals of species B. In such a case, we talk about incomplete lineage sorting.
Note that when we talk about 'incomplete lineage sorting', we are generally talking about specific genes as not all genes coalesce the same way when there is recombination and segregation (see below)
Recombination
Now the trick is that in the presence of recombination, different sequences coalesce differentially. It also means that when you look at two sister species, some sequences can show incomplete lineage sorting while others don't.
The presence of recombination therefore makes the claim false!
Do we recombine?
Yes, all of our genome recombines to the exception of two sequences

mitochondrial DNA (mtDNA)
Y chromosome not including the Pseudo-Autosomal Region (PAR)

mtDNA is maternally inherited (without crossover) and transmitted to all offsprings, while the Y chromosome is paternally inherited (without crossover) and transmitted to sons only.
So, is the claim true?
mtDNA
It is true that there was an ape who had two daughters. One daughter's mtDNA became the ancestor of all mtDNA we have in humans today, the other daughter's mtDNA became the ancestor of all mtDNA that exist in chimps populations today.
Of course, this daughter is the common ancestor of all modern mtDNA but is not necessarily the Most Recent Common Ancestor (MRCA). In humans, the MRCA to all modern mtDNA is called Mitochondrial Eve (mt-Eve or mt-MRCA).
Y Chromosome
The same claim is true for the Y chromosome (although I am not sure there was really not a single recombination event happening on the Y chromosome since). The MRCA to today's all Y chromosome is sometimes called Y-chromosomal Adam (Y-MRCA).
The names 'mt-Eve' and 'Y-chromosomal Adam' have of course been chosen in reference to the creation myth of Abrahamic religions.
Rest of the genome
The Y chromosome and mtDNA together represent less than 0.2% of our genome. The rest of our genome does recombine.
The claim does not necessarily hold true for 99.8% of the genome. I would therefore tend to think that the claim is misleading at best, wrong at worst.
Adam and Eve
We can call Adam the MRCA of all Y chromosomes today. Only Y chromosomes, not the rest of the genome. We can call Eve the MRCA of all mtDNA today. Only mtDNA, not the rest of the genome.
Of course, Adam and Eve did not live in the same time period and did not live at the same place. Adam and Eve never met. And of course, there were plenty of other humans around. They are in no way the first two humans.
Other popular source of knowledge
PBS Eons - The Two People We're All Related To

This is interesting. I will read more. I am struggling intuitively to understand the distinction between descent of particular DNA components versus of whole individuals. Shouldn't the question be answerable just by looking at a "tree" of individuals, without having to consider DNA? We might need godlike powers of historical observation, but if we had them there would be an answer at the individual level. So the DNA story may substitute for the lack of godlike history knowledge, but should it not ultimately tie back to individuals? (1/2)

(2/2) I.e., not who is the ancestor of which Y chromosomes, but just which individual(s) is/are the ancestor of which individuals. Separately, I'm confused about the coalescence argument. Consider times t = 0 ... N, and two individuals A_0 and B_0 at the "dawn of life," and each individual X_t asexually produces a child who will live at X_{t+1} and then dies. Then today I could have two individuals A_N and B_N who do not share a common individual ancestor. I believe you that this counterexample fails, but I don't clearly see what evidence we know that establishes its failure.

@Philip remember sex is involved with most individuals, you have two parents, 4 grandparents, 8 great grandparents, ect. As you go back eventually every individual in the population that reproduced is your ancestor. the ones that did not reproduce didn't pass on their genes. For a lot of asexual organisms "individual" as a concept kinda breaks down, a bacteria splits in half forming two, which daughter cell is or is not the same individual as the parent?

there might be a woman who first had the mutation that created the gene common to all mitochondria in humans, but she had to have sex with someone, and so do her children and both of them has to have parents, and grand parents, and so on and so forth. As you go back it becomes increasingly more likely with each generation that they will have an ancestor in common, If you go back far enough they basically have to have common ancestors because the population size is finite but the but the number of ancestors increases exponentially. most importantly.

It is easy to describe a scenario in which there is no single individual who can be called "the" ancestor of all individuals in a much later generation. Let's say there was, indeed, one individual female who had a mutant form of mDNA that occurs in all of us now; and also let's say that that particular mutation never occurred again (a BIG assumption!).  Indeed that female would be an ancestor to all of us; but certainly not the only ancestor. That one female's daughters and sons each carried only half of her genetic information; the other half came from their father(s); and each of those fathers had their own mothers.  Each of us is a genetic mosaic of a very large number of individuals.
Even if all humanity descended from one tribe of early hominids, with no cross-breeding between tribe members and outside tribes (very unlikely), we would all very probably carry genes contributed by almost all of the members of that tribe.

"Some of the information contained in this post requires additional references. Please edit to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted."  Please be more specific.  Which assertions require references?  This is very basic genetics.

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Why are nosebleeds easier to get in the winter?
I understand it probably has to do with the dry air, but what does dry air do to make nosebleeds so easy to get? For example, even gently blowing your nose can cause a nosebleed for some people during the winter.

The vast majority of bloody noses in healthy individuals arise from one specific area in the nose (on either side): Kiesselbach's plexus.

In the mucosa of the nasal septum (the cartilagenous structure separating the nose into two sides), there is an area where several arteries "meet", giving it an exceptionally rich vascular supply, called Kiesselbach's plexus. It is on the anterior surface, and exposed to dry air and trauma.
Bleeding typically occurs when the mucosa erodes for any reason, and the capillaries and venules (and sometimes arterioles) become exposed and subsequently break. The result is the familiar bloody dripping of a nosebleed.
Have you noticed that your lips chap more in the winter? Dry air and cols temperatures do that. The mucosa of your nose also dries out and suffers some damage. Not like your lips, but damage none the less. Damaged nasal mucosa is more susceptible to tears/trauma/erosion. If it happens in an area of rich blood supply, you get a nosebleed.
Anything that helps with the integrity of the nasal mucosa is going to help reduce nosebleeds. One can

run a humidifier in dry weather
avoid irritating by touching the nose or blowing nose too often
apply a very light layer of petrolatum or Bacitracin ointment to the inside of the nose covering Kiesselbach's plexus at night so the nose-breathing doesn't dry out your nose
use nasal saline spray to moisten and soothe the nasal membranes (don't rub the tip of the spray bottle against the nasal membranes, though)

*more serious or recurrent bleeding needs medical attention to rule out  other conditions that are associated with frequent nose bleeds.
Epistaxis

Perhaps a note that it's not always in the winter.  I used to get nosebleeds during the August-October period, which is when humidity is lowest where I live.

@jamesqf - good point. However, cold air holds less water (is dryer) than warm air in the presence of water (i.e. barring arid regions), so yes, it's more common in most places in the winter.

Might also depend on the amount of time you spend indoors or outdoors.  When cold winter air is brought inside and heated, it will be very low humidity - at least without some kind of humidifier.


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What dinosaurs live during cretaceous period?
I cant find website that shows all dinosaurs that lived during this time?
Tyrannosaur rex and triceratops I know but what else?

Wikipedia has a nice summary: https://en.wikipedia.org/wiki/Category:Cretaceous_dinosaurs

cant you make list of them that lived with tyrannosaur rex please

To see which dinosaurs lived alongside Tyrannosaurus I suggest you browse the dinosaurs list here: https://en.wikipedia.org/wiki/Hell_Creek_Formation#Dinosaurs , as T-rex was found in the Hell Creek Formation. It might not be a complete list but it is the best I know.


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What are the animals in these pictures?
I recently found some pictures of animals' skeletons. Does anyone know what species they are?

The pictures appear to be computationally generated or computationally enhanced visualizations (e.g.: change in color rather than in polygons around joints). Did the source perhaps include further images?

@tsttst Seems to be animal under X-ray.

@aircraft - They are not xrays. Just dramatically lit/shaded, maybe even computer generated, but not xrays.

The first, as @John said, is a water mammal: a seal, sea lion, something along those lines. The teeth are consistent with the Australian fur seal. The second, I have no clue. It's very light, fast, (I thought maybe a flying squirrel, but the 'hands' are wrong.) Seeing the teeth would help.

The top is some kind of seal (the flippers give it away) and the bottom is some kind of lemur (the long thin limbs and tail with the narrow skull) but that is the best I can do from just those photos. It might be a flying lemur but again from just the one photo without scale is difficult to say for certain.

the lemur's tail is longer than its trunk.

@aircraft There are many species of lemur with vastly different tail lengths, and we cant see how long the tail in the image is that well. Also your link is broken.


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How do you find probabilites of carrying an X linked recessive disease in a blank pedigree given only one phenotype?

In the above pedigree, the black square indicates the male
affected with Hemophilia which is a X-linked recessive trait. What is the
probability that the proposed child, which is a male (indicated as ?), will carry the disease?
I started off by trying to figure out the probability that the sister has an X chromosome carrying the disease, which I got as 10/16 (Since the mother must be XcXc or XcX and the father either XY or XcY; possible genotypes are XcX, XcX, XcXc, XcXc, XcX, XX, XcXc, XXc)
I then repeated the procedure for each generation and got the final answer as 9/16. However, the correct answer is 1/8. How do you obtain this? Are my assumptions flawed?
Source: https://biolympiads.com/wp-content/uploads/2016/08/inbo2009-Q.pdf

Assume the disease is rare. The parents of the affected male are thus probably X/Y and Xc/X. Their daughter (the sister of the affected male) has a probability of 1/2 of being a carrier (Xc/X). Her daughter also has a 1/2 probability of being a carrier. Her son has a 1/2 probability receiving the mutant X chromosome. Therefore, the probability that the son is affected is 1/2 * 1/2 * 1/2 = 1/8.
I can’t right now, but I’ll try and make it clearer with a figure tomorrow.


text:
Can anybody identify this plant?
I'm from Brazil. And I have this plant at home.
Can anybody identify this plant?

Strongly related: https://biology.stackexchange.com/questions/36542/what-is-the-name-of-this-flower

It's an Epiphyllum Oxypetalum. Epi is greek for around (epi-center) and phyto is plant, epiphytes are plants that live on other plants, for example rainforest plants that grow on the canopy of tall trees.
There are lots of hybrids and lots of colors.

It is a water loving cactus from Central America, I have some but I do not know the latin name. I asked a similar question.


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How much time does it take for an evolutionary change to take place?
I think I've read that in humans, it takes either 50,000 or 100,000 years for a mutation to fixate. But I've looked into the books I thought it mentioned it and I can't find it. I know there are theories that behavioral modernity has arisen before 40,000 years ago, and that modern humans evolved from Homo heidelbergensis, Homo rhodesiensis or Homo antecessor, some 100,000 to 50,000 years ago,  but I don't know if this implies the same. Anatomically moderm human . On the other hand, this other article (7 years old now)  says evolutionary change might take 1 million years (Not so fast).
How much time takes for an evolutionary change to take place in animals in general, but also in humans in particular? (if there is any difference between humans and the rest of the animals. I know mutations don't take the same time to spread in animals than in bacterias, for example)

I think the term you're looking for is "fixation". The fixation of a mutation is its presence in a population with frequency =1, that is every individual of that population has that mutation.

Are you arguing that it took 50,000 years for humans to cause the extinction of the Carolina parakeet?  Or that it takes 50,000 years for XDR tuberculosis to become common?

Any change in allele frequency is considered an "evolutionary change". So, you don't need anything to fix to get an evolutionary change.

But it seems not everybody uses it in that way, my question goes in the sense it is used in this link regardless of semantics.  https://phys.org/news/2011-08-fast-evolutionary-million-years.html . BTW, I've also seen it used that way it's used in the link, in a book

@Pablo well this popular article is awfully phrased! I can't really judge the content otherwise as the popular article fails to link to the original research paper from which they supposedly report the results.

Rather than time, you might want to measure in generations.  A human generation would be 15 years or more, rats may have 4 generations in a year, bacteria coupld perhaps manage 15 minutes or less...

Humans are known to have experienced a pretty significant bottleneck around  70,000 years ago, this alone will drastically increase the rate of fixation across that event. to the point of a single generation.

How much time does it typically take for a new mutation to fix in an animal population?
The answer can really take any number. It will all depend upon the size of the population and the selection coefficient on the mutation. If we assume neutral mutations, then we can use Kimura and Ohta (1968)'s result. They showed that the expected time for a neutral allele to reach fixation (given that it will reach fixation) is
$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0),$$
where $p_0$ is the initial frequency and $N$ is the population size. Replacing $p_0$ by $\frac{1}{2N}$ and you get
$$\bar t\left(\frac{1}{2N}\right)=-4N\left(\frac{1-\frac{1}{2N}}{\frac{1}{2N}}\right)\ln\left(1-\frac{1}{2N}\right)$$
which can be simplified
$$\bar t\left(\frac{1}{2N}\right)=-4N\left(2N-1\right)\ln\left(\frac{2N-1}{2N}\right)$$
Stick in any $N$ you want and you'll get your answer. Of course, this equations assume panmixie. In absence of panmixia, then it all depends upon the interconnectedness of the different populations. If some population are perfectly isolated, then a mutation will never fix in the entire species.
How much time does it typically take for a new mutation to happen and fix in an animal population?
The time to wait for the mutation to fix is typically quite negligible comparing to the time it takes for this mutation to happen. Let $\mu$ be the mutation rate. The number of mutations happening each generation is $2 N \mu$ and assuming they are neutral a fraction $\frac{1}{2N}$ of them will fix. Hence, the expected waiting time is $\frac{1}{2 N \mu \frac{1}{2N}} = \frac{1}{\mu}$. In humans, the average $\mu$ is of the order of $10^{-8}$ per site but there is a lot of variation among sequences.
So, if your mutational target is only a single site, then the expected time to fixation of a currently non-existing mutation is $10^8$ generations! If you are considering the entire genome as you mutational target is the entire genome, your mutation rate is of the order of $10$ and the expected number of generations is only $\frac{1}{10}$.

Perhaps just to add a source, the standard mutation rate in humans is approximately 0.5×10^−9 per basepair per year, and mitochondrial dna mutates quite a bit faster - so it depends what aspect of a human is being referenced. link  Cheers

@Aaron43 See edit


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"Immortal Genes" common to all organisms?
Author Sean B. Carroll mentions that there are about 500 genes common to all organisms. They have to do with the essential DNA machinery and so forth.
What are these genes? Where can I read more about this fascinating concept?
When you google immortal genes you get mentions of Sean B. Carroll. What term do others use for these genes?
"When we compare the genomes of Archaea, bacteria, fungi, plants, and animals, we find about 500 genes that exist in all domains of life... The functions of immortal genes are central... processes such as decoding DNA ... and making proteins. All forms of life have depended on these genes since the origin of complex DNA-encoded life early in Earth's history." (Making of the Fittest, pg 79)

I've not heard the term. However, "Housekeeping genes" are genes that are always turned on as a basic function of being alive.

That’s the term you get when a physicist writes about biology.

Please provide a reference with a preferably a link for Carroll's statement. Otherwise your question is unclear.

Ok I added quote from his book. I would LOVE some details on what these genes are or what term others use for them.

In order to expand my answer (did you read it?) in an appropriate manner, could you indicate how much biochemistry you know. For example, can you think of 100+ genes that would be required for ribosomal protein synthesis in any organism? Do you know what replication, transcription and translation are? Have you heard of glycolysis. If your answer is generally "no" then the expansion of my answer will need to be different from if it is yes.

their called housekeeping genes

Introduction
I believe that Sean B. Caroll is confusing:
• the minimum number of genes required for a viable organism
with
• those genes that are present in all organisms — so called ‘immortal genes’
I will deal with each in turn.
The minimum number of genes required for a viable organism
I have not read the book from which the quotation is taken. From its context and my knowledge I think that the author is mistakenly interpreting ‘the minimum number of genes required for a viable organism’ as ‘the genes present in all organisms’. This is because he seems to be referring to work from the laboratory of Craig Ventner on engineering mycoplasma.
Mycoplasma are among the smallest organisms capable of independent life. They have a genome of about 500 coding sequences, but as parasitic organisms they devotes some of these genes to their parasitic mode of life, while they lack others that the host provides.
The number of 500 may actually be too high: a figure of 300 is quoted in this description, who had plans of Ventner’s plans to build an organism containing a minimal genome containing only such essential genes. There is more on this in a Wikipedia article entitled Mycoplasma laboratorium. It should be noted that the word “immortal” does not appear in either account.
‘Les Immortels’ — genes present in all organisms
The poster would like a list of those genes essential to life, but I know of no such list. How would one go about composing one?
First, one has to set the rules. Do parasites, such as mycoplasma, which are dependent on their host organism, count? Do human beings count? We require amino acids and vitamins, but obtain them from food rather than synthesizing them ourselves. So although it is necessary that a self-sufficient organism have the enzymes for synthesizing the 20 amino acids of the genetic code, these are not all present in humans. I would suggest that we have to restrict ‘les immortels’ to self-sufficient organisms.
Second, one has to decide whether one is talking about a set of genes for accomplishing a function, or individual genes with a structural relationship in all living things that suggests a common identity. For example all cellular organisms (i.e. excluding viruses) must have ribosomes to synthesize proteins, but the protein complement of those ribosomes differs among organisms. Thus, the ribosomal proteins necessary to engineer a minimal mycoplasma may differ from those present in a bacterium such as Escherichia coli, and will certainly not be common to humans. I would suggest we would have to go for the latter.
Having made this decision, one  would get a team of undergraduate students to take all the genes in the genome of E. coli (or even of a mycoplasma) and perform BLAST searches to see whether they are present in representative organisms. Unfortunately I am no longer in a position to torment undergraduate students in this way, so I will have to start a list myself and encourage others to add to (or subtract from) it.
The List — a start
The genes for DNA replication, transcription of RNA and protein synthesis constitute the low hanging fruit here. My area is (used to be) protein synthesis, so I will start there:
Protein Synthesis
Large and small subunit and 5S ribosomal RNAs (3)
Ribosomal proteins (≤32)
Protein synthesis factors — EF1, EF2, IF1 and possibly others
Aminoacyl tRNA synthetases (20?)
tRNAs? — but all that is conserved is probably the anticodon (and sometimes not even that)
Accessory enzymes for protein synthesis:
Pseudouridine synthase
rRNA methylases?
DNA synthesis
B-family DNA polymerases?
RNA synthesis
? Evolutionarily related, but complicated because of multi-subunit nature
But if DNA synthesis is a problem, the reactions leading from RNA to DNA are surely not:
Enzymes of nucleotide metabolism
Ribonucleotide reductase (two subunits)
Thymidylate synthase
Uracil DNA-glycosylase?
Tetrahydrofolate reductase?
Enzymes for interconversion of nucleotides — Adenylate kinase? Nucleoside-diphosphate kinase?
Metabolism
This requires some work. One cannot specify either aerobic or anaerobic metabolsm, but in either case one needs oxido-reducto enzymes. Enzymes of hexose metabolism — hexokinase? Enzymes to metabolize key intermediates like glutamate and glutamine, and enzymes for introducing different groups in synthetic processes. This could make an interesting crowd-sourced project, or, failing that, a game for your next Biochemistry Christmas Party.

Aren't the number of genes common to all organisms and the number required in a minimal organism different concepts? Related, sure, but different.

@JackAidley — They are indeed. However, it is Sean Carroll — to whom the poster refers — who is confusing the two and actually refering to the number in a minimal organism. I tried to make that clear in my answer. Thus, a minimum set of genes might require 50 ribosomal proteins (say) but it may be possible to identify only a half a dozen (if that) that are common to all organisms. Likewise a system for replication and transcription is required, but the divergence between eukaryotes and prokaryotes may be such as to exclude common components (not my field).

I would be happier if you included that in your answer directly.

I have now edited my answer to address the valid point made by @JackAidley. The original answer was more directed to the poster and the extent of his biochemical knowledge, but the purpose of SE Biology is to provide answers of general utility, so the current answer refers to aspects of biochemistry with which the naive reader may not be familiar. The partial list is new. I realize it is scanty, but it is better than nothing, and nothing is what was there before.

I would suggest that we do not restrict ‘les immortels’ to self-sufficient organisms, because the question was not which genes are present in all self-sufficient organisms, but which genes are present in all organisms! Even parasitic bacteria have to replicate their DNA. However, I would exclude viruses (which are debatably organisms, and do not)

@user253751 — As I wrote, it’s pretty much a party game, although nobody else seemed to want to play. You can make lists of what you like, but if you include parasitic organisms it seems to me you are cheating unless you include the genes supplied by the host. And it seems obvious to me that whatever wording the poster used, he wanted to know what the minimum list was for self-sufficient life. Not that it matters what the poster intended, but that seems to me the more interesting question.

This statement is approximately correct.
According to the data in Zhang, 2018, as illustrated graphically by author Alex P.R. Phillips, there are 307 shared essential genes in the three domains of life.  That figure does not show shared nonessential genes - and I would question how "nonessential" a gene really is if it has been conserved in multiple groups since the last common ancestor of all life!  Additionally, that figure only covers major model organisms and there are probably a few that are present in other members of each domain.  Note that the statement you quoted was only about "500 genes that exist in all domains of life".  It doesn't say they can't be lost and replaced in some species.
The paper cited above is free, and if you have the patience I think you should be able to run down the updated list of all those genes in the supplemental data.

It seems likely that Carroll's claim is untrue, in fact there are a much smaller number of genes shared between organisms and genes that provide core functions appear to have independent evolutionary histories in many cases (source).
It is unfortunate that Carroll does not provide a reference for this claim, so I do not know where he was getting his data from but the book was written in 2006 which is the infancy of whole genome sequencing so that may be the cause for the error. But, even so, by 2003 evidence was pointing to a much smaller number, and even the earliest genome comparison papers (e.g. here) weren't finding conservation on the scale suggested by Carroll.
So, rather than "around 500" immortal genes, it appears that there is  a much smaller number of genes that both common to all life and share evolutionary history, perhaps 30 or so and, remember, these numbers can only ever go down as we sequence more species so it's entirely possible that it will turn out that there are no genes that are universal and share common evolutionary histories in all organisms.
You may wonder how this can happen when there are so many core functions that a cell must surely have to function. The answer appears to be that new genes able to perform these functions evolve, perhaps specialised to operate under particular conditions, and - for a time - the organism carries both versions of the gene until eventually losing the original gene in some lineages. You can see this pattern of evolution in organisms where an enzyme is known in two forms and some carry one or the other, while some carry both (here's detail on one such example).


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Can nitrate be an electron acceptor for NADH generated in the citric acid cycle?
Is the citric acid cycle aerobic or anaerobic? I know that the oxygen is required to accept the NADH electrons so that NAD+ could be regenerated. Nevertheless, if other electron acceptors, as nitrate (NO3–), are present, could they also be used to regenerate the NAD+? I am asking this because I read a thesis claiming that “acetly-CoA enters the citric acid cycle and through anaerobic nitrate-respiration a multiple amount of ATP is generated.” If you have some literature that you can share with me I would be really grateful. Thanks.

I have changed your title because it is misleading. Strictly speaking the chemical reactions of the TCA cycle are anaerobic because oxygen is not involved in any of them. But that is not your question. Your question is about electron acceptors for NADH produced in the TCA cycle. I have kept the question in the body of the text for you to modify if you like.

Yes, many microbes can use electron acceptors other than oxygen.
https://en.wikipedia.org/wiki/Anaerobic_respiration
https://www.sciencedirect.com/science/article/pii/S0168165611000289

As it stands this is not the sort of answer this site encourages. See the Help especially the section "Provide context for links". Your answer would be improved by (1) Emphasising that the TCA is intrinsically anaerobic, it is the process of reoxidising NADH that can involve oxygen or not, (2) That for all organisms have a single electron acceptor, in most cases (and in all animals) oxygen. At the moment your answer could be interpreted as certain microbes having a choice of electron acceptor.

@David is that not true?

Not that I was aware. I thought they were highly specialized, but I may be wrong. The point is to address this important question clearly in your answer, citing an example if I am wrong.

The redox potential of other oxidizing pairs differs from that of oxygen and water and therefore a different set of reactions must be used to obtain energy (pump protons) from oxidizing NADH with them.I am not a microbiologist, but it appears from  this that, as I would have expected, most bacteria that employ other electron acceptors are obligate anaerobes and will not therefore operate alternative modes of respiration. But some facultative anaerobes appear able to do this.


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Do dead cells always contain no nucleus?
If I examine a dead cell, can I be sure that it has not a nucleus?
And what about the other organelles?

If you're looking at cause of death by standard apoptosis, to initiate the process, cytochrome c will be released from the mitochondria, bind with apaf-1, and undergo a structural change resulting in what looks like a biochemical ninja star (figure 4). This will activate caspase-9 which will activate other executor caspases, eventually creating an avalanche of protein-degrading enzymes that will leave the structure and organelles of the cell looking like paper mache. Regarding the nucleus, the complexes of enzymes meant to maintain dna integrity and structure will be degraded, the DNA's network influence on the cell will become largely inert, and the dna will be condensed and broken apart by nucleases. The membrane of the nucleus is full of proteins and ribosomes, and these will be degraded too. If you are looking to simply identify an inert nucleus by its skeleton, you may not have much success either - here are a few good images from a nice study showing the progressive destruction of a nuclear structure.


text:
Negative spikes in neurons
I'm new to neuroscience research and came across a term called negative spikes (sometimes also used in conjunction with terms biphasic spikes or positive-negative spikes), but could not find what it meant from scientific papers. Can a spike occur in a negative direction (hyperpolarization from the resting potential first, followed by depolarization) or does this term mean something else entirely?

Please add context as to where you found the terms. What papers etc.

this question reminded me of: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804433/

Intracellular recordings of action potentials always show the same format with which you are familiar. There is polarisation which the stimulus reduces, a threshold is reached, there is a positive spike, then repolarisation, hyperpolarisation, a refractory period an a return to the baseline polarisation.
The term "negative spike" applies to extracellular recordings. These measure the potential between a point close to but outside the cell and a reference point. The inflow of cations into the cell causes a drop in extracellular potential, which appears as a negative spike in the recording.


text:
Organism with the greatest amount of gold as percentage of body mass
I've read that the human body contains trace amounts of gold:
http://www.tellmehowmuch.net/how-much-gold-is-found-in-the-human-body.html
http://web2.airmail.net/uthman/elements_of_body.html
Are there other species that are known to have significantly higher ratios of gold to body mass?
And while there seems to be no definitive answer about the benefit of gold being in the human body, are there any species for which gold has demonstrative bodily uses or benefits?

Acidothiobacillus ferrooxidans can gain metabolic energy by utilizing gold thiosulphate complexes (Reith et al., 2007); Micrococcus luteus can oxidize methane to methanol using gold-containing enzyme (Levchenko et al., 2002).
However, for most organisms, gold is toxic (Wietkiewicz & Shaw, 1981); some bacteria actively detoxify gold: Cupriavidus (Ralstonia, Wautersia) metallidurans, Desulfotomaculum sp., Desulfovibrio sp., Hyphomonas adhaerens, Plectonema boryanum, Pseudomonas aeruginosa Salmonella enterica,  Shewanella algae, Spirulina platensis (Reith et al., 2007).

Reith F, Lengke MF, Falconer D, Craw D, Southam G (2007) The geomicrobiology of gold. ISME J. 1: 567-584.
Levchenko LA, Sadkov AP, Lariontseva NV, Koldasheva EM, Shilova AK, Shilov AE. (2002) Gold helps bacteria to oxidize methane. J Inorg Biochem 88: 251-253.
Witkiewicz  PL &  Shaw CF III (1981) Oxidative cleavage of peptide and protein disulphide bonds by gold(III): a mechanism for gold toxicity. J Chem Soc Chem Commun 21: 1111–1114.

Thanks! Is there a known typical amount of gold as a percentage of body mass in any of these?

Shewanella algae is one of the bacteria that precipitate gold intracellularly. 3.2 × 10^15 cells of S. algae is able to create up to 1 mol of crystalline gold nanoparticles (see "Konishi et al., 2006" in Reith et al., 2007). As for other bacteria mentioned above, look into the papers cited by Reith et al., 2007 . . .


text:
Neanderthal and Sapiens DNA
From WIKI:

Modern humans and Neanderthals share 99.7% of their DNA

and

1–4% of the DNA of living non-African humans are found by the Max
Planck Institute to likely come from Neanderthals, a result confirmed
in 2012, and refined to 1.5–2.1% in 2014

What do they mean? If it is similar for 99.7, how it could be that 1.5%-2% is unique genes from Neanderthals?
The Africans do not have them, so African different from European in 1.5-2% ? But that's not true.

Q. “What do they mean?”
A. Two different things

“…share 99.7% of their DNA” is fairly straightforward.

This means that if you compare, base for base, the total DNA sequences of a group of Neanderthals with a group of humans — doing appropriate statistics — you will find, on average, 99.7% identity.

“1–4% of the DNA of living non-African humans…likely come from Neanderthals” is more nuanced.

This is because that 1–4% (generally thought nearer 2%) that is thought to come from Neanderthals could still be 99.7% identical to the human DNA it is thought to have replaced.
How can that be?
First let us assume that there are no genes unique to either humans or Neanderthals. (This may not be true, but the assumption emphasizes that we are considering the same genes.) Now suppose that after the divergence of Neanderthals and humans from their common ancestor the Neanderthals acquired a mutation that produced a new haplotype for a particular gene that spread to all Neanderthals. The percentage difference in DNA would be small, but the haplotype and hence the gene counts as Neanderthal. If it enters the European human population by interbreeding after emergence from Africa, then that gene is regarded to have come from Neanderthals. So the idea is that this is true for approx. 2% of non-African genes, even though the originating Neanderthal DNA may be 99%+ similar in sequence. Likewise, differences are observed between Africans and non-Africans in these gene haplotypes, even though the DNA sequence otherwise is very similar.
I have not discussed the evidence for this 2% gene haplotype difference here as I recently covered it in an answer to another question, specifically on that topic. (Hence my somewhat late interest in this question when it re-emerged.)

This answer is not essentially different from that posted by @John, but I have tried to explain it in biolgical/genetic terms rather than by analogy, in an endeavour to make my answer clearer.

start by checking to see if they are comparing the same thing, are they comparing base pair sequence, functional genes, non-functional genes, whole sequence or only the variable portions, one could even be comparing nuclear or mitochondrial DNA or both. I could not determine whether mitochondrial DNA latter was used in the listed estimate for last study.
the first is comparing exact nucleotide sequence while the second is comparing functional gene differences (for the listed numbers, they compare them several ways) so of course the numbers do not match. Note both are also comparing different reconstructed genomes, and with different methods no less.
imagine comparing two dictionaries, one person checks to see if definitions  match letter for letter exactly and ignores missing definitions, the other checks to see if they cover all the same words and give the same definitions considering them the same even if the exact wording and punctuation are different, of course the two people will get different percent differences.

Yes, the genes are the same, even between humans and chimps. They are talking about pairwise differences. Lining up 1000 nucleotides of DNA between the two species, 997 would be identical.

except they are comparing portions of a reconstructed genomes and saying the genes are the same can have two meanings they may match in base pair comparison or they may have the same functional gene, humans and chimps do not have all the same genes, there are unique genes in humans.

Almost no genes are unique to humans.

The 99.7 is a percent pairwise similarity. If it were percent genes shared, it would be much higher.


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Why can't cats run longer distances like dogs?
Cats can run about nearly 30mph. Their stamina, though, is for short distances. Why can't they run longer?
Can cats be trained to run longer distances like dogs? For instance, could their resistance improve by stair case training (running many times up and down the stairs)?

Amounts of fast twitch vs slow twitch muscles could be factor, cats are specialized as ambush predators so should have a lot of fast twitch.

Cats, both domestic and wild are, for the most part, ambush predators that catch their prey with bursts of speed. Lions and cheetahs do run down their prey, but not over long distances. Wolves chase their prey over long distances, sometimes for hours. This is a classic case of trade-offs. Humans have modified the behavior of domestic cats and dogs, but both still rely on the characteristics of their ancestors. You can build cat muscles with exercise, but you can't make them "dogs".

Canine elbow changed from allowing paws to swivel — which is important for grabbing and tackling prey — to keeping the paw more stable, which is important for long-distance running.
Meanwhile, cats maintained their tried-and-true method of ambushing prey, using quick bursts of sprinting to tackle startled beasts.(ref)
Cats and dogs diverged about 60 million years ago, and endurance adaptations for dogs started at least 40 Ma from mongoose like ancestors.
The forelimbs of African wild dogs show a combination of adaptations to endurance running, including a vestigial first digit and reorganized wrist muscles, passive spring action from a powerful ligament, and bigger muscles that store energy and provide stability. (ref)
You can see for yourself if you examine a dog's wrist and paw and check it's springiness, length, agility, grabbing ability... it's straight and springy for running.
Another know fact is that:
canines maintain a high mitochondrial protein turnover facilitating rapid adaptation to environmental extremes and energetic challenges (Miller et al, 2017, PLOS ONE 12:e0174874).
The cat's nasal channels are also less adapted to humidifying warm/cold air and tracking down prey for exhaustive predation.
Cats are typically forest animals and can climb trees better and specialize in fast attacks, including razor sharp claws where the chitin flakes a bit like flint.
You can see the cat's running adaptations when you consider it's jumping ability, climbing ability, reaction speed, attack poise, claw vs bite ferocity, limb agility, speed of movement, night vision.
They comprise a spectrum of ecological specialties that place them at different ends of the performance chart for much of their anatomy and biochemistry.

Given the diversity of cats and dogs, it is hard to generalize about the distances that cats and dogs can cover.
This question would be hard to answer even for dogs and cats of similar size, as there would be many confounding effects, such as the size of the legs, the size of the lungs, the basic metabolic rate and the motivation.
Training your cat could indeed allow it to run longer distances as its muscles develop and its amount of erythrocytes increases, but I wouldn't recommend pushing an animal too hard as it could result in exhaustion or death.

So train on the stairs could help then. I tried it out with treats my cat did 10x on 14steps that’s about 140steps he ran then he gotten tired so if he can run 2x as munch in month his stamina will grown higher and build muccel

Cats don't run long distances because their body temperatures rise quickly. This is because a cat's sweat glands are limited to a few parts of it's body, mostly it's paws.
Other mammals, such as dogs and humans have sweat glands all over their body and can therefore regulate internal body temperature for longer periods of time.

The part about dogs is untrue - they are similar to cats in this case, with the sweat glands being on the paws. They pant to keep cool...


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What are the abilities, sizes, and appearance of tyrannosaur rex?
Size
height 15-20ft tall
weight 7-9tons
length 40-42ft long
did the flim of jurassic park had some corrections of the reality I beilve there many things they gotten right on the trex

you really need to show some research of your own, you also need to be more specific about what you are asking, Are you just asking what is wrong with the ones in jurassic park?

I’m asking were the Trex in Jurassic Park flims were indeed right of their appearance size and abilities

You may want to change the question to reflect this.

The jurassic park rex is probably the best one ever put on film. the hands and skin are the biggest errors everything else is pretty good asinde from a few minor things.
It should probably be feathered but that is relatively recent discovery so they can be forgiven , how the feathers were distributed is anyone's guess. the weight estimates range from 5-9 tons with reality likey somewhere in between, 7-tons is a safe estimate for the largest ones.
The arms are a little too big and the finger position is all wrong. The fingers are held laterally (palms toward the midline) like a birds wing and with a lot less flex in the fingers and the arms would have been closer together. the production crew even admits they changed the arms to make it more intimidating.
They did make the rear portion of the head too narrow, it spreads out more with wide "cheeks"(jugal) improving the binocular vision and increasing the size of the jaw muscles. they did improve this in more recent movies. The base of the tail might be a little skinny too but that is nitpicking.
for scale and measurements use a scientific skeletal drawing like this.

As for behavior the only seeing movement thing is total fiction, but even the movie make it clear this is due to the genetic reconstruction not natural so no points lost. T-rex actually has a really good suite of senses with better hearing and smell than many other dinosaurs and binocular vision to boot. They would have head better vision than a human and a sense of smell comparable to a modern bloodhound. Hearing would have been good for a dinosaur but still inferior to a modern mammal.
The bite force we see on screen is light and dainty compared to what the animal could actually do, T-rex has the most powerful bite of any animal known.
40 mph is within the highest estimates of its speed but not unbelievable, 25-30 is more likely. T-rex does have some derived adaptations for speed (elongated interlocking compressed metatarsals, transverse processes on the caudals,ect) and was probably the faster and/or more maneuverable than other large theropod and it may have been faster as an adolescent. great lecture on T-rex anatomy.
Vocalization is an issue t-rex probably could not roar but it could have honked like a goose, and when you scale up a honk to T-rex size it will still end up sounding roar like, the roar from the movie is not that bad.
I am sure someone who has watched the movies more recently can recall a few other errors.

tyrannosaur rex roar could be possible since these dinosaurs were non avian birds they could roar. trex height 15-20ft tall so the height is correct and speed mostly 20mph


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What culture medium should we use for tap/drinking water bacteria?
We are a group of high school students from Manila who is performing an investigatory project on a topic that we chose which, at first glance, seemed simple, but turned out a bit complicated. We're trying to test the effectiveness of SODIS of solar water disinfection in killing bacteria.
I previously asked a  question here at Stack Exchange and we consulted our teacher about the answer we received. According to her, at our level, it is best to use culture media. Our testing will be qualitative. We won't be identifying the specific type of bacteria. Rather, we will observe culture media if anything grows in there.
She gave us an assignment to research about what medium to use. Due to inexperience and lack of knowledge on what we find on the internet, we resorted to ask here again.
For bacteria commonly found in tap water, what culture medium do we use? We found mentions of Legionella, Salmonella,  E. coli, and Anabaena sp. in our research.
In this article, we found different types of culture media. TSA captured our attention because it is a "general type." Nonetheless, we're not that sure about what "general" means if it means it can be used for the bacteria I mentioned above. There's also EMB that appears to be used in two of the bacteria we mentioned.
Edit:
It appears that not all culture media is good for student use. According to this article, only LB Agar, Nutrient Agar, and Tryptic Soy Agar can be used by students. Among these three, is there something I can use?

Usually when culture-based methods are used to test drinking water a range of selective culture media are used (media that favor the growth of a specific category of bacteria, e.g. the MacConkey Agar mentioned in the article you linked to). This is because the aim is to test for the presence of known harmful bacteria.
I would suggest that any of your suggestions (LB agar, Nutrient Agar or Tryptic Soy Agar) would work just fine.
On another note: How are you inoculating the agar? The concentration of bacterial cells in tap water is very low, to test for bacteria usually a large volume (~ 1 liter) is passed through sterile filter paper which is then pressed onto an agar plate to transfer the bacteria.

As an adjunct to your research, i would advise that you visit your local water authority to gain more insight into the process of testing water for bacterial contaminants using culture media. They will usually point you to a commercial lab that does the testing for the local water authority. That commercial lab will provide you a wealth of information, especially on why a particular medium or media is used to test local water samples.
Another source of information may be your local hospital. Visit their clinical lab and query if they have conducted water tests using culture media. They too will provide a wealth of information.

Would be better as a comment but seeing your rep, I understand why you could have posted this as an answer.


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Identify vegetable with stalks coming out of it
I know nothing more about this vegetable than the fact that it is safely edible, which a local vegetable vendor in South India told me. It's green (white inside) and has a strong smell resembling that of cabbage. It has these stalks coming out of folds in the outer skin, as well as a few leaves. STP identify.

It is a kohlrabi. The leaves are cut off. https://en.wikipedia.org/wiki/Kohlrabi#/media/File:KohlrabiinMarket.jpg

@ermanen You could probably post an answer.


text:
Why can't amylase break down glycogen?
Amylase is an enzyme that breaks down starch in the form of amylopectin and amylose. Both amylose and amylopectin are formed by alpha glucose joined together by (1-4) and (1-6) glycosidic bonds. Glycogen is no exception, just that it has more branching. However, why is it that a google search shows that it is hydrolyzed by Glycogen Phosphorylase rather than amylase? Also, how can amylase digest both (1,6) and (1,4) glycosidic bonds?
Any help would be greatly appreciated.

At an approximation the active sites of enzymes can be considered as having two aspects. The first relates to the catalysis — in this case the breaking of the glycosidic linkage. The second relates to binding the substrate. This review of the α-amylases by MacGregor et al. shows that there is a range of a-amylases, differing in this latter respect — their substrate specificity. In general there are binding sites for a varying numbers of glucose residues at either side of the bond being cleaved. This is shown in Fig. 3 of that review:

The important difference in the structure of glycogen and starch (amylopectin) — seldom mentioned in general biochemical or biology texts — is their patten of branching:

As this previous answer of mine to a different question explains, this results in a globular structure for glycogen granules in which only the ends of the chains are accessible. (The image below, from Protopedia, illustrates this better, especially if you imagine it in three dimensions.)

Hence the substrate-binding site of α-amylase does not have access to the residues that need to bind for it to perform hydroysis of glycogen, and, indeed, the enzyme that breaks down glycogen — glycogen phosphorylase — is specific for these free ends.
The α-amylases that can hydrolyse both α-1,4 and α-1,6 glycosidic links are quite few compared with those with specificity to one or the other type of linkage (see Table 2 of the MacGregor review, if you can obtain access to it). The impression obtained from following up two of the examples there is that the enzymes involved can exist in alternative conformations, the correct one of which is triggered by the substrate. An example is the glycogen debranching enzyme, the studies of which in Sulfolobus solfataricus and Candida glabrata can be read freely on-line. Although somewhat less directly relevant, the example of a Thermoactinomyces vulgaris neopullulanase is another variation on this theme.

So in summary it means that glycogen is arranged like a sphere so that only the ends of the glucose chain is exposed, hence amylase cannot work on it.

And that some amylase have active site flexible enough to accommodate both sort of linkages?

@user35897 — As regards the spherical form of glycogen, yes, and I have added another image (referenced). As regards my guess about flexible active sites, no, I was wrong. I seems that it is the enzyme overall that is flexible in being able to adopt alternative conformations. I have altered the last part of my answer with references to examples of studies with crystal structures. Good questions educate us all.

just a random afterthought but how does glycogen get digested as it goes through the gut to the small intestine, since glycogen phosphorylase is not produced in the stomach or small intestine? Some sources seem to tell me that amylase CAN indeed hydrolyze glycogen.

@user35897 — You are failing to differentiate between two different situations. One is the mammalian cell (e.g. a liver or muscle cell), from which amylase is absent, and where the breakdown of glycogen can be (and is) controlled by controlling the activity of the only enzyme in that cell able to do so — glycogen phosphorylase. The second is in the digestive system where any glycogen from a meal of meat is digested (or not). There it will presumably be exposed to, and succumb to, the same amylases that break down starch in food. [I mistakenly wrote GS, not GP in previous version of comment.]


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Practical Question about Evolution, Population Genetics and Speciation
North American cicada male of the genus Magicicada sing depending on the species at different times of the day and attract the females of the corresponding species. The species are very similar, but when crossing they have sterile (infertile) offspring.

In the species M. tredecim the time of the song is determined by the gene locus EARLYBIRD in an intermediate inheritance: The allele EARLYBIRD leads in the homozygous state to morning singing, the allele earlybird leads in the homozygous state to evening singing, heterozygotes sing at noon.
How does the frequency of the earlybird allele in the species M. tredecim change when the number of females of M. tredecassini increases? Does it increase, decrease, or does it remain the same?

I think it would not change the frequency of the earlybird allele, because they don't have a evolutionary advantage. But maybe it could also decrease the frequency, because infertile descendants sounds like a disadvantage? But I'm totally not sure and can't provide a real 'biological' reason since my thoughts are more like intuition.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. 2

@Remi.b : Thanks for the hint. I have written down my own thoughts about this question.

Good. I am retracting my close vote. +1

Infertile descendants indeed sound like a disadvantage. Individual must invest a fair amount of resources into making an offspring. Making sterile offspring is just a waste of resources as those offspring aren't going to pass on any gene further to any grandchildren.
If there is an increase of the tredecdssini females, then male tredecim that sing quite late are going to mate with many tredecdssini leading to the production of sterile offspring. There is therefore selection against the allele 'earlybird' leading to an increase in frequency of the 'EARLYBIRD' allele.


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Do viruses compete with each other or even infect each other? (Virus vs Virus)

I have read on a few websites that there can be competition between
the viruses in a host for replication, nutrition etc. Do viruses fight against each other, i.e. are there viruses that infect or attack other viruses directly or indirectly?
If yes, can this property help in curing or limiting hazardous viruses such as HIV
using less hazardous viruses which can be cured and can compete with
these hazardous viruses?

Can you please link to your websites and maybe provide direct quotes or a clear description of what you mean by "fight"?

By fight I mean can one virus destroy the other one by some method such as decoding the RNA

From what I understand virus on virus action is not particularly common but it isn't unheard of.
Consider the Sputnik virophage which

reproduces in amoeba cells that are already infected by a certain helper virus; Sputnik uses the helper virus's machinery for reproduction and inhibits replication of the helper virus.

Also consider the Mavirus virophage, which

is a double stranded DNA virus that infects the marine phagotrophic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus. Mavirus can integrate into the genome of cells of C. roenbergensis, and thereby confer immunity to the population.

As a last example, consider the Organic Lake virophage, which

is a double stranded DNA virus that infects the marine phagotrophic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus. [...] [It] preys on Organic Lake phycodnaviruses, which in fact may rather belong to Mimiviridae than to Phycodnaviridae.

So yes, viruses do at least occasionally attack viruses and inhibit their infectious potential and grant a sort of immunity. I'm not aware of any applications of this in medicine for now but maybe somebody else can add something to this if they know.

As TG2 mentioned, some viruses may exploit the presence of an additional virus, but viruses generally don't infect other viruses (as in a smaller virus injecting its DNA into a larger virus) simply because they lack the built-in resources and protein-machinery to replicate other virus species.
Natural selection causes each virus strain to retain only the genes it needs to replicate itself, which means the chances of being able to replicate a rent virus inside a fundamentally different virus are effectively 0 for all practical purposes.
Additionally, there's no reason for viruses to infect other similar (by surface structure or content) viruses because in the case of an infection, the virus particles would quickly cannibalize each other, collectively thwarting themselves.


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What is this (water-loving) bug?
For some time we've been finding these little fellows in our apartment:

They seem harmless enough, but finding them is a bit... annoying. I found the fellow above in the bathtub, and it's not uncommon to find more than one.
Unfortunately, some started to appear near the kitchen sink as well. Or outside of the bathroom on the floor (at least that's where we noticed them).
I think this thing prefers darkness over light, and seems to be drawn towards wet places or just water. These critters are also surprisingly fast.
What is it? Should we be concerned about a pest problem, or is this just a minor, unwelcome guest?
PS. We live in Poland.

It is a Lepisma saccharina or silverfish.
It is rather common and yes, it's harmless.

This answer would get more upvotes if you added a picture and perhaps addressed why the OP is finding them in wet locations in their home. In other words, it'd be good to "beef up" your answer a bit :).

@theforestecologist While you'd generally be right, as the OP I find the Wikipedia link to be a very good answer. After reading through the Wiki article I found it not surprising at all - the bug likes wet places, darkness and is fast (all 3 characteristics that I listed). No surprises then that I find the things in the bathtub or near the sink...


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What are the chances that Tyrannosaurus Rex could roar?
Tyrannosaurus Rex is now thought to have possibly had lips. Less of chance of it roar though I was told by a friend just because there are birds doesn’t mean they can’t.
Evolution isn't linear, just because one branch of a tree could/couldn't do something, doesn't mean 70+ million years later descendants could/couldn't do it too?

there's info on that here. https://www.washingtonpost.com/news/morning-mix/wp/2016/07/12/think-dinosaurs-roared-like-in-jurassic-park-the-truth-new-research-says-is-a-bit-wimpier/?utm_term=.868191bc02b2 The thoracic musculature uses bones that describe some kind of roar power if it is present.

birds and crocs can't that's called bracketing, which is not definitive but a good indicator.

Careful now: T Rex was not a bird, it was a non-avian theropod. Birds are dinosaurs but not all dinosaurs are birds. In the same way, tigers are cats but not all cats are tigers.
The argument that T Rex could not roar is not only based on none of its closest relatives being able to as you seem to indicate. Dinosaurs (and by extension birds) are archosaurs, a clade that includes crocodilians too and crocodilians are quite a bit more close to the basal form of archosaurs than T Rex was. Crocodilians can only sort of "hiss", not roar in the colloquial sense. And birds cannot roar. This is a decent start to a thought process but this isn't really the argument for why dinosaurs likely didn't roar in the past.
Researchers who have studied the potential vocalizations of prehistoric, non-avian dinosaurs have found indications that similar closed-mouth vocalization to those found in other living archosaurs are very probable: https://news.utexas.edu/2016/07/11/dinosaurs-may-have-cooed-like-doves
Closed-mouth vocalization is not really compatible with what people typically think of as roaring. It still allows a variety of sounds that don't necessarily (though perhaps probably) somewhat resembled crocodialian or simple bird vocalizations. So no, it's not impossible that some non-avian dinosaurs could roar but the current state of our knowledge is that they very likely could not.

so you are saying they couldn't roar at all since u say they could not in the end :(

I'm not claiming that they definitely could not. I'm saying that the current scientific consensus seems to be that they probably could not.

I guess they couldn't :(

Of course you have to ask yourself, if you scale a goose honk up to t-rex size, how different is it really from a roar.

a cooing T-rex :-)


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Pseudoautosomal regions of the X chromosome showing heterozgyosity
I've always had questions for myself about sex differentiation, mostly on account of an unusual history & puberty. I won't go into details, but needless to say it was unique.
My question is... I got results back from 23andme showing hetereozygosity at the beginning & ending of the X
I've been diagnosed as XY androgen insensitive & pseudohermaphrodite with mullerian structures intact.  Born with questionable stuff internally, only definitive thing is nothing male (no prostate, no seminal etc..)
They also did show a Y, but it was apparently missing half of it (though I've read thats not unusual for half of it to be --)
Can you have a hetereozygosity at the ends of the x and not have another x?
rs6644972   X   178624  AG
rs28475515  X   182276  CT
rs28463388  X   191998  TT
rs28669107  X   195014  CC
i6033542    X   200928  CC
rs6655397   X   201935  GG
rs7890186   X   202458  GG
i6033543    X   209741  CC
i6033544    X   215805  CC
rs28736870  X   220770  GG
i6033545    X   228250  GG
rs6603204   X   298440  GG
i6033547    X   301596  CC
rs2738344   X   310897  AA

A normal male can show heterozygosity in the "X" results of a 23andMe SNP test despite having only one X chromosome.  This is because there are very short regions at the ends of the Y chromosome, called pseudoautosomal regions, that match up with equivalent (homologous) regions at the ends of the X chromosome.
Because the pseudoautosomal regions of the Y are homologous to the matching regions of the X, the SNP results for those areas cannot be distinguished in the SNP tests, so the results appear along with the X results in "X" chromosome file.  The results in those two areas of the file can be either homozygous or heterozygous at each location.  Most of the locations in the "X" file are for  locations outside of those regions, so most of the file entries cannot report heterozygous results.


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What is the diameter of the measles virus?
I have searched countless studies. None have given this number. In fact there seems to be no details of any kind about the measles virus.

I'm voting to close this question as off-topic because questions like this are far too simplistic for Biology.SE; answering the question is as simple as Googling "measles virus diameter."

I believe this paper answers your question or at least comes very close to it: https://www.ncbi.nlm.nih.gov/pubmed/6540797
I'll reproduce the abstract here, with emphasis mine to indicate the relevant portion:

The molecular length of measles virus RNA and the structural organization of measles nucleocapsids.
Full-length measles virus RNA molecules isolated from purified virions or nucleocapsids and examined by electron microscopy were 5.12(+/- 0.12) micron in length, corresponding to a molecular weight of 5.2 (+/- 0.1) X 10(6). Purified virions examined by negative staining in the electron microscope exhibited a pleomorphic range of particle sizes varying in diameter between 300 nm and 1000 nm. Purified nucleocapsids had dimensions of 21 nm (diameter) X 1254(+/- 7) nm (length) and a central core of diameter about 5 nm. Full-length nucleocapsids were composed of 204 (+/- 3) protein discs. The pitch of the nucleocapsid helix was calculated to be 6.1 nm and the helix angle, alpha, to be 8 degrees 16'. Approximate volume calculations indicate that each enveloped virus particle contains multiple nucleocapsids.

In case of unfamiliarity with the term "virion", see: https://www.britannica.com/science/virion
In case of unfamiliarity with the adjective "pleomorphic", see: https://en.wikipedia.org/wiki/Pleomorphism_(microbiology)


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How many genders are there?
These days it is often contested how many genders is there. So my question is how many genders is there and is it unnatural for evolution to generate multiple genders.

this is a much better fit for the social sciences.

this is a bad question as shows complete lack of googling beforehand. I suggest you do some research and come back, asking "hey here is what i know, here is what i don't understand"

Sex vs Gender
Sex is defined by the anatomy of an individual. The majority of people can safely be categorized as either male or female. There are exceptions and limit-cases of course such as intersex people for example.
Gender is a social construct. It is therefore not the role of a biologist but the role of a sociologist to address the details of the concept of gender. I am therefore not trained to discuss these points but I will just say a few introductory words.
The gender can either refer to a social role based on the sex of the person (gender role) or personal identification of one's own gender based on personal appreciation (gender identity). The two most common genders are male and female which are named after their sexual equivalent. However, there are other types of genders. Btw, you might want to make sure to avoid confusion between gender and sexual orientation. It is also important to distinguish between "gender role and "gender identity"
Have a look at wikipedia > Sex and gender distinction for more information.
Note that, in biology, as we are not dealing with the social construct of the gender, we tend sometimes to use the term 'gender' as a synonym of 'sex'. Using the term gender instead of sex also has the advantage in biology to avoid the confusion between 'sex', 'sexual reproduction' and 'sexual organ'. I will below use the term 'sex' and 'gender' as defined by sociologists.
Answering in the text

These days it is often contested how many genders is there. So my question is how many genders is there[?]

There is no true answer to this question. There are as many genders as we want to as it is a social construct. There are only two sexes (and limit cases).

is it unnatural for evolution to generate multiple genders.

For reasons explained above, the question makes no sense. But let's replace 'gender' by 'sex' and rephrase your question as

is it unnatural for evolution to generate multiple sex?

There are species with a number of genders different from two. There are of course also species where single individuals have carry organs of both sexes. There are species where reproduction is asexual. There are species with sex but very little sexual dimorpisms (thanks @TimonG.), there are species with sexual reproduction but not sexes (sometimes mating types), etc... So, no it exists.
In humans however, there are only two sexes (plus limit cases).
Sex and sexual orientation
Of course, sex and sexual orientation are not the same thing. While there are only 2 sexes in humans (and as many genders as we want), there may be a lot of different sexual preferences. In fact, if we go into the details there are probably as many sexual preferences as there are people! Typically, we categorize those sexual preferences into a few sexual orientation. Note that there is nothing "unnatural" (whatever this term mean) to having a sexual orientation that differ from what the majority of the people with the same sex have.
You might want to read the post How can homosexuality evolve despite natural selection?

I think a noteworthy addition to this is that there are also species which do have different sexes but don't exhibit sexual dimorphism (outside of perhaps their genitals) or exhibit it to a much larger or much lesser degree than humans do. Physical and behavioral sexual dimorphism is present in humans but isn't a "biological necessitiy" in species which have sexes.


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What's the difference between a simple and 1-foliolate (unifoliolate) leaf?
How is a 1-foliolate leaf (e.g., Hardenbergia) different from a simple leaf?

Short answer:
Look for a pulvinus at the leaf-stalk/leaf-lamina junction.

Long Answer:
So from a strictly anatomical identification standpoint, this can be a bit confusing.
According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):

Simple: Undivided, as a leaf blade which is not separated into leaflets.

Where:

Leaflet: A division of a compound leaf

and

Compound Leaf: A leaf separated  into two or more distinct leaflets.

So the definition of a compound leaf is to have "two or more distinct" leaflets.
But wait...
From plantnet:

one-foliolate (1-foliolate, unifoliolate): a compound leaf reduced to a single leaflet, usually recognized by the articulated or jointed ‘petiole’, which is in fact a petiole plus a petiolule.

So what gives?
Perhaps this is due to a deficiency in terminology, as discussed (and corrected) by Jiménez-Saa 2011.
But, again Harris & Harris (2001) hint toward how this might arise [emphasis mine]:

Unifoliolate: a leaf theoretically compound, though only expressing as a single leaflet and appearing simple.

So there is still a fundamental difference between the two.
Structurally, we can see the difference at the basal joint of the foliar structure:

Simple or unifoliolate: The leaf is undivided...with (unifoliolate) or without (simple) an articulation between the leaf lamina and leaf stalk. [source]

Put differently:

Unifoliolate leaf is usually recognized from a simple leaf by the presence of a distinct joint or a pulvinus at the lamina-petiole junction, which is in fact a petiole plus a petiolule.

Note: Pulvinus = a distinct enlargement/swelling at the base of (sometimes at the apex of) a petiole or of a petiolule.

Note: a discussion about the developmental evolution of unifoliolate characteristics in Cercis canadensis is discussed here.


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Why do animals have fur and feathers?
Does it give them protections from harm?
Sphynx cats, being furless, can get hurt from thorns if they go through bushes
So I'm assuming it's more like defense from animals biting them.
A lion mane is attraction for females and protection on the neck since most predators go after the throat.
Why do only lions have manes for protection and not other cats like domestic cats?

Could you specify one question? Fur and feathers, or the lion mane?

Im justing asking the fur and feathers for animals gives them protection from predators simailr of lion Manes for their neck

short answer insulation.

you have to think this out for yourself Gian, read some stuff. It's mechanical and thermal.  you have to read a lot about evolution of fur and feathers, you'd learn a lot!!!

The nice thing about studying evolution is that questions like this can be answered with replicates of history. There are two groups of homeotherms; Birds, and mammals. Both these groups require an enormous amount of food to fuel this self-generated heat. Body heat is too expensive to throw away. So fir and feathers are convergent examples of insulation to keep this hard-won heat in. That there are many examples of feathered dinosaurs that could not fly implies that feathers were not originally for flying.

but whats the purpose can the fur and feathers also be protection from wounds from predators like the claws wont get to close to the skin

@Gian: Of course.  Evolution is not simple engineering, where something only does one thing.  For instance, a mammalian ancestor probably evolved fur for insulation.  Later, some species evolved it futher as protection (thick fur), camoflage, sexual adornment (the lion's mane), weaponry (rhinoceros horn), &c.  Birds went even further, evolving insulating feathers into flight structures & sexual adornments like the peacock's tail.

@Gian the technical term for what jamesqf is explaining is called exaptation.

...also... in the case of lions it looks like the evolution of the male's larger mane has been influenced by additional factors other than heat regulation, as described in this article: http://science.sciencemag.org/content/297/5585/1339

oh so fur is for tempter not protecting from claws from other animals like defense. in the flim Jungle Book Shere khan mention to Mogli he has no fur or others as fur was more of protection from predators. Mogli being human with out any defense of protection wouldnt survived from tiger claws and sharp fangs through his skin. If he was covered with fur he will be protected

@Gian: Much as I appreciate Kipling, he's not an authority on animal biology, at least in the rather egotistical voice of Shere Khan.  Fairly short fur isn't much protection against claws: just ask my dog :-)

I'm more up on hairs than feathers so I'll answer with respect to fur -
PFA Maderson in American Zoologist, 1972, suggests that mammalian hairs began as mechano-sensory organs and later gained sufficient density to function as insulation -

A chance mutation led to subsequent multiplication of the originally
  sparsely, but spatially arranged papillae, causing the induction of a
  sufficient density of "sensory hairs" to constitute an insulatory body
  covering.

This is a function which has not been lost - it may be a defining characteristic of mammalian hairs that they act, via follicular nerves, as sensory organs. In humans the density of follicular nerve supply is especially high, enough for W.Montagna, "Evolution of Human Skin", 1985, to liken them, regardless of size or location, to the dedicated feeler hairs - vibrissae - of related apes - which makes the sensory function the principle one most of the hairs on modern humans serve. As I suggest they probably are the principle function of hairs of other "hairless" species like Hippopotamus, Elephants, Mole Rats - which, like humans, are not actually hairless.
A whole range of functions besides sensory became possible once hairs evolved, including insulation, water shedding, protection from direct sunlight and physical abrasion, visual signalling/communications and dispersal of pheromones. Mammals managed to evolve and use them all. Manes in lions are probably signalling (of male sexual maturity and sexual fitness) rather than protective.


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What directs macromolecules to their cellular locations
For example I know that after transcription a mature mRNA is sent outside of the nucleus through the nuclear pore and then it goes to ribosome. But as for the free floating ribosomes that are out somewhere in the cytoplasm, how does the mRNA get to those organelles? Is there something else that attaches to the mRNA to help it? Even then I don't understand what force is helping a large molecule (mRNA) find and even larger macromolecular assembly (the ribosome).

I have changed your title to remove the anthropomorphic implications.

Once a eukaryotic mRNA enters the cytoplasm, in most cases it is probably the cytoplasmic concentration of the eukaryotic translation initiation factors that determines whether or not a specific mRNA is translated on the ribosomes.  The concentration of ribosomes in the cytoplasm tends to be quite high, and I think the same is true for the eIF subunits.  The short answer to the first part of your question is therefore: diffusion and the law of mass action.  The last sentence of your question is unclear (to me) and should probably form the basis for two separate questions.

This is fairly often question for molecular biology

how does the mRNA know exactly how to get to those organelles

The secret to understand it, is that nothing knows where to go. Different molecules have different affinity to each other. Molecule A likes molecule B, but not molecule Y. Inside the cell, thermal fluctuations causes disorder that drives molecule A to bump into all kinds of molecules, including Bs, Zs, Ys, and others. However, when stumble upon molecule B, molecule A will very likely form some sort of stable complex with it. One example, is ribosome and mRNA.
When mRNA and ribosome join into complex, their inner parts can be considered in the same fashion: they will jiggle a lot around, but most likely jiggle will produce polypeptide, not, let's say DNA, or not cause mRNA to fall away from the ribosome.
So, you can say that mRNA tries to go everywhere it can, without any clear direction, apart from the fact that it will most likely form something stable (i.e. useful) with ribosome. Or maybe it will be mRNA degradation protein, such as ribonuclease.
PS: "will very likely form some sort of stable complex" means that in some reasonable time mRNA will find and bind to ribosome. However, it might take billions of years for ribosome to bind DNA and produce some sort of polypeptide.