texts: How do adenoviruses interact with muscle tissue that it makes them acceptable as vector viruses?

texts:
From what I understand certain attenuated adenoviruses are popular as a vector virus, meaning a virus that is used as the active agent in a vaccine to infect cells and trigger a helpful immune response.
Of course, this use assumes that the vector virus can indeed infect cells and cause them to replicate the target protein in the first place. From what I can tell, how adenoviruses attach to cells and their receptors is imperfectly understood and furthermore live adenoviruses seem to often prefer infecting cells in organ tissue, not muscle tissue, so what makes researchers confident that adenoviruses are effective as vector viruses when injected into a muscle?


texts: How much genetic divergence must there be to yield two different species?

texts: I read that humans are a few percent Neanderthal. So how much difference between egg and sperm is needed for there to be no offspring. That is, for there to be two different species? Is this a measurable quantity or just a random genetic mismatch?


texts: From what stage can you speak of an inflammation?

texts:
Imagine you hit your foot at a table leg and it hurts a while or you got a tiny graze. Those injuries aren't an infection but could these things still be called an inflammation?

Is it necessary that in both cases cells are damaged to induce a cascade of hormones? Or with other words, is there always an inflammation when cells are damaged or is needed more?


texts: What is the conversion between r and FST?

texts:
From Schonman (2013):

...allele A can only invade under Hamilton’s condition  R=$F_{ST}$ > C/B.

From Harpending (2002):

The best general definition of the coefficient of relation $R_{XY}$ between individuals X and Y is (Bulmer, 1994) $R_{XY}$ = $F_{XY}$/$F_{XX}$, where $F_{XY}$ is the kinship between X and Y and $F_{XX}$ is the kinship of X with himself [..]
[..] $F_{ST}$ is just the coefficient of kinship between members of the same deme [..]
[..] $F_{Self} = \frac{(1 + F_{ST})}{2}$  [..]

This means, unless I am mistaken, that if I take Harpending's equation and substitute $F_{ST}$ for $F_{XY}$ and substitute 1/2(1+$F_{ST}$) for $F_{XX}$, I can calculate within-deme relatedness: 2*$F_{ST}$/(1+$F_{ST}$).
Yet Schonman says R=$F_{ST}$?
What am I doing wrong here?


texts: Gene distance and Recombination Frequency: Mechanism

texts: Why is the recombination frequency higher if the genes are farther apart?


texts: Does anybody know which plant (or tree) is this?

texts:
Thus one has teased me a lot. This is just a small plantlet, the actual one went about 5 feet in height before we had to cut it. Whenever we cut it, it grew back within weeks. And soon small plantlets grew near it in a radius of about 3 meters. Today, we called 2 men to take off its root. They dug a hole about a foot deep and discovered that its roots had spread all across our garden. All the people we asked gave us different speculations of what plant it could be, but nobody was sure. Does anyone here know about it?

Data:

It has lots of thorns, even in its roots!
This plant is about 25 cm in length.
Its leaves are about 4 mm long and 1 mm wide.
A compound leaf is about 1.5 cm long.

Location: Northern plains region, India


texts: Longest pathway from sensory to motor neurons

texts:
How long is the longest pathway a neural signal can take starting from a
  sensory neuron and ending at a motor neuron (without loops)?

[This is a purely theoretical question concerning only the synaptic connectivity of neurons, not the propagation of real signals.]

The number I am looking for must be greater than 8 because there are 6 layers in the cerebral cortex and 2 layers of motoneurons: upper motor neurons and lower motor neurons.

The question then reads:

  How long is the longest pathway from a sensory neuron to layer I of
  the cerebral cortex?

  How long is the longest pathway from layer VI of the cerebral cortex
  to an upper motor neuron (which may lie in the brain stem)?

  How long can be "detours" inside the system of layers of the cerebral
  cortex?

I assume that the cortex is not strictly layered, so that a neuron in layer $i$ normally projects on a neuron in layer $i+1$ directly, but possibly also via $N$ interneurons. Theoretically, the upper bound for $N$ is just the number of neurons in the brain, but in practice will be much smaller. To get a sensible number, it may be necessary to neglect detours that are too long because they are too sporadic and/or useless. (But how to define and quantify sporadicity and usefullness in this context?)

If my question doesn't make sense in the way I ask it here: How could I improve it to make it sensible?

[Of course, I am not looking for exact numbers but only for estimates, resp. estimates of lower and upper bounds.]


texts: Why does the olive tree produce a bitter tasting fruit?

texts:
What is the survival value for the olive tree to produce a bitter tasting fruit, even when it is ripened?

I realize some fruits and berries are species specific, i.e., meant for specific animals to eat and disperse the seed widely. Is this the case of the olive?


texts: How many human proteins are very well characterized?

texts:
Following up on How many human proteins have a solved 3D structure?,is there a list of very well characterized human proteins / protein complexes?

My criteria for "very well characterized" includes, at least:

a high quality 3D structure
known activity in vivo
known associates in its activities in the cell
kinetics of its activity
regulatory elements for expression
etc..., and
(probably most importantly) a general consensus among experts that it is well described

This list would most likely include such proteins or protein complexes as:

P53,
polymerase alpha, and
the nuclear pore complex,

to name a very small number.


texts: Are there any bacterial lineages which are particularly well adapted to becoming endosymbionts?

texts: Is there any particular bacterial lineages which contain a large number of endosymbiotic species and that inhabit a large range of eukaryotic hosts? To me, this would seem to suggest that they are particularly well adapted to becoming endosymbionts.


texts: I recently came across an article saying that fruit flies use alcohol to deter parasites. The researcher was quoted as saying there have not been any studies on the effect of human alcohol consumption on parasites. Is there any research being done on this? Another related question I have is whether the fruit flies can tolerate higher alcohol concentrations than mammals/humans.


texts:
I'll keep this as brief as I can. I am an engineer and I have an idea for an early detection system for the Zika virus. I want to build it. However, first I need to do research on how one detects Zika in mosquitos.

I am under the impression that to detect it in a human you would wait for the appropriate antibodies to appear in the blood. I am assuming that I would need to culture anything I get from a mosquito.

Can someone point me at any research material they can find? All of the search terms are to ambiguous for mere non medical mortals like myself.


texts: Can someone ID this moth seen in Bellandur, Bangalore?

texts: Picture taken near Saul Kere. You may need to zoom in.


texts:
Can we change our dopamine baseline levels? High dopamine levels improve alertness, problem solving, but may also cause anxiety and aggression.

I've read that smiling and laughing, eating certain foods, or having unexpected rewards can elevate dopamine levels in the brain. I also read that expecting a reward in the future (such as an upcoming vacation) elevates dopamine levels. Can these actions, if repeated over a prolonged period, increase baseline dopamine levels? Or will dopamine return to original levels once these actions are stopped?


texts: Can you vaccinate against bacterial diseases? Are there existing vaccines for such diseases?

texts:
I have the (maybe wrong?) preconception that we only vaccinate against viral diseases, and that there can only exist vaccines against viruses. I think the idea comes from the idea that only for viral diseases are you becoming immune after contracting the disease, not for bacterial. The question Is there a vaccine against the plague (Yersinia pestis)? made me think that I don't really have a justification for that, seeing that the mechanisms for combatting viral diseases and bacterial diseases should be the same (is that right?).

So, is it possible to vaccinate against bacterial diseases? Do we have existing vaccines for any bacterial disease?


texts: Restriction enzymes, how are the recognition sequences determined?

texts: How were the recognition sequences (e.g. GAATTC of EcoRI, GGATCC of BamHI) characterised? Text books only list the recognition sites but never the methodologies used to determine the sequences.


texts:
I read article about alcohol harm where written that child may bear with birth defect cause mother used to drink alcohol 10 years ago so egg cell stay damages that long.

I don't believe that human egg cell wait for such long time until activated.

How long human egg cell grow up until sperm fuse it?


texts: Do all Gram negative bacteria cause septic shock? If they don't could they if you attacked them with an antibiotic that could lyse the cell? For example any antibiotic that attacks the cell wall, although I suppose that could be difficult with the gram negative wall, not to many gram negatives are susceptible to a wall attack.


texts: Do plants take in the same amount of CO2 as they release?

texts:
There are many claims in the media that trees remove more carbon dioxide form the atmosphere than they release back into the atmosphere. By what chemical pathway can this occur?
The law that matter is neither created nor destroyed surely applies as shown by the chemical pathway in the photosynthesis and respiration process.

6CO2 + 6H2O + sunlight energy.  -----> C6H12O6 + 6O2
C6H12O6 + 6O2.                  -----> 6H2O + ATP (energy) + 6CO2

Thus the SAME amount of 6CO2 taken in is released, in order for the plant to have formation of the ATP usable energy for plant tissue creation, so photosynthesis cannot happen at a  more rapid rate than respiration. If that happened, then yes, more CO2 is removed then released, but that would leave an unbalanced equation.
I am not arguing the story further down the road of tree tissue and carbon sequestration/storage.


texts: Relation between carbon dioxide assimilation and the ambient and intercellular partial pressures of carbon dioxide

texts: So, water-use efficiency (and carbon assimilation rate) is correlated with ambient CO₂ concentration (Ca), and  carbon isotope discrimination Δ is correlated with Pi/Pa (partial CO₂ pressure, intercellular and atmospheric, respectively) in C3 species. If the Ca increased, would that result in decreasing Δ? In other words, would increasing ambient CO₂ levels result in less discrimination towards the ¹³C isotope, in C3 species? And if that's true, is my math sound?


texts: Where can I find datasets containing large phylogenetic networks?

texts:
There are many datasets out there for phylogenetic trees, one can example can be found here.

However, I couldn't find something for phylogenetic networks. According to Wikipedia:

  A phylogenetic network or reticulation is any graph used to visualize
  evolutionary relationships (either abstractly or explicitly)2
  between nucleotide sequences, genes, chromosomes, genomes, or
  species.2 They are employed when reticulation events such as
  hybridization, horizontal gene transfer, recombination, or gene
  duplication and loss are believed to be involved.

Of course a phylogenetic tree is a phylogenetic network, but phylogenetic networks can be thought of as rooted directed acyclic graphs, meaning that more complicated evolutionary structures can be captured.


texts: Why do eggs lack an endoplasmic reticulum?

texts: Trueman's Elementary Biology book I found says that the endoplasmic reticulum is absent in eggs, but no reason is given. Why is it absent?


texts: We saw this leech like worm in Kerala, India. Can anyone identify it for us? I saw it today, 10th September. It's about 6 to 7 centimeters long. It was very still, didn't move while we went close and took a picture. Thank you.


texts: Insect Identification. Moth or dragonfly or?

texts: Found on the exterior wall of my house taking cover from the rain it seems. Wingspan is approximately 5cm. I live in the South SF Bay and it has been rather cold and rainy this week.


texts:
I observed Phyllanthus reticulatus is sleeping during nights. I want to plant this species indoor under a UV device.  Do these plants sleep under ultraviolent rays?

(Sleeping means leaves are close to each other)


texts: Beyond the Stanford HIV database, what other databases out there provide a dataset linking virus/bacterial genotype to quantitative phenotype? I'm looking for high quality datasets to test machine learning pipelines. My own searches usually yield only databases that curate mutations related to drug resistance class ("resistant, possibly resistant, susceptible), but not quantitative information in a standardized form like the Stanford database.


texts: Is there a difference between NADH and NADH2?

texts: I've been reading a lot about the oxidative dissimilation etc, and often I see different sources use NADH and NADH2 in the same reactions. One source uses NADH and another uses NADH2 in the exact same way. Is there a difference or is it just a different name for the same substance?


texts: What is the proper format for genus and species names in latin?

texts:
When using the latin nomenclature for a fish in printed materials (such as Sander vitreus for walleye), what is the correct capitalization of each word?

In this example, should 'S' be uppercase only, or both 'S' and 'V' be upper/lower case?


texts: Inoculating agar plates with microbes suspended in sterilised water?

texts: We were having a problem with our experiment (culturing microbes on homemade nutri agar) so we decided to change our set-up. It already cost us quite some money. So, we saw this procedure. Can anyone tell if this is legit? Thank you!


texts: Where is sialic group in gangliosides that form ABO blood groups?

texts:
A ganglioside is a molecule composed of a glycosphingolipid (ceramide and oligosaccharide) with one or more sialic acids (e.g. n-acetylneuraminic acid, NANA) linked on the sugar chain. (source: https://en.wikipedia.org/wiki/Ganglioside)

Gangliosides form ABO blood groups.

Do gangliosides always contain sialic acid? If true, then where is sialic acid in blood groups?

Structural formula of ganglioside GM1a:

Blood Group Antigens:


texts: Are these birds in video real? What are they called?

texts:
I recently came acroos this video   :  https://m.facebook.com/story.php?story_fbid=1053324651468913&id=492140647587319

I want to know whether these birds are real or edited? If they're real,  what are their names?


texts: Why do SRIs help in serotonergic neurotransmission?

texts:
Serotonin reuptake inhibitors (SRIs) block the action of the serotonin transporter (SERT) which, according to Wikipedia, leads to an increase in serotonergic neurotransmission.

Now this book summarizes serotonergic neurotransmission as follows:

  [The neurotransmitter] binds to specific receptors on the postsynaptic cell, thereby
  generating a postsynaptic electrical signal [...]. The transmitter must then be removed rapidly to
  enable the postsynaptic cell to engage in another cycle of
  neurotransmitter release, binding, and signal generation. [Neurotransmitters are removed by] reuptake into nerve terminals [...].

So my question is the following: If, as stated in the quote, the transmitter must be removed rapidly, shouldn't an increased amount / binding potential of SERT actually be a good thing because if there are more transporters, the process of removing the neurotransmitter is much faster? And consequently, why would blocking the SERTs help in serotonergic neurotransmission? Is it because the neurotransmitter must remain in the synaptic cleft for a certain amount of time? Is it because the reuptake takes place before the neurotransmitter could bind to the receptors of the postsynaptic cell? Or ist there yet another reason?


texts: State of voltage gated sodium channels in depolarised potentials

texts:
Case 1

We learn in Physiology that during the depolarization phase in the membrane, more sodium channels tend to open as the membrane potential increases i.e., less negative. This is a kind of positive feedback which leads to the action potential and explains the threshold of depolarization that is required for action potential.

So in short, as the membrane potential becomes less negative sodium channels tend to open.

Case 2

On the other hand there is famous graph from Bertram Katzung, Susan Masters, Anthony Trevor-Basic and Clinical Pharmacology, Edition 12. which shows the dependence of the sodium channel function based on the membrane potential preceding the stimulus.

To quote,

  The fraction of sodium channels available for opening in response to a stimulus is determined by the membrane potential immediately preceding the stimulus. The decrease in the fraction available when the resting potential is depolarized in the absence of a drug (control curve) results from the voltage-dependent closure of h gates in the channels.

Both these cases look pretty contraindicating to me. But I attempted to explain this by the three stages of the Na+ channel.

Case 1 - may be addressing the transition from closed to open channels, i.e., opening of the m gate. (I'm just hypothesizing here so correct me if wrong)

Case 2 - as mentioned in the book, talks of closing of the h gate leading to inactivated gates at higher membrane potentials.

Do case 1 and case 2 happen one after another? Are the voltage ranges for each different? Is my explanation for case 1 correct?


texts: What causes inhalation during breathing?

texts:
I have read here that the two major inhalation muscles are the (1) diaphragm and the (2) external intercostals.

Additionally, inhalation can also be caused by (1) expansion of the abdominal cavity, or (2) movement of the pelvic floor.

I thought that inhalation was caused by muscles that essentially cause the intra-thoracic pressure to drop, thus causing air to flow into the lungs to fill the absence, like a straw. This is what I thought caused us to inhale.

MY QUESTION

If my understanding is correct, then do the muscles cause this drop in pressure? Which spaces within the trunk experience this drop in pressure? If not, how exactly do these muscles facilitate inhalation?


texts: Why can I see a light flicker when it's in my peripheral vision?

texts:
When I'm looking at an old CRT monitor or a worn fluorescent lamp, but not directly in the center of my gaze, the light from it seems to flicker. When I focus my gaze onto the monitor or lamp, the flickering stops.

Why can I see a light flicker only when it's in my peripheral vision?


texts: History: Do evolutionary and ecological processes occur at the same timescales?

texts:
Classically, it was thought that evolutionary processes occurred at a much slower pace than demographic/ecological processes. Nobody, ever thought about incorporating both processes into the same model as they were assumed to occur at different time scales. We slowly came to realize that this way of thinking is quite wrong and many demographic/ecological changes (demographic expansion for example) directly affect evolutionary processes and even more important that evolutionary processes can directly influence demographic/ecological processes. I take for example Kirkpatrick and Barton (1996) who investigated how dispersal load (fitness decrease due to maladaptive alleles brought to local populations by dispersal) affect the "evolution" of the species range limits.

Who (what) are the main authors (articles) that allowed for this switch in our viewpoint about the interrelations between evolution and demographic/ecological processes?

Dennis Chitty might have been an important author to establish the viewpoint that evolutionary processes can influence the probability of survival of a population. However, I know a little bit about his work only because he was professor at my department (way before I even arrived in the department) and he might therefore not be the most important author of all.


texts:
As telomerase works by adding new nucleotides complementary to the RNA it contains, it cannot work for the complementary strand.

Say telomerase X has RNA complementary to the 5' to 3' strand it cannot elongate he telomere for the 3'to 5' strand.

So does a cell have 2 types of telomerases ? One for 5' to 3' and another for 3' to 5' ?


texts: How do prokaryotes perform cellular respiration without membrane-bound organelles?

texts: In order to survive, prokaryotes such as bacteria need to produce energy from food such as glucose. In eukaryotic cells, respiration is performed by mitochondria, but prokaryotic cells do not have membrane-enclosed organelles. How do prokaryotic cells respirate without mitochondria?


texts:
Per the United States Department of Agriculture (USDA) an invasive species is defined as:

  non-native (or alien) to the ecosystem under consideration

  whose introduction causes or is likely to cause economic or
  environmental harm or harm to human health

Corn in the Midwest, USA (often referred to as the Corn Belt) would seem to satisfy the first requirement as an invasive species as it is not native to this area.  Regarding the second requirement, it could be argued that corn in the Midwest causes environmental harm because it is in place of many indigenous plants that many other animals rely on to survive.  For example, habitat loss is considered a cause in the decline of the regal fritillary (Speyeria idalia) butterfly.

A Google search brought me to this Q&A site where many argued that corn is not an invasive species because it cannot survive or spread by itself without human intervention.  I tend to agree with this logic but it does not seem to be within the scope of the USDA definition.

Should corn be considered an invasive species in the Midwest?


texts: What is the ultimate source of ADP/ATP in humans?

texts:
I am teaching myself Cell Biology from the internet. Despite my usually good Googling skills, I'm stuck in a loop with this question.

Q: What is the source of ATP?

A: ADP

Q: What is the source of ADP?

A: ATP

At first I thought that ATP synthase actually created ATP from scratch as intimated here:

  ATP synthase is an important enzyme that creates the energy storage
  molecule adenosine triphosphate
  Wikipedia

I then realise that ATP synthase doesn't create ATP so much as convert ADP.

My Question

Can humans synthesise ADP/ATP from scratch. If so, where are these phosphates made and if not what food source provides them and how? Also, where do we get the phosphorus?

Thanks


texts: Can human perception differentiate between monochromatic and polychromatic light?

texts:
Maybe monochromatic is not the right word, what I mean is light consisting of a single wavelength (i.e. a spectral color) versus light composed of photons of multiple wavelengths (intermediate color).
For example, suppose we had a single, violet "laser" and a set of "lasers" combining into a purple color.*
Is it possible to combine the latter light sources such that their composite would perfectly match the violet one such that both look the same to a human eye (assuming perfect alignment)?
And would they look the same to all human eyes?
My guess is a no, because people might have different susceptibility to red and blue hues, and their aggregation functions may differ as well.
* Apparently, there are alternative definitions to distinguish the two colors (purple is reddish, violet bluish), but I am referring to the ones found in Wikipedia: Purple being an intermediate color and violet being a pure spectral color.
Interesting article on color perception in the animal kingdom:
https://arstechnica.com/science/2020/06/experiments-show-hummingbirds-see-colors-youve-never-dreamed-of/


texts: Why does abnormal mitosis takes place in the cells of tapetum?

texts:
I know that the tapetal cells present in the anther are binucleate. I also know this means that after karyokinesis the cell does not divide itself and instead form a syncytium.  This occurs due  to abnormal mitosis, but I don't find a reason for abnormal mitosis to occur.

What is the reason for abnormal mitosis to occur?


texts: Resources for interesting facts about biology

texts:
Are there resources for interesting or fun facts about biology, for example:

fastest animal/bird/insect
largest organ in human body
largest virus
largest genome
largest de novo synthesized genome
largest protein
longest experiment done so far
most expensive experiment done so far
biggest discovery by luck
...

You get the idea. It would be nice if these is a curated "database" for all these interesting facts that might be fascinating to lay people as well.


texts: Difference between fertilin and fertilizin

texts:
I am confused between fertilin and fertilizin.Are these two same or different?
Here are a few sources i referred

Julian Lombardi (auth.) - Comparative Vertebrate Reproduction-Springer US (1998)
Page 210

Richard E. Jones - Human Reproductive Biology, Third Edition-Academic Press (2006)
Page 244

Bioregulators of Reproduction
edited by David Jagiello

google book image link

Please help me know how they are same or different ,specify their functions in detail and thanks for your help in advance !!!


texts: Proteins that are strongly overproduced in E. coli and S. cerevisiae?

texts:
I'm looking for some pointers to proteins that produce at really gigantic levels in E. coli and yeast (S. cerevisiae).  Can anyone point to some champion proteins?

Even in inclusion bodies and non functional, just cases where the yield is very high - how much of a given protein can a liter of E. coli or S. cerevisiae make?

I've seen bands on gels like this, but I've probably not seen the champions:

It would be great if you could cite and discuss the plasmid/promoter used and whether codon optimization or other such tricks made a difference.


texts: How to build SEG in your personal environment?

texts: I'm trying to implement SEG (Wootton & Federhen,1993) in my MATLAB and Python environment. From this oriinal article I cannot figure out what I need to build my script. Are there any related article that explains the various steps to build this algorithm (from the mathematical point of view)?


texts: Increasing estradiol (E2) hormone from ovarian follicles prior to ovulation has been hypothesized to play a critical role for induction of pheromones. These pheromones render females sexually receptive to males to facilitate mating. An investigator performs experiments in sheep in which females are gonadectomized, then treated with E2 or vehicle alone and allowed to breed. What can be the hypothesis


texts: Are insects attracted to near infrared light?

texts:
Do insects see near infrared light?  If yes, are they attracted to it at night, as they are to visible light sources?

I am building something similar to a home-made trailcam with a Raspberry Pi camera.  Currently I use an incandescent light source.  Obviously, it attracts lots of bugs.  I was wondering if the same is going to happen when I switch to an infrared light source.  This would be 850 nm or 940 nm, as these types of LEDs are commonly available.


texts: What's a reasonable time constant for a mathematical model of a neuron?

texts:
Background
I've been studying various mathematical models of neurons. So far I've covered the classic Hodgkin-Huxley model (to describe the potential difference of a single neuron) and the integrate and fire model for two neurons (to describe the voltages of interacting neurons). I am now studying a firing-rate model which describes the firing rate of neurons, not their voltage.

All of these models include a time constant $\tau$. For the Hodgkin-Huxley and integrate-and-fire models $\tau$ tells us how fast the channels and pumps open/close in response to an action potential.

I am currently working with a two-neuron system of one excitatory neuron and one inhibitory neuron. It is described by the equations

$\tau_E \frac{dV}{dt} = f(v_E, v_I, \theta)$

$\tau_I \frac{dV}{dt} = g(v_E, v_I, \theta)$

where

$v_E$ is the firing rate of the excitatory neuron
$v_I$ is the firing rate of the inhibitory neuron
$\theta$ is a set of constant parameters.
$f$ and $g$ are linear WRT $v_E$ and $v_I$

I have fixed all parameters $\tau_E$ and $\theta$ leaving only $\tau_I$ to be varied. Certain values of $\tau_I$ cause stability while others cause instability.

For the parameters $\theta$ that I'm using I have found that disregarding the possibilities of $\tau_I<8$ and $\tau_I>791$ greatly simplifies the analysis (because of the way the eigenvalues of the Jacobian matrix work out). I also have reason to believe that it might be alright to disregard these values.

All of the $\tau$ time constants in all the examples I've seen so far have been around $10ms$.

Question
$791$ seems very high, but is it so biologically unreasonable that it can be completely ignored? What's to stop one neuron being $1000$ times more responsive than another one given there's such diversity in neuronal structure and function over all types of neurons? Are there examples of this?

$8$ seems completely reasonable for a time constant. Surely values under $8$ can't be disregarded completely?


texts: How does kinesthetic work and with what do we sense this?

texts:
I know that kinesthetic and proprioception are different things but, in contrast to proprioception, I don't know how kinesthetic works.

A broad explaination as well as very specific(but explained for 17 year olds) would be nice.


texts: Mushroom Identification: White mushroom growing on tree (South America)

texts:
Near the place I live in I noticed a little white mushroom growing on a tree trunk (a dead palm tree). I was curious to identify it, but from the little I learned so far white mushrooms are the worst to identify. I’m on Brasil, near the tropics in an Atlantic Forest predominant area, and I haven’t yet found a field guide for my region (if anyone knows any, or a field guide from a region that grows similar mushrooms I’d love to hear suggestions).

Also, I'm very novice when it comes to mushroom identification (still learning the basics), so if I missed some important characteristic, or misinterpreted something that can be spotted in the pictures I'd love to hear it. The whole point of identifying this mushroom is learning.

Below are some characteristics I noticed and some pictures from the mushroom:

Region: Brazil southeast coast, state of São Paulo, predominantly Atlantic forest
Grows in very small colonies, but every fruiting body comes from an individual point (No Cespitose)
Presence of Volva
No presence of partial veil (No Annulus)
Pileus Color: White with some brown spots
Stipe Color: White
Wasn’t able to get a spore print, but when it grew old (at least I think that's what happened) and shrunk it looked like the spores where brown as can be seen in the pictures
Narrows gills? (The fruiting body is small, so maybe relatively speaking it isn't narrow)
Fruiting body leaves white stain in wood
Margins of the Pileus are cracked

There's a new colony growing, so I might be able to collect a sample once it grows big enough and gather more information, as a proper spore print, since my guess of the spores being brown might be a mistake (maybe those brown things in the dead mushroom are not spores).

Pictures:

Older colony

Recent colony

Shrunk fruitbody


texts: How do I import FASTA files into Haploview?

texts:
I'm trying to produce a haplotype network and so have decided to use the software haploview. However I'm having some problems importing my sequences into the software.

I Have my sequences in a FASTA format but I can't find a way to convert this into a format that haploview accepts.

Does anyone have any ideas how I can get from a FASTA format file (e.g. >Az01|Female|Azores AGGATCT...) to a phased haplotype format (Az01    Azores    0    4    2    2)?


texts: Do mitochondria simply automatically convert glucose to ATP?

texts:
I wonder whether there is any intelligent decision-making in mitochondria in the timing of their operation.

Do they simply begin ATP production as soon as the correct reactants are present?

Or, because they have their own DNA, do they have more complex strategies that vary to benefit the mutual cooperation with the host cell? This assumes that the simple circular DNA is performing higher level decisions in switching.


texts: Can anyone help me identify this spider found in Cochabamba, Bolivia. It is quite small. This photo shows it on a normal mortar layer between brick.


texts: Definition of "structural underdominance"?

texts:
In Stathos and Fishman (2014), the authors refer to the concept of structural underdominance. The first time they mention it is in the first paragraph of the second page (left column) and the term is followed by some kind of definition in parenthesis. It is written:

  Furthermore, artifical doubling of chromosomes in sterile plant hybrids can sometimes restore normal meiosis and fertility (Stebbins 1950), a pattern diagnostic of structural underdominance (heterozygote inferiority).

In addition to how they use the term "Structural underdominance" in this paper, the above definition is confusing to me.

Is structural underdominance a specific type of underdominance (heterozygote disadvantage)? Is it the evolutionary process by which a population is lead to diminish the average underdominance along their loci? Is it a predisposition of the genetic architecture to display underdominance when a chromosomal rearrangement occurs? In short the question is:

What is the definition of "structural underdominance"?


texts: How can a polar molecule pass through polar channels of proteins in the cell membrane?

texts:
To transport a polar molecule through the nonpolar cell membrane, a protein with a polar channel is needed to allow it to diffuse. However, if the molecule is polar and the channel is polar, wouldn't the molecule just be attracted to the polar amino acids and "stick" on the inside of it?

I may be thinking of this totally incorrectly, so please bear with my ignorance!

Thanks in advance :)


texts: Abiogenesis: Beyond the research journals as a lead in to discussions on evolution

texts:
I just came across this abstract:

  Aminoacyl-tRNA synthetases (aaRSs) are responsible for creating the pool of correctly charged aminoacyl-tRNAs that are
  necessary for the translation of genetic information (mRNA) by the ribosome. Each aaRS belongs to either one of only two
  classes with two different mechanisms of aminoacylation, making use of either the 29OH (Class I) or the 39OH (Class II) of the
  terminal A76 of the tRNA and approaching the tRNA either from the minor groove (29OH) or the major groove (39OH). Here,
  an asymmetric pattern typical of differentiation is uncovered in the partition of the codon repertoire, as defined by the
  mechanism of aminoacylation of each corresponding tRNA. This pattern can be reproduced in a unique cascade of successive
  binary decisions that progressively reduces codon ambiguity. The deduced order of differentiation is manifestly driven by the
  reduction of translation errors. A simple rule can be defined, decoding each codon sequence in its binary class, thereby
  providing both the code and the key to decode it. Assuming that the partition into two mechanisms of tRNA aminoacylation is
  a relic that dates back to the invention of the genetic code in the RNA World, a model for the assignment of amino acids in the
  codon table can be derived. The model implies that the stop codon was always there, as the codon whose tRNA cannot be
  charged with any amino acid, and makes the prediction of an ultimate differentiation step, which is found to correspond to the
  codon assignment of the 22nd amino acid pyrrolysine in archaebacteria.

Granted, this is a few years old, but I often find myself having to admit that "I don't know" when at the root of discussions on evolution.  That is, once abiogenesis has occurred, we can go on and explain the rich diversity of life, but sadly we really don't know much before that critical step.  Generally, those satisfied with "magic" as an answer posit their myths and fables, whereas I'd rather try to actually find out what happened.  Sadly, as the abstract shows, you actually need a level of education to understand papers such as this that is generally well beyond those who would deny the reality of evolution.

Does anyone have a collection of papers on abiogenesis that are more accessible and understandable to laypeople?


texts: Which Lactobacillales (Lactic acid bacteria — LAB) strains are capable of degrading starch?

texts:
I've been researching bacteria strains but am having trouble finding amylolytic LAB strains with amylolytic and lactic acid producing character. The only species I've found, that are capable of amylolysis (correct me if I'm wrong) are Lactobacillus amylovorus, Lactobacillus manihotivorans, Lactobacillus plantarum.

If any, what other LAB strains provide amylolysis? Also, can anyone verify if the above strains also meet the criteria?

Edit
The keyword here is strains. Many species can degrade starch but most strains cannot.


texts: What exactly is extreme heterozygosity and how does it work?

texts:
What does the concept of "extreme heterozygosity" mean?
I first encountered this concept in "The Drunken Botanist". They describe that when planting a seed from, say, a 'red delicious' which was pollinated by another 'red delicious' does not guarantee growing another 'red delicious' tree. The author goes so far to say that the new tree may have almost none of its parent traits, and may barely resemble any other breed whatsoever. They argue this is caused by extreme heterozygosity.
I later found the concept of extreme heterozygosity the Wiki page for "apple"

This is because seedling apples are an example of "extreme heterozygotes", in that rather than inheriting DNA from their parents to create a new apple with those characteristics, they are instead significantly different from their parents.

On a PNAs article on Extreme genomic variation referencing extreme heterozygosity

We conclude that the extreme heterozygosity in C. savignyi is caused by a large effective population size and not an elevated mutation rate.

My understanding of population genetics (allele frequencies and patterns of dominance)
I understand homozygous diploid pairs, like pp or PP, and heterozygous pairs like pP and Pp, and hetero/homozygous dominance and recession. I also found an interesting paper on sea squirts to work through later that suggests why extreme heterozygousity is popular in large population sizes.
What I can't seem to find is exactly how "extreme heterozygousity" works. How is this different than ordinary heterozygous? Is there an entirely different context I'm missing out on? The only way I can imagine a more "extreme" heterozygosity is with triploid mismatched pairs, which can't be right. So how does the process work and what exactly defines it?


texts:
Why does this plum/apricot hybrid look like brains?

Notes:

Here's a photo of what a normal fruit on the tree looks like.
Location is Zone 5, east of Toronto.
There are about 20 other fruits on the tree. This the only fruit on the tree that has this problem.
The date is June 26, 2019 (although plants have been delayed by about 3 weeks this year due to unusually cool and rainy weather).
I have had lots of disease problems on my prunus this year due to the wet weather.


texts: What's the benefit of the average human body temperature?

texts: Why would the body choose a resting temperature of 36.1c to 37.2c? It seems a very inefficient mechanism of survival considering the typical ambient temperatures on Earth. If there is a benefit to needing to continuously do extra work, what is it?


texts: Need to identify this insect and ways to eradicate it

texts:
I need some help in identifying this unknown insect that was found in my kitchen.

Thanks in advance.


texts: What species is this fast-moving spider?

texts:
This is a frame from a recent recording:

Location

Forest in Central Europe at around 1pm.

Abiotic factors at the time of recording

Temperature = 23°C
Humidity = 38%
Wind = 6 km/h

Description

Approximate size = ~3 cm including limbs
Semi-transparent limbs and cephalothorax, opaque abdomen
The abdomen presents a pattern which reminds me of the coat pattern in giraffe G. camelopardalis tippelskirchii
its general morphology makes me think it might be part of Pholcidae family but I'm not entirely sure because the height of the abdomen seems a bit too bulbous on the Y axis
web structure rather irregular

Observed behavior

Very short reaction time (dropped a piece of leaf on top of its web), very fast moving spider. I can't provide a better estimation for the speed, but here's is the 3rd frame after the one above (on the previous two frames it just very slightly flexes its limbs):

And one frame later it's already gone.

Internet search

Google image search: no results using the first image you see in this post
Google text search: different sentences like "long-legged transparent forest spider" only returned the usual daddy long legs you can find at home in urban areas.
Finally I tried https://spiderid.com/spiders/ selecting white and brown but none of the displayed spiders matches anything that resembles the frame above.

Any help will be much appreciated. I guess the pattern on the abdomen is key to identify this species but I haven't had a lot of luck while looking for abdominal spider patterns.


texts: How much DNA of mitochondrial origin is incorporated in main cell's DNA?

texts:
And especially three points :

in which chromosomes is it located (especially for the human case) ?
how do we know about it ?
does the proportion and composition vary a lot from one eukaryot to another ?


texts: Colonial Cells Demonstrating Cell Specialization

texts: Are there any living examples of cellular colonies demonstrating very primitive cellular specialization?  If so, what do we know about how they assimilate?  How independent are the individual cells and what do we know about their behavior (for example, do they, perhaps, migrate to different colonies in certain proximities)?


texts: Simple question.  Do male skunks (striped skunk, eastern US/Canada if it matters) have teats?  Occasionally want to identify road-kill, but don't know if teats are diagnostic for females.  I believe they are for racoons.


texts: How do NSAID's work and what are the differnces between COX-1 and COX-2?

texts: NSAID's work by slowing down the COX enzym, but how do does enzymes cause pain? because I've read that they're also needed for the body and do "good" things.


texts: How is Calcium regulated in myocardic AP and plateau phase?

texts:
The plateau phase is maintained by influx of calcium and outflux of potassium in the second stage:

My conjecture is that calcium transforms between two phases

ionated phase (free calcium from i/c SR and e/c Ca-ATPase)
non-ionated phase (bound to some proteins).

The initial form can be ionated.
The process of deionisation occurs only in all-or-nothing cases - I see no evidence that this process can be continuous in my data.
My another conjecture why this deionisation can occur is because of the vortexes in the diastolic phase of ventricles (T wave; blood bouncing back to the tricuspid valve).

Which sources can correspond to this non-ionated calcium more?
My conjecture is e/c Ca more because longer travelling distance and entry involves accelerative movement.
Actually, this can differ depending on the situation at hand.

The accelerative movement can also contribute more to ionisation process so the situation can be reverse in some cases.
How is Calcium released from Sarcoplasmic reticulum?
Steadily or in accelerative motion or in a vortex.

How are Calcium forms regulated during action potential of myocardial cell plateau phase?

Keywords: Local Ca2+ signaling in health and diseases.


texts: What is the impact of the invasiveness of the European Starling in North America?

texts:
Currently there is a campaign to eradicate the European Starling from North America because of its threat to other species. Are there actual data regarding the extent of the ecological risk to native species, and are there data on the effects of the current eradication programs (are they working)?

Background

In North America, there an estimated 140 million European Starlings, or about 45% of the global total. The species was introduced to the continent over 100 years ago when only 120 or so were released in the New York area. Those few have quickly spread across the whole continent, competing easily with other native birds of similar type, especially for nesting holes, because they are naturally far more aggressive. It is currently listed in the IUCN List of the world's 100 worst invasive species. Annually, the US kills over 1 million of them with the sole purpose being extermination. There is even a specific poison commercially available. However I am having difficulty finding data to show how invasive the Starling really is in North America and the extent of the ecological risk to native species because of their presence. I would also be interested in data showing the impact of current control methods (do they actually reduce the impact on native species?).


texts:
Background: I'm currently performing research in mathematical biology,
specifically on the treatment dynamics of HIV and TB co-infection.

Question: Can a person infected with TB disease, who are undergoing treatment for it, infect a person with no history of TB bacteria in their body?

Reformulation: In other words, is there a similar analogue for TB as for HIV, wherein an HIV+ person undergoing treatment for HIV will have a lowered viral load and thus have negligible chances of infecting a person with no history of HIV?

Please note that my model does not incorporate latent TB because it would become too complicated to analyze. I am focusing only on TB disease because only it is infectious.

Thanks for any help.


texts: How does the body repair extracellular damage caused by glucose?

texts: So we know that glucose is an aldehyde that can cause cell damage to the lysine and arginine residues on proteins through the Maillard Reaction (among other damaging reactions that glucose participates in). Since everyone needs glucose to survive, though - I'm wondering - how does the body repair damage to its proteins+blood vessels that are caused by all this glucose? I'm especially interested in the blood vessels, as the damage to blood vessels is common in diabetics.


texts: What are these near microscopic white bugs from my comb?

texts:
I saw a whole bunch of white bugs crawling on my comb in the medicine cabinet, they didn't photograph well but I did manage to get a bunch of them in mineral oil and eventually take some micrographs.

The good news is that a dermatologist says I'm not infested with anything and, after nuking the bathroom with poisons and cleaning products, they haven't come back.

Here's 3 different specimens at 40X and 100X.  The live ones seemed to be in the 0.2 to 0.8 millimeter range.

(Click for larger images)

What are these things?


texts:
Can you tell me is there any good softwares and tutorials which can be used to learn DNA Origami. I am new to this and want to learn from basics.

Advance thanks for your help

edited: INSILICO


texts: What is the smallest difference in light wavelength that the human eye can detect?

texts: Is there a lower limit to the difference in wavelength (colour) our eyes can detect? If so, is this consistent between individuals? Are there any other traits correlated with precise colour vision?


texts: Is there any in silico analysis method to predict post-translational modification sites on a given protein?


texts:
I am relatively new to Physiology, and I've just learnt about muscle tone.
I however find it difficult to understand the electrical changes that initiate (and/or accompany) muscle tone in smooth muscles .
To be specific, I know that action potentials(AP) cause muscle contraction (just like they cause nerve impulse propagation), and I also know that smooth muscle tone is a result of irregular contractions of the muscles at rest.
How then can these muscles contract when no AP is generated at rest?
PS: This question has been edited to achieve more clarity.


texts: Does DNA helicase or topoisomerase actually "unwind" DNA?

texts:
I am reading through my textbook (Genetics, Brooker 4th edition) and the summary it gives seems imprecise for the functionality of helicase and topoisomerase.

The following is an exerpt:

At each replication fork, DNA helicase unwinds the DNA and topisomerase alleviates positive supercoiling.

Is it proper to say that helicase "unwinds" DNA? In other places in the book, it says the function of helicase is to separate the two strands of DNA, and topoisomerase "relieves the supercoiling" caused by the strand separation activity of helicase.

Pardon my ignorance, but it seems rather like helicase actually induces more winding, and topoisomerase (gyrase) actually unwinds DNA.

Is this just a case of poor wording, or does helicase actually somehow unwind (untwist) DNA? I am finding this particularly frustrating because virtually every resource I can find says that helicase unwinds DNA, but based on the mechanisms they offer, it definitely does not "unwind".


texts: Can the human eye distinguish colors in the periphery?

texts:
In the back of my mind I have the idea that human eyes can't notice the color of objects in the far periphery, and that any subjective perception of colors is done by the brain that tries to fill in the color percept.

Is that true?


texts:
If a scientist is observing a single cell under a microscope, and then realizes that the cell has died, is it possible to bring that dead cell back to life?

For my inquiry, let's assume that the death of the cell has occurred without disease or external circumstances.

Has such process ever taken place in a lab before? Thx.


texts: Can we just replace pasteurization with simple irradiation for most (if not all) foods? (For example, such as milk, to sterilize and preserve flavors)


texts: What is the Edward O. Wilson fuss about?

texts:
I have just read this article on E. O. Wilson and I don't understand what the difference is between what he is arguing and "standard" natural selection.

I read "the extended phenotype" some years ago and from what I vaguely remember that argued that everything about selection comes down to genes: they are the units of what is inherited and drive everything else (and their reach can be quite surprising).  At first glance that seems inconsistent with the article, since it mentions "group selection".  But when you read the details it includes things like

  Group selection begins when a colony of creatures develops a behaviour
  that gives it a competitive advantage over other groups. Initially,
  this could be down to a random genetic mutation.

which sounds like it's gene-based too (and examples seem to come from ants and the like which I thought were closely genetically-related across a colony too...).

So what is the fuss about?  And how will it be resolved?

Maybe the difference is easier to explain in terms of some difference between mathematical models?  If so, that's fine (I hope - it might make more sense than jargon in a field I am unfamiliar with ;o).

[Is this too "general public" for this site?  Apologies if so.]


texts: Can we artificially increase human growth using HGH?

texts:
Robert Pershing Wadlow was a man who lived in the first half of the twentieth century. He had hyperplasia of his pituitary gland, which caused him over-produce human growth hormone (HGH), and as a result, he grew to nearly 9 feet (2.75m). He had difficulty managing his body size and died at age 22, with no sign that this growth was slowing down.

HGH can be used for medicinal purposes, and it seems that doctors prescribe it for conditions like chronic underdevelopment and HGH deficiencies.

Putting aside ethical or government regulation issues, is it theoretically possible for someone (like a "fully grown" adult) to artificially grow beyond their genetic potential by providing them with regular doses of HGH? If not, what was different about Wadlow's case?


texts: Can fireflies species be identified with their wavelength?

texts: I was wondering if we could ID male fireflies using their wavelength? A bit like how we use UV light to ID species of scorpions.


texts:
Hi, in this agarose gel photo (70 volts, 3.5uL Gel Red in 30ml of TBE, 1% Agarose, 1 hour run), I've checked the digestion of a large plasmid (15Kbp, one cut site). The theory says that the digested plasmid (linearized) should migrate slower than the supercoiled form of the uncut one (bigger band of the Undigested Plasmid). In my case the digested plasmid is faster than the undigested one.
I've found that my digested plasmid could be single-stranded (http://bitesizebio.com/13524/how-to-identify-supercoils-nicks-and-circles-in-plasmid-preps/). Do you think that could be the case?


texts: Can polystyrene sulfonate bind calcium or sodium in the gut? How?

texts: Polystyrene sulfonate is used as a potassium binder to treat hyperkalemia in traumatic rhabdomyolysis, acute and chronic kidney disease. It is listed as an ion-exchange resin that can also remove sodium or calcium from solution, but is also available in sodium salt or calcium salt form. How might this work?


texts: Does cow urine have medicinal properties?

texts:
It is a common belief in India that cow urine has medicinal properties.

It is said to be anti-biotic.

It cures diabetes, cancer and many other diseases if not all.

Because this is biology I would like to focus on the anti-biotic property and set aside other claims cos they many be related to medicine and not biology.

Is it anti-biotic?

Does urine not cause infections?

Especially since it is applied the belly of new born babies by orthodox Hinuds.


texts: same osmotic pressure of different solution

texts:
For example, There is a sugar solution with concentration $A_{1}$, how to determine the concentration of a NaCl solution which produce same osmotic pressure as the previous sugar solution toward animal's cell?

Is this ratio various between different kind of cells?

NOTE: the unit of concentration is not important between mass/vol or mol/vol. Because when one is known, the other is easy to compute.


texts:
I assumed a virus to be something with a very specific geometry,
similar to a crystal, but more complex.

In an answer to
What is the size (diameter) of the SARS-CoV-2 virus? some SARS-CoV-2 virus particles are shown.

It looks like they do not have the same geometry.

They may be soft and influenced by external forces, but they could also be of different, but similar shape. Also, they could simply be defective in some way.

I assume a structure of the size of a virus is not rigid. Assuming no external forces, would multiple exemplars  of the same kind of virus have the same shape?
Can a virus have a different molecular arrangement, but be equivalent for biological purposes?


texts: Genetic variance for a behavioural trait among human populations

texts:
From this article from The Guardian:

  We instinctively assume that differences in behaviour that are in fact due to culture must be linked to – even caused by – characteristics of appearance. That is what the traditional notion of race is all about. But genetics has found no such innate origins of behavioural differences between “races” – and it is highly unlikely, given what we know about genetic variation, that it would. (my emphasis)

Because the term "race" is so poorly defined and because this categorization has been and still is an immensely important source of hate and discrimination, I will use the term "human populations" (despite the term being at least as vague). The fact that the term categorization into "races" does not make in any way a good representation of the partitioning of the genetic variance in human populations (e.g. see this post) is irrelevant to our discussion.

Are there any study who investigate the partitioning of genetic variance for a behavioural trait (e.g. drug dislike, aggressiveness, agreeableness, openness, reading performance, etc...) among "human populations" (defined one way or another)? Did they find a significant correlation? What is their correlation coefficient?

The article I refer to says

  We instinctively assume that differences in behaviour that are in fact due to culture must be linked to – even caused by – characteristics of appearance.

In no way, do I expect that the phenotypic variation used to define races could "cause" much of an eventual genetic structure for a behavioural trait. I know it is a politically sensitive topic. Let's raise above it and discuss the evidence.

Estimating partitioning of genetic variance

If need be, see this post for a definition of heritability.

I realize that estimating the partitioning of genetic variance is a difficult endeavour and can easily be confounded with other sources of phenotypic variance such as the ones caused by social and educative systems. Any article that does its best to estimate a correlation coefficient between a behavioural trait and "races" is welcome.

Behaviour

Of course, the term "behaviour" is not perfectly defined. This has never prevented us from massively using this concept in biology and I don't think it should prevent us from using this vague categorization of phenotypes to answer the current question.

What behaviour am I interested in? ... pretty much anything that one might want to call behaviour. I am not particularly interested in behavioural differences that might be directly cause by a difference in the prevalence of a specific disease.

In the book IQ and the Wealth of Nations, Lynn and Vanhanen attempts measures of IQ among countries. These methodology has been highly criticized. I double that IQ could be considered as a behaviour but, while I would welcome anyone to include such work in an answer (along side its criticisms on their methodology; e.g. Witcherts et al., 2010; see also Rindermann 2007), I would rather like to focus on evidence that are not directly focused on IQ. I am fine with evidence that are on behavioural traits that somehow relate to our intuitive notion of intelligence (e.g. reading performance, spatial abilities, ...). This answer in the post Genes and Intelligence is very relevant and lists three articles that looks for loci that explain some variance in IQ.


texts: Formaldehyde turns plantar region of feet red?

texts:
I'm a freshman med student and I've noticed that on all the feet (and hands) of deceased people that I've worked with, the bottom of the feet always turns red and also the inside of the palm? Why is this?

Thank you.


texts: How does human body deal with inert solid material in the bloodstream? For example, if there is a powder of glass injected into our bloodstream, will the white blood cells do anything or will kidney excrete these materials? Thanks.


texts: Why didn't the human Cerebrum evolve to have granule cells like the Cerebellum does?

texts:
The Cerebellum is much smaller compared to the Cerebrum yet it contains more than half of the total neurons contained in the brain.

That's mainly due to the granule cells in the Cerebellum which allows it become so densely packed with neurons.

But why is the Cerebrum not like that? Why isn't it as "compressed" as the Cerebellum? Doesn't it make sense for it to be more smaller and compact?


texts: Does the magnitude of gene-expression changes decrease the more downstream a gene is from the origin of change?

texts:
If I have a decrease or increase in expression in one gene, will the decrease/increase in expression in the downstream genes always be of a magnitude lower than the previous ones, or can they be higher?
I’m thinking in terms of signal propagation in a network. If I, for example, knockdown gene $X$ to 40% of its basal level, and it influences genes $Y$ and $Z$ in the following manner:
$$X → Y → Z,$$
Will I expect genes $Y$ and $Z$ to suffer lower decreases/increases than the previous gene, for example:
$$X: 40\% ~⇒~ Y: 60\% ~⇒~ Z: 80\%$$
Or could I have a scenario where a small change in one gene’s expression can lead to higher magnitude changes in downstream ones, for example:
$$X: 40\% ~⇒~ Y: 20\% ~⇒~ Z: 10\%$$
I suppose that in some networks the signal will always decrease in magnitude the farther it is from the source, but I’m wondering if, in a biological network, that will also happen and consistently in each step. I read papers with knockdowns all the time, but I never stopped to analyse if knockdowns always create lower magnitude changes in downstream genes or not. So I was wondering if this intuitive notion holds empirically or not.


texts: It is known that some viruses embed themselves in the human genome. Is there a mechanism by which human genes can be transferred to other animals or plants by means of viruses shuttling them from humans to other organisms?


texts: Interpreting Allele frequency and allele count

texts:
In the following vcf file, the AF allele frequency of ALT allele  is 1.0. Does it mean that it is not a true SNP of interest? Does it also mean that ALT allele always occurs and REF allele never occurs in the population?

Also not sure how allele count AC=37 is being calculated.

Chr1 pos=565286, REF=C, ALT=T, Info AC=37; AF=1.0 Format GT:AC:AF:NC Child=1:11:1.0:+T=4,-T=7 mother=1:26:1.0:+T=8,-T=18,

Cheers,
Ambi.


texts: With over 400 chromosomes, does mitosis in a species of butterfly happen in the same way as in humans?

texts:
The beginning of the Ars Technica article Gene editing crunches an organism’s genome into single, giant DNA molecule begins:

  Complex organisms have complex genomes. While bacteria and archaea keep all of their genes on a single loop of DNA, humans scatter them across 23 large DNA molecules called chromosomes; chromosome counts range from a single chromosome in males of an ant species to more than 400 in a butterfly.

Thanks to @Remi.b for tracking down Lukhtanov (2015) The blue butterfly Polyommatus (Plebicula) atlanticus (Lepidoptera, Lycaenidae) holds the record of the highest number of chromosomes in the non-polyploid eukaryotic organisms.

Does mitosis happen in this species of butterfly cells, and if so, does the process that separates the pairs take place in a similar way mechanically to the way it happens in mammal cells such as the 23 pairs in human cells even though there seems to be almost twenty times the number of individual chromosomes?

Has the mechanics of this process ever been imaged or visualized?

above: from here and here.

above: " Image of the mitotic spindle in a human cell showing microtubules in green, chromosomes (DNA) in blue, and kinetochores in red." from here


texts: Is it possible to contract the plague by kissing a wild chipmunk?"

texts:
I watched  this cute video and I came to conclusion that the lady in the video is putting her life in danger. She kisses a wild chipmunk.

As I know, they have fleas, and fleas have a black plague. Am I right? But maybe the risk of infection in contact with just one chipmunk is low?

How dangerous is such behaviour?


texts: how to make plasma cells adhere to the bottom of a microplate?

texts: I am isolating single plasma cells by FACS sorting into 384-well plates, with the intent to assay the supernatant and clone H/L chains from positive wells. The efficiency of the PCR is however low, because the medium must be removed, yet many plasma cells get sucked up during medium removal. Is there any way to make plasma cells adhere to the bottom, and therefore withstand sucking? I am thinking of poly-L-lysine, gelatine, or similar things - but I do not know whether these would be effective, or even tolerated by the plasma cells.


texts: What model of epistasis best fit the reality?

texts:
In theoretical population genetics, it is very common to have to assume a model of epistatic interaction. The two most common models are the additive model and the multiplicative model.

Additive model

Under the additive model the fitness $w$ of an individual carrying all $n$ mutations of effects $[s_1,s_2,...,s_n]$ is

$$w=1-\sum_{i=1}^n s_i$$

, which becomes $w=1-sn$, for the special case when $s=s_i \forall i \in [1,n] $

Multiplicative model

Under the multiplicative model the fitness $w$ of an individual carrying all $n$ mutations of effects $[s_1,s_2,...,s_n]$ is

$$w=\prod_{i=1}^n (1-s_i)$$

, which becomes $w=(1-s)^n$, for the special case when $s=s_i \forall i \in [1,n]  $

Old observation

In Population genetics: a concise guide, Gillespie reused data from Mukai (1968) to plot the following graph

, where the additive $\left(w=1-sn\right)$ and multiplicative  $\left(w=(1-s)^n \right)$ models correspond to the two lines that poorly fit the data. The line that best fit the data is a quadratic model of synergistic epistasis

$$w=1-sn-an^2$$

In all cases, $s$ and $a$ where estimated from these data. We probably have better data and better studies today.

Question

What model of epistatic interaction would you recommend?

Here are some clarifications if needed

Consider $n$ mutations. The fitness of an individual carrying only the first mutation is $1-s_1$. The fitness of an individual carrying only the second mutation is $1-s_2$, etc... the fitness of an individual carrying the $n^{th}$ mutation is $1-s_n$. What is the fitness of the individual carrying all $n$ mutations? Of course, there is no single answer to this question and it will depend on the epistatic interactions between these loci. However, there is probably a general trend that a theoretician would like to consider in its assumptions.


texts: Glass petri dish to replace plastic petri dish?

texts: I never use a glass petri dish before, but I just wonder if I can use it to replace for plastic petri dish because it can reusable. The only thing I worry is , in a Fridge's user manual, it said that do not put glass container into the freezer (usually -20 oC) because it can be damaged/break and even explode. So do a glass petri dish have any special design to prevent this damage?


texts: Why does a centrocyte have a cleaved nuclei? Is there a biological reasoning behind this phenomenon or is it the nature of the centrocytes? Does the selected centrocytes proliferate too?


texts: Why do humans suffer anxiety when they view "Trypophobia trigger images"?

texts:
When you type Trypophobia Trigger Images in google, you see a variety of images with irregular lumps and bumps among some more gory images.

Many people report that these images induce phobia like symptoms of anxiety.

Why do we get anxious when exposed to these images? What advantage is there to be had from this response?

I find the reasons like this ABC news report on ants and spiders. But still didn't get it any info from it.


texts: How do aminoacyl-tRNA synthases distinguish between similar amino acids?

texts: How do aminoacyl tRNA synthases recognize the right amino acid for their tRNA? What is the structural reason behind the selective recognition? I have difficulty in seeing how, for example, leucine and isoleucine can be selectively recognized by different binding pockets when they exhibit similar hydrophobicity, molecular volume etc.


texts: Is olfactory input processed by the thalamus? I know olfaction is the only sense that can bypass the thalamus, but are there cases where the input can project to the thalamus?


texts:
During a trek through a small forest-type area on the main island of Hawaii, I came across the following plant:

It did not cover very much area from what I could tell (there was a continuation of the bed just behind me from where I took the picture). I believe it was near Punalu'u Beach but I can't say with certainty.

It's creepy, looks like a tractor load of snakes got loose, and something I find fascinating. Could someone tell me what this cactus-y, bed of vines-like plant is?


texts: How to send many samples to a lab for testing mosquito-transmitted diseases?

texts:
I am doing a project for the science fair in my school on mosquito-borne diseases in Panama. We want to collect mosquitoes from three different areas in the country to document what diseases they had, which place had more diseases, which species was more common, etc.

We will take a dead mosquito, document which species it is and, with a special tool, extract the blood that the mosquito had extracted from their host and put it in a small container to test for disease. We want to extract 300 samples per area of the city (900 samples in total) to have the best results. The problem with this is that we can not send 900 samples to a laboratory for testing and I do not think we can collect fewer samples because the results will not be as good. One idea we had was to put the 300 samples in the same container so we only have to send 3 containers to a laboratory.

Will mixing 300 different blood samples from mosquitos in the same container affect the results, especially if there are any diseases? If this wouldn't work, what other procedure could we do to avoid having to send 900 samples to the lab?


texts: How did the nucleobases in the Murchison meteorite form?

texts:
The Murchison meteorite is an important piece of evidence for abiogenesis, because it contained nucleobases from extraterrestrial origin, as this Wikipedia article explains.

  These results demonstrate that many organic compounds which are components of life on Earth, were already present in the early solar system and may have played a key role in life's origin.

My question is: How did these nucleobases arise? Is it possible for these nucleobases to have been synthesized naturally from simpler molecules in a specific environment, like in the Miller-Urey experiment for amino acids?


texts: Animal reproduction when resources are scarce

texts:
(This question is aimed at animals that take care of their young, e.g. dolphins.)

As I understand it, most animals reproduce if possible. The only way they don't is because they run out of resources. I'm wondering how this shows up in practice:

Do they simply not have sex? If so, does this mean they don't have sex drive?
Do they conceive and then let their children starve to death?
Do they fail to conceive (that is, are there biological changes to a mother who's not getting enough food such that she is no longer fertile)?

Option #2 seems the least likely to me because presumably pregnancy involves a cost to the parent, and with resources already scarce this would be a waste; however the plot of White Fang does indeed involve this situation (I have no idea how scientifically accurate that book is however).


texts: Are bacteria incapable of producing cytokines such as interleukins?

texts: As far as I understand, bacteria cannot produce cytokines such as interleukins. However, I have not read an explanation as to why they cannot. Perhaps it has to do with an evolutionary limitation. Yet, if this is the case, why would bacteria be incapable of acquiring new functions such as cytokine production during their evolution, especially intracellular bacteria which reside within immune cells. If bacteria have not been able to acquire this function, then maybe it has to do with a biological constraint (size of the proteins, amino acid composition, machinery or bioenergetic capacity). If anyone knows the exact reason or has a knowledgeable explanation I would really like to read it. Thanks.


texts: Why does the colossal squid range over only the Southern Ocean?

texts:
Wikipedia's article on the colossal squid gives the distribution as in the Southern Ocean only.

It makes sense for many animals found in the Antarctic to not also be found in the Artic even if the environments are similar, simply because there's no way for the species to get from the Antarctic to the Artic. However if colossal squids can range more than a kilometer under sea level, then by that depth, the ocean should look the same in every direction: it would be so dark and cold that there's no easy way to tell if one is on the equator or under the North Pole. In other words the squid should be found in every ocean, not just the Southern Ocean.

What is wrong with this reasoning?


texts: Why didn't the polar bear change its color from white to black during evolution to absorb heat?

texts: Polar bears are white in color and white color is not a good absorbant of heat. Why then didn't they evolve a black color to absorb more heat?


texts: Do you use Pippin prep? We would like to buy it, but we need more info. What is the expiration date of kits for Pippin prep? Thanks!


texts:
Here's an interesting question I've been trying to figure out:

My annotations are in red. So far, I've figured out:

We know 630 colonies survived when plated with ACD antibiotics...meaning they picked up the a/c/d resistance alleles, but remain wild-type for the b allele. The genotype would be "a b+ c d". Because SO MANY (630!) colonies seemed to inherit a/c/d together, and b completely separate from them, I would say b is the gene quite distant from the 3 other genes.

However, I've unsure about how to proceed and determine the probably order of the 3 others genes: a, c, and d.

Here's my hunch: B--------------------C-D-A.

I'll explain:

Well, I looked and saw 942 (many!!!) picked up A/D together. So A/D are probably adjacent.
Then, 786 (many, but fewer) picked up C/D together. So C is further from D than A is far from D. The question becomes: is it "C---A-D" or is it "A-D---C"?
The insight comes in with 640 (still fewer) picked up A/C together. That means A is actually quite FAR from C, because more distance = more recombination events that could split them up. So between the "C---A-D" or "A-D---C" listed above, it's more likely "A-D---C".
Okay! We know B is far from the other ones, BUT is it like "B-------ADC", or is it like "ADC-------B"? Well, let's look: picked up B/C together is 51, but picked up A/B together is only 46. That means A is a little FURTHER from B than C is further from B, since 46 < 51.

This led me to my proposed answer: that the order is "ADC---------B", or if you just flip it around, its equivalent: "B---------CDA".

How's my reasoning? This stuff can be pretty confusing; am I approaching it from the right angles? Thanks so much; really appreciate it!


texts: Why do sparrows jump instead of walk when they are not flying?

texts:
I want to talk about sparrows, one of the most common birds around the world. I noticed that when one slowly walks into them (so that they are not frightened enough to fly away), these tiny birds would jump away, rather than walk away, as if they are not able to walk.

Why?


texts: Does the pyloric sphincter contract after ingesting only liquid?

texts:
At university, I was told by one of my fellow students that the reason why eating before going on an alcohol laden night out was a good idea, was because the pyloric sphincter contracted once food was in your stomach, and only let it into your lower intestines gradually. Their theory was that if you then drank alcohol, it would also sit in your stomach (with your food) and would only be let into your intestines gradually as the food was allowed through, thus slowing your rate of inebriation. Drinking on an empty stomach would conversely not cause the pyloric sphincter to contract, thus allowing the alcohol to enter your intestines at a much faster pace. However, I've been trying to find some online sources to corroborate / disprove this, and I'm having problems finding any information on it at all.

So my question is: does the pyloric sphincter stay relaxed if only liquid is consumed on an empty stomach?


texts: Why did translation develop a specific codon for initiation?

texts:
The translation of mRNA is initiated by a specific methionine-accepting tRNA at a specific initiation codon, usually AUG (complementary to the tRNA anticodon). However translation at suitable (albeit unphysiological) conditions in vitro does not require a specific initiation codon or a specific amino acid, so it is not difficult to envisage an earlier stage in the evolution of the translation apparatus in which this specific initiation system was absent. Instead there might have been random initiation or initiation from the 5′ end of the mRNA.

A specific initiation codon puts constraints on the sequence of the mRNA and adds an unnecessary amino acid to the N-terminus — one that is sometimes unwanted and needs to be removed.

  What advantages can one envisage for initiation at a specific internal
  site, rather than at, say, the 5′ end of the mRNA?

I appreciate it is impossible to prove which factor was actually responsible during evolution, but by soliciting concrete explanations I trust that this question is as valid as the original from which it is derived (see Footnote).

FOOTNOTE

This question has been expanded from one part of a three-part question posted some time ago on “Why is AUG the Initiation Codon?”. This recently resurfaced, and as nobody had answered this particular part, and as it is site policy to ask one question at a time, I decided to remove it from the original and repost it here so it could be considered on its own merits, without the distraction of other questions such as the choice of codon or of methionine over other amino acids. I shall contribute an answer with some thoughts of my own, but, of course, anyone can join in.


texts: Are the irises an exact match in a human's set of eyes? Assuming the eyes are healthy with 20/20 vision.


texts: Synaptic pruning and selective elimination during adolescence

texts:
How does Synaptic pruning occur during pre-adolescence, adolescence and post-adolescence, after there is blooming overproduction of synaptic connections until the years of late childhood, and how does during this stage of brain development, "selective elimination" of synaptic connections occur, which is depended on the activity of synapses which are involved in  primary functions?

Also, why, how and to what extent does the brain, after approximately age 6, receive the urge to cut back certain synapses?

Update 1: what exactly is triggered before and during adolescence, so that the brain receives the urge to perpetrate synaptic pruning? I know how synaptic pruning is carried out, I am however very intrigued in the specific processes that occur, from the signal that the brain receives to do it, to why exactly it occurs in such an early stage of life


texts: What exactly makes red meat (probably) unhealthy?

texts:
It seems generally agreed that (even fresh, unprocessed) red meat is at least somewhat bad for human health.  But why exactly is this the case?  It's difficult to find any attempt at an explanation, especially for anyone not too familiar with diving deep into the medical literature.
Is it because the myoglobin in red meat is carcinogenic or otherwise harmful? That would seem to be the most direct explanation, and there are a few studies on this, but they don't seem to be widely cited in discussions on health effects of red meat.  If that is true, would it mean that one should avoid dark, myoglobin-rich fish and poultry such as tuna and ostrich just as much as mammal meat?
Is it only because red meat tends to be more fatty?  In that case, would leaner cuts of red meat have the same health effects as white meat?
Or is it possible that there is some deep genetic reason why the flesh of mammals is more harmful than the flesh of birds and fish for human consumption?  (I had wrongly assumed this was a strange idea, but acvill's answer gives a plausible explanation.)


texts:
I'm studying a TCGA dataset trying to find correlations between gene expression and clinical data which might shed light on some pathways. One column of the clinical data provides a list of chemotherapy drugs the patient received and I'm pretty sure there's a wealth of possibility in this column but I don't know anything about how chemotherapy drugs work or what kinds of things it makes sense to classify about them.

I'm making a spread sheet that will have the following columns:

Drug_Name
Number_of_Patients_Received
Mechanism
Associated_Drugs

But I don't know what else is important to know about these drugs. What would you think is important to know to help understand how these drugs might have played an interactive role with the pathways. Also, if you have any recommendations of online resources, I'll appreciate you mentioning them with a short explanation of what I might find there.
But my primary question is else should I look up about these drugs to help me understand their role/impact.


texts: What specific sensory nerves act as receptors for "pins and needles" (neuropathy)?

texts:
According to this excellent answer, the difference between "pain" and "pins and needles" (neuropathy) is that different receptors (sensory nerves) trigger in reaction to different stimuli.

Different types of pain receptors (hot/cold, pressure, etc.) send pain signals to the brain.

Different receptors are responsible for sending neuropathy signals to the brain. These receptors are usually triggered when the nerve receives a shortage of blood flow.

According to the Wikipedia Article on Sensory Receptors, there don't appear to be any nerves that produce pins-and-needles sensations to the brain...

So I ask: What are the specific types of nerves/receptors that send "pins and needles" signals to the brain? What are they called?

I would imagine that it either has to be a specific, specialized receptor that (perhaps) starts firing if its senses "something is wrong" (such as decreased bloodflow to the area, etc.), or it's that all sensory receptors are capable of firing "pins and needles" signals under special circumstances.


texts: What is the correct value of Neuronal Resting Potential - is it -65mV or -70mV?

texts:
Some books show the resting potential of neurons as -65mV, such as Neuroscience: Exploring the Brain, Fourth Edition (2016, published by Wolters Kluwer).

However, a majority of internet sites, including Wikipedia, show the resting potential as -70mV.
Which one of these is the correct value, and why is there this small difference?


texts: Sugar metabolism in preserved/cryopreserved livestock semen

texts:
I wonder how can semen use di/tri-saccharide (e.g. sucrose, trehalose, raffinose) for spermatozoa metabolism in preservation/cryopreservation of livestock semen, since the semen itself never bring any enzyme to breakdown those sugars and the extender used also don't contain enzyme needed?

Is there any other way to breakdown sugar without enzyme, or is there any component in the extender which can substitute the enzyme function?

Thanks in advance.


texts:
Does anyone know where I can find a machine-readable version of the phylogenetic trees from APG III?  I'm looking for something that contains the full tree structure, including unnamed branches.  (i.e. not merely a list of which families are contained in which orders.)

The trees at the APG III site are graphic images -- not easy to turn into a data structure.


texts:
I saw a decimal-sized dot walking on my hand. I wanted to know what this is, so I got it onto some paper and sandwiched below a piece of clear tape so I could keep it in place and photograph it. However it's so small that even with my camera lens almost touching the specimen, I can't get a great photo. It's small, about 0.8mm long, beige or gray or brown with a pattern on the back. It's a little smooshed from the tape so it's hard to tell if it has 6 or 8 legs and is an insect or an arachnid. But hopefully based on the shape, size, and pattern it can be identified.

Location is southern California.

Update: I now believe this to be a rat mite or bird mite. I'll include some additional photos that were better quality (photos were taken with a close-focus camera, mites were on printer paper underneath Scotch tape, back-lit by an LED light):


texts:
If  father has hemophilia, mother is a carrier of the disease, then
  what is the probability of having a normal daughter ?

My question: Should the probability of having a daughter be also multiplied ? Should the answer be 0.5 or should it be 0.25 ?


texts: What are the roles of cadherins in epithelial mesenchymal transitions?

texts: I know that cadherins control the expression of cancer cells involved in the epithelial-mesenchymal transitions, but I was wondering exactly how the process worked.


texts: How to find the radius of gyration for a protein?

texts: While going through the paper titled "GEOMETRIC ANALYSIS OF THE CONFORMATIONAL FEATURES OF PROTEIN STRUCTURES" by Manish Dutt, it talked about finding the radius of gyration of each protein structure. I am unable to understand how the radius of gyration has been obtained for the entire protein. I first find the root mean square distance between the centroid and the C alpha atom. Is the average of these distances the radius of gyration?


texts: Can anyone identify this chrysalis? (Identified)

texts:
It's about 5 or 6 cm long. It's on the outside (north facing) wall of my garage about a metre above ground level.

Photo taken in Thailand near Hua Hin (about 12N 100E) in December 2014.


texts: Are there any confirmed cases of melanism in snow leopards? I am aware that melanism is much more common in Jaguars and Leopards, both often called black panthers, but I cannot seem to find any info on melanism in snow leopards.


texts: What is the biological relevance of RIPPLE phase in membranes?

texts:
I was reading about ripple phase in bilayer lipid membranes which is described here as a meta-stable state between lamellar tilted crystalline and lamellar fluid state. It is also known that ripple phase exists just below the phase transition temperature $T_m$. The figure below is from this article.

I have 2 questions here:

1) Is ripple phase a stationary structure or does it propagate in space as a travelling wave? (Since they have crystalline structures inbuilt will the fluidy defect propagate?)

2) Secondly and more importantly will ripple phase gets exhibited above transition temperature $T_m$ if the lipid interacts with some molecules like protein etc?

UPDATED QUESTION:

What can be the possible biological significance of Ripple phase in membranes? Will formation of ripple in membrane initiate any relevant processes, since membrane curvature itself is changing? I will be really helpful for any resources related to this.

I am citing an experimental biological work related to Hsp12 protein interaction with DMPG membrane in yeast which reports ripple phenomenon well above the usual transition temperature. Paper here.

NOTE: I was initially confused about whether to post this in biology.SE or physics.SE. I got more tags here. So posting it here.


texts: Where can I find an at least Semi-Comprehensive list of what biochemical reactions Acetyl-CoA participates in?

texts: Acetyl-CoA has a number of biochemical roles in the body and I'm curious as to whether anybody knows where I can find at least a semi-comprehensive list (i.e. comprising all the major roles in the human body it serves) of the biochemical reactions in which acetyl-CoA partakes in the human body.


texts:
In Kurt Vonnegut's novel Galapagos, a certain mammal species, due to drastic and peculiar environmental changes, evolves (among other features) a smaller and smaller brain.

Has this ever happened? Are we aware of any species whose ancestors had remarkably bigger brains?


texts: Source for an upper bound in the number of genes based on mutation rates

texts:
So I've found myself referring in an answer once again to the idea that complexity (insofar as it's a quantity for which "number of genes" is a proxy) has an upper bound, limited by Muller's ratchet-related processes. The idea being that if harmful mutations happen faster than natural selection can cull them, the genome will accumulate harmful mutations and the organisms' fitness will degrade over time; and that this imposes an upper bound on the size of a functional genome, because the number of harmful mutations that can happen obviously depends on the size of the functional genome (i.e. how many bases there are where a mutation would likely be harmful).

I knew about Muller's Ratchet, and when referring to it I usually refer to the Wikipedia page for it. But I first came across the concept that this defined an upper bound on complexity (as opposed to being a huge paradox of evolution and a plausible reason for sexual reproduction) in this Less Wrong post (it might have been edited since I first read it).

I've pretty much adopted this concept as a thing that happens; it makes sense to me, and I have seen other references to such an upper bound limited by mutation rates from biologists, for example most recently in this talk by Nick Lane (at 39:15).

However whenever I talk about this in discussions or debates and look for sources I cannot find an easy-to-link source that presents this argument, as seen from within the field of biology. The Wikipedia page on Muller's ratchet only talks about it in the context of asexual reproduction and LessWrong isn't a biology source. The post claims that George Williams makes this argument in his book Adaptation and Natural Selection, and that may also be what Nick Lane is referring to in the video, but a book is hard to refer to online and I would expect such a powerful concept to have more material about it anyway.

Is this concept actually the consensus in the field of biology, or evolutionary biology failing that? Either way, where can I find good, preferably linkable, sources explaining the concept or debating it if it isn't the consensus?


texts:
Why can we not regenerate cartilage in our ear and nose, while bones and flesh can heal?

What makes it so resistant to regeneration. Can we artificially create it in the lab?


texts: Effect of sex-ratio on the effective population size

texts:
As stated on this wikipedia article, the effective population size $N_e$ when the sex ratio differs from $\frac{1}{2}$ is

$$N_e = \frac{4N_mN_f}{N_m+N_f}$$

I understand the biased sex-ratio decreases the effective population size and the formula is quite simple. However, I would fail to prove that this formula is right.

Can you demonstrate to me that $N_e = \frac{4N_mN_f}{N_m+N_f}$ is true?


texts:
Would electroporation be successful on a one/two-celled mouse embryo? If it would, what buffer could be used and what percentage of cells would be viable?

Thank you.


texts:
if the evolution makes the species better then why the leaf and trees are not black??

black colour absorbs more ligth than simply the green color so a black plant should make photosinthesis better then why aren't the plants black ?


texts: How can Pyridostigmine have the indication of Myasthenia?

texts:
I am thinking how pyridostigmine can be used in the treatment of myasthenia gravis.
Its similar compound (neostigmine) is also anticholine esterase.
This compound has the indication of myasthenia gravis but with the stimulation of the nicotinic receptor.

I cannot understand how pyridostigmine is causing the effect.
Probably, pyridostigmine is similar to neostigmine in structure, which can be why more pieces of information is about neostigmine than pyridostigmine.

How can pyridostigmine have the indication of myasthenia gravis?


texts: why do some cells in the body prefer necrosis to apoptosis as a means of cell death?

texts: There are many programmed cell death pathways, but some cells show a greater preference for some over the other. I'm wondering as to why if necrosis is an inflammatory response that causes damage to neighboring cells, why some cells would prefer this as opposed to a more controlled mechanism such as apoptosis or even autophagy.


texts: The effect of sugar on rate of yeast Respiration

texts:
In my experiment, I am investigating the effect of different types of sugar on the rate of respiration of immobilized yeast (yeast trapped in calcium alginate balls). I am looking at glucose, fructose, sucrose and maltose.

Research leads me to believe that the disaccharides will perform the worst as they require enzymes to breakdown into monosaccharides and so will require more time to digest and this have a slower rate of reaction. In contrast the monosaccharides will work the best for the opposite reason.

Can anyone offer any insights into this hypothesis? Any helpful background theory that would support/discredit this.

Thank you.


texts: What are the brain structures directly on top of the brain stem?

texts:
I have been trying to learn the anatomy of the brain, and some information on their functions, through an iPad app called 3D Brain.  Whilst going through the different parts, I have noticed that one area doesn’t seem to be mentioned.

If you look at the image below, you get the brain stem (colour highlighted and labelled).

Going from the brain stem upwards, I am then trying to identify the structures in medium grey which sit on top of the midbrain.

I have seen that the bulbous areas left and right are the basal ganglia.

What are the rest of the structures?  I would like to know what all the mid grey structures are in the first image, but I am especially curious to know what I have drawn around below.


texts: What kind of red/green/black, spiny caterpillar is this?

texts: It's red and lime green with black on its back and a few white spots as well. Found in Tulsa, Oklahoma (USA).


texts: What is the effect of extra-cellular potassium concentration on heart rate and conduction velocity?

texts:
If the extracellular potassium concentration surrounding a myocyte increases, then the potassium gradient accross the cell membrane decreases, and therefore the resting membrane potential will become more positive.  Similarly, if extracellular potassium decreases, the resting membrane potential will be more negative.

With this in mind, how does the heart rate change when extracellular potassium concentration increases/decreases?


texts: How does one calculate how to dilute a solution to working strength?

texts: If I'm loading a 3.5ul PCR onto an agarose gel, how do I calculate how much of the 6x loading dye to add?


texts:
I'm looking at a paper that uses several sequence logos to illustrate the consensus sequence of certain sites.

Here is the most important of the sequence logos I'm interested in:

The explanations I found about the exact meaning of this visualization were rather abstract and mathematical. I understand that the height of the letter stack is indicating in some way how strongly conserved that position is, but I have some difficulty judging the absolute values.

When are the positions considered to be significantly conserved? The paper where this data is from mentions the positions 5 and 6 as characteristic for the consensus sequence, which is not really obvious to me from this graph.

How do I interpret the absolute value on the y-axis? What does it actually mean if position 16 has around 0.6 bits of information?

I'm not so much interested in an exact mathematical treatment, but a general guide on how to read these graphs and how to interpret them in practice.


texts:
I have seen this bug/worm twice on my dog's leg after taking him for a walk this week. I think that this is a leech, but my mom disagrees because she says leeches are not found where we live but are found around beaches. We live in Carmel Mountain San Diego: Google Maps.
The closest beach is around 15 minutes away.
The bug is approximately the size of a fingernail, and it did not do anything when I picked it up.

EDIT: We were just walking around my neighborhood, nowhere jungle-ish at all.


texts: Epistasis Across Chromosomes and Individuals 'Homozygous for Interactions'

texts:
Apologies for any failures in nomenclature. I'm a mathematician who is making a foray into genetics for a masters thesis. Specifically, I'm generating artificial diploid genetic sequence data and phenotype data based on known epistatic interactions.
Primary Question
I am familiar with the concept that having multiple copies of a single allele (e.g. one from each parent) can actually increase expression and thereby change the quantitative phenotype (at least in some cases?). Can this also happen with epistatic effects? For example, consider the case that locus 1 ($L_1$) and locus 2 ($L_2$) exhibit some positive interaction ($\beta$) on the trait ($Y$).
$$E[Y]=\mu+\beta(L_1L_2)$$
If both chromosomes contain the allele in question at both loci, then does this individual exhibit more of a trait increase than if he only had one chromosome with the epistatic alleles?
Secondary question
Can alleles interact epistatically even when they are present on different chromosomes? e.g. assume allele A at locus 1 interacts with allele B at locus 2. Individual has A at locus 1 and b at locus 2 on chromosome 1. He also has a at locus 1 and B at locus 2 on chromosome 2. Do A and B from the different chromosomes interact? My intuition is yes but I want verification.
Many thanks!!!


texts:
I'm wondering about a few technicalities of crossover in meiosis. The point of crossover is to create new chromosomes that don't have the same allele combinations as the original two chromosomes. Usually, the chromosomes are cut at the same place on both chromosomes, and each piece is then stitched to that place on the other. This is to avoid unequal recombination, a scenario in which one chromosome has several instances of a gene and the other no instance at all. I'm wondering how the molecular machinery knows where to cut.

So here's my question: How does the molecular machinery choose where to cut a chromosome for recombination?

This question has two parts: At what type of place does it occur (does the machinery choose a completely random place, regardless of where genes start and end, does it just cut at the start of genes, or does it do something else)? Given that it happens at this type of place (e.g. start of a gene), how does it decide that it will cut here (the start of this gene) and not there (the start of that gene)?