How is DNA testing used to differentiate between different species? How is DNA testing used to determine that specimens belong to different species, rather than being subspecies, or members of the same species?
Usually the definition of species is about the ability to produce fertile offspring under natural conditions. How are markers chosen that indicate individuals are different species?

Or does this process occur the other way around? Are species identified as being different, then DNA used to identify which members are which?

Statistics of divergence
You can compute various statistics of group divergence. Typically you could consider the pairwise number of differences between any pair of individuals. For example the following two sequences
ATATATCCTGTGTCA
AAATATCTTGTGTCA
has 2 differences.
Obvious or obscure grouping
Often, individuals really group together quite naturally (if you perform a principle component analysis you will see clearly defined groups) but sometimes the groups are quite blurry.
The definition of species is arbitrary
Whether the grouping is blurry or not, it is often quite arbitrary how much two groups need to be different in order to classify them in different populations, different subspecies or different species, different genera, etc...
The problem here is more a problem of definition than a technical problem. You should have a look at this post to understand the issue behind the definition of species.

My attempt at a high school level explanation
Explain what a phylogenetic tree is
First draw a phylogenetic tree. Explain what they mean:

A node is an common ancestor
A leaf is a extant species (if the leaf gets to the top of the tree)
All species are related but some are more related than others..
Introduce the concept of sister clade
Explain that every species in a sister clade is equally related to the all the species in the other sister clade by highlighting their common ancestor.
Explain that no extant species is the ancestor of another species as the ancestors are the nodes.

You can get a short introduction to phylogenetic trees here on Biology.SE or here on Understanding Evolution.
Methods to reconstruct a phylogenetic tree
Let them wonder how we could get to know what the true phylogenetic tree is.
Suggest using phenotypic data and make them realize and if you put all the yellow flowers together, or the flying organisms (insects, birds, bats, squirrels) it won't work very well. So phenotypic data can sometimes be misleading. So explain that we can use genetic data by counting the number of pairwise differences. Let's consider the three different sequences
species A: ATCTCTG
species B: ATCTCTT
species C: AGGCATT
It sounds like the first two sequences are more closely related than any of them are to the third sequence. You can draw the tree for these three species.
Molecular clock (optional)
Knowing the rate at which mutations occur, one can date since when two lineages diverged based on genetic data. You will probably have to learn a bit more about molecular clock for yourself. You may ask a for high school explanation in another post.
Within population diversity (optional)
Recognizing the existence of genetic diversity within population is key to all evolutionary processes so it is good to let them understand the existence of such diversity early on.
Of course there is genetic diversity within a species that renders everything a little bit more complicated. For example, some of you have blue eyes while others have brown eyes (assuming there is variation for eye color among your students), this is due to the fact that the DNA sequence within each of you is a little different. Not as different as it is between humans and chimpanzee but a little bit different.
Genetic data to group populations into species
Then, you can say that genetic data can allow us to tell groups apart. You can show a PCA type of plot (without really explaining what a PCA really is) with colors. Each color correspond to a population (insiste on term population and not species). Something like

and then argue informally that light-yellow, green and red populations are probably different species while all the other populations seem to belong to the same species.
Problem with the species definition
If you really want to bring the question of the how to use genetic data to tell species apart, then you will first have to destroy their concept of species! For that, you should first have a look at this post. You will have to

Introduce the biological concept of species
Explain why this concept does not work for asexual species (hopefully they know that many species are asexual).
Give an example of another issue such as the classical (yet rarely observed) example of ring species (see here on Biology.SE or here on wikipedia)

Then, get back to the PCA and ask, how different two populations must be for them to be called different species? And make them realize that this is rather arbitrary. We can tell they are different lineages but it is up to everyone to decide what we want to call a species. However, very often vague intuition about how different a species should be is good enough.


Can hepatitis B also infect vaccinated persons? If a person is vaccinated against hepatitis B: Is there any chance that he also gets the infection by physical contact? Is it a congenital disease or not (if the parent is hepatitis positive is the offspring is also affected or not)?

It is possible but the chance is somewhat low - 10%.

You can check to be sure that the level of surface antibody in your blood is efficient by a simple blood test.

The Hepatitis B vaccine is very effective at preventing Hepatitis B virus infection. After receiving all three doses, Hepatitis B vaccine provides greater than 90% protection to infants, children, and adults immunized before being exposed to the virus.

In highly endemic areas, Hepatitis B is most commonly spread from mother to child at birth (perinatal transmission), or through horizontal transmission (exposure to infected blood), especially from an infected child to an uninfected child during the first 5 years of life.

Find more about this here:

http://www.who.int/mediacentre/factsheets/fs204/en/

You can find all about Hepatitis B vaccine on the CDC's website:

http://www.cdc.gov/vaccines/vpd-vac/hepb/public/index.html


How different are these terms: Phylloclade, Phyllode, Cladophyll and Cladode? We started with Plant Morphology in class (specifically, the morphology of angiosperms).

My teacher's provided us with the following terms and their definitions.

  Phylloclade

  A modified stem that is flattened or cylindrical and capable of unlimited growth. They are green and capable of photosynthesis. Examples include; Opuntia, Epiphyllum, Casuarina, Euphorbia.
  Cladophyll (also called a Cladode)

  A modified stem capable of limited growth. They are green and capable of photosynthesis. They bear an axillary bud at the their middle, from which flowers develop. Examples include; Ruscus, and some Asparagus species.

 No mention of the term "Phyllode"...yet.

Now I'm sure I understand the definitions provided, however, I'm beginning to seriously question the validity of those definitions.

Apparently, these terms aren't documented very well, and after two hours of constant Googling, I arrived at:

  Phylloclade (From the Wikipedia page of the same name)

  Phylloclades and cladodes are flattened, photosynthetic shoots, which are usually considered to be modified branches. The two terms are used either differently or interchangeably by different authors. [Examples provided]: Ruscus, Phyllanthus and some Asparagus species.
  Cladophyll (From the Wikipedia page for "Petiole")

  In some plants, the petioles are flattened and widened, to become phyllodes or phyllodia, or cladophylls and the true leaves may be reduced or absent. Thus, the phyllode comes to serve the functions of the leaf. [Examples provided]: Some Acacia species.

This is annoying, seriously.

According to the definitions provided by my teacher, we're dealing with something called a "Phylloclade" and something else called a "Cladophyll" (= "Cladode"). They don't mention the term "Phyllode", though.

Based on the Wikipedia definitions, however, we're dealing with something called a "Phylloclade (= "Cladode", if you ignore minor d̶i̶s̶r̶e̶p̶a̶n̶c̶i̶e̶s̶  differences in their definitions, which are mentioned later on in the Wikipedia article), and something else called a "Cladophyll" (= "Phyllode")

My questions:

1) What are the correct definitions of the terms "Phylloclade", "Phyllode", "Cladophyll" and "Cladode"?

2) Are the examples (provided in my notes and the Wikipedia articles) actually relevant/correct? For example: Does Ruscus possess  Phylloclades (as suggested by the Wikipedia article) or does it possess Cladophylls (as suggested by my teacher)?

3) Building on question (1): Does "Phylloclade" = "Cladode", and "Cladophyll" = "Phyllode"?

Apart from the discrepancy of the cladophyll term I can say that both your teacher and the wiki page are correct.

If you read the Wiki page carefully it states that

  Phylloclades and cladodes are flattened, photosynthetic shoots, which are usually considered to be modified branches. The two terms are used either differently or interchangeably by different authors.

(As you have also quoted)

This is simple because both phylloclades and cladodes are stem modification for photosynthesis and xerophytic adaptation as well. So in this context they are interchangeable

Also if you have further read the article it states why the terms are interchangeable and why not. The different levels of definition are given:

  Definitions of the terms "phylloclade" and "cladode" vary. All agree that they are flattened structures that are photosynthetic and resemble leaf-like branches.

  one definition, phylloclades are a subset of cladodes, namely those that greatly resemble or perform the function of leaves,[2] as in Butcher's broom (Ruscus aculeatus) as well as Phyllanthus and some Asparagus species.

The definition given by your teacher can be interpreted by these two definitions stated in the Wiki page:

  By an alternative definition, cladodes are distinguished by their limited growth and that they involve only one or two internodes.[3] By this definition, some of the most leaf-like structures are cladodes, rather than phylloclades. By that definition, Phyllanthus has phylloclades, but Ruscus and Asparagus have cladodes.

  Another definition uses "phylloclade" to refer a portion of a leaf-like stem or branch with multiple nodes and internodes, and "cladode" for a single internode of a phylloclade.

But phyllode is a leaf modification, specifically a modification of the petiole for photosynthesis and a xerophytic adaptation to some extent. (Source is the Wiki page itself)

So to conclude

phyllode is completely different from phylloclade and cladodes.
Taking the type of morphology of the plant into consideration and the definition used, phylloclade and cladodes may be used interchangeably or may not be.


Trees growing around objects vs pushing them away. Where is the threshold? If a tree grows against a taut wire then the tree will grow around it, eventually enveloping the entire wire. This often scars the tree, and if the wire is thick enough, it will interrupt nutrient flow and cause more significant damage.

But if the tree grows against a larger obstacle, such as a wide board, the tree displaces the obstacle as it grows.

As a real-life example of this, I have a large pine tree on my property next to an old wooden building. The tree, as it grew, pushed hard enough against the building's eaves to bend a 2x4 piece of lumber five inches out of the way. When that 2x4 finally met the rest of the building, the tree could no longer move the board and started growing around it.

Where is this threshold? I assume it can be described as a simple pressure (force over area), and that it is dependent on the specific type of tree. Is this tabulated somewhere?

Specifically, I wish to hang a 40lb (18kg) weight, permanently, from a branch of an ~80ft (~25m) lodgepole pine. I intend to use some sort of wider material in between the cord and the branch. It would be great if I could simply run the cord through a larger-diameter pipe and position this pipe over the top of the branch. But if this wouldn't be sufficient then I'll use boards (or similar) to distribute the weight. I won't be constricting the entire circumference of the branch.

I know that mounting a bolt into the tree would be better, but that isn't an option for me in this case.

I don't want to do this: (!)

image source

Since you asked for the science I'll try to give a scientific but simple explanation.
Trees (and plants) become wider and taller over time. This growth is due to cell division and cell elongation from meristematic cells (analog to stem cells in animals).
The stem (upper part of a plant) becomes wider because is it constantly creating new vascular tissue from the cambium. The cambium creates xylem to the center of the tree and phloem to the outer parts. The bark that peels off is the phloem and other tissues irrelevant for the explanation. Here you can find a good illustration.
Since the tree adds new xylem all the time the, cambium gets further away from the center of the tree.
When the tree pushes against a wire, the wire cuts and kills the phloem cells and after that the cambium cells. But the plant has mechanism to regenerate the cambium ring and that's why the tree continues to grow there. In the photo the wire is already in the xylem section.
When the tree pushes against a wall there is a barrier in the whole section. Either the wall collapses (or, more commonly seen, the sidewalk rises) or growth in that sections stops.
I saw graphs of cells having up to 3MPa of turgur pressure but the actual pressure you should check is that of the bark which can be higher or lower. It changes between plants species, sections of plants and plants itself so the best is to simply check.
I wouldn't hang a weight from a tall tree. Trees get diseases and many times you only see that they are rotten from the inside when it is too late.


Are added yogurt cultures harmful to the gut? I have read somewhere that the live culture added to yogurt acting as "healthy" gut bacteria are actually synthetic and harmful.

Any truth to this? If so, what are some alternatives to getting good gut bacteria?

I'm not sure what you mean by 'synthetic' gut bacteria, so I can't address that. is yogurt harmful to the gut? I believe the answer is no.

Women (and their doctors) have long known that taking antibiotics can result in Candidia (a yeast infection). Physicians have been advising women taking antibiotics to eat yogurt with live cultures, including lactobacillus spp. and bifidus spp. In keeping with today's movement towards evidence based medicine, Natural Medicines Comprehensive Database rates effectiveness based on scientific evidence according to the following scale: Effective, Likely Effective, Possibly Effective, Possibly Ineffective, Likely Ineffective, Ineffective, and Insufficient Evidence to Rate.

The effectiveness ratings for (just) LACTOBACILLUS are as follows:

Likely effective for:

  Diarrhea in children caused by a certain virus (rotavirus). Children with rotaviral diarrhea who are being treated with lactobacillus seem to get over their diarrhea about a half day earlier than they would without this treatment. Larger doses of lactobacillus are more effective than smaller ones. At least 10 billion colony-forming units during the first 48 hours should be used.

Possibly effective for...

  Preventing diarrhea in children caused by antibiotics.
  Preventing diarrhea in hospitalized adults. Drinking a specific beverage containing Lactobacillus casei, Lactobacillus bulgaricus, and Streptococcus thermophilus (Actimel, Danone) twice daily during antibiotic treatment and for a week afterwards significantly decreases the risk of developing diarrhea.
  -Preventing diarrhea due to traveling. Taking a specific strain of Lactobacillus rhamnosus, Lactobacillus GG (Culturelle) seems to help prevent diarrhea in travelers.
  Preventing diarrhea due to cancer treatment (chemotherapy). There is some evidence that patients with cancer of the colon or rectum have less severe diarrhea, less stomach discomfort, shorter hospital care, and require fewer chemotherapy dose reductions due to GI side effects when they take a particular strain of Lactobacillus rhamnosus, Lactobacillus GG (Culturelle).
  Colic in babies. Taking a specific Lactobacillus reuteri product seems to be more effective than using the drug simethicone.
  Lung infections. Children ages 1 to 6 years who attend daycare centers seem to get fewer and less severe lung infections when given milk containing lactobacillus GG or a specific combination product containing both Lactobacillus acidophilus and Bifidobacterium (HOWARU Protect).
  Treating a bowel condition called ulcerative colitis. Some research suggests that taking a specific combination product containing lactobacillus, bifidobacteria, and streptococcus might improve symptoms.
  Treating irritable bowel syndrome (IBS). There is some research showing that certain strains of lactobacillus, but not others, can improve symptoms of IBS such as bloating, and stomach pain.
  Treating vaginal infections caused by bacteria (bacterial vaginosis).
  Treating and preventing eczema (atopic dermatitis) in infants and children who are allergic to cow’s milk.
  Helping prescription medications treat Helicobacter pylori (H pylori) infection, which causes stomach ulcers.
  Treating diarrhea caused by the bacterium Clostridium difficile.

Though some of the recommendations are for specific probiotic formulations, one can achieve similar results by reading yogurt packages and mixing types to assure coverage with the proper bacterial spp.

National Institutes of Health


What kind of bird is this and what does it eat? My father found this little guy in one of the tractors of where he works (in the fields) i’m not sure what species of bird it is and what it eats. It just keeps chirping not stop and I have no clue what so ever to what it eats. If anyone knows please tell me, I don’t want to see him starve to death.

Based on the photo, it looks like you have a fledgling American Goldfinch (Spinus tristis). Here's a photo of an adult female feeding a young goldfinch. This link has dietary information.

I would suggest contacting your local Wildlife Rehabilitation Centre or leaving the young guy where he was found. He could of jumped the nest a bit early, but typically the parents are always nearby.


What are the sites of nutrient digestion and absorption in the human GI tract? Where does nutrient digestion and then absorption take place for different nutrients along the alimentary tract?

The saliva from your mouth will slowly start to digest starches.

Then the stomach specializes in digesting protein with enzymes and its highly acidic content.

The small intestine will digest proteins, starchs and carbs (with the help of the enzymes traveling from the stomach).

The liver and pancreas secretions will join in the small intestine will help break down fats and complete digestion.

The small intestin is responsible of absorbing the vast majority of digested nutrients and the water is then mostly absorbed by the colon.

Source: Your Digestive System and How It Works


What is this spider? Two black stripes When I opened my front door, there were five of this type of spider sitting on the door. I can't quite find anything online matching the two black stripes on it's back.

I vacummed them up before I realized I should identify them, so the above picture is the only one I have available. (I like spiders, but there were too many.) I'd feel more comfortable if someone could identify the spider and determine it's threat level.

Details:

Inch or so longer
Brown
North East Wisconsin
Wooded Area with little to no grass
Mile away from lake Michigan
Jumpers
Party of about 5
Door was in direct sunlight

Judging by the stripes, it's most likely a wolf spider.

If they didn't have a web I would say they're almost certainly wolf spiders, since they don't build webs. Like most spiders in North America, they are harmless to humans.


How to learn and memorize animals classification to get an intuition about them? I would like to have a good intuition on how close is what animal to which one and how large each group is by number of species and population. I was wondering if there is a good website with good demographics and graphs that could help me memorize it because it's really so hard to make up the tree myself from wikipedia pages!

Another alternative is the Tree of Life web project, which includes species richness information in the lower levels of the tree and allows reasonably easy navigation of subtrees. You can find the animal portal here.

EDIT -- another alternative, which is in active development, is this integration of Wikipedia and the Open Tree of Life Hyperbolic Tree.


Passing on the DNA of old age I've often pondered the fact that we only pass on the DNA of our youth. Any mutations to our DNA that occur after having children, that may help us to respond to getting older, are not inherited. Do older parents pass on a different, perhaps more learned "quality" of DNA? Anyone know the answer to this?

It is good thinking you're doing here!

Only mutations happening in the germ line can be passed on

Mutations that happen in an individual hand (or any other soma line) will not be passed on the the offspring. Only those happening in the soma line can.

Mutations are random

What I mean here is that it is not because someone is old that all of sudden the mutations that would happen in this person would be beneficial for old people.

Age dependent "quality" of genome being passed on

You are asking

  Do older parents pass on a different, perhaps more learned "quality" of DNA?

You seem to misunderstand how natural selection works. An individual alone does not get selected over its lifetime to become better (at least not in the sense of what is meant by "natural selection"). You need a population for selection to happen.

In the females as the pool of ovules is being set early in life. In males the spermatozoids keep replicating during the whole lifetime of the individual. Hence, in males, but not in females, the number of new mutations being passed on to their offspring should increase with age and it does.

In humans the mother transmit on average 15 new mutations and the father transmit on average $25+2(g−20)$ new mutations, where $g$ is the age of the father (Cochrane and Harpending, 2013; this approximation holds only for men older than 20 years of course).

As the vast majority of mutations are neutral or deleterious, the "quality" of the genome being passed on should decrease with age unlike you expected.

Efficiency of selection decreases with age

The fact that after a given age, one does not reproduce anymore (among mammals, this is particularly true for women) does affect the selection pressures on the genetic variants that affect age specific fitness. e.g. A mutation that will reduce health at young age will be quite strongly selected against while a mutation that affect health at old will not.

When talking about this discrepancy between selection pressures at different ages, the concept of antagonist pleiotropy often comes into the discussion. Pleiotropy is the phenomenon where one locus affect several traits.

The idea of age-specific antagonist pleiotropy is that a mutation that will increase health at a young age by a factor $s$ but decrease it at an old age by the same factor $s$ will be selected for. Such process can cause a population to evolve toward lower lifespan. The antagonistic pleiotropy hypothesis is one of the most important hypothesis that we have for the evolution of senescence.

Evolution of senescence

You might want to have a look at the posts:

Why does evolution not make our life longer?
Why do we age? or Do we have a theory of senescence?


mRNA Transcription from Nuclear DNA How does a cell "know" the coding strand vs. the non-coding strand of DNA during transcription of mRNA?

This is determined by the promoter -- the DNA sequence to which RNA polymerase binds. It's assymetric, and the polymerase binds in a specific orientation, that determines the strand and the direction it will go once elongation begins.


Are there land animals that use gill-like organs instead of lungs? Among aquatic, water-breathing animals, gills and other continuous-flow breathing methods dominate over lungs and other storage-based breathing methods as in land animals. Notably, axolotls have gill-like structures around their heads which use a high surface-area structure heavily vascularized with capillaries to breathe water.

However, it seems all air-breathing organisms use storage-based breathing, air-breathing fish included, as lungfish use their swim bladders as lungs, a clear example of storage-based breathing.

Are there any land organisms that use continuous-flow breathing methods over lungs?

Terrestrial crustaceans are land animals that use gills (or gill-like structures) for gas exchange, though these gills must be kept moist for efficient respiration.

Specifically, animals like hermit crabs have a branchiostegal lung that looks like gill tissue but is better adapted for absorption of oxygen from air instead of water.


Why do we assume that the first humans were dark-skinned? According to the article Dark skin and blue eyes: How Europeans once looked:

  It is widely accepted that Man's oldest common forefather was dark
  skinned, and that people became more pale as they moved further north
  out of Africa into colder climates with less sunlight.

I thought that humans' oldest common ancestor was light-skinned, because

Dark-skinned people have white palms and soles, but light-skinned people have more consistent skin tones. This suggests that light skin is more ancestral and dark skin evolved to protect skin from the sun.
Bonobo chimpanzees, our closest primate cousins, look like they have light skin under black hair.

I understand we all originate in Africa, but I thought that the environmental conditions in Africa were different from today. How do we know that the first humans were dark-skinned?

The first modern humans evolved about 200.000 years ago in Africa. When they lost their body hair (or at least most of it), they needed some other protection of their skin from the sun - otherwise they are prone to develop melanoma. Melanin is such a protection, and the rate of melanoma is much lower in dark skinned people.
There is also a nice correlation between latitude and skin color - the more to the north (and to some degree to the south as well) you get, the lighter the skin color of the population gets. The reason for this is likely the better ability to synthesize Vitamin D (for which you need sunlight on the skin):

The evolution of human skin coloration.
The evolution of human skin ans skin color.
Development of different human skin colors: a review highlighting
photobiological and photobiophysical aspects.
North-South gradients of melanomas and non-melanomas: A role of
vitamin D?

The lightening of the skin occurred after humans moved to Europe:

The Timing of Pigmentation Lightening in Europeans

And we even know, that this occured more than once, since the genetic reasons for lighter skins are different between europeans and light skinned asians.
A lot of this we know via sequence comparisions of genes involved in pigmentation, there you can trace mutations and see, where they show up first and how they migrate over time. One very good example is the melanocortin-1-receptor (MC1R), which is mutated pretty often in europeans (mutations in this gene are generally associated with lighter skin and hair color; people with red hair carry certain mutations in this gene) but its under selection pressure to not mutate in africa (there are almost no known mutations in MC1R for africans). Another example would be a mutation in the SLC24A5 gene, which is exclusively found in europeans, but not in asians and which accounts also for lighter skin. I stop here for the moment, if there are more specific question, go ahead.

The genetic architecture of normal variation in human pigmentation:
an evolutionary perspective and model
Genetic Variation at the MC1R Locus and the Time since Loss of Human
Body Hair
SLC24A5, a putative cation exchanger, affects pigmentation in
zebrafish and humans.


T7 vs pBAD promoter strength How do pBAD and T7 promoter strengths compare when pBAD is induced under conditions which would lead to its highest strength? Are there any papers that compare the two inducible promoter systems?

The exact numbers depend on the protein.
In my hands, I would say between the pAraBAD and a pLac-T5 you can expect some fold improvement and pAraBAD and a pT7 promoters you can expect about an order of magnitude… but there are two big caveats.
First, pET and other T7 driven plasmids do not work in K-12 strains (without the pTARA) so BL21 is generally used. BL21 is much better generally than K-12 strains (more primary metabolites cf. omics paper) for a lot of things including protein expression. The chaperone balance is difference, so you will get differences from that too —if you have used the TAKARA plasmid team you will have notice how quirky protein expression optimisation can be.
Second, if your protein has a cofactor you have a major problem. FeS clusters, PLP, heme or even O2 (for maturation of GFP, say) become rate limiting and overexpressing the protein can make it highly toxic and you might be in a bigger pickle than with a lower level promoter. In my thesis, I added pyridoxine to a pBAD expression, because it gave an improvement.

Footnote: If the expression levels are really bad, changing promoter might not be that great as the assumption of linearity might not hold.
If heterologous and not codon optimised, consider using pRARE.
If insoluble, consider using ethanol shock and the TAKARA chaperon plasmid team.
If oxygen sensitive, alas, doing expression and purification anaerobically.


Background (null) distribution for higher observed frequency of an allele I am testing the hypothesis that being heterozygote at a certain gene locus, say X, increases the chances of having the good allele of X compared to being homozygote. I have data of more than 6000 individuals with their zygosity for gene X. What could be the background distribution of allele frequency for testing the hypothesis if the observed frequency of good allele is more in heterozygotes compared to one expected by chance.
Thank you so much.

I don't really understand your hypothesis you want to test. Here are two things that may help you.

Test if allele frequency is the one expected from the genetic and demographic properties

The expected allele frequency is not that easy to calculate as you need much information. You need to know the mutation rate, the population size, the migration rate, assume random mating and most importantly know the selection coefficient associated with this allele. Once you've got all that, you'll find the equation in the old paper Wright 1937.

How to test?

Maximum likelihood ratio test is probably the way to go.

Test if heterozygosity is the one expected from the allele frequency

Now if you want to test if heterozygosity is not the one expected, it is much easier. The expected genotype frequencies are given by Hardy-Weinberg rule (see here for explanation on Hardy-Weinberg's rule and see here for the assumptions of this rule).

In short, for a bi-allelic loci with allele frequencies $p$ and $1-p$ the three genotype frequencies are $p^2$, $2p(1-p)$ and $(1-p)^2$, where $2p(1-p)$ is the frequency of heterozygote.

How to test?

You can simply do a chi-square test or a binomial test.

  I ask if being heterozygote increases the odds of carrying a certain allele compared to being homozygote. So can I just compare the allele frequency in two populations (hetero- and homozygotes) using fisher exact t

Oh ok. If I understand you correctly, you have two loci. One for which heterozygosity is the variable of interest, while for the other locus, the variable of interest is the presence / absence of a certain allele is that right?

Sounds like your question is a pure question of statistics, not biology. Stats.SE is the place to go to but I will still try to address your question now that I started.

You can do a simple chi-square test you have the following 2 by 2 chi square table with the count of individuals in each cell

$$\begin{array}{c|c|c|}
 & \text{Homozygote} & \text{Heterozygote} \\ \hline
\text{Allele 1} & w & x \\ \hline
\text{Allele 2} & y & z \\ \hline
\end{array}$$

Now, that works well if you consider only a single, randomly picked allele per individual but that would reduce your sample size. If you pick both haplotype per individual, then I am not sure of whether you might suffer from pseudo-replication. In such case, you could do a logistic regression with a nominal random effect that is the individual ID. They will be better than me at giving you such advice on stats.SE though.


Myopia & the Blur Effect I know myopia is caused by elongation of the eyeball. When the eye is too long, light entering the eye balls falls in front of the retina instead of on it.

However I do not quite understand how this leads to the "blur" we observe. If part of the light entering the eyeball "misses" the retina shouldn't the observed effects simply be a reduction in the brightness of the object - as if I were standing in a less illuminated place? For example, if I take off my glasses in broad daylight my retina is getting a far greater dose of light than when I'm indoors (wearing my glasses) under artificial lighting. Yet the world still looks blurry outside (without glasses) and clear indoors (with glasses).

What causes the blur effect? If less light is hitting the retina it should simply look less illuminated, not blurry.

You have some misconceptions about visual acuity. You need to understand how lenses work to understand why objects up close are blurry in myopia.

Sure, if one elongates the orbit, blurring will occur, but that's not usually the cause unless it's in childhood. As we age, the elasticity of the lens has more to do with it.

Light comes in through the pupil. The amount of light is what determines brightness; too little, and we can't see, too much and we look away. In between we "see". Being able to focus doesn't have any effect on brightness; the size of the aperture does, however (the aperture in this case being the pupil.)

Blurriness is caused by where the light rays striking the object we're looking at come into sharp focus in out eye. Sharpness falls within a very small range, then once the range is exceeded, the image becomes progressively blurrier because the rays scatter again. This is why looking through a pinhole improves our vision: less scatter. If your pupil could constrict down to a pinhole, that would be pretty amazing, but it can't.

The purpose of the lens is to focus the image. It can do so (with the help of ciliary muscles) by changing shape. But it can only change shape within a range. If it cannot change shape enough to focus the image where it needs to be - on the retina itself - you have blurry vision.

That's why additional lenses (or changing the contour of the cornea) help.


Mechanism of Myosin Head Bending in Cross Bridge Cycle Power Stroke Phase What is the mechanism of bending of myosin head during the power stroke of the cross-bridge cycle of the muscle contraction? Does this have anything to do with the protein's 3-D structure i.e. folding of protein in space? I would prefer a physics explanation down to either the classical electrical dipole or quantum mechanical interaction amongst the proteins. I want to know what exactly produces the force that powers the bending. I am pretty sure that the force can only be electromagnetic. The question is how the force is manifested in the bending.
Any references for further reading are appreciated.

Introduction:
This is going to be quite a long answer. To have an introduction to the topic, you can have a look at articles from Wikipedia and RCSB Protein Data Bank.
The exact mechanism of physical interactions in myosin head during powerstroke cycle are not yet known. The only thing we definitely know about how release of Pi from myosin causes conformational changes (and hence, force) in it, as given at MJC website is:

This is a very basic description of the powerstroke cycle, so we'll move ahead for more detailed explanation of physical interactions during the cycle.
Details:
I have found three theories regarding physical interactions during the powerstroke cycle. Let's discuss them one by one.
THEORY 1: I could not find much explanation about physics of the cycle, the only thing I could find was at the JBC website (emphasis mine):

Mutation R759E in the myosin converter domain results in biochemical and biophysical defects as well as aberrant muscle structural and physiological properties. The central portion of the converter domain is encoded by exon 11e in indirect flight muscle (Fig., green), and the converter interfaces with the exon 9a-encoded relay domain (Fig., blue). Molecular modeling indicated that residues 508–511 in the relay loop are located near the converter residue 759 and defined weak and strong interactions of residues 509 and 511 during the rearrangements of the relay loop that are affiliated with the mechanochemical cycle. Furthermore, Ile508 can be cross-linked to Arg759 in Dictyostelium non-muscle myosin II when they are each substituted by cysteine. Therefore, we hypothesized that specific amino acids in the relay domain interact with converter residue 759 and that second site mutations in the relay residues may suppress the defects associated with converter mutation R759E.

They couldn't give much explanation of the physics involved in it. Maybe this is because I missed it or because there hasn't been much research on this because Dissecting the molecular mechanism of muscle myosin function in vivo has proved difficult. as said at JBC website.
THEORY 2: This theory, given at PNAS, provides a more detailed view of the physics, so we'll have a more thorough explanation of it:

Molecular motors produce force when they interact with their cellular tracks. For myosin motors, the primary force-generating state has MgADP tightly bound, whereas myosin is strongly bound to actin. We have generated an 8-Å cryoEM reconstruction of this state for myosin V and used molecular dynamics flexed fitting for model building. We compare this state to the subsequent state on actin (Rigor). The ADP-bound structure reveals that the actin-binding cleft is closed, even though MgADP is tightly bound. This state is accomplished by a previously unseen conformation of the $\beta$-sheet underlying the nucleotide pocket. The transition from the force-generating ADP state to Rigor requires a 9.5° rotation of the myosin lever arm, coupled to a $\beta$-sheet rearrangement. Thus, the structure reveals the detailed rearrangements underlying myosin force generation as well as the basis of strain-dependent ADP release that is essential for processive myosins, such as myosin V.

Just so that you know what it is, let me add a few points about Molecular Dynamics Flexible Fitting:

The molecular dynamics flexible fitting (MDFF) method can be used to flexibly fit atomic structures into density maps. The method consists of adding external forces proportional to the gradient of the density map into a molecular dynamics (MD) simulation of the atomic structure. For examples of MDFF applications, visit the websites on Mechanisms of Protein Synthesis by the Ribosome, Dynamics of Protein Translocation, Molecular Dynamics of Viruses, and Intrinsic Curvature Properties of Photosynthetic Proteins in Chromatophore.

Now, returning to the main point (results & discussion sections):

The equilibrium and rates of transition between the Strong-ADP and the Rigor states vary greatly among different myosin isoforms and predominantly determine how long a myosin motor can remain bound to actin in the absence of load. This kinetic tuning must be achieved by structural differences in the regions that we have seen to change in our Strong-ADP structure as well as regions involved in stabilizing the lever arm position...Our structures show that the Loop 1 conformation alters in the transition from Strong-ADP to Rigor. Thus, different sequences likely favor one conformation over the other, or promote the transition from the ADP-bound conformation to the Rigor conformation, providing a structural basis for this kinetic tuning.
For myosins, such as myosin V, that function in a cell as two-headed, processive motors, the length of processive runs and the initiation of processive runs are both enhanced by “gating” of the heads. For a two-headed molecule with both heads simultaneously attached to actin, gating refers to the fact that a lead head is essentially stalled in an ADP state strongly bound to actin, until the rear head is detached from actin by binding MgATP. This gating is attributable to the strain dependence of MgADP release. Although we do not know whether some of the subdomains of myosin may be deformed by strain, our Strong-MgADP actomyosin structure clearly reveals that strain must prevent the rearrangement of the $\beta$-sheet from the Strong-MgADP conformation to the Rigor conformation, based on the data presented in Results. Preventing this rearrangement is thus the basis of gating.

For better understanding, you should also see this video (same website) which shows animation of different conformations of myosin in different stages of the cycle:

The transitions are animated by direct morphing between the three structures Pre-Power Stroke (PPS), ADP state, and Rigor. Starting with the PPS conformation, myosin first rearranges to allow phosphate release without much change in its lever arm. Then, the first step of the powerstroke consists of a large swing of ∼58° of the lever arm toward the ADP state. The actin-binding cleft [between the U50 (blue) and L50 (white) subdomains] is closing for this transition, leading to the only state of the actomyosin cycle, which exhibits high affinity for both actin and the nucleotide. The second step of the powerstroke occurs upon ADP release and ends in the Rigor state after an additional lever arm swing of 9.5°.
THEORY 3: This theory gives even more detailed, but a bit different from the previous one, view about how the energy, released by ATP hydrolysis, is stored in myosin head. It is called Rotation-Twist-Tilt (RTT) energy storage mechanism. See this:

According to the mechanism, ATP hydrolysis in the catalytic site rotates the top of the regulatory domain, which, being connected to the coiled coils of the S-2 region, causes twist between them to increase, and leads to the twist in the myosin head. Since, at the time of hydrolysis, the myosin molecule is not bound to the actin filament, the head is free to rotate and tilt. The increase in twist is instrumental in storing the energy of ATP hydrolysis, while the rotation and tilt of the myosin head brings it sufficiently close to the actin so as to form the actomyosin complex. Untwisting of the coiled coils and the subsequent untilting and constrained reversal of rotation of the head cause the power stroke. This strain decreases the energy of interaction between actin and myosin and thus enables ATP to dissociate myosin from actin. The system is now in such a state that after the next ATP hydrolysis event, the myosin head can bind to actin, and thus, a new contractile cycle can be initiated.

The original paper of RTT mechanism (by Nath and Khurana, 2001) is available here. Since the detailed mechanism is too long, I am not posting it here. You can read the full process, just remember to have a pen and paper with you!

Conclusion:
All of the above theories provide an in-depth view of the powerstroke cycle. However, I'd still conclude that the exact physics behind the powerstroke cycle is not yet fully known, only the transitions in conformation of myosin head have been observed and interpreted to some extent.
References:

Myosin head: Wikipedia
Myosin: RCSB Protein Data Bank
Journal of Biological Chemistry: Mapping Interactions between Myosin Relay and Converter Domains That Power Muscle Function
Proceedings of the National Academy of Sciences of the United States of America: Force-producing ADP state of myosin bound to actin
Theoretical and Computational Biophysics Group: Molecular Dynamics Flexible Fitting
Cell Movements: From Molecules to Motility
Molecular mechanisms of energy transduction in cells: Biotechnology in India II
Molecular mechanism of the contractile cycle of muscle; Sunil Nath and Divya Khurana, March 2001


What are some potential consequences for attempting to cure Type one Diabetes? Type one diabetes has been in my family for a few generations. As a carrier and having a mother with the disorder, I've done a lot of research on it. As I am completing my High school Biology course, I've gotte a better understanding of how the disorder may be treated. (Stem cell therapy, gene replacement, etc). Here's a hypothetical scenario: Scientists develop a modified virus that contains a normal person's beta cell genetic makeup, injects it into the pancreas, and reproduces. The virus and beta cells reproduce, and the body detects the virus, but not the beta cells. (or neither, and the virus is not harmful). The beta cells create insulin, and the Diabetes is cured. Would this work, and would this hurt the immune system? Would it be possible for the scientists to blunder and either create too potent a virus or too much of the virus?

High school biology apparently failed to teach you that many conditions, like type I diabetes are not classically Mendelian. The term "carrier" does not apply to you...you are just someone with a predilection who hasn't developed the condition (but who might...I have heard of someone developing type I diabetes in college)

  Scientists develop a modified virus that contains a normal person's
  beta cell genetic makeup,

How much DNA do you think you can cram into a virus?  Not having the right beta cell DNA is almost certainly not the cause of type I diabetes, anyway.

  The virus and beta cells reproduce, and the body detects the virus,
  but not the beta cells.

How do you think the immune system responds when it detects a virus?  Hint, it kills the hosting cell.

A virus that induced a small percentage of pancreatic alpha cells to undifferentiate and redifferentiate beta cells might work...but you would still have the same immune system that went agro on your beta cells the first time.  They might do the same when exposed to new beta cells.  And there is a fine line between undiffernetiated cells and cancerous cells.


Are the inverse problems of Systems Biology impossible to solve? I have heard Sydney Brenner give a talk [0] on how the entire program of Systems Biology is suspect because, according to him, a chap named Hadamard showed that inverse problems are impossible to solve, or something to that effect.

I find it somewhat odd that no one seems to be paying any attention to this, and many are blithely carrying along trying to reverse-engineer biological organisms. I personally think that this reverse-engineering effort has its place, but Sydney Brenner doesn't seem to think so, and advocates tackling only the forward problem. Here's an excerpt from an abstract to a similar talk of his:

  ... This notion of computation is, in my opinion, the only valid approach to biological complexity and is opposed to many of the ideas underlying what has come to be called systems biology, which is very fashionable today. It will be shown that systems biology attempts to solve inverse problems — that is, obtain models of biological systems from observations of their behaviour — whereas, what I call computational biology, continues in the classical mode of discovering the machinery of the system and computing behaviour, solving a forward problem.

Is Brenner simply wrong on this or is there something to his objections?

[0] Sydney Brenner, Much ado about nothing: systems biology and inverse problems, 2009.

The answer is mostly no, and this is not as disruptive a statement as it seems to be.

I think Brenner has a point of course and he is not the only one who wonders whether the systems biology can create a holistic model of living things.  Still I wouldn't take this to mean we should stop doing systems biology research.

At 18:30 brenner illustrates the inverse problem with some examples 1) can you create a drum from only the sounds that come from the drum? (no he says). 2) can you solve the molecular structure of a molecule from a diffraction problem (no he says).

Of course we can do both of these, but the point is valid as we need to have an idea of what a drum looks like.  If we did have even a glance at a drum, this lets us build a model (cylinder of diameter d, height h and with a drum head of a tension t and material properties alpha beta, etc) from the sounds is a lot of work, but it could be done.

The problem of solving a molecular structure from diffraction intensities alone has also been solved for small molecules in the 60s I believe by so-called 'direct methods' which don't work well or proteins and larger molecules.  Still the point is that you had to have a good mathematical model of molecules and diffraction to get to direct methods, MIR, MAD and other diffraction only methods. Sorry I can't go into details here...it might bore you to death if you don't care about crystallography.

In both cases the statement is that you need to have that model - what does a molecule look like, what does an x-ray do when it encounters a crystal? In order to get there.  Which makes total sense and I agree with.

I wouldn't read too much into this though, because in practice this has never been done, yet Bragg started with just the diffraction pattern and drew in models from other fields of study.  Given the nature of the proof described, no scientific discovery has ever happened in a mathematical vacuum and systems biology will not either.

Rather I would read this talk as saying that the models we are using for action are not very good yet.  What is happening is that synthetic biology (engineering approaches), experimental observation, and intensive modeling (the 'inverse' and 'forward' approaches Brenner mentions) are all happening at once and are informing each other.

Its hard to imagine that data from inverse approaches can't be an important part of any solution to biology.  Its also looking likelier that a mathematical model alone of biology will be difficult or impossible to find also.  What is currently (IMHO) working is a framework that is both conceptual (and not entirely quantitative) as well as analytical (mathematical) and data driven.


How do signalling molecules find their receptors at large distances? I have been baffled with this question approx. for a dozen of years for now.
There is a default "lock & key" mechanism of action assumed for the interaction between a signalling molecule and its receptor, but while applying a bit of combinatorics and biophysics to it I find the following inconsistencies.

Suppose a long-lasting neuropeptide is circulating in a CSF or blood macrocirculation. Or suppose a norepinephrine or other neurohormones are released by hypothalamic and pituitary cells into the macrocirculation for sympathetic or parasympathetic signalling. Accroding to the logic of "lock & key" mechanism, in order for a "key" signalling molecule to activate its "lock" receptor an active site of this molecule - the molecule partition which directly reacts with the receptor as it is generally not the whole molecule which reacts with the receptor - should come in direct contact with the relevant active site of its in-membrane receptor. So by such combinatorial logic, if there are thousands of receptors on outer membranes of cells in CSF or vessel endotelium along the way of which this "key"-molecule is travelling, this molecule should try to "lock into" every such potential "lock" receptor in order to "check" if this is the right "lock". In other words, while travelling across long distances such "key" signalling molecules should not just float in CSF or blood vessels as is generally depicted, but slide across all outer cell membranes in CSF or across vascular endotelium in blood or lymph circulation in order to "check" every potential "lock" receptor for finding their relevant receptors for eventual activation. It is definitely not the case, but it the result of applying combinatorial "lock&key" logic.

Somehow it seems (for myself, at least) that it is just assumed that a "key" molecule released at distances which are millions> of times larger than the molecule size should just "lock" for granted into its appropiate receptors throughout the organism. But suppose a "key" molecule travels in CSF or interstitial fluid in the vicinity of its appropriate membrane "lock" receptor, but with the molecule's reaction (active) site pointed away from its receptor or at an angle. Should the "key" molecule not then react with its "lock" receptor?? Is there a minimum effective reaction distance established between a "key" molecule and its "lock" receptor in order to effectively activate the receptor?

The latter argument holds true also for small distance 20-40 nm synapses with molecules released in it whose size would be minimum 1000 times smaller than the synapse size. Should a neurotransmitter molecule not react with its receptor in a synapse if the molecule's active site would be pointed 180 degrees away from the receptor's active site?

Yes, any individual ligand may have the wrong orientation to interact effectively with an individual receptor, but so what?  There are typically thousands of each type of receptor on a single cell1 and there will be many molecules of a given ligand present as well.

For your synapse example, I suggest looking up:

How many neurotransmitter molecules will be present in a synapse
How many receptors will present in a synapse
How many of those receptors need to be bound to get a signal

I think that will help you make sense of this phenomenon and I encourage you to post a detailed answer to your own question!

You might also want to look into molecular dynamics simulations ...

1: Milo, R., & Phillips, R. (2015). Cell biology by the numbers. Garland Science.


Is there any kind of "unintended consequence" in evolutionary systems? In the social sciences, unintended consequences is a term used to describe an unexpected positive or negative effect of a particular action. This is obviously the wrong word to use in the context of evolutionary systems but I am looking for something that has a similar concept. It may be related to concepts in dynamical systems theory.

For example, if we look at one trait or a group of traits, we may be able to see how this adaptation benefited a population. However, the mutations that occurred along the way would no doubt alter other systems/properties of the organism. In many cases these effects would be negligible. I am looking for any cases where the effect of one set of adaptation leads to another comparably impactful (either positive or negative) effect for the population.

The following is more theoretical and controversial but I am particularly interested in larger, more complex traits such as behavior (which may be considered the product of many different evolutionary adaptations and molecular changes) and any "unintended consequences" that could occur as a result of such a behavior. For example, empathy may be considered a very complex trait that has an evolutionary advantage (post hoc we might say it evolved because it allows specific kinds of communication in social groups) but it may also cause populations to react incorrectly (with regards to survival) in threatening situations when an empathetic response is not the most optimal response. I realize I am treading in vague territory here and it may be controversial to reduce empathy down to the molecular level as I have done in this example. But if there is any work at least related to this idea on a basic level I would be interested.

In summary, I am looking for either the term that describes this sort of analysis, if it exists, or some major examples that may help me do further research on the topic.

Preamble
Evolutionary systems do not have these exact terms as far as I'm aware (although I'm not a behavioral expert) This mainly is because generally speaking we must stop thinking about traits in terms of "advantageous" or "intentional consequences" when discussing evolution. However there are countless examples where a seemingly detrimental evolutionary trait flourishes, or when a seemingly beneficial trait can be exploited by other species. Here I point out two simple, well known examples that might be what you're looking for.
Physiological disease trait emerges
The most well known is sickle cell anemia (SCA); a disease that also reduces susceptibility to malaria. In areas of the world with high instances of malaria, there are also high instances of SCA (Piel et al 2010).
Behavioral altruistic trait exploited
For behavioral studies I think humans would be too vague... (okay, I know very little about sociology) But there is one story that springs to mind from another animal. Birds are ideal models for behavioral studies.
The cuckoo and warbler are an endless evolutionary arms race in terms of camouflage and behavior. The cuckoo parasitises the nest of the warbler with a single egg in a clutch of 3 or so warbler eggs. The warbler parents will watch the newly born cuckoo kick the other eggs out of the nest, and then continue to feed the cuckoo chick thinking it is their own. The reason is thought to be because the warblers respond to the feeding call of their chicks (altruistic, albeit from parent to chick), however the cuckoo chick can mimic this call much more intensely than an entire brood of warbler chicks (altruism is exploited)(Davies et al 1998). By the end, the tired parents are feeding a chick three times their size.


How long do the periods of systole and diastole last? The background to this is i'm doing some work using ECGs for an animation of the heart and i'm having trouble defining the end points of these periods, particularly diastole. Currently, the only information the animation uses is the time (in seconds) when a R peak was detected in an ECG.

So i was wondering what the normal lengths of these periods are and what could affect the lengths of these periods.

I assume that the lengths of the periods is mainly affected by pressure/blood volume and not electrical activity so an ECG won't tell you how long these periods are (unless a heart beat is interrupted by another?). Is that assumption correct?

On a side note: what would happens to the heart physically if there is a large gap between beats. Does it sit relatively still during that period?

EDIT:

My original post could have worded better, so: I want to know specifically about long it takes for the ventricles to physical contract and relax. How would i determine the length of these two periods in seconds and where could i find the "normal" lengths of these periods? in the cause of relaxation, i'm wondering about what to do when there is a substantial gap between heart beats.

The following image from wikipedia answer what you need. You can check corresponding page for details.

The top part shows the details of the different processes during a heart beat. Corresponding to these events the ECG reads are marked. As you can see the distance between the T wave ( the small bump after the QRS complex) and the next P wave corresponds to the diastole. As you can see the pressure changes correlate well with the electric reads from the heart. This wiki page has great descriptions of the features of the ECG and the corresponding events.

For example P to QRS corresponds to the conduction of stimulus from the sine node to AV node, or QRS depicts the rapid depolarization and repoliarization of the ventricles. This latter leads to strong muscle contraction and this causes intaventicular pressure rise, that is followed by aortic pressure change.

Edit: Sorry, for missing the key point, I totally misunderstood what you needed. I'll try to correct my mistake (I'll leave the previous info as it may be useful for others) The authors of this paper did a really nice work on modeling and measuring left ventricle contraction time and other things.

The reference: (Beyar and Sidman 1984)
Long story short: the contraction of the ventricle depends on the initial amount of blood (preload), aortic blood pressure at the end (afterload), and intial contractility. The results are summarized in three tables:

As you can see in the last columns, the ejection time varies with the parameters. The ejection time that is required for the ventricle to push the blood out to the aorta. Under normal circumstances a complete heart cycle is about 0.8s (or 800ms) this pie char shows the time ratio of main events. (Image taken from: tutorvista.com)

Note that complete cardiac diastole is when all the heart muscles are relaxed (this can be shortened if higher heart rate is required).

According to wikipedia

  Isovolumic relaxation time (IVRT) is an interval in the cardiac cycle, from the aortic component of the second heart sound, that is, closure of the aortic valve, to onset of filling by opening of the mitral valve. A normal IVRT is about 70 ± 12 ms, and approximately 10 ms longer in people over forty years. In abnormal relaxation, IVRT is usually in excess of 110 ms.

Isovolumic relaxation is when the muscle relaxes, yet the volume of the ventricle remains the same, thus only the internal pressure changes (it is analogue to isovolumic contraction - when the volume is unchanged, but pressure is built up, this happens at early ventricle contraction).


Why there is Cp/Ct (crossing point) value for negative sample in COVID-19 RT-PCR? I am from IT/ Engineering background and have some confusion in RT-PCR. So far my understanding we extract RNA from test specimens and transcribed it into complementary DNA (cDNA), and inside PCR DNA double helix is separated. Then primer a short nucleic acid sequence that provides a starting point for DNA synthesis with the target sequence and multiples the target DNA.
Since a higher cp value indicates a negative result but why negative results have cp value? Why it cross the threshold when it does have any target sequence (viral DNA)? Fluorescence is the measure of target DNA right??
In extraction, RNA is extracted does only COVID viral RNA is deducted? What happens to other viral and human RNA?
I have seen result were we have low cp value and test result is negative, the reason for this was because curve do not have Sigmoid function. I need more explanation on it.

PCR is highly specific (meaning it amplifies only the DNA the primers bind to), so the results in general are good. But: Due to the exponential nature of amplification, even very small mispairings can lead to the amplification of a very small amount of DNA and subsequently to a fluorescent signal. There are basically two ways of getting this amplification (except from the desired one): Contaminations and primer self-amplification. The first one should be clear, the second one happens when primers are able to bind to themself (or the complimentary one). This usually shows up late in the PCR, which is the reason why you assign a Ct-value to it after which you do not expect any meaningful amplification result anymore.

Depending on the method, you extract all RNA from your sample and translate it into cDNA. However, for the amplification in the PCR you need primers that fit to this cDNA. And since these primers have been proven to be highly specific (meaning: they bind absolutely no other sequence, not even from closely related viral species) we can be sure that any signal which is about the criteria mentioned in 1. comes from viral RNA and shows an infection. See the reference for one of the often used PCR tests.

Without seeing the curve, I cannot say anything specific about it. In general a real-time PCR curve follows a sigmoid shape. This gives some information about the way the reaction progressed over time. If it looks differently, something may have either happened to the reaction or to the sample. It may contain a PCR inhibitor, the sample can be contaminated or something else. I wouldn't trust such a result and repeat it with a new sample.

Reference
Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR


Can anyone help confirm this tiny insect larvae? Can anyone help identify this insect larvae?

Found: UK, autumn, in a bed.

Size: less than 2mm

The bed was searched thoroughly and no others were found, but is there likely to be more of them?

Thanks!

Can anyone help identify this insect larvae?

This is a varied carpet beetle larva, which belongs to the species Anthrenus verbasci.

A. verbasci. larval form, left; matured beetle, right.

  The bed was searched thoroughly and no others were found, but is there likely to be more of them?

It's difficult to say, though, generally, ~40 eggs are produced at a time, and they can remain in the larval stage for 8 months to almost two years.

At any rate, the University of California Agriculture & Natural Resources, and this website, both provide solid information about this insect, and outline measurements that can be taken to protect your home from it.


Using perceptual adaptation for enhancing realism of VR/other entertainment I am quite a fan of the recent oculus rift VR glasses, but it does have several flaws over normal vision, most notably a much less wide field of view, the so-called screen door effect because of too low resolution (example 1, example 2) and often also a certain latency between head movements and corresponding view angle change.

Could one, in theory, create glasses which have these limitations to wear during everyday life to adapt to them, and later have the benefit of a more "realistic" experience?

I know making the glasses is not trivial, I'm just asking about whether the perceptual adaptation part would even work as intended, what timeframe I could expect to adapt in, and how stringent the wearing of them has to be (is waking up without them ok, or should sleep be blindfolded, etc).

Does anyone have experience/advice/knowledge on the subject, maybe even links to prior applications?

Adaptation to altered vision is probably most well-investigated using prism-glasses. Prism glasses can shift the visual horizontally, for example by 20 degrees (Redding et al., 2005):

The use of horizontal shifting goggles has been investigated intensively to treat the symptoms of attentional neglect. Neglect occurs due to unilateral parietal brain lesions. For example, a lesion in the right hemisphere may induce left-sided neglect, where the left part of the visual field is seen, but simply not processed and neglected (Rosetti et al., 1998). Wearing prism goggles for approximately 6.5 hours/day, over the course of 2 weeks has been shown to reduce the symptoms of neglect significantly by as long as 17 weeks(!) after treatment (Frasinetti et al., 2002).

For the treatment of a neurological disorder such as neglect adaptation to prism glasses is great. However, treating healthy controls with comparable methods may induce unwanted side effects. 15 min of prism exposure has been shown to lead to several degrees of error in pointing tasks, for up to two weeks after the adaptation in normally sighted controls (Klapp et al., 1974).

To mention some studies closer to your question: in a virtual reality experiment subjects wore a head-mounted display that shifted the virtual position of their eyes. Their performance on a hand-eye coordination task first decreased by ~40% and then increased again with ~30% after adapting to the display. After taking the display off, there were transient after-effects, that impacted eye-hand performance (Rolland et al, 1995; Biocca & Rolland, 1998). In other studies wearing a head-mounted display longer lasting discomfort was reported in 5% of the subjects (Cobb et al., 1999) as well as binocular stress after removal of the display (Mark Mon-Williams et al., 1993).

Although the latter studies did not report serious after-effects, the more rigorously performed studies with the prism glasses have shown long-standing effects after visual adaptation. Hence, although the performance with virtual-reality head-mounted displays and comparable devices will undoubtedly increase after adapting to them, visual functions in everyday life may correspondingly be compromised.

So although this answer may not be addressing all your practical questions, I would say it is not advisable to let one actively adapt to head-mounted displays, or other wearable virtual-reality glasses that change visual function in the first place.

References
Biocca & Rolland, Presence 1998; 7:262-77
Cobb et al., Presence 1999; 8:169-86
Frasinetti et al., Brain 2002; 125:608-23
Klapp et al., Perception & psychophysics 1974; 15: 399-400
Redding et al. Neurosci Biobehav Rev 2005; 29:3, 431-44
Rolland et al., IEEE Proceedings of VRAIS 1995
Rosetti et al. Nature 1999; 365:166*9


Calibration curve for single radial immunodiffusion When we draw a calibration curve for single radial immunodiffusion, the curve does not pass through origin. Instead, there is a y intercept. Why does that happen ? Shouldn't zero antigen give zero ring diameter ?

When the radial immunodiffusion method is used to measure antigen concentrations in samples, a plate or slide is set up using agarose containing an antibody or antiserum. Holes are punched out of the agarose to form wells into which antigen is dispensed. The antigen diffuses out into the agarose and when the antigen/antibody ratio is favourable an immunoprecipitate will form as a ring (immunoprecipitin ring). The final diameter of the ring is proportional to the initial concentration of antigen.

Addressing the question: isn't this simply explained because the values on the Y axis are squares of the diameters of the rings, and this includes the well into which the antigen is dispensed?


Deciding between chi square and t test I am always so confused whether to do a chi square test or a t test in the sums given by my biostats teacher. Does anyone have a simple rule to decide this?

This is a very subtle question and I encourage you to read the Wikipedia articles on these different subjects (t-test, chi-squared test, p-value, etc) because the authors worked hard to combat common misconceptions about these commonly used statistical tests. Here is a rather oversimplified rule-of-thumb for these different tests:

t-test: Used when you are looking at the means of different populations. For example, you might want to determine whether the difference in the mean gene expression level between treated and untreated cells is different, or if the gene expression level of cells in a certain environment differs from what you would expect in a null hypothesis. Assumptions: You are assuming that the populations you are looking at are normally distributed. The variance of the populations is not known (that would be a Z-test), but it is assumed that the variance of each population is the same. Finally, for the t-test to work, the samples of the data from the two populations are assumed to be independent.
$\chi^2$ test: Several possibilities for this. The most common in biology is the Pearson $\chi^2$ test, which is used when you are looking at categorical data, like the number of pea plants with white or purple flowers and round or wrinkled seeds, and trying to see whether the number of individuals in each category is consistent with some null hypothesis (such as the number in each category you'd expect if the genes for flower color and seed shape are not linked). Assumptions: The data points were randomly and independently gathered from the population, and you have a reasonably large number of samples.

I'd hate to have made a huge mistake, so please edit my answer and/or contribute your own if you think I am completely misrepresenting these topics!


What is the name of this flowering plant? My mother is in hospice, and this beautiful flower is outside her window. She would like to know the name of "her" flower.

The flower is growing in Eastern Kansas and we are approaching the first day of summer here

It looks like a variety of canna lily. There are several flowers that have opened on the tip of your plant, as in the photo below.


Is there redundancy in the auditory system like there is in the visual system? In the early visual system, there is a great deal of overlap between retinal ganglion cells, which results in redundancy of the signals that neurons carry to higher visual processing areas in the brain.

Is there a similar type of redundancy in the early auditory system?

There is certainly redundancy in the auditory system, well demonstrated by Gal Chechik et all

It is also clear that there is pronounced intersensory redundacy, involving auditory systems here

Another article discusses clear auditory redundancy in adults when participating in a task to discriminate between two sounds as quickly as possible

...the auditory system maintains and tolerates functionally independently represented redundant and contradictory predictions.

In terms of redundancy in development, it seems there have  been shown links in mice discussed by Dr Thomas Braun

Hope this helps!


Why structures of many proteins are still unknown? https://www.learner.org/courses/biology/textbook/proteo/proteo_3.html
Despite advances in techniques for determining protein structure, the structures of many proteins are still unknown...

My question is why? We have many researchers all over the world. We know what our 3 billion DNA is. The governments invest billions of money into medical research. We should have sufficient human resources and technology.
What's stopping us determining structure for all proteins? We need more money? We need more people? We need better technology?

The gold standard for determining protein structures is x-ray crystallography. However, in order to perform x-ray crystallography you have to obtain your protein in crystalline form. Many proteins are not soluble in water, so crystallization is difficult or impossible. See this answer for information about the difficulty of crystallizing trans-membrane proteins.


Can a human be made with ovum but without sperm? This article says that scientists were successful in making a mouse using only a sperm and no egg (ovum). The article also states that this procedure could be applicable to humans.

However, I want to know why didn't they try with only an ovum?

Can a human be made only with an ovum, i.e. without sperm?

Nice question! It is actually very difficult to do so because humans, obviously, are far more complex than some animal species which naturally show parthenogenesis. Just to mention, there are female-only animals also present in nature, such as New Mexico whiptail, which reproduce only by parthenogenesis, meaning that it is not as impractical as one might think.

There have been many parthenogenesis tests on mice and monkeys, but they usually result in abnormal development. This is because mammals have imprinted genetic regions, where either the maternal or the paternal chromosome is inactivated in the offspring in order for development to proceed normally. A mammal created by parthenogenesis would have double doses of maternally imprinted genes and lack paternally imprinted genes, leading to developmental abnormalities. It has been suggested that defects in placental folding or interdigitation are one cause of swine parthenote abortive development.

During oocyte development, high metaphase promoting factor (MPF) activity causes it to arrest at the metaphase II stage until a sperm fertilizes it. The fertilization event causes intracellular calcium oscillations, and targeted degradation of cyclin B, a regulatory subunit of MPF, thus permitting the oocyte to proceed through meiosis. The most precise and exact mechanism is not known yet.

But this does not mean that it is not possible. Actually, it has been done quite a few times; once on June 26, 2007 by International Stem Cell Corporation (ISCC), and once (controversially) on August 2, 2007 by Hwang Woo-Suk. Even the procedure for parthenogenesis (in swine though) in lab is available. To initiate parthenogenesis of swine oocytes, various methods exist to induce an artificial activation that mimics sperm entry, such as calcium ionophore treatment, microinjection of calcium ions, or electrical stimulation. Treatment with cycloheximide, a non-specific protein synthesis inhibitor, enhances parthenote development in swine presumably by continual inhibition of MPF/cyclin B As meiosis proceeds, extrusion of the second polar is blocked by exposure to cytochalasin B. This treatment results in a diploid (2 maternal genomes) parthenote Parthenotes can be surgically transferred to a recipient oviduct for further development, but will succumb to developmental failure after ≈30 days of gestation.

The major problem with parthenogenesis in humans is the abnormal development of embryo. This has been accounted by a phenomenon known as genomic imprinting. Genomic imprinting is the epigenetic phenomenon by which certain genes are expressed in a parent-of-origin-specific manner. For example, if the allele inherited from the father is imprinted, it is thereby silenced, and only the allele from the mother is expressed. The death of diploid parthenogenetic or androgenetic mammalian embryos is determined by the absence of expression of the genes of imprinted loci of the maternal or paternal genome, which leads to significant defects in development of tissues and organs. How this exactly works is not known yet, but it is supposed that it evolved to prevent parthenogenesis. Bi-parental reproduction is necessary due to parent-specific epigenetic modification of the genome during gametogenesis, which leads to non-equivalent expression of imprinted genes from the maternal and paternal alleles. Thus, genomic imprinting seems to be ineffective during normal reproduction.

As a side note, in the article you refer to, the researchers did not just mix two sperms and produce diploid zygote or something like that. In the procedure, they injected a normal sperm to the above explained abnormal embryo, which later on proved to be viable. They, thus, showed that these kind of embryos can also become viable if they get fertilized by a sperm within time.

References:

Abnormal development of embryonic and extraembryonic cell lineages in parthenogenetic mouse embryos; Karin S. Sturm, Margaret L. Flannery, Roger A. Pedersen
Parthenogenesis - Wikipedia
Patient-Specific Stem Cell Lines Derived from Human Parthenogenetic Blastocysts; E.S. Revazova, N.A. Turovets, O.D. Kochetkova, L.B. Kindarova, L.N. Kuzmichev, J.D. Janus, and M.V. Pryzhkova
Genomic imprinting is a barrier to parthenogenesis in mammals; Kono T.
Genomic Imprinting and Problem of Parthenogenesis in Mammals; E. S. Platonov
Mice produced by mitotic reprogramming of sperm injected into haploid parthenogenotes;
Toru Suzuki, Maki Asami, Martin Hoffmann, Xin Lu, Miodrag Gužvić, Christoph A. Klein & Anthony C. F. Perry
Stem cell fraudster made 'virgin birth' breakthrough; Silver lining for Korean science scandal; 3 Aug 2007, Christopher Williams


How correlated are the lengths of tendons in different part of a human body? How correlated are the lengths of tendons in different part of a human body?

E.g., if the we consider two humans, A, and B. Human A has a patellar tendon of length 2 cm, and human B has a patellar tendon of length 1 cm, i.e. twice shorter. Should we expect all tendons in human A to be approximately twice larger than in human B?

I couldn't find studies analysing clearly enough tendons size, but a couple of sources show that they are probably correlated:

One study found correlation between dimensions of Achilles'tendon and other ankle tendons (see table 2).
Another study found correlation between height and dimensions of some tendons (see table 2).

Anyway, since correlation is not very strong, I doubt if the effect found is just the obvious correlation of dimension of all body parts to the general dimension of body - that is, bigger people tend to have bigger tendons, bigger bones, bigger livers, and so. It would be interesting to do a regression analysis of tendons dimensions taking in account body dimensions and other tendons dimensions. This way we could be able to see if people with some bigger tendon (compared with people of the same body size) tend to have other bigger tendons.


Do Acyl Carrier Proteins and Conenzyme A have similar reactivity? In terms of the reactions they undergo are they roughly equivalent groups?

The acyl groups ligated to CoA and to acyl carrier proteins are actually attached to the same group (a phosphopantetheine group) as shown below, and so have very similar reactivities (i.e. group transfer potentials).


How does MSMA kill crabgrass with only minimal damage to lawn grasses? I use MSMA (Monosodium methyl arsenate) to kill crabgrass in lawns. I am not certain of the mode of action.

How does this chemical work? How does it target the annual grassy weeds, without damaging the lawns much?

Please consider this a sort of comment — I tried looking up for articles related to MSMA mode of action but almost all the articles are about its toxicity in mammals.

By what I understand, trivalent arsenates act as phosphate analogs and therefore interfere in phosphorylation reactions including DNA synthesis [Ref].

The weed is affected perhaps because of its relatively higher growth rate. Also the already established lawn grasses would have good population size to regrow out of the damage.


Relationship between nerves and axons I just wanted to get a realistic viewpoint of our nervous system. I understand arteries and veins, but I wanted to know how similar our nervous system is to that?

I understand we have neurons (please correct me if I am wrong) all over the surface of body. Whenever we feel a touch a neuron fires a response, and that response travels through axons (myelin sheath).

My main question is what a nerve exactly is. Is it a long axon? How many axons (same thing as neuron body?) are in a nerve? I am sure it depends on different nerves.

I will go through your list of questions below:

I wanted to know how similar is our nervous system to [the circulatory system]?
They are very different, but as in every comparison of very complex systems, there is some overlap. The circulatory system carries fluids, the nervous system electrical signals so they are functionally not alike. However, both systems run throughout the body and have a more or less central control unit (the brain and heart respectively). So there is a structural similarity. I reckon they are as much alike as a city's sewer system and electricity grid.
I understand we have neurons (please correct me if I am wrong) all over the surface of body.
That is correct
Whenever we feel a touch (stimulus arises) a neuron fires a response, and that response travels through axons (myelin sheath).
Tactile stimulation may result in firing of one or more neurons, dependent on the intensity of the stimulus. Larger stimuli will, obviously, recruit more fibers. Stronger stimuli will evoke stronger responses (increased firing). Axons indeed conduct the neuronal responses, like an electrical wire conducts electrical current. Longer axons are often myelinated (insulated). Not all neurons related to touch are myelinated, however.
So my main question is that what exactly is a nerve?
A nerve is a bundle of axons that carry related functional information. Typically, nerves conduct information originating from locations closely located together in the body, and generally they convey this information to a localized spot in the body as well. For example, the optic nerve carries information from the photoreceptors (related information) from the retina (localized source) to the brainstem (localized target).
Is [a nerve] a long axon?
A nerve contains many axons. 'Long' or 'short' is rather subjective.
How many axons (same thing as neuron body?) are in a nerve? I am sure it depends on different nerves.
Neuronal cell bodies are typically located outside a nerve. Nerves contain varying numbers of fibers. For example, the auditory nerve harbors the axons of the spiral ganglion cells that transmit auditory information from the inner ear to the brain. It contains between 31k - 32k (myelinated) fibers in normal-hearing humans (Spoendlin & Schrott, 1989). In contrast, the optic nerve, which carries visual information from the retina to the brain, contains some 1.3 million (myelinated) fibers in young human adults (Jonas et al., 1992)

References
- Jonas et al., IOVS 1992;33:2012-8
- Spoendlin & Schrott, Hear Res 1989;43:25-38


How would a plant sprout and grow in a zero gravity environment? Have any experiments been carried out involving sprouting and growing plants in a zero gravity environment? If so, what was the outcome? How did the plants sprout out of the soil without gravity? Did they grow outward or toward light sources?

There have been several experiments in growing plants in microgravity (strictly speaking, we do not achieve "zero-g" since astronauts remain in orbit about the Earth).

Changes in plant growth due to the influence of a gravity field is sometimes called gravimorphogenesis. More specifically, gravitropism is a differential growth response of plant organs to gravity. For example, roots grow downwards (positive gravitropism) and shoots grow upwards (negative gravitropism) on Earth.

Studies (e.g. 1) suggest that in micro-g, there is no preferred direction; roots may grow "up" and shoots "down".

It is thought that this growth response is due to the relative distribution of auxin in the plant. On Earth, auxin will preferentially move down into the root-tips due to the location of amyloplasts in the root-cap cells. In micro-g, amyloplasts do not settle at the "bottom" of the plant, therefore there is a more generalized distribution of auxin, and therefore there will be no preferred growth direction.

In addition, changes in plant gene expression as a response to micro-g environments are also being investigated (2) and suggest that auxin transport inhibitors may block the activation of the auxin responsive promoters in Nicotiana spp. (tabacco).

(1) Mechanisms in the Early Phases of plant Gravitropism CRC Crit Rev Plant Sci. 2000 ;19 (6):551-73  11806421  Cit:65

(2) Transcription Profiling of the Early Gravitropic Response in Arabidopsis Using High-Density Oligonucleotide Probe Microarrays, Plant Physiol. 2002 October; 130(2): 720–728.
doi:  10.1104/pp.009688


How does Oedipus complex fit in the evolutionary theory? This is somthing that really makes me curious. How is posible that trough a  evolution process the best posible candidate is the one that falls in love whith his progenitor?

It doesn't.  The Oedipus complex is one of Freud's theories to explain human behavior, not something that is endorsed by the fields of psychology or psychiatry.  Freud had a lot of interesting theories, some of which remain core concepts in psychology, and some of which have been marginalized or rejected.

There are some professionals who feel it has merits for consideration, to one degree or another, but if you look at publications by the APA (American Psychological Association) and Psych.org (American Psychiatric Association), you won't see in their practice guidelines.

APA: http://psycnet.apa.org/journals/pst/32/4/535/

Wikipedia: http://en.wikipedia.org/wiki/Oedipus_complex#Criticism

If you're asking how might it fit with evolution if it were to be true, that's more of a philosophical question - which perhaps is the better angle from which to approach the question.

In "survival of the fittest" - "fittest" is better described as "those who most successfully reproduce and produce offspring that are also highly successful in reproducing."

Reproducing with one's immediate family results frequently in severe birth defects, the opposite of "fit."  Those who want to reproduce with their mother but don't, and reject all other mates, will not reproduce.  Not "fit."  The only possibility similar to the oedipal complex is that males choose mates that are like their mothers.

What is true is that we often marry someone similar to our parent - but it is not a result of an actual oedipal complex.  Freud wrote the oedipal complex in part to try to explain this phenomenon.  But there are better explanations - we are attracted to that with which we are most familiar, to that which makes us feel comfortable, to that which makes us feel warm and fuzzy.  Our definition of beauty is largely shaped by family faces - because that is what you are surrounded with as your mind develops.  Etc etc.


Can the same target gene be regulated differently by the same transcription factor under different conditions? I'm very new in biology and doing more computational analysis. I'm confused with the type of interactions between Transcription Factors (TF) and target genes.

Is it possible that the same transcription factor interacts differently with the same target gene under different conditions?

e.g., TF1 up-regulates Gene1 under condition 1 while TF1 down-regulates the same gene Gene1 under condition 2
Does the above example take place in biological systems?

I can only think of different TF complexes which are regulating the gene Gene1 under different conditions with different effect. However, it would be great to know if, in case TF1 does not participate in any TF complexes to regulate Gene1 under certain conditions, it is then possible that "TF1" regulates Gene1 differently under different conditions?

Short answer - yes but probably somewhat rarely.

Transcription factors aren't necessarily limited to being either repressors or activators. In practice they mostly do one a lot more than the other - e.g. if they have an 'activation' domain then they will mostly activate, but they can still do the opposite, directly or indirectly.

A single TF will often regulate different genes in different directions. This can be due to indirect effects - our activator activates a repressor which then switches off a gene. It can however also happen through direct means - for instance a factor might bind a repressing or activating domain at different locations, or displace different factors.

Most of this variation is probably specific to the target gene, so factors are probably more specific in their effect on a given gene. However, since our factors action depends on other genes,and different genes will be active in different conditions, there's no reason a factor couldn't do different things under different conditions while at the same location - perhaps one condition activates a repressor that binds with it, or a stronger activator that it competes with.

It's a matter of ongoing research, but I would expect this kind of thing to be the exception rather than the rule. In general complex interactions between TFs at a given location seem to be rarer than more or less additive effects.


Do chromosomes uncoil in interphase II? During interphase II, there is no S phase in which DNA replicates. However, in this stage, do the chromosomes remain wound? Or have they unwound into chromatin form, and recondense during prophase II?

In many cases the chromosomes do undergo some dispersion, they do not reach the extremely extended state of the interphase nucleus, this all happens in telophase -I. It would be correct to refer to the stage between two meiotic divisions as interkinesis which is generally short lived.

The prophase-II is initiated immediately after cytokinesis, usually before the chromosomes have fully elongated.


Can Blood Types Change? I recently heard a radio show where two callers claimed that their blood types had changed. One caller claimed that he was born O-, but recent tests said he was A+. Another caller claimed to change from AB- to AB+. Both callers claim that they had multiple tests before and after the change.

What I noticed is that both cases claim a conversion from Rh- to Rh+, or from type O to some other type. These could potentially be explained by a person carrying a gene for Rh factor or some other blood type, but failing to express the protein. Then the gene starts expressing, changing their blood type.

Of course both stories could be false, intentionally or otherwise. This is purely anecdotal evidence, and one caller claimed that her blood type change was due to extraterrestrial interference. I couldn't find any better documented cases of blood type changes after a quick search on the internet, so I thought I'd ask here.

Are there any documented cases of a change in blood type?

Blood group antigens are either sugars or proteins found attached to the red blood cell membrane. ABO blood group antigens are the most clinically important antigens because they are the most immunogenic. As red blood cell antigens are inherited traits, they are usually not altered throughout the life of an individual. There have been occasional case reports of ABO blood group antigen change in malignant conditions,ABO antigen alteration associated with acute myeloid leukemia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5242122/

https://www.ncbi.nlm.nih.gov/pubmed/15135601 ( B to O change)

https://www.ncbi.nlm.nih.gov/pubmed/22270426 (New laboratory procedures and Rh blood type changes in a pregnant woman.)

A bone marrow transplant will replace the cells which make your blood cells with cells from the donor. Over about 3-4 months (life span of a red cell), your blood will become your donors type.


Why do living things go belly up as they die? I have seen birds, lizards, frogs, fish, etc in various places on their back dead. May be insecticides cause them to flip over but I do not believe every upside down creature died by poison as stated in this question's answer: Why do cockroaches flip over when they die? and the roach question only covers roaches and insecticides. My question covers all animals not affected by poison that are belly up.

Other than poisoning is there any other reasons like DNA programming on behavior or muscle spasms that cause this?

limbs are light weight compared to bodies, if you knock an animal around (and it has no active correction AKA is not alive) it will tend to end up on its back just due to where its center of gravity is.


Why do some trees in California have dead brown leaves but also new green leaves? It's Autumn 2015, and I just saw a tree that had mainly dead brown leaves but also some new small green leaves growing. Why didn't the tree just keep its old leaves? Does it think we are in spring already?

EDIT: To be clear, I had always thought that in autumn that all the leaves of a tree would fall off together, as a preparation for winter. It seems silly that the tree would then immediately grow some new leaves when it just decided to let all those previous leaves die. Why not just use that same energy to maintain those leaves?

I've taken some photos of the leaves and the trunk for help with identification.

More images of the tree can be seen at this Imgur link

Whether trees are deciduous or evergreen, their leaves don't last forever; they need to be replaced at intervals.  The process of photosynthesis depletes the chlorophyll in the leaves, so that needs to be replaced and this is a significant metabolic cost to the tree.  Therefore, whenever a tree is experiencing metabolic stress, it will slow down the chlorophyll replacement, and let the leaves die to save energy. It's metabolically cheaper to simply let the leaves die -- after removing the most precious nutrients -- and then regrow new leaves as needed, than to keep repairing the leaves that aren't needed because the tree is resting for other reasons.

In temperate areas, where there are well-defined seasons, this typically happens in the fall, and deciduous trees let their leaves die all at once in the fall.  In tropical or subtropical regions, where trees could photosynthesize all year, leaves may drop all year round (as with evergreen trees, like conifers, in temperate regions).  Often, though, their leaves will reflect metabolic stresses on the tree, such as drought.

(The Wikipedia article on "Deciduous" makes the point that this can be very localized, related to very local environmental differences that could only affect a single tree.)

Much of California is a subtropical region, and it has been experiencing severe drought for some time, so it wouldn't be surprising for a tree to have reached a point where its leaves have all had their chlorophyll removed.  On the other hand, as the El Nino event of 2015 increases, rainfall in California is returning, so it would also not be surprising for a tree to have recovered from drought enough to start making new leaves.

If your question is why the old leaves didn't fall off before the new ones started to regrow, it is probably simply a matter of timing.  The tree doesn't really "care" if the leaves fall or not, so long as they're not using up its resources, so there's no reason to force them off.  The new water supply may have arrived fairly shortly after the degree of drought that caused the tree to shut down the leaves.