texts: Are changes in flexibility from stretching due to changes in the nerves or the muscles?

texts:
For many people, stretching repeatedly over a period of time improves their flexibility. I want to know whether this improvement commonly seen is due to a change in the nerves or the muscle’s material properties.
Are the changes in flexibility seen on the order of minutes/hours to weeks/months due to changes in the nervous system's reaction (e.g. reflex habituation) or changes in the viscoelasticy properties of the muscles (e.g. muscle length via serial sarcomere number)?

Excerpts:
To help answerers, I want to provide a few excerpts from two sources. The first source is from 1998.

"This article reviews recent findings regarding passive properties of
the hamstring muscle group during stretch based on a model that was
developed which could synchronously and continuously measure passive
hamstring resistance and electromyographic activity, while the
velocity and angle of a stretch was controlled. Resistance to stretch
was defined as passive torque (Nm) offered by the hamstring muscle
group during passive knee extension using an isokinetic dynamometer
with a modified thigh pad. To simulate a clinical static stretch, the
knee was passively extended to a pre-determined final position (0.0875
rad/s, dynamic phase) where it remained stationary for 90s (static
phase)."
“A significant decrease was observed for energy (30%) and
stiffness (13%) in the dynamic phase, and passive torque in the static
phase. However, the observed decline in the variables measured was
transient and they returned to baseline within 1h.”
“Long-term stretching (3 weeks) increased joint range of motion as a result of a
change in stretch tolerance rather than in passive properties.”

Source: Magnusson, Stig Peter. "Passive properties of human skeletal muscle during stretch maneuvers." Scandinavian journal of medicine & science in sports 8.2 (1998): 65-77.
The second source I want to cite is The Complete Guide to Stretching by Christopher Norris. Paraphrasing pages 56-58, he says stretching can affect the following:

Habituation – when the stretch reflex becomes desensitized and the
reflex doesn’t activate as easily when stretched
Muscle stiffness – a muscle has an elastic recoil when stretched. The degree of this
recoil is the “muscle stiffness”
Stretch tolerance – the amount of discomfort induced by a stretch that a person can endure
Serial Sarcomere Number (SSN) – a muscle can lengthen or shorten in length
when the number of sarcomeres change

Norris also notes that the first 3 criteria usually change on the order of months (called “acute” or short-term) while the SSN tends to change on the order of years (called “chronic” or long-term).


texts:
There are typically hundreds of retroviruses found in healthy human beings.

Are retroviruses then cytotoxic? (In other words, are they able to kill or damage other cells).


texts:
Are there any documented cases of extinction of a species of fungus? I imagine it would be hard to detect something like this.

Edit: documented by humans when it happened and/or induced by humans.


texts: What determines the number of chromosomes an organism carries?

texts:
This is an extension of this question about What limits chromosomal length?.

I am wondering what could be the specific reasons behind the number of chromosomes an organism carries. In other words, what drives the number of chromosomes and is there anything "stabilizing" the number of chromosomes.

Of course I am not talking about multiple copies of the same chromosome, i.e. trisomy, but rather the reasons behind the partition of the genetic information into a defined number of chromosomes.

From the question I referred to, chromosomes have an upper length limit which is based on their physical size, i.e basically they must be shorter than half of the spindle arm axis and they probably also have a lower limit. Yet it is unclear to me if any non-random equilibrium exists between chromosome number and length other than just being bound by an upper and lower limit in size.

Also let's restrict this question to diploid organisms to avoid organisms such as the Oxytricha trifallax which has 16,000 chromosomes but is also ampliploid or plants such as wheat which can be tetraploid.

I tried to search in the literature and couldn't find a satisfying answer. Also I had in mind the example of the Hela cells which have completely shuffled chromosomes yet still exactly 46.


texts: Why is compensatory negative supercoiling generated in a positively supercoiling ccDNA?

texts:
I was reading DNA replication in E.coli in Lehninger Principles of Biochemistry 6th Ed. and stumbled upon the following --

  The tight right handed wrapping of DNA around DnaA oligomeric complex induces an effective positive supercoil. The associated strain in the nearby DNA leads to denaturation of AT rich DUE region.

Edit:

Yet again I have come across the following in  in Indian Molecular Biology books which certainly contradict Lehninger.

Binding of DnaA protein to oriC initiates unwinding of the DUE by introduction of negative superhelical turns.

I've done a little more research and found this paper, which clarifies the problem I previously had:

  As a right-handed ATP-DnaA spiral would be expected to
  wrap DNA into a positive supercoil, adjacent DNA regions would be
  subjected to compensatory negative writhe (Fig. 6d, left). Although
  any superhelical strain generated by DnaA-mediated wrapping would
  be expected to spread throughout the topological domain that con-
  tains the origin, it may preferentially affect the nearby DUE, which is
  unstable and prone to spontaneous unwinding (Fig. 6d, top arrow).

Changed question: Why is this negative supercoiling generated in a positively supercoiling ccDNA?


texts: Do the pH and other ions affect the hydrolysis of ATP

texts:
ATP hydrolizes to ADP and phosphate in a strongly exergonic reaction and is used for energy transfer and short-term storage in cells.

ATP is stable inside a cell, so a significant activation energy must be necessary for the reaction.

However, the English Wikipedia article implies that stability of ATP is not a given, but depends strongly on the properties of the surrouding solution:

"ATP is highly soluble in water and is quite stable in solutions between pH 6.8 and 7.4, but is rapidly hydrolysed at extreme pH." and
"ATP is an unstable molecule in unbuffered water, in which it hydrolyses to ADP and phosphate."

How does the pH affect the hydrolysis of ATP?
Why is it even relevant if the solution is buffered or not? (Do the ions stabilize the molecule somehow?)
Are there other effects that influence stability in animal cells?


texts:
As I understand it, plasmids, like mitochondria, have their own genetic material and are capable of self-replication.

According to Wikipedia: Plasmids are considered replicons, units of DNA capable of replicating autonomously within a suitable host. However, like viruses, they are not classified as life. Plasmids are transmitted from one bacterium to another through conjugation. Unlike viruses, plasmids are "naked" DNA. However, some classes of plasmids encode the conjugative "sex" pilus necessary for their own transfer.

My understanding of that is that a bacteria gets their plasmids not because of the replication of their circular chromosome, nor because that chromosome have genes to code for the plasmid (I don't really know if that's possible), but because of the self-replication of their own plasmids.

So, my question is how the first plasmid got into the first bacteria, if they are not in their chromosomes? Were they a virus other prokaryotic cell that had circular DNA, and got phagocytosed by that bacteria ?


texts: What plant is this? (Found in South Thailand)

texts: Have tried to recognize with PlantSnap App, no results.


texts:
What is a membrane holding potential? I have come across this term but haven't been able to find a definition.
From "Voltage-gated sodium channels as therapeutic targets in epilepsy and other neurological disorders", legend to Figure 4:

Voltage-dependent and frequency-dependent inhibition of voltage-gated Na+ channels by Na+ channel blockers (A) Inhibition of Na+ currents by phenytoin is dependent on membrane holding potential. The top traces show currents evoked by depolarisation to 0 mV, with control (a standard physiological saline solution) and with 50 M phenytoin. In each of the four pairs of current traces, the larger trace is the control. The traces on the left were elicited from a holding potential of 130 mV, whereas the traces on the right were from a holding potential of 65 mV. The control current at 65 mV is smaller, due to greater inactivation induced by the more depolarised holding potential. Moreover, phenytoin is a much more effective blocker at the more depolarised holding potential. This is more evident in the bottom traces, in which the amplitudes have been scaled so that the control currents are the same size. (B) Phenytoin block builds up during repetitive channel activation. The graph shows normalised current amplitudes of whole-cell Na+ currents over the course of depolarising pulses to 0 mV, from a holding potential of 85 mV, applied at 2 Hz. Red dots indicate discrete measurements. Dashed line indicates a baseline to monitor decline in amplitude. (C) Voltage-dependent and frequency-dependent inhibition of Na+ channels by phenytoin and other antiepileptic or local anaesthetic drugs with a similar mode of action (green diamond) are qualitatively explained by a modulated receptor model. In this model, the drug binds with higher affinity to inactivated channel states than to resting channel states. Biophysical and molecular data suggest that the modulated receptor site is within the inner vestibule of the ion-conducting pore.


texts:
What logic do anti-darwinists provide for refuting the proofs( by proof I mean the fossil records) of darwinism ?

Is it the missing links?

If yes then , what do they make of the fossils which are present?

Note : I'm not being hostile to the anti-darwinists, I'm just very curious.Also I really want  to see it directly from an anti-darwinist (i.e. answer from an anti darwinist highly preferred)

If there's any problem in my question please inform me.


texts: What Evidence Do We Have For the First Mammal?

texts:
Edited for a less broad question, I've retained my original question in the event anyone wants to try to answer it

Narrowed down question

According to evolution we should all share common ancestors, straight to the very first cell. I am trying to find evidence for these ancestors. So therefore as a start, what fossil evidence do we have for the first official mammal to roam the earth? What was the defining moment and change from whatever it was before to a mammal?

Original question

I'm just doing some research for my biology class and I was wondering
what evidence we have for the elusive "change of kinds" question? And
for clarification, I define kinds as the branches of life (essentially
birds, reptiles, mammals, amphibians, fish, etc etc). Do we have
evidence for the common ancestors that link the vastly different
species we have? Because obviously a human, tortoise, jellyfish, and
say tarantula are vastly different, each their own distinct "kind",
but according to evolution there should be common ancestors and many
distinct species leading up to them. We all came from one thing. Man
and primates came from one thing. Mammals came from one thing. Where
do we get that distinct change of a kind, from say a fish to mammal?

There should theoretically be tens of thousands of in between links
and species that were what led to everything today, correct?
Therefore, we should have mountains of fossil evidence to support it,
yet from what I've researched I've found very lacking evidence and
generally just see posts insulting creationists and skimping the
question. So by asking the question myself hopefully I'll get a
legitimate and clear answer that is the truth.


texts:
I am working on a protocol to ligate cfDNA, extracted from blood, into some vector. I have looked into the literature but I cannot find any detail about the status of the ends of the cfDNA. Are they blunt or sticky? What is the enzyme responsible for cutting the genomic DNA into cfDNA?

I know I could blunt it anyway and proceed with a blunt-ligation. However, the amount of cfDNA I have is limited and I would like to avoid purification steps. So, if it tourn out that it is already blunt-ended I would save a step in the process.

Also, protocol aside, I really would like to know more about the cfDNA molecular details and which enzyme is generating it.

Any hint is very appreciated.


texts: Open Source Variant Caller comparable to GATK Haplotype Caller?

texts: Is there a Variant Caller comparable algorithmically and in performance to GATK Haplotype Caller but Open Source Compliant (non-restrictive use)?


texts: Master Catalog of all Fossils / Literal Fossil Record?

texts:
Is there a website or other resource that catalogs all fossils ever found? Basically, is there a literal "Fossil Record"?

Where do scientists gather their results from excavations? Are they just scattered in various peer-reviewed papers in science journals?

I'm imagining something like manuscripts and master texts. You have some researchers who analyze manuscripts to produce the text of that manuscript in electronic form, for instance. Then, other researchers take these various readings and assemble a master text, taking into account the variations and attempting to recover the original work.

By analogy, this would be like when a paleontologist at a dig site submits a paper about his/her findings to a science journal. Is there another group of scientists who look at all of these papers and compile a "master text" of the fossil record?


texts: Is diarrhoea advantageous to the microbe?

texts: Diarrhoea is a common side effect of many feco-orally transmitted bacterial infections. How does diarrhoea help the pathogen? Should it not have a selective evolutionary advantage? Do all symptoms of the disease need to have a selective advantage for the pathogen? All I can think of is that a more liquidy stool would lead to further ease in feco-oral transmission. Is this true?


texts:
I know that veins carry oxygen.

Veins look blue because the oxygen-depleted blood in them is blue.

Is this true??


texts: What is the percentage of people living in England in 1500 AD whose lineage is still alive?

texts:
This sounds a bit random, but it stems from a lecture in statistical genetics which I attended a while ago. We were shown a population lineage graph from which it was clear that most lineages eventually go extinct. The further you go in to the past, the smaller the percentage of the individuals living at that time whose lineage is still alive today. This probably makes sense in the context of evolution.

So I am curious about the speed of that process in human populations. I am aware that this speed, quite possibly, varies over time and geographically. Are there any estimates about that speed in European populations? To be more specific, I would take England at 1500 AD as a starting point. What is the percentage of the people living in England at that time whose lineage still exists?

EDIT

I am very grateful to @Richard Erickson for the reference to the Galton-Watson process. It is really fascinating that +70% of all known Chinese family names have become extinct. It would be really interesting to know more about the speed of the process of extinction - in particular in European populations.


texts: Does adenylate cyclase stimulate or inhibit acid secretion in the stomach?

texts:
I am confused about my teacher's notes.
"Acid secretion is stimulated by ACh, gastrin and histamine.
Histamine stimulates adenylate cyclase which increases cAMP production."

When I looked this up apparently gastrin decreases AC (adenylate cyclase) production. If histamine and gastrin both stimulate acid secretion why does one increase and the other decrease AC?

Also in her notes the acid secretion inhibitors are acid, protein, fat as they cause the secretion of CCK and secretin and these stimulate AC. But I thought AC stimulated acid secretion not inhibited it?

Thank you.


texts:
Many animals can become mentally ill, but I could not find any account of animals showing schizophrenia, not even apes. I could only find this, but it seems very vague.
Is there any evolutionary explanation of why only humans have schizophrenia?


texts:
I came to analyzing population genetics data from the background of a theoretician and a computer biologist but not with the standard tools that a bioinformatician (or empiricist in population genetics) know of. I have a fairly good knowledge in R and in programming in general.

I am looking for a course/tutorial for learning bioconductor (and other R tools for analyzing genetic data). A course/tutorial that is short, dense and assumes the user has good knowledge in programming. I am happy with both a video or a written tutorial although I would slightly prefer a written tutorial. I typically aim at analyzing data on structured populations such as the average number of pairwise differences among population, or graphing the site frequency spectrum per population, etc..

There are a fair number of such tutorials. Can you please give me recommendations?


texts: In vitro transcription, contamination problem

texts:
I am using a RNA which is in vitro transcripted before I started my project. It turned out it is not prepared properly and has DNA contamination.

Instead of perform the in vitro transcription again, I want to try to clean it with DNase treatment and LiCl precipitation afterwards. Do you think would that work?

And second thing, in vitro transcipted RNA is in different dilutions, so I have a little bit of stock (maybe 5 uL) which is around 200 ng/uL and I have other dilutions 1 and 0.1 ng/uL. I would like to clean all of them. Do you think if I just mix all of the dilutions with the stock and determine the concentration and do the rest? Is it appropriate?

Thanks!


texts: Real-world examples of Darwinian extinction

texts:
Darwinian extinction (also known as "evolutionary suicide") refers to processes of selection-driven self-extinction, i.e. the cases where natural selection causes the extinction of an evolving population.

In the literature, there are many models of life-history evolution and (to a lesser extent) experiments with bacteria in which Darwinian extinction has been demonstrated. However, I couldn't find anywhere real-world examples (i.e. not from models or experiments) of Darwinian extinction of complex organisms within more or less constant environment.

Do we know of such examples?
And if we do, could you please refer me to them?

Edit: A mechanism of the Darwinian extinction could be, for example, the emergence of ”selfish” strategies w.r.t frequency-dependent selection, which are beneficial to individuals when rare, but may result in a deteriorating environment and smaller population size once they become common.


texts: DRD4 genes and their connections to Dopamine 2 subtype

texts: I am trying to find out how the DRD4 gene correlates with the dopamine 2 family subtype receptor in the brain. Does a certain amount of methylation of DRD4 affect how much Dopamine is present in the brain?


texts: Can any one identify this insect from Lokhandwala, Mumbai India?

texts: I found this insect on my bed. I have never seen such creature before. Can any one identify this?


texts: What would life expectancy be in the western world in the absence of Ischemic heart disease?

texts:
In 2012, the leading cause of death was Ischemic Heart Disease.  In 1st world countries, what is the life expectancy for people who do not die of Ischemic Heart Disease?  I'm interested in the USA, but I'm happy for you to provide information on other 1st world countries if USA data is unavailable.

My motivation for asking the question is a curiosity of how much our life expectancy would increase if IHD was abolished.


texts: Does a higher body temperature slow the corona virus down?

texts:
The corona virus appearantly does not like high temperature:
High Temperature and High Humidity Reduce the Transmission of COVID-19
Also it seems that higher body temperatures helps the immune system to work better: Elevated body temperature helps certain types of immune cells to work better, evidence suggests

Should therefore someone who suspect they may have the corona virus or possibly another cold virus and do not experience fever try to elevate their body temperature slightly (say 0.5-1 degrees celsius) by dressing extra warm?

This is postulated here.

Does this sound plausible to you?


texts: Do hairs in the ear respond to things like shampoo?

texts: Shampoo and conditioning products make claims to be the end all be all in hair care. I doubt that they are so advanced "growth formula/anti-breakage/oily treatment". Have any of the claims been shown to be valid? Assuming a positive response do they have application for restoring the hairs used for hearing?


texts: Is all of the DNA used by genes (encoding DNA)?

texts:
My intuition tells me no, since only 1.5-2% consists of exons, so this statement would be wrong.
The correct statement would have to be: only about 1.5-2% of the whole DNA is used by genes (encoding DNA).

Am I correct in this assumption?


texts: Whenever I have any cut in my lips ,it gets healed in 2-3 days so why do lips get healed faster as compared to other body parts?


texts: Why there are two rounds of cytosine de-methylation in mammalian development?

texts:
I assume that the key biological meaning of cytosine de-methylation during germline development in germline progenitor cells is to reset imprinted genes and then set methylation pattern on these genes according to the gender of the embryo. (this is simply my best guess, so if there is an alternative interpretation, please mention it in the answer)

This de-methylation procedure is dangerous, because DNA-demethylation affects a lot of different regions and some transpons get de-repressed. So there is a risk of novel transposon insertions. However, since it is important to set imprinting in your own gamets properly, the embryo takes this risk.

But I don't understand why does de-methylation in mammalian development happen twice. Well, the first round it is not as deep and, I am guessing, that the transposons are probably not affected very much during the first round, so the risk of novel transposon insertions is not as high. However, since the resetting of imprinting marks is happening in the second round anyway, why does the embryo bother the first time around at all?


texts: Induce plasmid acquisition in bacteria to make them susceptible to antibiotics

texts:
Is it possible to use plasmids as a way of creating antibiotic susceptibility in bacteria.

For example; in Microbiology, an introduction 13th edition by Pearson , Page 230 "the researchers traced the drug-resistance plasmid to a plasmid found in E.coli that resided in the volunteers before the study".

I was wondering if it is possible to induce plasmids that make those bacteria susceptible.

They have to be in a first instance good for the bacteria, for example an enzyme that allows the bacteria to use a compound. But  through an antibiotic it would make that enzyme catalyze useful compounds of the bacteria, working the antibiotic as a cofactor of such enzyme.
Is it possible?
I was thinking on it as a "trojan plasmid".

Thanks.

Edit: Linking to this question: Could plasmids and conjugation mechanisms be used against antibiotic-resistant bacteria? , it talks about those "trojan horse" plasmids referring them in a way that seems to be linked to a bactericidal function, if instead the  plasmids are linked to a good survival rate in one situation (example, 36°C) but to a bacteriostatic situation ( temperature goes up to 39°) or such a way like hemoglobin works with CO, it's fundamental for us but selection hasn't worked to get through this problem and still binds to the molecule.

This type of coevolution in Wolbachia https://en.m.wikipedia.org/wiki/Wolbachia makes the host insect susceptible to needing the bacteria for reproduction despite being good in some environmental conditions it induces infertility in others.

Or inducing variants of genes that are still with functionality but trunked under certain conditions, if those conditions aren't present in the environment, the gene variant could spread without causing problems competing with the original variant until those environmental conditions are met reaching an equilibrium in which a % of the population could be used as a target of that antibiotic.


texts: What is the equivalent of shutter-speed in Human eye?

texts:
I just learned that in video cameras, every frame of the video has its own shutter speed.

And I know how frame-rate in human eye works out, well, not completely, hence the question.

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

  The human eye and its brain interface, the human visual system, can process 10 to 12 separate images per second, perceiving them individually.

How much (or what is the equivalent of) shutter-speed in those individual images?


texts: intravenous (IV) in the tail vein of an anaesthetized mouse

texts:
I trained myself to do intravenous injection on live mice. However, on anaesthetized mice you don't see the flux of your product showing that your injection was successful. In the same way, on live mouse a slight back pressure can be used to pull blood into the syringe to confirm proper placement in the vessel before injecting. On anaesthetized mice, I really have difficulty to obtain blood. All my following experiments rely on this injection, so I really need to be sure that the injection was successful and I have no choice that to do the injection on an anaesthetized mouse. Of course I warm the animals before injection to dilate the veins but I don't know how much I can warm an anaestethized mouse.
I thought to put a catheter before anesthetization the mouse but I don't know if it will stay in place until the mouse is anaestetized.
Do you have any tips?


texts: can dissolving be endothermic process. I have a container with glucose(solid state) and added water and found the container getting colder. was wondering there is no reaction(just a physical process) and why would it absorb heat.


texts: Can signals travel "backwards" in the sensory pathway?

texts:
My understanding of the "sensory pathway" is that its a linear, directional pipeline as follows:

Nerves (fire various signals depending on the type of sensors they are)
Fibers (transmit signals from nerves to spinal cord)
Spinal cord (transmits signals from fibers to brainstem)
Brainstem (transmits signals from spinal cord to brain)
Brain (the somatosensory cortex register signals as pain/pressure/temperature/etc.)

So again, my understanding is that sensory nerves are 1-way sensors, and that once they fire a signal, its 1 and only ultimate destination is the brain.

So, as a precursor to my question, if anything I have stated is incorrect, please begin by correcting me!

I read that pinched nerves in the back and neck can cause neuropathy ("pins and needles") all over the body: hands, feet, face, etc.

But how can this be? If my understanding of the sensory pathway is correct, then a pinched nerve in one's neck should only send "pins and needles" signals directly to the brain; it should not at any point forward/relay signals on to any other areas of the body.

To state that a pinched nerve in one's neck could possibly cause neuropathy in their arm, then that insinuates there is some connection between the pinched "neck nerve" and the nerve(s) in the arm that are experiencing the pins and needles sensation.

In fact, unless I completely misunderstand the entire sensory pathway and how pain signals transmit, this implies that a pinched nerve sends signals out to the spinal cord, down the spinal cord and into, say, an arm, and that the sensory receptors in the arm subsequently react to these signals.

How is this possible?!? Is there some kind of feedback mechanism at play where nerves in the neck and back can relay signals on to other areas of the body, instead of just feeding directly into the "spinal cord => brainstem => cortex" pipeline?


texts: Why is post-vaccination fever for 4CMenB so frequent?

texts:
When considering the introduction of 4CMenB vaccine, the Joint Committee on Vaccination and Immunisation said:

  The sub-committee noted that the clinical trials data suggest that
  when  4CMenB vaccine is given concomitantly with other routine
  childhood  immunisations a substantially increased frequency of
  vaccine-induced  fevers should be expected. Vaccine-induced fever
  rates may be similar to  those associated with whole cell pertussis
  vaccine used in the past.

What is the likely explanation for the higher rate of fever for 4CMenB in comparison with other vaccines?


texts: I have read that every 120 degree rotation of the F1 complex of ATP-synthase can be split into a 30 degree rotation and a 90 degree rotation. In between these two are dwell times, the one before the 90 degree rotation been called the ATP-binding dwell time and the one after been called the interim dwell time and that both of these fall of exponentially. I cannot, however, find a derivation of the probability density function of these dwell times, or there exact form. If anyone knows such a derivation or where to find one this would be much appreciated.


texts: How to calculate the percent of mitochondrial heteroplasmy

texts:
How do people calculate the percent of mtDNA heteroplasmy?

Does 7% heteroplasmy out of 10 cells, represent a mutation found in the same position on the genome among 700 mtDNA genomes out of 10,000 mtDNA genomes assuming there are 1,000 genomes per cell?

Thanks for helping me understand this concept a little better.


texts: How do I stimulate a neuron extracellularly, specifically the sphenopalatine ganglion

texts:
Apologies if this is too basic of a question, but I am an electrical engineer, just getting into neuromodulation/neurostimulation.
For my senior project, I am trying to make a device that stimulates the sphenopalatine ganglion. I have read as much as I can online, but some basic questions seem to not be answered. Answers to any of these would be really really helpful, as well as any resources to continue my research:

When I'm trying to 'stimulate' a neuron, I am really trying to trigger an action potential, correct?
Can I just send current across the exterior of the membrane to trigger an action potential?
Is is possible to stimulate a neuron without piercing the membrane? I know an action potential is the voltage across the membrane, so how can I change that voltage without piercing the membrane?
I believe I need to record the action potentials of the neuron, to make sure that my device is targeting the correct location and working properly, is this possible without piercing the neuron?
From the literature, I found that a 10 Hz electrical pulse works best for the sphenopalatine ganglion stimulation, but I am not sure how frequency plays a role in this.

Sorry again if that is a lot, but I am new to the field and have a lot of questions. Thanks in advance for any help!


texts: How deep in the soil can a seed be placed and still develop into a plant/tree?

texts:
The selected answer to How does a plant grow before photosynthesis is possible? indicates that a sprout grows beneath the soil using the food stored within the seed.

Does this limited ready food place a restriction upon the depth to which a seed may be placed and still develop into a plant? What depth will be best applicable for a given plant/tree seed? Is there a mathematical relationship known?


texts: Why guard cells need to turn malate into postassium malate to become turgid?

texts:
According to the Active Potassium Transport Ion concept given by Levitt et.al, stomata open due to turgidity in guard cells. It seems that guard cells turn the starch produced by photosynthesis into malate (which is a stable solute and should increase the osmotic pressure of the cell) but then go on to invest energy to exchange the hydrogen ions of malate with potassium ions.

Thus guard cells basically invest energy to turn malate into lots of potassium malate (so that water will enter due to increase in osmotic pressure), but why should such a process evolve if they can become turgid by just producing lots of malate?


texts: Why are my calculations for O2 requirements of daily metabolism so far off?

texts:
When I attempt to calculate the O2 necessary for a day of metabolism at rest (for an imaginary average human) and compare it with the expected O2 consumed per day my results differ by a factor of 3. I don't expect it to be 1 to 1, but a factor of 3 makes me think that I am missing a fundamental concept.

For our fictional human, I'm starting with the values for 1 MET. Specifically:

RMR (kcal / kg / hr) = 1
VO2 (mL / kg / min) = 3.5

I then define the weight of my human:

weight (kg) = 70
RMR (kcal / hr) = 70
VO2 (mL / min) = 245

And convert to more useful units:

RMR (kcal / day) = 70 * 24 = 1680
VO2 (L / day) = 245 * 60 * 24 / 1000 = 352.8

At this point, my understanding is that consuming 352.8 L of oxygen should produce somewhere in the ballpark of 1680 kcal at rest. My next assumption is going to be that aerobic respiration of glucose is accounting for all of the energy throughout this day of rest. I'm aware this isn't reality, but I wouldn't expect it to be 3x off. I'd guess that either this assumption is wrong or I'm misunderstanding something in the following math.

Let's start with some more constants regarding cellular respiration.

ATP creates 7.3 kcal / mol
An average of 30 ATP are generated per glucose (glycolysis, krebs, etc)
6 O2 are required to aerobically metabolize 1 glucose

Given the energy to ATP ratio, we can compute the ATP necessary per day. I should note that the result here is about twice as high as reference numbers I've seen so I am suspicious.

ATP (mol / day) = 1680 / 7.3 = 230.1369863
Glucose (mol / day ) = 230.1369863 / 30 = 7.671232877
O2 (mol / day) = 7.671232877 * 6 = 46.02739726

To convert the O2 requirements for our ATP from moles to liters, we use Avogadro's law at standard pressure (100 kPa) to conclude there are 22.712 liters per mole in a gas.

O2 (L / day) = 46.02739726 * 22.712 = 1045.374247

And finally, we can see that my calculation says that you need 1045.37 liters of oxygen to produce 1680 kcal of energy through aerobic respiration, but earlier I computed that you should only need 352.8 liters using 1 MET as my basis. There were assumptions made in there, but these results make me think that I am still misunderstanding a fundamental concept.


texts:
There is a spider on the window of my office that I've been trying to identify for the past few days but can't quite figure it out. My coworker thinks it's a Furrow Orb Weaver but I'm not sure. My office is located near Raleigh, NC and unfortunately I'm on the third floor and the spider always faces away from me, so these are the best pictures that I could get.

[


texts: Are there any resources out there for TFBS (transcription factor binding site) predictions for the yeast (S. cerevisiae) and S. pombe genomes? Even if these are only de novo predictions, I would like to have access to them.


texts: How does this diagram illustrate carbon cycling in lakes?

texts:
Could someone please explain the following process to me:

This process refers to carbon cycling in lakes and is described in the context of $CO_2$ flux from lakes into the atmosphere. GPP is gross primary production, $CO_2$ is carbon dioxide, R is respiration, and OM is organic matter. I realize that this question may be rather simplistic to some but my basic knowledge of any biological/ecological processes is rather limited. So, basically what I am asking is

have I written this process correctly?
how can this process be described?


texts: I know that papain is a proteolytic enzyme present in papaya. It is often used to tenderise meat.  What is the function of papain in papaya?  Is papain sweet? Does it function as an antibiotic?


texts: What proof do we have that visual attraction to other humans is a natural biological trait?

texts:
There's another question answered that relates to this, but the sources don't show enough evidence of how it is a natural biological trait that we're born with.

Even though there's evidence that culture influences some of our behaviors on visual attraction towards other people, is there any evidence this stems from something that is a natural biological trait?


texts: Why don't bees sting hornets for defense?

texts: Why don't honeybees sting hornets for defense when their hive is attacked? It seems like a good weapon against bigger animals - why not against hornets?


texts: Shannon diversity index: Pi relates to all found species, or number of species by site?

texts:
I am trying to dig into Shannon's species diversity index to compare the species diversity between different sites. For this, I need to calculate the 'relative abundance of species within the community'[details here][1]. What I do not understand is if this relative abundance relates to all species in a sample, or all found species?
In my example, I have in site1 6 species: a, b, c, d, e, f and in site2 two species: g, h. Should I calculate the proportion by species by site relative to 6 and 2, or to 8 (6+2, as species do not overlap between the sites? This is dummy example, likely species will reoccur).

If calculated by total number of species (8): Shannon H = 1.11 and 0.820,
if calculated by total number of species by site (6 & 2): Shannon H = 1.29 and 1.26.

I wonder which one is correct? The general trend is the same (site1 is more diverse then site2) but differences between indices seems quite large.
Dummy example to calculate Shannon's H step by step with dplyr. The commented out mutate allows to change if distinct number of species and their sum will by calculated by site or by total.
# Create dataframe with two sites and 6 and 2 different species. Area indicate abundance of species.
d<- data.frame(site = c(rep("s1",6),  rep("s2", 4)),
               species = c(letters[1:6], letters[5:8]),
               area = c(59,12,11,10,5,3,
                        10,5,21,20))

# Calculate sum of the area
# calculate distinct number of species, vary if the distinct area calculates by sum or by total??
d %>%
  mutate(species_n   = n_distinct(species)) %>%   # !! should 'mutate' by placed before the grouping variable or after?
  mutate(species_sum = sum(area)) %>%
  group_by(site) %>%
 #mutate(species_n   = n_distinct(species)) %>%
 #mutate(species_sum = sum(area)) %>%
  mutate(spec_pi     = area/species_sum) %>%
  mutate(pi_ln       = abs(log(spec_pi))) %>%
  mutate(sp_shannon  = spec_pi*pi_ln ) %>%
  mutate(shannon_comun = sum(sp_shannon))


texts: I've been thinking of culturing Cutibacterium acnes (old name is Propionibacterium acnes) for a thesis topic of mine on the comparison of the efficacy of local antibacterial topical skin care products but I have no idea how to culture it. I haven't encountered any definite instructions on the process in culturing it aside from it being an aerotolerant anaerobe and requring an anaerobic incubator.


texts: Why does high EDTA concentration cause swelling of platelets?

texts:
According to this textbook, high ( >2mg/ml of blood) EDTA concentration causes swelling of platelets which lead to their fragmentation.

I know that high concentration of EDTA increases plasma osmolarity which leads to cell shrinkage , as is the case in all other blood cells, but why does it have opposite effect on platelets? Why osmotic effects aren't seen in platelets?


texts: Why has the human eye evolved to become sensitive only to the visible light?

texts: The human eye has evolved to become sensitive only to visible part of the electromagnetic spectrum. Why? Why is infrared vision disfavoured for us by evolution but not for some other animals? I am not an expert of biology but curious.


texts: How does a protein molecule enter a cell through the cell membrane?

texts:
I can't find a good explanation as to how a whole protein molecule enters a cell membrane. Is it through endocytotic vesicles, with the help of ATP? How does this occur?

Thanks for the help!


texts: QA/monitoring in recombinant vaccine manufacturing

texts:
On a16z[0] podcast on vaccines[1], an interesting tidbit came up: vaccine manufacturing in cell cultures is expected to hit a major challenge in terms of quality control due to unpredictable behaviour of cells.
The issue was mentioned only in passing during the podcast, specifically Rajeev Venkayya[2] said:

First of all, we need to see if these vaccines can be scaled up from a manufacturing standpoint very, very quickly. And not just be produced at scale but also produced with a reproducible high quality.
This is one of the biggest challenges that you run into when making biologics at large scale, particularly when we're talking about hundreds of millions or even billions of doses.

I'm wondering how monitoring and quality assurance looks for cell cultures in an industrial setting. What are practical examples of what can go wrong with a cell culture that affect the final output (e.g. a vaccine) and how does one detect these issues? Is cytometry involved for "cell interrogation" or some more specialized methods are used?
I tried researching this question on my own, but quick googling didn't yield much. I'm a software engineer with deep learning experience, I look at this issue from a computer vision point of view and wonder if anything my field could do to contribute to solving this issue.
[0] a VC firm with a science leaning
[1] which is very good! https://a16z.com/2020/08/14/vaccines-vaccinology-renaissance-covid-pandemic-beyond/
[2] board member of Coalition for Epidemic Preparedness Innovations


texts: Proof of mechanisms and causal relationships in biology

texts:
Statistical methods in biology are strongly encouraged: they are quantifiable, unbiased, and usually the only ones that are accepted as evidence.

However, it doesn't seem like the whole picture.

Say, someone wants to prove the hypothesis that wings are used for flight. He (or she) conducts an experiment: takes two groups of birds, ties up wings of all birds in one of the groups, then throws them out of a window and gets statistically significant data that birds with tied wings do not fly.

However, strictly speaking, he didn't prove that birds use wings to fly: only that birds with tied up wings didn't fly when thrown out of window. Or, as they say, correlation does not imply causation.

To tie the hypothesis to the results, he might include a paragraph in the discussion that "wings have large area, there are muscles that can flap them etc" - in other words, explain how wings could be used to fly. However, this explanation isn't statistical, or quantifiable: he just wrote a "story", perhaps used some common sense - but last time I checked, it's not evidence.

And that's pretty much what happens in every paper on biology: when they try to prove some mechanism, they include an experiment results and stats for a single aspect that is related to the mechanism (which, obviously, cannot explain the mechanism on its own), but then, when it comes to discussion, they just drop all the numbers and start explaining the phenomenon "logically" and eventually come to the conclusion. To be honest, they could've done no experiment at all and just went to explanation straightaway.

So what I wanted to ask:

Is there such a method of proof in biology as "proof by explanation", or something like that - when the author just explains the causual effects from, say, physics perspective and comes to a conclusion? Perhaps, even something similar to mathematical proof? Does this constitute valid evidence?
Are there any formal requirements for such proof? Perhaps, some way to quantify it or reduce to a "formula" of some sort?
Say, I wanted to publish a paper about some new protein that affects testosterone production. If I did no stats at all, or experiments like trying to remove the gene for the protein from some individuals and seeing what happens in comparison to control group, but instead just extracted and described the structure of the protein, identified the binding sites to some testosterone precursor, and explained how it can affect the testosterone production chemically, would it be a valid paper?


texts: Why is thymine rather than uracil used in DNA?

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


texts: Substitute 25mM dNTPs mix with 10mM dNTPs

texts:
I need to make a solution of multiple compounds, one of them is dNTPs. The recipe calls for 20 μl 25 mM dNTPs in a 1250 μL master mix. Unfortunately I do not have it available at that concentration, can I substitute 25mM dNTP mix with 10mM mix?

TECHNICAL DETAILS

$dATP: C_{10}H_{13}N_5O_{12}P_3Na_3 - MW=557.2$
$dCTP: C_9H_{13}N_3O_{13}P_3Na_3 - MW=533.1$
$dGTP: C_{10}H_{13}N_5O_{13}P_3Na_3-MW=573.2$
$dTTP: C_{10}H_{14}N_2O_{14}P_3Na_3-MW=548.1$

Would it be 50μL of 10mM dNTPs to substitute the 20μL of 25mM dNTPs?


texts: How does Tylenol relieve pain without making me drowsy?

texts: So I have a crown that popped out and has been killing me, I've lived on a steady diet of Tylenol since it popped out. I've noticed that aside from killing most of the pain from the tooth, the tylenol hasn't made me particularly drowsy, which to my understanding was how most pain killers work. If it doesn't just put me to sleep, how does tylenol work to numb pain?


texts:
Is it possible to introduce a microorganism to a colony of black mold that will kill off the black mold entirely and permanently? Is there a common microorganism that likes to eat them and is harmless to us?

In other words, I ask if there's a way to get rid of the mold biologically, maybe a different mold that at least won't stink?

Alternatively, will getting a UV lamp to shine in the opening once in a while be an optimal solution?

I also read that copper sulfate is a popular fungicide with plantations, will it kill and prevent the mold from coming back? Could this ruin the AC with corrosion or be harmful to people if it will be airborne?

I ask this because I have black mold in my AC and I can't take it apart and disinfect it.

PS: it's probably Aspergillus, they're black and make these white structures like in this picture:


texts: How does antibody structure relate to function?

texts:
I know that antibodies have 2 binding sites (as Y shape) so they can bind to 2 pathogens for agglutination. They have a hinge, heavy and light chains, constant and variable sections on these chains.

But how do these structures (and any obvious structures I have missed) relate to the function of antibodies?


texts:
Is there any evidence for the validity of RNA/DNA supplements?

I've recently been seeing advertisements for RNA and DNA health supplements in the form of a pill, which claim to perform some rather miraculous functions within the body, though I can find no scientific validity behind this. There are some very respectable companies including Holland and Barrett selling this stuff and I can't see how this would provide any health benefits.

Are there any studies on this? If not, may someone care to speculate if there could be any health benefits to RNA/DNA supplements or is this just a terrible gimmick?


texts: Nomenclature of substrates for DNA synthesis

texts:
I have read in my school textbooks that both deoxyribonucleoside triphosphate and deoxynucleotide triphosphate are used in DNA Replication as substrates.
However, it is unclear to me whether the terms refer to the same molecule as one uses the term nucleotide and the other uses nucleoside. What confuses me is that nucleoside is a compound with a purine or pyrimidine base and a sugar and a nucleotide is the same but with the inclusion of a phosphate group.
Is it possible that the “deoxynucleotide triphosphate“ is used in artificial DNA replication as in PCR, and “deoxyribonucleoside triphosphate“ is the natural substrate for the replication of DNA within cells?


texts: Why HIV need integrase enzyme to integrate their DNA into host cell?

texts: In gene transfer by microinjection, the gene of interest is injected into the nucleus of host cell without using integrase enzyme. So why does HIV need that enzyme? Why they not just place their DNA into the nucleus and let it stay there?


texts: Can heritability be deduced from a correlation coefficient?

texts:
I am trying to understand the concept of heritability and from what I can gather, the heritability of a factor (say birth weight) must be closely related to the correlation coefficient of that factor when you do a linear regression of the factor between parent (say mother) and child.

So my question is this - is it possible to calculate the heritability from the correlation coefficient, and if so, what is the formula.


texts: connect three coding sequences with IRES

texts: To express two proteins at once in mammalian cells, expression vectors carrying an IRES (internal ribosomal entry site) are available. Does anyone know any attempt to express three proteins using two IRESs or more. The third gene may be expressed very low, but it may be acceptable depending on experiments if it works.


texts: Are there medical imaging devices to look inside artery? If yes, what is there sensitivity i.e. smallest object they can detect?


texts: Have there been attempts to identify Chomsky's "language mutation" in humans?

texts:
I'm not versed in either biology or linguistics so please forgive any naiveties I may commit.

I've learned that Noam Chomsky thinks that language is a result of a single genetic mutation in humans. It would be a mutation allowing the human brain to conceive of natural numbers as I understand. Have there been any (even speculative) attempts by biologists to locate that mutation in the human genome and/or in time? Is it even feasible?


texts: Do beneficial viruses exist? If so, what examples are there?

texts:
Typically, people call viruses some kind of organic compounds that cannot reproduce autonomously and which lower the fitness of their hosts. Even the word "virus" means "venom" in Latin.

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

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

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


texts: Cytochrome Oxidase activity in neuronal cells

texts:
The abstract of this article says

"...the entire neuron is often not metabolically homogeneous; most of the oxidative activity is usually found in dendrites."

Why would the activity of cytochrome oxidase be localized in the dendrites of the cell? Is it because it has a greater surface area (more channels and such) compared to the rest of the cell?


texts: Do the four cells produced by meiosis each divide into four cells again?

texts: In the beginning of meiosis, there is one cell. During meiosis, 1 cell divides into 4 cells. Does each of these 4 cells divide each into 4 more cells?


texts: Does Batesian mimicry rely on constant reinforcement?

texts:
If the species being mimicked, the monarch butterfly, for instance, were to become extinct, would the species mimicking it loose all of the benefit gained by their Batesian mimicry immediately?

I realize that the Monarch may be a poor example as it is a Müllerian mimic with the Viceroy butterfly, however their ranges do not overlap everywhere. Would the extinction of the monarch reduce the ranges of Batesian mimics to that of the Viceroy?


texts: Why does methylation not occur in viral DNA? Can viral DNA undergo the process of methylation? If not then why does this process does not occur in viruses?


texts: How is "fine mapping of pelvic regulatory region" done in the stickleback PitX1 paper?

texts:
I'm working through this paper for a class. I'm a bit confused by the methods they used in one experiment.

So the researchers are studying spine development in stickleback fish. They noticed some fish have spines and some do not. They have a good hunch that spine development is under control of PitX1. They work out through cross breeding spined/non-spined fish that spine development is regulated in cis.

They then attempt to find what piece of intergenic DNA regulates PitX1 expression. And this is their explanation of how it was done:

"To further localize the position of the cis-acting changes, we looked for the smallest chromosome region co-segregating with bilateral absence of pelvic structures in a cross between pelvic-complete (Japanese marine (JAMA) and pelvic-reduced (PAXB) fish, 13). High resolution mapping identified a 124kb minimal interval, containing only the Pitx1 and Histone 2A (H2AFY), genes, which showed perfect concordance between PAXB alleles and absence of the pelvis"

The attached picture is the accompanying figure, where part A refers to this experiment and part B refers to a promoter bashing experiment later.

I have no idea what it means to "look for the smallest chromosome region co-segregating with bilateral absence of pelvic structures in a cross between pelvic complete and pelvic reduced fish". I assumed they did at QTL mapping, but spines appear to be a mendelian trait. Since QTL mapping is done on polygenic traits, it wouldn't work.

Could anyone shed some light on this experiment?

It's captioned: "(A) VISTA/mLAGAN alignment of Pitx1 candidate region from pelvic-complete stickleback (SALR), medaka and zebrafish. Red peaks, >40% sequence identity in 20bp sliding windows; grey bars at top, repetitive sequence; An external file that holds a picture, illustration, etc.
Object name is nihms-215525-ig0003.jpg symbols, microsatellite markers ..."


texts:
Extensor digitorum and extensor digiti minimi both insert into the extensor hoods of digits 2-5 (or just 5 in the case of e. digiti minimi).  In every source that I can find, extensor pollicis longus & brevis insert directly into the base of the distal and proximal phalanxes respectively.

Does this indicate that the thumb does not have an extensor sheath as the remainder of the digits do?


texts: Primary cilia: what cell types have non-motile cilia that migrate?

texts:
My understanding is that there are two broad categories of cilia: motile and non-motile (also called primary.

Examples of the former include sperm flagella and the cilia of epithelial cells that line the airways.

Examples of the latter are mostly single cilia that protrude from the cell and act as an antenna, usually packed with certain receptors (HH pathway, Notch pathway etc.)

In the inner ear, a primary cilium called the kinocilium extends out of the center of the apical side of hair cells and migrates to the lateral side over the course of a few days. This cilium is non-motile, it is simply anchored to a basal body which is pulled to one side of the cell.

Does anyone know of another such example in any other tissue? A single non-motile primary cilium whose basal body migrates along the apical plane of the cell after docking with the cell cortex.

Thanks.


texts:
I took this picture in central Mexico. The insect is about 1mm in size. I found lots of these dead on a desk, so many that at first I thought they were just dust. I assume they came from a plant that was above the desk.

Does anyone know what it might be?

EDIT:

I found the culprit walking nearby! I guess that verifies what others pointed out: It seems to be the molted cuticle of an aphid. (sorry for the poor quality of the pictures)

Thanks a lot!


texts: If a dead animal is electrified, will it decay?

texts:
I was walking past some power lines today, and a flying fox (like a small furry bat, for those who don't know Australian fauna) had grabbed onto two adjacent power lines, completing a circuit, and as such died due to electrocution.

That got me thinking about whether or not the animal would decay in this situation. As far as I understand it, decay is caused by bacteria and other micro-organisms. Could they survive in this high-voltage environment? If not, will this poor flying fox be perfectly preserved until the next blackout occurs?


texts:
I'm not sure all heavy metals are toxic, but most are.

Some may be present as insoluble compounds, or otherwhise hard to get into an organism, but that's a side aspect.
For example, I would count copper as toxic, even if some salts are triggering to vomit just too quickly to swallow poisonous doses.

So, in this sense, are they all toxic?
Is the toxicity based on the same mechanism?


texts: What should be the distance between plant promoter and gene?

texts:
I am trying to clone a rice gene under a different endogenous rice promoter.I will be cloning the CDS of the rice gene.So I wanted to know what is the minimum or maximum distance I should put between the rice and the promoter so that I can get good expression levels.

Should I check the expression of the construct in E.coli before transforming it?

What should steps should I follow before finally transforming the construct into rice?


texts: How does electroporation mediated recombination work?

texts: For yeast and other organisms, DNA can be readily taken up into the cell naturally or through membrane disruption. What does applying a voltage to cells do exactly that allows more recombination to occur?


texts: Is the bulbourethral (Cowper) gland turned on during puberty or is it on at birth?

texts: I am trying to find information about the bulbourethral (Cowper) gland and if it gets turned on during puberty or not. I tried asking several other online sites and they said they couldn't help. I don't know where to ask or where I could look up the answer.


texts:
I sometimes read of "inhibitory synapses". But I understand that when the neuron is inhibitory, all of its synapses will be inhibitory (so it is a property of the neuron, not only the synapse) - is that correct?

How is this experimentally tested? I did not find an estimate of how many outgoing synapses inhibitory neurons typically have, but I assume that it might be thousands. So how do we know for all of its synapses that they are inhibitory?


texts: Does the genetic sequence of SARS-CoV-2 end with 33 A's?

texts:
Looking at the DNA (or RNA?) sequence of the Covid-19 virus here: https://www.ncbi.nlm.nih.gov/nuccore/MN908947.3

I notice it ends in 33 a's. Does the virus really look like that, or is it some artifact of the sequencing process, or some sort of padding to round out numbers?

Here's the last few lines:

29761 acagtgaaca atgctaggga gagctgccta tatggaagag ccctaatgtg taaaattaat
29821 tttagtagtg ctatccccat gtgattttaa tagcttctta ggagaatgac aaaaaaaaaa
29881 aaaaaaaaaa aaaaaaaaaa aaa


texts: How much current various kind of body tissues can tolerate without any serious damage?

texts: Human body can tolerate some amount of current. How much current (and duration) various kind of body tissues can tolerate without any serious damage?


texts: What happens to H+ when Glycerate 3-Phosphate is converted to Triose Phosphate?

texts:
The conversion from Glycerate 3-Phosphate to Triose Phosphate requires:

$ATP \rightarrow ADP + P_i$

$NADPH \rightarrow NADP + H^+$

So what happens to the $H^+$?

Is it in-effect "recycled" back to the Light Dependent reaction.


texts: Is mating between human and non-human primates theoretically possible?

texts:
I wonder if it is theoretically achievable to produce living offspring between a human and a non-human primate. Great apes have 24 pairs of chromosomes compared to our 23, however, it is known that a mule is made from a donkey (62 chromosomes) and a horse (64  chromosomes).
Are there other reasons why this human/non-human primate hybrid can't survive?


texts: Why have plants evolved to photosynthesize glucose instead of another molecular compound?

texts:
I think this question can be broken down into two sub-questions:

Why do plants produce $C_6H_{12}O_6$ as opposed to another molecule following the formula of $C_nH_{2n}O_n$? Why not $C_8H_{16}O_8$, $C_4H_{8}O_4$, or any other of the many possible variations? Does it likely have something to do with stability or some other property that glucose has that many other variations on the formula do not?
Why have they evolved to produce a molecule following the formula $C_nH_{2n}O_n$ at all? In short...why carbohydrates as opposed to another family of compounds?

My assumption is these are questions that have been researched extensively in biology and evolutionary biology and have at least tentative answers.

I'm looking for either your best hypothesis or a currently popular hypothesis within the relevant scientific disciplines. I understand there is likely no "definitive" answer, but probably at best pretty good hypotheses.


texts: The effects of coffee as a stimulant are quite well-known. What are the mechanisms by which coffee helps prevent sleepiness? I have heard of the presence of caffeine, but what does it actually do inside our body?


texts: Automatic cropping of collimated digital X-ray images

texts:
Do you have any suggestions for a library which offers an algorithm to crop digital X-ray images automatically?

We receive full-size images (43x43cm) from a detector, independent of the collimator settings. If the collimator has been closed to 10x15cm, we need to crop this area. This should be done automatically, so that the user does not even see the full-size image because it contains a lot of information which is not needed.

Now we are looking for a good library which offers such an algorithm. This sounds like a simple task, but depending on the dose and the collimation, it can be pretty hard to detect the collimated area of the image. Therefore, we are looking for a professional solution rather than implementing it ourselves.

Any suggestions?


texts: Pelleting bacterial cells using centrifugation and getting proteins in the supernatant

texts:
Do significant amount of proteins from cells find their way in supernatant during pelleting? If the answer is yes then I see two ways in which protein can be in the supernatant
.

1) Through lysis during pelleting
2) Through leakage of protein from cells during pelleting

if significant amount of lysis occur during pelleting then obviously protein will be there in the supernatant due to lysis alone. However, If most cells (like 98%-99%) remain intact  then only by leakage significant amount of protein can be in the supernatant. Both way can also contribute. Which is the case?


texts: Would oxygen levels be stable without photosynthesis?

texts:
I learned how the CO$_2$ cycle works in several biology classes, high school, elementary school, geology, and physics. Then today there was an article published in the NY Times claiming:

  ...it is a myth that photosynthesis controls the amount of oxygen in the atmosphere. Even if all photosynthesis on the planet were shut down, the atmosphere's oxygen content would change by less than 1 percent.

I'm really confused. If the earth naturally has 20% oxygen in the absence of photosynthisis, why did it spike durring Great Oxygenation Event? I reread that several times. There's no citation; no further context that can explain this. If this were coming from the climate change denier camp, I'd just shrug it off, but the credentials would say otherwise. It's in the NY Times and Nadine Unger is an atmospheric chemist at Yale.

My guess is that this is simply a misleading paragraph with a grain of truth. The question is, where is that grain? How long would the atmospheric oxygen content remain at within 1% of the current level if we turned off photosynthesis?


texts: What causes skewed ladder bands on an agarose gel?

texts:
I frequently ran into an issue where the bands of my ladder become skewed. What causes this?

Here's an example: 0.7% agarose gel, 100V, 60 minutes. Same problem occurs with 1%. I loaded 10 ul of a 20 ul PCR reaction.

As you can see, the problem is not smiling per se. The lanes themselves are fairly vertical and straight. Just the bands themselves appear warped. What could cause this issue?


texts: Why deoxyribose for DNA and ribose for RNA?

texts: Why is DNA made out of deoxyribose and RNA made of ribose? Why can't they both use ribose or deoxyribose? I think that the deoxyribose gives an advantage in storing genes, the job of DNA and ribose is better dealt with outside the nucleus...but why?


texts: How much of my ancestry comes from each grandparent?

texts: Three of my grandparents were Eastern European, back at least several generations. I recently discovered that I am less than 25% Eastern European, the rest being Western European and other. How likely is this?


texts: What's it called when a male seahorse gets "inseminated"?

texts: I am looking for the scientific term for the process where a male seahorse receives eggs from the female. For example, we usually say, "the male inseminates the female with sperm." What is the correct term to use for seahorses? Would you say "the female inseminates the male with eggs", or is another term more appropriate?


texts: Why do epithelial cells arrest in response to serum?

texts:
Primary epithelial cells, for example human mammary epithelium, fail to proliferate (arrest) in serum-containing medium. Therefore, a common growth medium for epithelium contains pituitary extract instead of serum (Hammond et al, 1984). This may be related to the fact that epithelium is normally not in contact with serum in the body.

On the other hand, many epithelium-like cell lines grow well in serum, and most tumor-derived cell lines are cultured this way. But it can be difficult to establish such lines from epithelial cancers: often, only fibroblasts grow out of tumor explants in serum-containing medium, while the (epithelial) cancer cells do not. In contrast to epithelium, fibroblasts increase their proliferation when exposed to serum, and this process is well studied (Iyer et al, 1999).

Why does epithelium arrest in response to serum? Are any mechanisms known? Is there any study of epithelium gene expression response to serum? Why is the behavior of epithelium so different from that of fibroblasts --- is there a physiological explanation, perhaps related to wound healing?
Is this true for all types of (human) epithelium?
Should we consider epithelial-like cells growing in serum to be adapted / selected? Have such cell lines then lost some part of the epithelial phenotype? Is this a serious artefact?

Any pointers to literature would be appreciated!


texts: Why can't we move our toes and some fingers separately?

texts:
In our feet, other than the large toe, the other toes cannot be moved separately. If we try to move them, then all the four toes move together. We cannot move each toe by itself.

Same thing occurs in the hands of some of us, where we cannot move the little finger by itself. While folding the little finger, the ring finger before that also has to be folded to some extent, and vice-versa.

An explanation to the problem with the ring finger and the little finger can be found here.

The phalanges make the toes. Are the phalanges of the small toes connected, such that we cannot move them separately?


texts: The Proofreading Function of Coronavirus Polymerases

texts: I have heard that the Coronavirus family have a proofreading and editing function in their polymerase enzymes which can recognize and excise mutations. This is obviously disastrous for the population of infected individuals. Is this true, and if so, would it be possible to knock out the proofreading and editing subunit selectively so that the mutational burden would progressively increase in the viral population ?  Could this then lead to something like Muller's Ratchet and dampen the virulence in the population or would there still be a mechanism to remove the mutated viruses from the population and retain the virulence over time?


texts:
Why do the eyes of this cat have different colours when viewed from different angles?

Both of the eyes of this cat appear yellow when looking straight at the camera.

However, when the cat looks at an angle to the camera one eye appears green. Unfortunately, the cat is not mine and I don't have many more pictures of it.
I have also noticed that my own eye which appears dark brown from straight on, looks lighter when viewed from an angle.
Why does this happen? Is there a special property of the iris that lends itself to such behaviour? In this website, it is mentioned that the colour of the iris varies with the angle at which it is viewed but no explanation is given.


texts: RNA seq and using of Poly(A) or non-Poly(A) based amplification of RNA

texts:
I'm studying "Deep sequencing the circadian and diurnal transcriptome of Drosophila brain" Hughes et al., 2012. I've got some problems with the materials and methods.
Before RNAseq, the authors amplify RNA. They use two kits: Poly(A) based and non-poly(A) based. For the samples Poly(A) based amplified they do a sequencing to generate 100 bp paired-end and for the samples Non poly(A) based they do a sequencing to generate 75 bp single-ends.
I read in the strategy:

Total RNA was amplified, and ribosomal RNA was depleted, using a non-poly(A)-based amplification kit, which significantly diminishes the 3' bias in downstream libraries used for RNA-seq (see Methods).

I don't understand why they use both kits. Actually, they say that they want to asses the bias introduced by an alternative amplification methods BUT the following sequencing is not the same in both cases so there is more than one parameter which change between the two protocols so I don't understand how they can compare.

For the poly(A) based I understand that the rRNA are not polyadenylated so they remove rRNA from the amplified sample. However, don't they remove non-coding RNA too (long or short)?

For the non poly(A) based, I don't understand how they remove the rRNA but I understand that since they don't select the RNA according to their poly(A) tails they keep the rest of the RNAs which are not kept in the poly(A) based amplification.

When I look to the RUM statistics, I see that there are fewer total aligned reads in non-poly(A) based: 70-80% (non polyA) and 80-90% (polyA). So it seems like we lose some information with non-poly(A) based.

To sum up, why the authors use Poly(A) and non-poly(A)? Why do they show all the rest of the results from the non-poly(A) amplification since they have less aligned read? How do they compare since the following sequencing is not the same? How the rRNA are removed in both techniques and especially in non-poly(A)?
I didn't find the protocols kit with exactly the same name but here are the links to the protocols which are closer (I think).
http://www.mscience.com.au/upload/pages/nugen/nugen_ov_rna_seq-brochure.pdf
http://excilone.com/client/document/ug-arcturusE%E2%80%9E%C2%A2-riboamp%C3%82-hs-plus-amplification-kit-user-guide_38.pdf


texts: How can bats achieve good resolution with wide beams?

texts:
I have been reading about the echolocation system in bats. papers state that bats tend to produce a sonar beam that has a beam angle (-3db) of about 30-40 degrees. This would be considered a wide beam given the fact the sonar sensors used by robots have beams 15-20 degrees or down to 10 degrees with multi-sonar.

As the beam width increases, the azimuth resolution decreases. Yet, bats have good navigational capabilities and good object discrimination in azimuth. How is that achieved? what is the technique used?

I searched hard but what I found is that they rely on the timing between two ears. however, given the complexity of the environment and the multiple echos that return, how is it possible to correlate which echo in the left ear belongs to which in the right ear?


texts: Prevent clumping of bacteria in my media so that I can measure turbidity?

texts:
Forgive my naivety, I'm an undergraduate Chemical Engineering student doing research this summer into growth rates of various combinations of bacterial isolates.
I have about 9 isolates from a toxic leachate, and I am looking into finding combinations of these 9 isolates which degrade the leachate the fastest. I have also have the general consortium of what was growing in the leachate.
I am trying to compare the growth rates of my isolates (and combinations) to this growth rate in order to demonstrate some increase in treatment efficiency. (The idea is that a faster growth rate in the leachate demonstrates a faster breakdown of the leachate)
My current way of measuring growth is to fill a 96-well plate with some known volume of leachate and inoculate the appropriate isolates into the appropriate wells. This is my community matrix. Then I run my plate reader (TECAN) for 72-hours in order to measure the turbidity change over time, as an indirect measure of leachate breakdown.
The problem is that many of my isolates and combinations of isolates, including the consortium clump when they grow, meaning that the plate reader I am using does not measure the growth the way I'd like it to.
Here is an example of a good growth curve of Brevundimonas diminuta growing in my leachate, which I consider good:

Here is my "growth curve" of my consortium, the bacteria have a tendency to clump here:

Essentially, I am asking if there is a way for "force" my bacteria to grow in a planktonic fashion?
More information:
These are my isolates:

Brevundimonas diminuta
Streptomyces sp.
Lysinibacillus sp
Alcaligenes sp.
Pseudomonas sp.
Pseudomonas fluorescens
Paenibacillus sp
Pseudomonas fluorescens
Stenotrophomonas chelatiphaga

These and the consortium grow the way I want them to in M9 salts supplemented with acetate, all planktonic, and measuring their growth in that is very easy, but I want to demonstrate a growth curve in my leachate. I don't know a way to do this on a scale which the 96 well plate reader allows me to do. I can get 32 different combinations out in a single plate if I grow them in triplicates.
A post-doc has been trying to measure a decrease in ammonia flourescence in the plate reader, but has had less luck than me.


texts: Please identify this little and soft white creature. Since childhood I am seeing this things flying in my surroundings and nowadays they are seen occasionally.


texts: Why I have to pee more often in low temperature?

texts: I realised that I have to pee more often in winter or simply the temperature is low. Is there any scientific explanation, or just simply psychology?


texts: Why does Thiamine pyrophosphate have phosphates?

texts: The reactions that Thiamine Pyrophosphate(TPP) catalyses are associated with the thiazolium ring. Why is pyrophosphate a part of the structure of TPP then? What benefit do the additional phosphates give TPP? Is there some reaction with TPP that does not center on the thiazolium ring?


texts: Research papers that demonstrate work done on other species with honey bee pheromones

texts:
I found research where Queen mandibular pheromones (QMP) emitted by queen bees were used to find their affects on Drosophila melanogaster. However, I am curious to see if the QMP from bees have been used in other social insects like wasps or termites. Can you please guide me to any research papers on the same?

Since the eusocial queen pheromones among different species are more or less composed of the same hydrocarbons, treating wasp workers with honey bee QMP should have the same effect on worker wasps as it would have had on honey bee workers.


texts: Insect identification (Brazil, orthoptera?)

texts: This insect appeared in my indoor yard, in southeastern Brazil. The body is roughly 2cm in length and it makes very distinct beeping sounds, in a pattern that sounds almost like morse code, unlike the crickets I've seen around here. Any ideas?


texts: What determines the physical location of differentiated cells in an organism?

texts:
Exposition:

As a little kid, I always thought of DNA as being a description of how to build an organism. For example a human DNA would have "Add two legs and two arms", a dogs DNA would have something like "put a tail here". Now, at school, I have learned that DNA codes for proteins, for structural proteins, enzymes etc. But how does a growing fetus actually know where to put the different parts of the body?

Examples:

For example, why don't I have retinal cells growing on my feet? Why is my cerebral cortex not in my mouth? And where is the information stored that humans do not have tails, or that elephants have trunks?

Summary:

What determines where different cells should be located, and how is that information stored?


texts:
This insect bumbled into my bedroom last night - can someone ID it for me? I'm mainly curious because I'd like to know if it poses any danger to my cats (who were very eager to add it to the menu).

It was about an inch and a half to two inches long, and when I picked it up to toss it outside it made a loud squeaking noise. I live just outside of Cape Town, South Africa (but I'm not a native, so I don't know all the species here).


texts: How do I name a binding antibody? “Binding antibody to”, “binding antibody against”, or “anti-[antigen] binding antibody”?

texts:
I'm translating a text that describes how an immunogenicity of a drug is measured by assaying the levels of binding antibodies to the drug. Or is it "against the drug"? I'm wondering how to name these antibodies. Let's say the drug is cetuximab, and I'm writing the title of a document section:

  Assay of binding antibodies against cetuximab in serum.
  Assay of binding antibodies to cetuximab in serum.
  Assay of anti-cetuximab binding antibodies in serum.

I googled for "binding antibodies to" and "binding antibodies against" and got only several dozen results for each of the two options. Therefore I came up with "anti-[name of the antigen] binding antibodies", but don't know how to google for it, hence my question here. Would option 3 look nice to a native speaker?

P.S. Alas, it is exactly "binding antibodies to" in my Russian text. I cannot omit the adjective "binding" before "antibodies"..

  Связывающие антитела к цетуксимабу.

I quote from the Wikipedia page on neutralizing antibodies:

  Most antibodies work by binding to an antigen, signaling to a white blood cell that this antigen has been targeted, after which the antigen is processed and consequently destroyed. The difference between neutralizing antibodies and binding antibodies is that neutralizing antibodies neutralize the biological effects of the antigen, while binding antibodies flag antigens.

My authors use the adjective "binding" to distinguish binding antibodies from neutralizing antibodies, just like in this paper, for instance: BAbs and NAbs. Another section in my document gives the results of an assay of NAbs against the same antigen.

Explanation of the difference between binding and neutralizing antibodies from the FDA:

(ADA: anti-drug antibodies)


texts: Which process is needed to complete male reproductive development?

texts:
In order to properly complete male reproductive development:

A. primordial germ cells must begin Meiosis I in utero.
B. Sertoli cells must produce testosterone.
C. Dihydrotestosterone must masculinize Wolffian duct derivatives
D. the paramesonephric ducts must degenerate
E. the metanephros must form the genital epithelium

My attempt:  I think the answer is C because testosterone turns into DHT which then masculinzing the wolffian duct.  Other people I am studying with claim the answer is D (which is true) except that I dont think the loss of the paramesonephric duct is needed to complete male repro development.


texts: Why does enteral carbohydrate yield higher energy than parenteral?

texts:
The following is written in a well-known textbook of surgery:

  Each gram of enteric carbohydrate provides 4.0 kilocalories (kcal) of
  energy. Parenterally administered carbohydrates (eg, intravenous
  dextrose) yield 3.4 kcal/g

What is the explanation for this?


texts: We know geckos can climb vertically or even upside down a surface like glass. But can they do that on wet glass?


texts: Which sex of trees bears fruit? The males or females? And what specifically cause that one to bear fruit. Is it the same as it is with blossoms in trees?


texts: How would extraterrestrial organisms be categorized?

texts: Suppose we find bacteria on Mars, we sequence its genome, and find it is genetically similar to $E. Coli$. Would we categorize it in the $Escherichia$ genus? Or would we put it into a seperate system of classification?


texts: Cloning a gene of an organism with an nonsequenced genome

texts: What would be the best protocol to clone a gene about 5kb in size? The genome is not sequenced, but the gene itself very similar to orthologous genes of organisms with known sequences.


texts:
I always see these Lumosity ads on TV, and I personally feel they are just trying to "sell me something". I did some layman's research (wikipedia) and read that "Studies of Lumosity's effectiveness have shown mixed results".

Does anyone with knowledge on the topic of learning know if the "brain games" they post are simply games? I guess the proper question would be:

Can games like the ones Lumosity offers increase cognitive ability?


texts: What tests are available to detect C. Botulinum/Botulinum Toxin in fermented meats?

texts:
I am interested in the preparation of fermented dry-sausages (salamis, summer-sausages, etc) where due to the humid anaerobic atmosphere inside the salami. It is a good environment for C.Botulinum spores to grow.
The mainstream food safety practice is to use Sodium/Potassium Nitrate or Nitrate + Nitrite, which are suspected carcinogens.
I would like to prepare fermented dry-sausages without Nitrate usage and test the finished product after for the presence of C.Botulinum?
Salamis are usually 10-50cm, and if I were to consume or sell them it is viable for me to test each salami. Thus, I am also interested in the viability of taking a few cuts out of a salami to test for C.Botulinum presence, would a small cut on the sausage be sufficient, or it might be that there is a growth of C.Botulinum in a small part of the sausage not throughout the whole sausage making testing a sample not likely to reveal whether or not other parts of the sausage have C.Botulinum.
Also concerned about whether lack of C.Botulinum is sufficient proof that the salami is clear, or whether the bacteria might have died off after producing the toxin. The same concern about whether if there is toxin production should it be throughout the salami or in isolated pockets making testing a small sample from a large salami not viable.
Based on this situation what would be a test that is will allow me to detect whether a salami is likely to cause botulism?
Is it as simple as some gram stain and an optical microscope?


texts: How long does it take for memory to disperse after death?

texts:
1: There seem to be cases where coma patients with a non-active brain (i.e. flat EEG) have regained full consciousness. => Apparently memory and knowledge are stored independent of brain activity.

2: There seem to be animals (e.g. hamsters) that can be frozen to complete organic inactivity and will regain full functionality after being thawed. => Apparently the stored memory does not depend on blood flow and other support.

3: From this I assume that quickly cooling a human brain to a temperature low enough to avoid decomposition would preserve the state of that brain that corresponds to that human's memories, knowledge, cogntivie abilities, and maybe consciousness at the time of cooling. => With the proper technology that "content" is theoretically retrievable.

Q: How long would that state remain after death in a brain left at room temperature?

Or in other words: How long does it take for decomposition to destroy memory?

Addendum:

The fact that the stored memory may not be accessible with current means is not relevant to my question. We cannot access the information stored in Linear A, but this unretrievability does not delete the information.


texts: Why is the IC50 an interesting measure for in vitro cancer drug screenings?

texts:
Large-scale in vitro screenings  of (potential) cancer drugs are done to access their effectivity depending on the actual transcriptome of a tumor cell line. Databases like GDSC or CCLE supply data of these experiments.
For each drug - cell line experiment they provide an IC50 value: The concentration of the drug needed to kill of 50% of the cancer cells in vitro.
Why is that value interesting? The value simply depends on the toxicity of the compound. In these databases cytotoxic snake venom would probably be the seen as the best cancer drug, but it would not be a great idea to give that to patients.
Cancer drugs work by killing of cancer cells faster than normal cells. Therefore, I think these IC50 values lack normalization/ comparison to the IC50 of healthy cells. Without this I feel the databases are useless.
Where am I wrong?


texts: What’s this fungus growing in supersaturated salt solution

texts:
As a hobby, I’ve been trying to “grow” crystals of from supersaturated solutions of aluminium potassium sulphate.

I noticed that my solutions are also rather successful at growing a type of fungus.

The fungus grows bigger and bigger in the saturated solution and leaves behind yellow spores as the salt solution evaporated (see photos).

I’ve always thought that salt is antifungal and anti bacterial, and I’m surprised to see that there is a fungus actually growing bigger in a supersaturated salt solution.

I have tried boiling and filtering (with tea mesh filter so the spores probably got through) the salt solution, but the fungus keeps coming back, so the spores survive boiling too, unless there are spores floating around my room.

Is there a way to identify what sort of fungus it is? What sort of fungus is it likely to be? Have I bred a type of super fungus? Is my life in danger by allowing this to grow?

I live in Sydney, Australia if that helps with identifying the fungus.


texts: What is the relationship between the oxygen affinity of hemoglobin and the maximal oxygen uptake (VO₂ max) of the human body?

texts:
I was curious about whether any of the numerous documented human hemoglobin variants conferred a quantifiable athletic advantage but the only thing I've found of any relevance is the relative oxygen affinity of each hemoglobin variant. From the bit of research I've done it seems to be the case that a higher oxygen affinity causes the hemoglobin to hold onto oxygen more tightly and not release it into the plasma at the same rate as normal hemoglobin, leading to the body overproducing red blood cells to compensate for this (erythrocytosis). On the other hand, lower oxygen affinity causes the hemoglobin to release oxygen more readily, leading to the underproduction of red blood cells (anemia).
Assuming the quantity of blood cells were normalized between the two (so the consequent erythrocytosis/anemia is mitigated) would the lower oxygen affinity confer an increase in maximal oxygen uptake? How about higher oxygen affinity?


texts: If we sequenced the genome of every species, would all phylogenies agree?

texts:
The Tree of Life is still up for debate. Most of this debate seems to be due to a lack of genomic information, but that deficiency is decreasing rapidly with advances in technology and sequencing power.

Hypothetically, if we knew the genome of every species, would we resolve all phylogenetic debates? If not, what would still be up for debate?


texts:
What does the word "refractory" in "refractory period" refer to?

I know what it means "refractory period" (both, absolute and relative) in the action potential graph, but I don't understand what the meaning of "refractory" in this context is. What is it refractory for?


texts: When a muscle contracts, but not all the muscle fibers are activated, what happens to the remaining muscle fibers?

texts:
I understand how motor neurons work, but I would like clarification on what exactly is going on when a muscle contracts. For the sake of simplicity, let's just use the bicep as an example. If I do a bicep curl with a weight that is the maximum weight my bicep can lift, all the muscle fibers in my bicep will be activated and contract(more or less). If I remove the weight and do the same bicep curl, now only a small percentage of the muscle fibers in my bicep will be activated and contract, because that extra force isn't needed. But, the whole bicep muscle is still contracting! It must be, otherwise wouldn't the other muscle fibers staying at regular length prevent the bicep from contracting?

So the only thing I could think of is that the unactivated muscle fibers are pliant and DO contract, they just don't initiate the contraction, but instead go along for the ride. So if you looked at the level of sarcomeres, in the activated muscle fibers, the myosin heads pull on the actin, causing contraction. In the unactivated muscle fibers, myosin heads are NOT pulling on the actin, but the sarcomeres are still contracting, due to the forces from the activated muscle fibers. Is this a correct interpretation of what's going on or am I wrong?


texts:
I understand that in PCR we're able to amplify only selected portions of the DNA... however despite reading it from multiple sources, I cannot figure out how this selection actually takes place.

I know that by using proper primers, one each for coding and template strands, we can direct the DNA polymerases to specific sites to start with. I also understand that these primers make the replication proceed in opposite directions, towards each other. Like follows:

However, I wonder what makes the replication terminate when the polymerase reaches the primer at the other end? Because as far as I understand, replication should continue indefinitely until the physical end of the sample strand is reached... such that we may decide the starting points but never the ending points.


texts: Amplification technique for proteins similar to PCR for DNA?

texts: I know PCR can be used to amplify a tiny sample of DNA in order to perform experiments. Is there a similar technique to use on a protein sample? More specifically, I'm not interested in "cutting" up the protein but simply making more of the original sample.


texts: What is the meaning of "E-value" in the BLAST search?

texts:
After reading many pages, I still do not understand the definition. Can someone use simple words to explain me that?

https://en.wikipedia.org/wiki/BLAST
This expectation or expect value "E" (often called an E score or E-value or e-value) assessing the significance of the HSP score for un-gapped local alignment is reported in the BLAST results.

If a lower E value means closer results to the query sequence, what is its difference to "Sequence Identity Cutoff"? http://www.rcsb.org/pdb/search/advSearch.do?search=new


texts:
The school textbook of my daughter (the textbook is written in German) describes the five kingdoms of life: prokaryota, plants, fungi, animals and "Ursprungliche Eukaryoten". These are defined as "single cell organisms with real nucleus and other specialized organoids, both autotrophs and heterotrophs". No Latin name is given.

I am somewhat confused, as I know that there are both multi and single cell varieties between algae, and these used to belong to even particular taxon within algae (a single cell Rhodella, for instance, not just belongs to plants but also specifically belongs to red algae). Also, there are unicellular fungi like yeast that used to be fungi (and, OK, protists used to be a separate group that probably also belongs to "Ursprungliche Eukaryoten"). Are they all pulled out of they groups into this new kingdom in this system?

The summary of the proposed classification schemes over history can be found at https://en.wikipedia.org/wiki/Kingdom_(biology)#Summary . Which scheme, if any does this taxon correspond? Is something missing in that table?

The textbook is Training Gymnasium - Biologie Mittelstufe Band 1, Harald Steinhofer (2013), ISBN 978-3-86668-709-7, seen here. The description in question is on the page 16.


texts: is it possible to use electroshock to temporary stop gross motor functions directly on the neural pathway?

texts:
Is it possible to modify that procedure and use it to send a small electroshock on the specific neural pathway and temporarily stop that gross motor function?

  When the microphone detects unwanted noise—such as a humming airplane engine—it sends a sound wave into the headphone speakers that is 180 degrees out of phase with the bothersome sound. Consequently, the two waves cancel each other out, resulting in silence._

i would like to know if that procedure can be modified with electric currents in the human nervous system, so body movement is stopped, without stopping organs and damaging the body by sending the current directly in the nerve, canceling out the signal.


texts: Why do DNA and RNA have the functions they have?

texts: I know that there are two most important directions of genetic information transfer in living organisms: DNA->DNA and DNA->RNA. The first is replication, and the second is transcription. I wonder if there is a reason for this choice of directions. According to this article, all other directions are possible. Why do we use DNA for example? RNA is capable of self-replication since it happens in viruses. And why do we use RNA, not DNA, as messenger molecules? Is it just an accident or is it possible to explain why this is the right way of doing it?


texts:
I am working on a tool for SNP calling in polyploid plants. To test my method, I need a list of housekeeping genes common in almost all plants. For my case, these genes must be single copy (ie each HK gene should have no paralogs).

Briefly I need a list of genes that are:

House keeping
Single copy
Common in almost all genomes, or genomes of a taxa

Any help is appreciated.


texts:
Though a number of animals have been going extinct at alarmingly quicker rates (so called anthropocene extinction), a number of 'star'  threatened animals are still alive.  Which of the following charismatic endangered species is modeled or expected to die off soonest: polar bear, panda, black rhino, african elephant, mountain gorilla,bengal tiger/ tiger.

Where can I find population projection models for each of these species?

Mountain gorillas  have the current smallest population,  but polar bears are clearly in  a lot of (and quickly widening)  trouble due to melting ice. African elephants are seeing species loss due to poaching,  and drying conditions making food/water scarce,  which could also speed their decline, but they have the largest of the populations.

Since WWF and other conservation organizations use these charismatic species to 'sell' conservation and raise interest, awareness and funding,  losing one (or many) of these species could affect conservation considerably. This will either be positively via a reactionary  disappointment by the public or negatively by losing a "poster species".


texts: Synthesis of immunoglobulin Fab fragments: Where can I learn about Fab?

texts:
I wanted to know the chemical reaction involved in Fab synthesis. I looked everywhere for it. No luck. I know I will find it here.

All I know for now is:

Fab is a monovalent fragment that is produced from IgG and IgM, consisting of the VH, CH1 and VL, CL regions, linked by an intramolecular disulfide bond.

Molecular basis of Fab will make more sense.


texts: How to do a nucleic acid or genome and amino acid search

texts: I have been looking to find a database where i can search for genome and amino acid search. Are there any open source databases available for the same.


texts: Can an organism exist as a single cell but come together as multi-cellular during certain times?

texts:
I am trying to remember a particular segment from a BBC special, about a single celled species. However, at certain times all the individual cells came together to form a structure, not unlike a mushroom, to scatter something like spores into the wind. Afterward, the individual cells separated and continued on as individuals.

Am I remembering this incorrectly? Is this even possible?


texts: What is this passage trying to say about Darwin's difficulty in explaining variation?

texts:
This passage, from the book "How humans evolved" by Robert Boyd, says that one of the problems Darwin had at the time was that he struggled to convincingly explain how variation could be maintained; this was needed to theorize that evolution is the result of cumulative adaptations over many generations. According to the book, there are four problems, one of them being that selection removes variation:

  For example, suppose the environment changes so that individuals (finches) with
  small beaks are less likely to die than those with large beaks. The
  average beak size in the population will not decrease because there
  are no small-beaked individuals. Natural selection destroys the variation needed to create adaptations.

I understand the idea, but don't really understand what the example is trying to illustrate. The example seems to be saying if small beak finches survive better, then there would be no small-beaked finches...?

The second difficulty Darwin had was in explaining how animals "might evolve beyond it's range of variation (?)"

  Selection can cull away some characters from a population, but how can
  it lead to new types not present in the original population?

The bit above I understood; however, I struggle to see the point of the example that was given for it:

  How could elephants, moles, bats and whales all descend from an
  ancient shewlike insectivore unless there were a mechanism for
  creating new variants not present at the beginning?

Please help rephrase or explain again what these two difficulties actually are, or help make sense of the two examples that the book gave.