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Does alcohol really helps to get substances get faster into the bloodstream?
I saw the video where Arnold Schwarzenegger cooks some protein cocktail and adds Austrian Schnapps to the mix, saying that it's to make everything get faster to the blood. Is it true or some kind of a joke?
One person said this:
Alcohol inhibits protein synthesis, which is necessary for muscle building. It affects Glucose, which is needed for energy and recovery, so in this aspect it'll stunt your recovery and energy. For workouts, it dilates your blood vessels forcing blood into limbs and leaving core colder, what this means is that you'll loose performance. The article mentions that this mainly affects endurance
He says about effect of alcohol, that's a good question too.
And what about actually getting stuff faster into the bloodstream?

The total conclusion of all studies of alcohol is that moderate alcohol consumption has no beneficial effects on health. Some studies said a bit of alcohol is good for you... Most alcohol is metabolised by an enzyme in your liver cells known as alcohol dehydrogenase (ADH). ADH breaks down alcohol into acetaldehyde, and then another enzyme, aldehyde dehydrogenase (ALDH), rapidly breaks down acetaldehyde into acetate. Some people drink the wrong alcohol for covid... which ADH enzyme instead turns to Acetone or Formaldehyde.

About 20% of alcohol is absorbed right through the stomach after drinking.  This means alcohol could have a rapid effect on other aspects of digestion.  Specifically, it could affect the rate of gastric emptying, which would then affect how quickly other food is digested.  I found one paper which I think supports a faster rate of emptying, but another that says the rate of emptying is reduced.  This one says it is the sex of the volunteers that determines this.  They actually went on to look at the menstrual cycle.  Did I say this was one of the weirder batches of PubMed results I've seen lately?  You can find many more studies of alcohol and gastric emptying on PubMed, examining disease conditions and animal models.  I suspect that overall, considering the small sample sizes and heterogeneous results, it would be easiest to classify this use of alcohol among the myriad natural supplements for which there is "insufficient evidence of efficacy".


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Fuel from photosynthesis
I was reading how plants make use of sunlight, CO2 and some other stuff to make energy. So why can't we create artificially engineered bio solar panels which will take sunlight, C02, water and other things and give us energy (maybe electricity or heat etc). So basically instead of solar panels which are made of silicon or something we can have bio panels made of organic materials. Then we need to supply it with water and it will convert sunlight into electricity.
I googled this on the internet and I don't find anything relevant in this regard. So I am assuming there must be a very good reason we are not trying to do this. I want to know if there is any research going on in this regard and if not why this idea is not feasible.

Here is one group working on it. There are others, of course.

What you are suggesting is an organic photosynthesizer,but that's not necessary when you already have plants that have genetically adapted for millions of years just to be suitable for this very purpose.
 Of course,artifical photosynthesis already exists,essentially using the same process;photons,chloroplasts,calvin cycle,photosystems 1 & 2,etc.It utilizes the general concept with photoelectrochemistry,so basically just replacing the organic tools with artificial photoelectric cells,which also uses h20 and light.What you are asking is why we have not developed genetically engineered organic matter to produce higher efficiency.As a matter of fact,GMO plant's already exist with immunity,though I have not heard of GMO that catalyzes photosynthetic reactions,and best not,because genetic engineering is still at it's best a new field that is too complex,for example,the general GMO is to incorporate the bacterial enzyme cas9 to cleave away specified DNA to alter an organism's genome,such as inhibiting receptors to cannabinoids,or to fight pests with substances that are not harmful to humans,etc.But it has consequences,such as permanence of that edited genome,so if the organism/plant reproduces,the progeny would also exhibit the same GMO properties.
 Photosynthesis is a complicated series of reactions that uses complicated enzymes and such.For example,the enzyme rubisco that changes co2 to energy rich molecules such as glucose,from highly unstable phosphoglycerates.Artifical photosynthesis is quite new,but it also uses the same fuel;co2,h20,and light,not sure if it uses biological nutrients like soil,but the process also uses Nicotinamide adenine dinucleotide phosphate,or NADP+.It is used for anabolic reactions,so it builds up molecules,vice versa are catabolic reactions,which is when enyzmes break down lipids and molecules in metabolism.Albeit I do not know for sure if this molecule has the same purpose in artifical photosynthesis,but for general photosythesis,yes.NADP+ also absorbs electrons for independent and dependent reactions to generate ATP and NADPH,etc.
 I hope this simplifies some things.CONCLUSION:we do have artifical photosynthesis,but gmoed photosynthesis may be harmful to a plant's heredity if we damaged it's genome,causing potential harm.
  Artifical is quite similar to organic,so I guess you say they are biopanels,using h20,co2,and light.

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Understanding a Chromosomal formula in a karytope analysis
I am reading a medical reporting results of a karyotype analysis. On it it is written:

Chromosomal formula
46,XX,del(7)(q11q36)[12]/46,XX[13]

I understand that 46 is the number of chromosomes, XX refers to the pair of sexual chromosomes, del(7)(q11q36) means a deletion on the long arm of chromosome 7 spanning the bands 11 to 36.
What do [12] and [13] mean?

Cytogenetic nomenclature is standardized in the International System for Human Cytogenetic Nomenclature. Unfortunately it is not free and my institution does not have access. However, looking at a preview of the 2013 version in Google Books, it would seem that the number in square brackets is the number of cells scored with that karyotype.

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Known ways to modify the genetic structure of the 13 loci used in CODIS
After reading the answer to Does our DNA change during our lives?, I was wondering if and how it would be possible to change the structure of the 13 loci that are used in the CODIS database, in such a way that forensic biometrics would not be able to identify/verify you anymore.
I have read about DNA chimeras, and cases exist where a bone marrow transplantation altered the DNA, depending on the sample that was taken. However, are there any other known ways to alter DNA, such as cancer, radiation, etc?

What do you think will happen, when you alter you DNA in this way? Short: No, it's not possible.

Well the nuclear plant example is of course ridiculous, but I'm wondering if cancer or aging may have an effect which is of high enough significance to circumvent DNA tests.

To cause enough mutations to make the DNA a mismatch would assuredly result in the death of the person long before the sample were obtained. The answer is still no with cancer.

@Chris I disagree that it is necessarily impossible. New techniques such as CRISPR-Cas allows for directed mutagenesis of specific loci, and if you can predict in advance the tissue they are obtaining the DNA from, it is not implausible for a modification to be carried out (for example using retroviral-induced modification).

@MarchHo In all cells of the body so that forensic biology cannot identify you? That'S impossible.

@Chris / March Ho: Any pointers to research papers about this, or do you know this from own experience?

@Michael Forensic biology works with a number of different markers which are located throughout the genome. If you want to change your genetic fingerprint, you need to change all these regions in all your cells. Otherwise you will leave a trace which makes you identifiable.

@Chris , yes I agree, so my question is if it is possible to change these (13) markers.

@Michael Depending on the source you look at, you body has something like 3,4 x 10^13 cells (or 34 trillion). See here for example. How do you want to change all these cells? No, that impossible.

@Chris, I edited my question. I understand that it is impossible to change them all, but cases are known where a bone marrow transplantation caused certain samples to have a different DNA than other samples, of the same body. I'm looking for other ways to accomplish that, maybe more creative, but scientifically proven.

This is important when you look at blood. A lot of forensic biology is done on lost hairs, dendruff...

So for blood it is possible, but for hairs, dendruff, saliva, etc, there are no known (proven) cases?

I have edited my question to be less opinion-based. I'm looking for scientific sources where it has been proven that it is possible to alter DNA structure of the 13 loci used in CODIS. Bone marrow transplantations are known to alter the DNA structure of the blood significantly. Blood transfusions as well, but here, the impact is temporary. In case you still feel it is too much opinion-based, I'm open for suggestions.

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The effect of salt, pH and temperature to the salivary amylase
If I prepare the following set of tests, incubate for 15 mins, then add 2-3 drops of iodine solution to each test tube:
Salt test (1ml starch solution + 0.5 ml enzyme + 1ml 1M NaCl, incubate at 37 oC
Acid test (1ml starch solution + 0.5ml enzyme + 1ml 0.5HCl), at 37oC
Alkaline test (1ml starch solution + 0.5ml enzyme + 1ml 0.5M NaOH), at 37oC
Temp test (1ml starch solution + 0.5ml enzyme + 1ml H2O), place in water-bath
(75oC)
What is the effect of salt, pH and temperature to the salivary amylase? I don't know what exactly how salt effect.
high temperature will denature the enzyme.
How about salt?

Sounds like a homework question to me. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

At extreme pH (too acidic or too alkaline), the salivary amylase will be denatured.
At salt, the addition of salt will affect osmolarity and hinder the reaction.

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Meaning of some unit of measurement of kinase activity
I need help knowing what $cpm \times 10^3$ means in Figure 4(C) of this paper (https://www.sciencedirect.com/science/article/pii/S0022202X15323149#f0010). It appears to be a unit of kinase activity.

It is not a specific unit of kinase activity, rather a general approach taken for following reactions where there is no change of colour. The abbreviation cpm stands for counts per minute and is a measure of radioactivity.
In this particular example a radioactive phosphate has been incorporated in the ATP of the protein kinase assay. If the protein kinase is active with the substrate, the phosphate will be transferred from the ATP to the substrate peptide/protein. If the sample mix is loaded on a SDS-PAGE gel, a scintillation counter can be used to measure the radioactivity of each band and one will be able to  show how active the protein kinase has been in phosphorylating it's substrate.

Great answer! Is there a way to approximate the mass of the active enzyme based on cpm? Thank you very much!

As a follow-up, what exactly is being counted per minute? Thanks!

Each count is one ionisation event at the detector. Assuming an excess of substrate, I guess you could use it for concentration determination of you had a standard curve to compare to.

Are these assays called "Radioligand binding assay"?

I think it would be clearer to call it a radioactive protein kinase assay, radioligand binding assay to me is more about protein-protein interactions

or "Radiobinding assay" as described here? https://en.wikipedia.org/wiki/Radiobinding_assay


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Difference between stem cell "expansion", "repopulation", and "self-renewal"?
From this paper (link:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4130805/), I read "Thus G-CSF results in the expansion of phenotypic HSCs in the bone marrow with reduced repopulating activity and self-renewal capacity."
If expansion meant population-expansion, then would that not mean the same thing as repopulation? Likewise, self-renewal occurs through asymmetric cell-division in which a parent cell divides into two daughter cells; or it can occur through symmetric cell-division in which a parent cell divides into a progenitor cell and a daughter cell. In essence, both types of cell-division maintain or increases the population of stem cells; hence, "self-renew" or "expand". Clearly, I am missing something here with the terminologies. Please help! Lastly, I thought phenotype is a noun, then what does phenotypic even mean?

will you be still interested in a few days time?

@PolypipeWrangler: Yes! Please help! I need this.

I will read paper this weekend

After an hour of reading the paper (from 2014), if you can I recommend instead reading the below review article (from 2020). the 2014 article uses difficult to understand language.
Eric M. Pietras; Inflammation: a key regulator of hematopoietic stem cell fate in health and disease. Blood 2017; 130 (15): 1693–1698. doi: https://doi.org/10.1182/blood-2017-06-780882
https://ashpublications.org/blood/article/130/15/1693/36384/Inflammation-a-key-regulator-of-hematopoietic-stem
I found this by pasting your article's title into google scholar, hitting "cited by", sorting by date, and browsing until I found a review article.
The point of treating with G-CSF is that the stems cells divide, and can be recovered from the blood for stem cell treatments.
"expansion" . Here means an increase in the numbers of cells. But in plant biology it has the literal meaning of cells growing larger.
"phenotypic HSCs". Using the adjective phenotypic, the cells express the phenotype of HSCs. So the cells behave like HSCs
By itself, G-CSF makes the the HSCs divide for a while, then they stop dividing. That is, they become "quiescent".
This state of quiesence can then be interrupted. If the mice are treated with antibiotics to kill intestinal flora (or if mice are used that are germ-free), then the HSCs continue to divide.
The article calls this process of getting the HSCs to divide again "mitigating the G-CSF-mediated HSC repopulating defect"

So to paraphrase the in-quotes from the 2014 paper, G-CSF causes the expansion of bone marrow HSCs with the phenotype of low repopulating or self-renewal capacity? Since G-CSF causes BM niche HSCs to exit quiescence. I am assuming that the 2014 paper distinguishes BM niche HSCs from BM HSCs.

Perhaps say "eventual phenotype". The HSCs that divide after treatment with G-CSF, seem like normal HSC but eventually stop dividing and become insensitive to G-CSF.


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Gel electrophoresis and foam

I've never seen this kind of thing happen. What might trigger this??

Looks like an agarose gel. What buffer did you use? Did you happen to clean the tank (incompletely) using a detergent?

Gas bubbles are foamed by electrolysis of water, generating bubbles of hydrogen gas on the negative electrode and oxygen gas on the positive electrode.
As for the foam itself... I am guessing there is some form of detergent in the buffer. Some electrophoresis buffers do contain detergent.


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Do lack of sleep affects the process of digestion?
Many times due to lack of sleep I felt discomfort in digestive tract.Why did it happen?Do lack of sleep affects the process of digestion?


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Are there situations where in vivo results work better than in vitro results would have shown?
Basically, if I have poor in vitro cell line results but decided to test them in vivo in a mouse anyway what are the possibilities of having better results in the in vivo live mouse model that I would have never known otherwise from the in vitro results?
Links are appreciated

This is a very broad topic and massively depends on the specifics of your hypothesis.

Differences between in vitro and in vivo results are (unfortunately) very common!
Somehow, all failed clinical trials (and many preclinical trials) are large-scale examples of the discrepancy between promising in vitro and actual in vivo results - which also highlights the fact that even from one in vivo system (e.g. mice) to the other (e.g. humans), there can be significant and unpredictable biological differences. It is the opposite of your case, in which you expect an improvement when moving to live animals, but it is also more common.
By essence, your in vitro culture will be unable to recapitulate key processes like:

Signals provided by the natural extracellular matrix. Your cells are probably grown on polystyrene, but that substrate is far from the complexity of the natural molecules that surround cells in vivo: stiffness, immobilized signaling molecules...
Information provided by other cell types. Organs are formed of many dynamic subpopulations (stem cells, immune cells etc), some unknown, that interact and control cell behavior at the tissue scale.
Fluctuating information like biological cycles and behaviors (circadian rythm, sleep, food intake...)
Many others like for instance immune processes, (de)activation of small molecules by enzymes in unrelated organs (liver) or plasma...

All these factors can change your result in unpredictable ways, making them either better or worse. But, and that is important, more often than not, complex biological systems tend to make things worse, as they introduce extra noise, buffering effects etc. so more often than not, things will not be as good in a real animal as in a Petri dish. It can get better, sure, but it is extremely unlikely!
That is one of the main reasons why people do in vitro work first: it is faster, cheaper and more ethical, and failure in vitro is usually a good predictor of downstream failure in vivo.
Please, don't cherry-pick an answer that tells you otherwise! It's easier and more comforting to think that everything is going to work if you just move to animals, yes, but you will most likely waste time, money and animal lives for identical results. My (unsolicited) advice is to build a better in vitro model, that will reduce the possible differences between cell results and animal models: can you mimic a biologically relevant environment by adding a protein/sugar matrix to your cells? Can you find primary cells that will behave more naturally than immortalized cell lines? Can you make mixed cell cultures to improve the adequation of your model with reality? If you do all this, then your results should be much more reliable and you will have a better idea of what to expect in vivo.


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How do molecular biologists determine biochemical pathways?
I'm new to this community, so hopefully this is the right place to ask this question.
I know my question is really general, but in all of my biology courses we are merely taught the chemical pathways of common reactions in cellular metabolism, but we're rarely told how these reactions were determined or discovered. What approaches do molecular biologists take to determine what molecules are involved in what reactions, what order the reactions take place, where they take place, etc.? Some of these pathways involve tons of steps, huge molecules, and a bunch of enzymes and proteins, and I just don't see how anyone could have pieced it all together. For that matter, how is the molecular structure of anything in the cell determined? For example, what was the setup of the experiment that determined that TNF-R1 even existed on the surface of the cell membrane, and that it triggers the apoptosis pathway? Another example is photosynthesis -- I could see how maybe we could find PS1/2, cytochrome complexes, etc. in a soup of blended up cells, but how in the world did we figure out what each one does and in what order?
The average cell is just so tiny and complex that it doesn't seem like there's any feasible experimental design that could lead to the discovery of these things. Please enlighten me!

You might find the answers you seek in the autobiography of Arthur Kornberg: “For the Love of Enzymes: The Odyssey of a Biochemist”

Welcome to SE Biology. What research have you done on this topic? First, molecular biologists had nothing to do with determining biochemical pathways, it was chemists — first called physiogical chemists, then later (in English-speaking countries) biochemists. This should give you a clue how they went about it. How does a chemist study a reaction? How would a chemist determine that yeast converts glucose to carbon dioxide? What's the next step from studying live yeast? And after showing A goes to Z, how would you look to see if there are B, C and D in between? With this in mind, search.

Have fun. Remember, Rome wasn't built in a day, and that the initial slow and limited progress was built upon by others as technological advances allowed new methods to be used. And, though cells may be small, you can get enough compounds (and enzymes out) with lots of them (e.g. yeast cultures, rat livers and kidneys). Enzyme preparations didn't have to be pure to yield information. And at the time the pathways of central metabolism were worked out (before and immediately after WWII) they didn't know anything about DNA (and probably didn't even think about it).

@David It's really quite fascinating how recent (late 20th century) the majority of this information came to light. I've always taken it for granted and assumed it was discovered hundreds of years ago, like many of the things we learn in the classroom.


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Is it possible to create a biological radio?
If someone had taken the genome for a basic single or multi-celled organism, and had the understanding of genetic code to write his own program, is it possible on a fundamental level to create the organelles necessary to emit an electromagnetic signal at a frequency that isn't widely used by modern day electronics (noise concerns)?

Welcome to Biology.SE! This type of question are off-topic here. You might want to give it a try on WorldBuilding.SE

Note: Bioluminescence is a type of electromagnetic signal. Gymnotoid fish use electric signals to communicate (mainyl for courtship if I am not mistaken). Electric discharges (e.g. eels) might count too. Also, any neuron that fires causes an electromagnetic signal. You don't need to do any genetic engineering to get an animal that produce an electromagnetic signal! You should clarify what you're looking for.

Albeit interesting question, what @Remi.b refers to are the additional senses of magnetoception and electroception. However, i think your are talking about something else. Please clarify.


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how much can changing light enter the eye shap what you see?
Does it change the shape and how objects are seen or does it just stop you from seeing certain things?

Needs clarification: what is "it"?  "changing light"?  What do you mean by "changing light"?

Now that I reread it its really poorly writen. I'm guess I'm talking about light manipulation. How can manipulating light change how you see. Like changing how much light get in the eye changing  the angle. Will these manipulation change how we see and how? Will it just stop us from seeing and nothing more or is that some how linked to hallucinations?

I'm interpreting your question to be: "How much can changing the light entering the eye change the shape of/how objects are seen? Would manipulating that light just stop you from seeing certain things?"
Manipulating the light entering the eye is the exact premise of a virtual retinal display (VRD):

From Wikipedia –  A VRD is a display technology that draws a raster display (like a television) directly onto the retina of the eye. The user sees what appears to be a conventional display floating in space in front of them.

Google Glass and other technologies (virtual reality headsets, heads-up displays) operate through relatively similar projection mechanisms. Light defines everything the eye sees (outside of hallucinations, and even those can be induced by flickering light). Also, the way your brain processes visual information (photons received by your eyes) can be "tricked," which is discussed in this BBC article. Finally, your brain's ability to process visual information can be altered by external forces (e.g. drugs, motion, or even strong magnetic fields).

Thanks also for the link to other information.  This is exactly what I was looking for. Sorry for the bad explanation.


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Is there a critical size for a bacteria colony forming?
I am a maths student doing a project based on modelling bacteria and phages. In one of my models the bacteria population reaches a population size of ~450 cells.
Would a colony of bacteria this size be at risk of completely dying out if there was an environmental change (e.g. pH or UV)?
Also, is there such a thing as a critical colony size? e.g. if a colony of a certain type of bacteria falls below this critical size then the probability of a colony forming would be very low.

Welcome to the site!  What type of bacteria? How much of a change? What environment are they in currently?  And pH or UV is two questions; it would be best to [edit] down to just one to make the question answerable.  Thanks!

Can you be more specific about what your goals are in your simulation? We would need to know a lot more about the kind of model you're talking about to know what the significance of a particular number of bacterial cells is. "Colonies" of bacteria are generally artificial and arise in the lab because we grow cells in isolation or near-isolation on nutrient plates under controlled conditions. Such cells are growing as fast as they can; it's not like they need a critical mass of cells to survive.


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How are neurons selective towards specific stimuli?
I've read several papers that mention that there are specific neurons that are activated for specific things (e.g. neuron A activate only when horizontal lines appear, neuron B activate when certain sound appear, etc).
How does this happen over time (unless the neurons are "born" with certain "affection" towards stimuli) and what is the mechanism that allow it? I understand that it's probably not some conformational change in proteins since the activity has to be really fast- so how can an electrical signal be selective?

Sensory receptors and neurons get their selectivity from physical processes and their position in space. For example, photoreceptor cells in the retina respond to light in a specific position in space because the lens and structure of the eye directs light incoming in a particular angle to a specific spot on the retina. Sensory receptors in the skin can sense touch in a particular place because that's where they are located. Hair cells in the cochlea respond to particular frequencies of sound because the membranes in the inner ear vibrate at different frequencies along the length.
For selectivity to lines of a particular orientation, neurons combine receptive fields of retinal cells, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception
The "LGN" (visual thalamus) cells pictured here have receptive fields that look a lot like the retinal ganglion cells that carry output from the retina. For simplicity, you can think like they are the same. These cells are excited by light in the center (red), and inhibited (indirectly) by their neighbors (blue) (there are also "off-center" cells that respond in the opposite way, preferring dark in the center and light in the surround).
If you add up a bunch in a row, you can make a cell in primary visual cortex (V1, the green cell) that responds to edges. If you summed up the receptive fields of cells in a different orientation you'd get selectivity to a different orientation of lines. The key feature to making selective receptive fields is which cells are connected to which.
These receptive fields are created in development by spontaneous activity in the retina and eventually by actual visual input when the eyes open. The process is pretty complex and occurs in multiple stages, but you can start with a review like this one:
Huberman, A. D., Feller, M. B., & Chapman, B. (2008). Mechanisms underlying development of visual maps and receptive fields. Annu. Rev. Neurosci., 31, 479-509.
Higher in the visual processing hierarchy you will find increasing complexity as receptive fields of different types are combined and recombined.


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Mutated and unmutated PCR product
If I have a mutated colony containing the fusion protein, mCherry instead of the stop codon TAA, and an unmutated colony which does not contain the protein. Why will the PCR products of the two colonies have the same size?
I thought that since the mutated colony contains the protein instead of the stop codon, this would cause this product to be larger in size than the unmutated product. However, from experimental data it shows that both products are of same size. Could someone please explain why this is?
Thank you!

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, your question should show evidence of prior research and some familiarity with the relevant area of biology. Note that it is extremely unlikely that you have replaced the stop codon with a protein. ——— Please do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

If mCherry was successfully cloned replacing the stop codon, you would indeed expect a fusion protein that is about 27 kDa larger than the original protein.
However, with a PCR you are not testing for the full length protein, but rather for a part of the target gene sequence.
The length of the PCR product very much depends on the position of your primers: If both primers are targeted at your unmutated sequence, the product size will not change by adding mCherry behind the targeted sequence. The product size of the PCR would only change, if one primer is located before or in your unmutated protein and the other one behind mCherry. This would probably result in a very large PCR product and hinder the PCR reaction from being effective.
To check for correct integration of mCherry, you would need to design a primer pair with the forward primer in your unmutated protein and the reverse primer in mCherry. This should result in a product in the fusion protein colonies, but not in the unmutated ones.
Alternatively, you could sequence your products.

Whoever gave a -1 to my answer, could you please explain why?


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Normal ECG/EKG Measurement?
I'm getting started using ECG using a 3 lead system by iWorx. I have place the leads on my two wrists and the ground on my ankle and have recorded some data into the provided LabScribe 3 software using the ECG template. Can anyone help me interpret what I'm seeing?

It doesn't look like the standard QRS I see in my textbook, but it's so regular (this is just a snippet) that I don't believe I'm seeing artifacts.
Any insight would be greatly appreciated.
Thanks!

What do you want to know? It looks fairly straightforward. Wandering baseline causing some artifact, maybe a short P-Q Interval, everything exaggerated throughout. Is this what you're asking?

it does look OK, that is P, QRS and T waves are present (means you alive). Weirdness might come from insufficient or incorrect filtering, namely, it seems that T wave is too intense.

If no one answers here, you might request admission onto the Google Plus ECG community. And post this same question there; there will definitely be someone who can help you there.

downvoter! leave a feedback.

How can an ECG be recorded from the wrist? ECGs pick up the electrical activity from the heart muscle? Where is the wrist signal coming from?

These sites provide useful info for understanding EKG signals:
https://ekg.academy
https://www.practicalclinicalskills.com

If you're looking for an explanation of the parts of the waveform you recorded, here's an annotated version:

I hope that helps you map it back to the "standard" QRS you saw. The AV delay is the time between the depolarization of the atria and the ventricles.
I agree, the T-wave is too intense. I'm not familiar with a 3-lead ECG that connects to the wrists--I'm more familiar with chest ECGs. I'm guessing the large T-wave is an artifact of measuring through the wrists (hopefully it's not indicative of a health condition such as Hyperkalemia). It looks like your resting heart rate is around 52 BPM--that's healthy.
The signal itself comes from the heart muscles. It takes a number of milliseconds for the electrical impulse to travel from the sinoatrial (SA) node to the atrioventricular (AV) node, down the His bundle, and finally to the Purkinje fibers in the ventricles. It takes this long because the movement of charge is caused by ions in the cells physically moving. That change in charge is conducted (via normal electrical conduction, such as you see in a wire) through the tissue and muscle to the electrodes on the wrists--this conduction is effectively instantaneous (in this case, it's electrons "pushing" each other, not ions moving within cells as in the case of the heart's electrical system). ECGpedia has some good background on this.

The ECG system takes the voltage from your right wrist (call this VRA), and subtracts it from the voltage at your left wrist (call this VLA), so that Vlead I = VLA - VRA.

So, in summary, the signal you're seeing is produced by the heart's conduction system, not the muscles in your wrists. Muscle noise would manifest itself as noise or random spikes in the ECG.

+1, but where on earth does this signal come from you think?


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What (open) software there are for simulating behaviour of human (cortical) neurons?
Is there any reliable open-source software for simulating the behaviour of human cortical neurons? I am looking for serious software, so let's assume I have access to a computer with more than 10,000 computing cores.
What I would like to do is to scan a subject's brain with MRI, record EEG during a simple task (e.g. listening to tone pips), project the EEG data to the cortical surface calculated from the MRI (solve the so-called electromagnetic inverse problem), and once that is done try to simulate the behavior of the cortical neurons at the "active" regions.
This simulation part is new to me, the rest I know quite well. All hints and ideas are welcome!

I just know NEST, but how would you get the map of the connections ?

Thanks for the feedback! Yes, of course you can do source localization, assuming there are a few dipoles (or under other simplifying assumptions), but it's difficult to connect to the neuronal level simulation as the OP wants to do. (Sorry. I don't know how to turn your answer into a comment.)

Perhaps I misread OP's question. Upon re-reading, OP only says "simulating the behaviour of human cortical neurons", I guess it could be larger scale model. I'm editing my answer.

There are a number of neural simulation programs available: Neuron, NCS, Genesis come to mind.  However, none of them have anywhere near the computing power to do even a halfway realistic simulation of a human brain.  You're looking at roughly 86 billion neurons, with something like 10K synapses each.

Sure, you can regularize your solution, and put extra constraints to get a better solution, but do you really recover the behavior of the cortical neurons with a thousand dipole model? Are dipoles the right representation for neural computation? We don't know the answer, but I'm betting they are insufficient.

No, not in the neuronal level. Because IMHO this is an ill-posed problem.

EEG combined with MRI won't have the resolution to do solve the inverse problem of neuronal network simulation. There are at least hundreds of thousands of neurons that would be involved in your specific behavioral task, and you have at most a few hundred electrodes. You'll have to make grossly simplifying assumptions about how the brain works to start any inference. You might learn something, but the claim would be somewhat weak.
Personally, I wouldn't work with EEG if you are interested in the mechanistic details of the brain. It is a very useful signal for some cognitive investigations (especially for humans), but the current technology lacks the spatial resolution.

Yes, in the coarse scale network level. (response to @sets' feedback)

If you don't care about micro-scale dynamics of the neural network, and want to model some population-wide activation that changes EEG, as @sets commented, there are various source localization & dynamical system models that you can use. I am not an expert on this, so see @sets' answer, or hopefully someone else will answer in detail.


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What is our skin made up of?
Again, it is a basic question. What is our skin made up of? is it made up of many cells arranged in a systematic way or is it just like any layer say of a book?? what is the difference? where is the living and dead thing coming into picture? is it the fact that skin can self-heal makes it living and in turn made up of cells??

The human skin is indeed made off a number of different layers, the three most important are epidermis, dermis and hypodermis (also called subcutaneous fat), see the figure (from here) for details:

All three layers can be subcategorized further, I'll only give a few details here. More can be found for example in the Wikipedia article on skin.
Epidermis: Top layer of our skin, is covered with the stratum corneum, which consists of several layers of dead cells, which protect the layers below. New cells of the epidermis are made at the border between dermis and epidermis and travel upwards (actually the top layers are worn off). The epidermis is the place where the pigmentation takes place due to melanocytes embedded in the keratinocytes of the epidermis.
Dermis: The next layer is the dermis where a lot of important functions on the skin happen. Sweat and oil are produced in the dermis. The feeling of the skin is also mediated in the dermis where the ends of the nerves are embedded. The hair roots of the hairs of the skin are also located here as well as the blood capillaries which supply the skin.
Hypodermis or Subcutaneous fat: The last layer is the hypodermis. It attaches the dermis to the underlaying muscles and bones and houses bigger blood vessels and nerves which go up into the dermis. The fat layer is also important for controlling the body temperature and storing fat reserves.


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Search engine for biological/medical/epidemiological science literature
I hope this question is appropriate for this exchange (I think it is too specific for meta?).
We are looking for a search engine that is capable of performing a search of all available biological/medical/epidemiological scientific literature (So more on the scope of Google than Elsevier or similar subscription services) and providing as many as possible of the following features:

Keyword search
Range of dates
Boolean terms (AND NOT etc.)
Option to download and sort
Email alerts.

Does anyone know of a search engine or service that has these capabilities? (A paid subscription is fine).
Thank you in advance for your patience.

Yes, this exists. The portal is called "Pubmed" and looks like this:

This portal allows you to search (have a look into the search-Faq) in various ways as well as getting email alerts, download your searches in different formats and so on. It indexes most (but not all) scientific literature for medicine, biosciences and all related topics and is probably the biggest database in this field. And its free.
Another possibility would be Google Scholar, which is focussed on scientific literature and can also be adapted to your personal needs. However, I usually prefer using Pubmed, but sometimes it is useful as well to use Google Scholar.


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Could someone explain the join in the SARS-cov-2 genome at location 13468?
I am having trouble understanding the reference sequence for sars-cov-2, NC_045512.2
Three nucleotides equals one amino acid, right? But the nucleotide at position 13468 seems to be used twice, so the sequence starting at 13463 reads:
tta aac ggg ttt ... which translates to LNGF
However, according to the reference, the translation is LNRV, so it's read as tta aac cgg gtt etc - like the c is repeated.
The reference says "join(266..13468,13468..21555)" but how does this work and why?

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

And if you think that's wierd, the transcriptional phase can get even more so because of the  error-prone RdRP: "For some nsNSV, like those of the Paramyxovirinae subfamily (e.g., measles, mumps, and Sendai virus) and Ebola filovirus, there is also a form of programmed transcriptional frameshifting (PTF). The most egregious example of this is parainfluenza virus type 3 (PIV3), where a stretch of 300-odd nucleotides in the middle of the P gene is translated in all 3 frames." https://rnajournal.cshlp.org/content/21/4/667.full

In the reference genome browser, it seems you are looking at the first Coding Sequence (CDS) line, YP_009724389.1, which shows the translation to LNRV...:

If you look lower down, you'll see a line for CDS YP_009725295.1, which shows translation to LNGF... as you expected.
So, these are two different interpretations of possible translations for this area of the genome.  Why does the first have the weird peptide sequence?  If you hover over the CDS line, the browser will pop up more information about it.  For the top CDS, that includes this comment: "pp1ab; translated by -1 ribosomal frameshift".  This suggests that someone believes that sometimes the ribosome translating the RNA glitches at that point and advances only 2 nucleotides instead of 3 after the "N" codon.  This shifts the interpretation frame as if there were another C present.
If you search for "pp1ab", you'll see it's mentioned in the Feb. Nature article on the sequence.

it seems there is one wiki article per coronavirus secondary structure  https://en.wikipedia.org/wiki/Coronavirus_frameshifting_stimulation_element


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Which is more efficient as a germicide: UVC, Ozone or combination and why?
I've read many contradictory info about ozone vs UVC light irradiation and cannot come to a conclusion, I am totally confused.
As it commonly known UV germicidal irradiation is very effective against bacteria, virus, molds, but in the disadvantages chapter one can read

Another potential danger is the UV production of ozone, which can be harmful to one's health. The US Environmental Protection Agency designated 0.05 parts per million (ppm) of ozone to be a safe level. Lamps designed to release UVC and higher frequencies are doped so that any UV light below 254 nm wavelengths will not be released, to minimize ozone production. A full-spectrum lamp will release all UV wavelengths and produce ozone when UVC hits oxygen (O2) molecules.

OK, ozone is a bad guy which can cause mutations, cardiovascular diseases and other bad things.
But then I read about ozone magic germicide abilities, that it can destroy all types of bacteria, water treatment, air purification and even cleaning of contaminated soils, and maybe even COVID-19.
So why they often advise against ozone?
I've found not so much science researches about comparative efficiency of zone and UVC, for example this which seems very dated (2003), and it says that UV is less costly but not as much universal and effective for water purification as ozone.
This one, more recent, clearly states the idea I also came to:

Vacuum-UV lamps with ozone production were found to be effective for inactivating various human pathogens.

Also I've found many comparative tables like this that confirms better ozone efficiency in all circumstances

We know that UV-lamps with wavelength below 254 nm produces ozone so why not to combine their strengths together?
So where is the truth in all these contradictory sources? How to filter out all those marketing fluff that ozone and UV-lamp sellers put into our ears?
P.S. I saw this question and it covers only part of mine.

Your question contains the word "efficient". The most efficient method is the one with achieves the goal with the minimum of effort or disadvantages. And that totally depends on what you want to do exactly.

If you have a surface like a lab bench, you use ethanol or iso-propanol because its cheap, quick, relatively safe to use for that purpose and dries up quickly without remaining substance.
If you have a cabinet to work with, you use UV irradiation because you can leave it on at night where it does not hurt your eyes/skin and it can pervade the small corners in the cabinet.
If you have a pool, you use ozone or chlorine because you have liquid water here so ethanol does not reach the desired concentration. However UV is also an option, for example for sewage treatment
If you have a small volume of liquid, you can use a microfilter because it's faster than using UV and does not split chemical bonds.
If yo have a living organism, you use antibiotics which are weaker (in comparison to the measures above) and more expensive but you cannot use the other measures because they would kill the organism

So both efficiency and efficacy of desinfection have to be chosen based on the concrete situation. There is not "the most efficient" way of disinfecting.

Yes, efficient for me is the ability to disinfect living quarters with lesser harm for humans

@Suncatcher still depends on the organism. Do you have rodents, parasites, fungus, bacteria, virus?

where? in my body or in the environment? of course they reside in my house. Let's assume the organism is weak


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Human somatic cells have 22 pairs of homologous chromosomes?
I am studying for my Bio class and I am stuck with questions that I came up with during this chapter of Meiosis. I understand that human somatic cell is made up of 22 pairs of autosomes and 1 pair of sex chromosome. I am confused about what made up each pair of autosomes? is that 1 chromosome from the father and 1 chromosome from mother made up 1 pair of autosomes in somatic cells? and therefore, since each pair of autosomes consisted of 1 chromosome from dad and 1 from mom, we can say human somatic cells consisted of 22 pairs of homologous chromosomes (not to mention the sex of the human), right?

@PolypipeWrangler 22.5?!  You can't have half a homologous pair.  But I get what you're trying to say and it's true... There are 22 homologous pairs and half the time there is a homologous XX pair.  The other half the time there's a heterologous XY pair, though even portions of those chromosomes are homologous...

Got it! thank you so much for the clarification!

Answer: *Yes  , human somatic cells have 22 pairs of homologous chromosomes
The human genome consists of 46 (2n*(22+1) ) chromosomes.
Most of our cells are somatic and diploid (2n), they have two homolgous chromosoms (called homologs, one "father" & "mother") these cells multiply by mitosis.
Reproductiv cells or gonosomal cells, (gametes; Sperm and eggcell(ovum)) are the product of meiosis ( a part of gametogenesis ) . These cells are haploid (1n), they only have one set of chromosomes (1n * (22+1)) which is a combination of "fater&mother". When 2 gametes  combine a diploid zygote is formed.
In both cases (Mei- and Mitosis) chromosome (pair (2n)oder single(1n)) number 1 -22 are called autosome , while
Chormosome number 23 is an allosome (sex chromosome), either Y (male) or X (female).
Since the gametes are haploid (1n) they have only 1 single allosome, egg cell always X , and  sperm cell either X or Y.
If the allosome (the 23 chormosome pair) of an human is hemizygot ( X–Y ), he is genetically male. Is the allosome pair X-X
,homozygot the person is genetically female.
Somatic cells can have therefore 22  pairs of homologous chromosomes the 22 autosomes. The allosome pair of chromosomes is not considert homologous but either "homozygot / homogametic"[XX] or "hemizygot/ hemigametic"[XY].


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What are these structures in blood from a nosebleed?
I decided to look at some blood from a nosebleed (not mine) under the microscope and took some pictures of the results. There many large orange structures interspersed within the blood cells and I'm wondering if someone knowledgeable can tell me what they are? Are they skin cells? What are the fibres inside them?

The first two images are x400 and second one is x100.

Could you estimate the diameter?

In the first picture it is roughly 100 microns if I use the RBC as a unit of measurement.

This is a mere guess: You see accumulations of airborne fibers (dust) that got caught by secreted lipid droplets within your nose.

This is rather old, but these are almost certainly dried droplets of blood that are on the outside of the slide/coverslip or possibly bubbles within the slide that have dried out internally due to heat exposure from the lamp. The patterns on the inside are crystalline deposits of salts from the plasma in the blood.
The reason I say that these are bubbles or droplets is that they are far too big to come from blood itself and have a halo around the outside. This is a diffraction pattern caused by interaction of the light with the surface of the bubble or droplet. They are also out of the plane of focus (compare to the RBCs), which makes them most likely on the outside or to be large bubbles between the coverslip and slide.  The rounded shape is exactly what bubbles or droplets look like under a microscope.
The comments mention that they could be part of something external from the nose itself (e.g. dust), but they aren't a biological structure - they are mostly too big and too inconsistent in shape or size to be an organism and the internal structures lack any consistency too. Dust is a possibility, but I would be very surprised to find dust at this concentration in a nosebleed sample unless sampled immediately after it starts in a very dusty environment. They could just be dust naturally accumulated on the slide/coverslip, but dust is normally clearish fibers or dark black spots in my experience.


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Does Tryptic Soy Agar (TSA) contain L-cysteine? (Question about Legionella)
I ask because Legionella sp. requires the presence of cysteine. If TSA does contain L-cysteine, is it sufficient to grow Legionella?

Legionella also requires other nutrients. Our general recipe includes ACES, Bacto Agar, Charcoal, Yeast extract, L-cysteine, ferric pyrophosphate, potassium hydroxide to make BCYE agar which is used to grow legionella.


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Why would a mammalian vector plasmid require an antibacterial resistance gene?
I have been trying to understand the composition of plasmids used in recombinant DNA cloning, such as this: https://www.genecopoeia.com/wp-content/uploads/2020/02/pReceiver-M35-051818.pdf
and I am wondering what purpose the ampicillin resistance gene has when transfected into a mammalian cell host (as it says it is for).
I understand that ampicillin resistance is used for selection in bacterial cells so that only transformed bacteria are grown as well as ampicillin being needed to prevent bacterial contamination among a mammalian cell culture, but I don't see why mammalian cells require a resistance gene to an antibiotic.
Thanks

It may help for you to look into how such plasmids are generally constructed, to understand why there is ampR. https://www.ncbi.nlm.nih.gov/books/NBK21498/

I think the assumption you are making is that the ampicillin resistance gene would save a purpose in the mammalian cells.
It does not.
As you said, it is only use during the cloning process to select the bacteria to replicate and produce more of it.
There is a resistance gene on the vector you posted which affect mammalian cells: neomycin. In this case, once transfected into mammalian cells, you could select only the cells with the plasmid by adding neomycin the cell culture medium.
Note: neomycin selection can take some time (4-5 days) and higher dose than for example puromycin. Hope this helps!


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Do we know if dogs are asymptomatic transmiters of sars-cov-2?
Dogs do not use mask when going for a walk nor they observe the security distance. On the contrary, they frequently join their noses, and put their noses where other dogs had put them before or had urinated. So, as they are our pets, it is important to know if they can be asymptomatic transmiters of sars-cov-2. Do we know it? At least, have we tested asymtomatic pets of people infected with sars-cov-2?

Related, and easier to check: do we know if some data associated to sars-cov-2 is higher among people with dogs at home?

It is the opposite, if the human is not infected then the probability that the pet (cat or dog) is positive is very low. To prove the infection they check that the animal is positive for > 4 days, because they are asymptomatic. If they'd find high viral load they would tell it (ie. very low viral load thus animals pets are not contagious). In contrary minks had symptoms and contaminated each other, same for a few tigers.

It may be too early to tell.
Testing of dogs in Wuhan found no infected dogs
"487 dogs including 90 beagle dogs, 147 pet dogs and 250 street dogs during the outbreak of SARS‐CoV‐2 were also tested serological negative."
from https://onlinelibrary.wiley.com/doi/full/10.1111/tbed.13577
This article mentions deliberate infection of five dogs. on this very small sample they suggest that dogs are not likely to become carriers.
"Coronavirus can infect cats - dogs, not so much."
https://www.nature.com/articles/d41586-020-00984-8
found by searching "dog" on LitCovid at https://www.ncbi.nlm.nih.gov/research/coronavirus/

I am assembling sources there https://biology.stackexchange.com/questions/92436/what-are-the-implications-of-tigers-being-susceptible-to-covid-19/92458#92458

I saw your sources too late. LitCovid is a great collection of papers too.


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

Your assumption that the mutations that occur during life are somehow beneficial and help us respond to ageing has no basis in fact. If you think otherwise please provide a source with evidence in support.

I'm voting to close this question as off-topic because it is based on a false assumption.

It is good thinking you're doing here!
Only mutations happening in the germ line can be passed on
Mutations that happen in an individual hand (or any other soma line) will not be passed on the the offspring. Only those happening in the soma line can.
Mutations are random
What I mean here is that it is not because someone is old that all of sudden the mutations that would happen in this person would be beneficial for old people.
Age dependent "quality" of genome being passed on
You are asking

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

You seem to misunderstand how natural selection works. An individual alone does not get selected over its lifetime to become better (at least not in the sense of what is meant by "natural selection"). You need a population for selection to happen.
In the females as the pool of ovules is being set early in life. In males the spermatozoids keep replicating during the whole lifetime of the individual. Hence, in males, but not in females, the number of new mutations being passed on to their offspring should increase with age and it does.
In humans the mother transmit on average 15 new mutations and the father transmit on average $25+2(g−20)$ new mutations, where $g$ is the age of the father (Cochrane and Harpending, 2013; this approximation holds only for men older than 20 years of course).
As the vast majority of mutations are neutral or deleterious, the "quality" of the genome being passed on should decrease with age unlike you expected.
Efficiency of selection decreases with age
The fact that after a given age, one does not reproduce anymore (among mammals, this is particularly true for women) does affect the selection pressures on the genetic variants that affect age specific fitness. e.g. A mutation that will reduce health at young age will be quite strongly selected against while a mutation that affect health at old will not.
When talking about this discrepancy between selection pressures at different ages, the concept of antagonist pleiotropy often comes into the discussion. Pleiotropy is the phenomenon where one locus affect several traits.
The idea of age-specific antagonist pleiotropy is that a mutation that will increase health at a young age by a factor $s$ but decrease it at an old age by the same factor $s$ will be selected for. Such process can cause a population to evolve toward lower lifespan. The antagonistic pleiotropy hypothesis is one of the most important hypothesis that we have for the evolution of senescence.
Evolution of senescence
You might want to have a look at the posts:

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


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How Does the Body Know a Finger is Fully developed?
When a baby is being developed inside the womb,
1) how does the baby's body know a finger, or any other part of the body, has been fully developed?
2) following question, how does it "stop" the development of that part? What kind of signals are being communicated here?
3) I have hairy arms. The length of the hair is almost the same length if i don't cut it. If it breaks, it grows back almost the same length. How does the body know the current length and how to stop when it reaches the "target length"? Is it the same "procedure" as the development of parts inside the womb?

Welcome to Biology.SE. The two first questions are related, the third question is quite different. Please always narrow down your post to a single question. Also, the first two questions are in themselves already quite broad. You might want to read a  bit more about developmental biology

For the third question, you might want to read related posts; Why does hair grow after trimming but remains at a constant length after a while? and Why can hair grow without limit while eyebrow cannot?

I am interested in the "communication part". I chose hair as an example because it regrows. I could have chosen anything that regenerates to the original shape in the body.

Is there a common "algorithm" the body follow for development and regeneration or is there different once for every scenario?

Yes but the case of hair is very different that the case of finger development.

Fair enough. The hair is a bad example,

Yes, there is some kind of "algorithm". Describing this "algorithm" would require writing a whole book. And in fact many people have been writing books on the development of organisms. This is why the question is too broad in my opinion. Your question sounds to me like the question "Can you explain to me how biology works?" might sound to you.

So Developmental Biology is the door for my question, yes?

Yes, it is! If you are interested in following a class, you can for example consider this MIT intro class. More introductory and less complete, there is also this Khan academy series of videos. Note: I have not attended any of these two classes, I just googled them so I can't comment on their quality but MIT classes tend to be pretty good. You could open a new post to ask for good ressources in developmental biology if you want to. Good luck!

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Have a nice stay!


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Psychrotrophic Bacteria
I want to know what gene or protein makes bacteria psychrotrophic, as opposed to regular bacteria that prefers warmer conditions. If you don’t know exactly, and you have suggestions as to where I can find the name of the gene, that would be great. I would also need the gene to be accessible so if anyone knows anything, please let me know. Thank you!

what is broader problem you are trying to solve? In other words, what do you want to achieve with this information? If you edit your question, adding these details, it might greatly help

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Also, what did you try in order to find the information you need? Can you give some example of psychrotrophic bacteria?


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Would preserving your Eyes from Light keep them healhty?
I read about why eyesight diminishes with age.
I am aware of the fact that there are different causes that can affect the quality of image received by our eyes and that being vague would not lead to a clear answer, but I will try to make it as clear as possible.
I am wondering if worsening of the ciliary muscle is affected by how much light the eye receives or at least how much we use it.
There might be other areas affected by high light intake. Because the title of the question might not be clear enough: I basically mean the following:
Is our eyesight determined to worsen with age or does it depend on how the eyes are "used"?


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I'm trying to identify this salamander-looking creature I found in my house today in Coos Bay, Oregon. It is about 2" long. What is it?

This is about 2" long. It is white on its underside and looks like a small salamander, except for it being white underneath. It is about 1/8th inch wide.

Search for  Larch Mountain salamander Plethodon larselli images; some I found look similar but this is very rare endangered species and Coos Bay is a bit south of the reported range (Columbia river gorge and north) and it's mainly a mountain species.  Size is right, color approximately right.

The body form looks more like a skink than a salamander. Close to a 5-lined skink (https://www.wildlifedepartment.com/wildlifemgmt/swg/t35p1/WMA/E_fasciatus_AT.shtml) but those aren't native to OR>

@kmm I think you may be correct, looks like there are scales which aren't present in a salamander (and apparently salamanders usually have 4 front digits).  Searching for images of lizards/skinks for CA/OR/WA doesn't turn anything up, and each state has high quality web sites for herps.  Maybe it's a juvenile form that is not well documented?

That is definitely a lizard, not a salamander. Salamanders don't have scales. It is a Northern Alligator lizard, Elgaria coerulea, in the family Anguidae.
https://www.inaturalist.org/check_lists/9307-Reptiles-of-Oregon
https://en.wikipedia.org/wiki/Northern_alligator_lizard

Is that typical coloration for the juvenile form?


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how food moves in horizontal coils of small intestines
This is a very very basic question, and I am looking at it more from point of view of physics. The small intestine is a highly coiled structure, which means it has horizontal coils as well. I can understand the vertical downward movement of food (when the person is in standing position) due to gravity, but how come the food can move in horizontal direction?
Any insights will be highly appreciated.
Thanks

Food moves thanks to Peristalsis through whole gastrointestinal system

@Mithoron closely related (and the answer is the same), but not a dup--this question asks specifically about the small intestine, whereas the other asks about swallowing

Food moved against gravity too, thanks to peristalsis.

@Luigi if another post has the same answer then this can be considered a duplicate. Note that duplicate doesn't mean a bad question; It just reduces redundancy of posts.


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Do cell membranes have more phospholipids in one layer than in the other?
Assuming the cell membrane to have a spherical shape, geometry tells us that the area of the inner leaflet is smaller than the area of the outer due to the difference in radius between them. Does this mean that the inner layer has fewer phosholipids? And, if so, how does it affect the fluidity relation between the layers?

The protein content and lipid type in each layer is likely to have a bigger impact on the number of phospholipids than anything.

Yes there is a difference in the number of phospholipid molecules because of the curvature. This is very evident when there is a lot of bending as in case of exocytosis (see here) but otherwise I do not think there would be an enormous difference in the number of phospholipids between inner and outer surface of the bilayer.
Assumptions:

Cell is spherical
Cell diameter = 1µm (overall)
Thickness of bilayer = 6nm
Width of a phospholipid molecule = 1nm

Difference in circumference of outer and inner layers = 2π(6nm) ≅ 37.7nm
So approximately 37 more phospholipid molecules in the outer layer in this cross section of the cell. This is just 0.6% of total number of phospholipids in the outer membrane.
I don't think fluidity will be compromised because of this - only if a layer is overpacked will the fluidity be affected.

Don't you have to look at the total area instead of the radius?

@MarchHo yeah.. I have to calcuate total area instead of circumference.. just a simplification. I should mention cross section.

These assumptions are sensible for vesicles, but I'm not sure if they translate well to cells. Have you any evidence that this is true for cells rather than vesicles?

@GoodGravy I guess cell is nothing but a huge vesicle. But I did say that this will matter the most in case of vesicles. Yes I agree that there are membrane proteins and cellular shape is not uniform. I can only extrapolate based on these assumptions. I don't think there are any studies for whole cell.


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Do our ears or brains gradually adapt to noise pollution?
Having lived in various places all over the world for the past 9 years of my life, one thing stood out to me throughout this time, and now in particular. From a quiet place on the countryside in Sweden, I moved to Manchester for my studies. When I first arrived there, I felt the city was very noisy, a feeling which gradually reduced as I presumably got used to the noise levels there. From Manchester I moved over to Saitama in Japan, an enormous city right next to Tokyo with a considerable amount of noise during the day, and buildings that have little to no sound insulation. With the exception of particularly loud noises, I again adapted to the sound levels in the country, which at the time, I felt was no more than a natural response in terms of how much attention we pay to the noise. If I'm distracted by work or other activities, I have little reason to dwell on the sounds of driving cars and talking people.
The thing I couldn't explain purely by the 'paying attention' argument however was when I moved back to the Netherlands, to an apartment with excellent sound insulation. My apartment is located in front of a somewhat larger road, and cars pass by almost consistently. However, when I moved in I could barely hear these cars driving past, something that stood out to me as fairly pleasant. I thought a little bit of ambient music would kill the sound of these vehicles driving past altogether.
Now skip ahead one month, and I can hear the cars almost as if I'm standing next to them, an exaggeration of course, but the sound is much clearer than it was when I moved in. I know that nothing has changed in terms of insulation and I know that no windows are open. Strangely the only thing that appears to have changed is the clarity in which I perceive this noise, as none of the other people whom I've asked seem to share the same opinion (that is, that the noise has grown louder). This made me wonder - does our hearing adapt to noise pollution, and if so, how does it work?

This is a fascinating case of sensory adaptation and neural adaptation. Another example of this would be when you stop smelling something after being exposed to it for long periods of time (as you probably know, this "long period of time" happens to only be a few minutes). A great representation of this happening with the nerves in the skin was done by Georg Meissner:

This image is from https://www.boundless.com/psychology/textbooks/boundless-psychology-textbook/sensation-and-perception-5/sensation-37/sensory-adaptation-160-12695/
When stimulus is applied, these nerves begin rapidly sending messages to the brain in the alarm period. The rate of these signals slowly start to decrease over time in the resistance period until they finally reach exhaustion and stop completely in, of course, the exhaustion period. Keep in mind that the time it takes for all this to happen varies greatly upon what type of cell it is (obviously olfactory cells have a much shorter exhaustion time than, say, hair cells (hearing cells)). After these cells have had a chance to recover (more like recalibrate actually), we can begin to hear/smell/feel/taste again.
I hope this helps.

Are the signals from the nerves themselves no longer being sent, or is the brain just choosing not to pay much attention to them?

In most cases it is the original nerve that sent the message that becomes exhausted (sensory adaptation) and no longer sends the message (or at least the message becomes so weak that the brain hardly notices it).

Very quickly and totally from the top of my head: Traffic noise is in many cases dominated by low frequencies, with the whole spectrum somewhat similar to a distorted 1/f function, with a few tonal peaks for exhaust noise and tyre/tread sounds. Now add the structure you are living in: "excellent sound insulation" in the EU is (still) dB(A)-focused, meaning architects and planners are aiming for a "wow" effect in noise reduction by eliminating that what's easy to eliminate - high and mid frequencies, ignoring mostly the low (and energy-rich) frequencies, which are incidentally the ones the A-weighing of noise is (historically) ignoring as well. As a result, you are basically living in what's known as a low-pass filter, one that is also "drawing" tonal peaks (resonances, room nodes) out of that low-frequency noise mixture. At first, your cochlea's short-term adaption mechanisms will do their job well and tone down signals that are not meaningful (MOC reflex).
Over time however, the presence of low-level tonal, continuous sounds can damage ("wear out") a specific sensor type necessary for this reflex to work. As a result, even inaudible LFN noise can, over time, lead to a distal sensitization effect. In many cases the culprit is actually not the traffic noise itself, but HVAC installations like heat pumps, A/Cs and gas turbines. The effect of "I can hear too much" (being aware of noises) as a result of sub-threshold LFN-exposure is known in the medical literature as a symptom of VAD stage I / II and in fact quite common in the urban population. Certain medications (Gentamycine, cis-platines) as well as organic solvents (acetone) and some disinfectants can speed up this process, which is non-reversible and poses a risk factor for suffering atypical (early onset) hearing loss later on... The "I hear too much" effect has been quite a solid indicator of long-term, low-level IS/LFN noise pollution.
To be on the safe side and to rule out a sub-threshold LFN-problem, you should an seek medical advice.
Sources:
Bakay, W.M.H., Anderson, L.A., Garcia-Lazaro, J.A., McAlpine, D. and Schaette, R., 2018. Hidden hearing loss selectively impairs neural adaptation to loud sound environments. Nature communications, 9(1), p.4298.
Branco, N., 2005. Clinical stages of vibroacoustic disease (VAD) for health professional continuous research. Mat. 12th int. sym. Lisbon, p.145.
Burt, T., 1996. Sick building syndrome: acoustic aspects. Indoor and Built Environment, 5(1), pp.44-59.
Ebner, F., Eulitz, C. and Möhler, U., Approaches for a comprehensive determination and assessment of infrasound effects in Germany. DAGA 2013 Conference Paper.
Findeis, H. and Peters, E., 2004. Disturbing effects of low frequency sound immissions and vibrations in residential buildings. Noise and Health, 6(23), p.29.
Kugler, K., Wiegrebe, L., Grothe, B., Kössl, M., Gürkov, R., Krause, E. and Drexl, M., 2014. Low-frequency sound affects active micromechanics in the human inner ear. Royal Society Open Science, 1(2), p.140166.
Paulin J, Andersson L, Nordin S. Characteristics of hyperacusis in the general population. Noise Health 2016;18:178-84
Waye, K.P., Clow, A., Edwards, S., Hucklebridge, F. and Rylander, R., 2003. Effects of nighttime low frequency noise on the cortisol response to awakening and subjective sleep quality. Life sciences, 72(8), pp.863-875.

I removed the medical advice and inserted a referral to an expert.

Maybe keep the referral to a certified acoustician as they will have the means to validate/rule out sub-threshold IS/LFN-immissions, whereas a ENT doctor will only see the effects (symptoms) which could also be the result of extended exposure to ototoxic substances like you would find them in nail polish remover...


text:
Examples of extant animals in a submature morphologically unstable evolutionary state?
I'm fascinated by evolutionary theory and the predictive aspect of it-the notion of an animal entering a strongly divergent state of evolution whereby it is evolving into a new form yet remains suboptimal, and is therefore undergoing rapid morphological change, and the idea that this allows us to project onto possible new variants of life.
To give a past example, the praying mantis is believed to have split from the cockroach around 250M years ago. During this period the mantis developed its upright stance, large range of vision and pronounced raptorial claws, and has seemingly stabilised into this optimal new form over the past 50M+ years.
The interesting thing is that this change could actually have been predicted by analysis of the animals evolutionary history, niche and further available advantageous adaptive forms.
Can someone give a good example of a current animal in this volatile state that we could make accurate projections for?
And please, no trivial answers like "everything is constantly in a state of evolution", I already know that and thats not I'm referring to.

Can you document the praying mantis example?

Theories based on a the discovery of a cockroach with nascent mantid features-Raphidiomimula burmitica. Though its really just an example...

Though I know a fair bit about evolutionary biology, I have no idea what you are talking about in the title when you write "submature morphologically unstable evolutionary state". Where does this language come from? It doesn't sound like anything I've ever read in the literature. Nor do I find it plausible that "The interesting thing is that this change could actually have been predicted by analysis of the animals evolutionary history, niche and further available advantageous adaptive forms." Which scientists argue this, in what papers?

I mean essentially an organism in a volatile state of evolution. The opposite of say, a shark or crocodile that has remained morphologically and behaviourally similar for millions of years.

Another example I can give you is that of early cetaceans as they colonised water. When assuming a fully aquatic future existence it would be easy to imagine hairless creatures with narrow streamlined jaws, and flippers, though these optimal forms would not be realised for many millions of years. That is a an example of a "submature" morphology. I'm interested in contemporary animals that we could make similar predictors for to some degree of probability.

Not sure exactly what you're looking for, but maybe the Giant Panda is of interest to you. The Giant Panda is an herbivore, but it has evolved from a meat-eating animal (the most recent common ancestor of Pandas and the other bears). It made the switch from omnivore to herbivore just ~2 MYA. According to wikipedia, pandas still have the digestive system of a carnivore. They can still eat meat and do not actually get much protein/energy from bamboo. Thus, you could consider them to be in a state of evolving from an omnivore into a more efficient herbivore


text:
Home bacteria culture at home?
Can simple bacterial culture be done at home using food agar as the medium (with some additives found in the store)?

what exactly are you trying to achieve?


text:
Gene expression: which allele is considered?
For human beings, we have two copies of each gene inherited from the parents. The question is, when referring to gene expression, which copy (or allele) is considered?

Could you explain what you mean by "when referring to gene expression". Do you mean in general conversation, in anlysing the results of an RNAseq experiment, or are you asking whether expression occurs on both alleles? At the moment this is quite unclear. You need to edit your question to make it more precise what you are after.

Genome assemblies usually feature a haploid set of genes, unless particular effort is applied to assemble separately the homeologs. With that said, the gene copy you have in the assembly is usually one of the two, and usually the one you had more genomic reads for.
In terms of gene expression, if you measure it by RNASeq you will get reads from both and both of the read pools will map on the same gene. The ones that come directly from it will map with no mismatches (ideally) and the ones that come from the homeolog chromosome will map with a few mismatches (probably).
The expression of the "gene" will therefore be the expression of both genes, summed together. If we consider it as the same gene, though, it doesn't really make a difference if you sum them up or count them twice separately; unless we are talking about specific homeolog silencing like the Xist mechanism, in which it is important to remember that one copy of the two is off.


text:
Are unsaturated fats antioxidants?
Unsaturated fats contain double bonds like carotenoids (which is an antioxidant), and from my understanding, what makes carotenoid an antioxidant is that its double bonds allow it to undergo oxidation, hence they can donate electrons to free radicals. Therefore, would this suggest unsaturated fats (especially those with more double bonds) are also antioxidants?


text:
Why is gel used in electrophoresis?
In analysing amino acids content in a protein through gel electrophoresis, What's the purpose of the gel? Wouldn't putting the amino acid in the gel prohibit the amino acid from dissolving into the buffer solution (which its pH controls the protonation and de-protonation of the amino acid)?

Just to be sure: You ask why the gel matrix is used to analyse proteins?

What research have you done to answer this question yourself? A Google search for gel electrophoresis of amino acids will give ample results. But your question is based on a complete misapprehension about the physical nature of the system. The gel is an inert and insoluble matrix which the buffer and amino acid solution permeates.

In gel electrophoresis, the gel is the mechanism by which macromolecules of different sizes are separated. By loading the gel with amino acids (or proteins or DNA), you start all of the samples equally, and then push them through a gel using a salty buffer solution that is electrified.
The gel has a certain concentration of a polymer (commonly agarose or polyacrylamide) that acts as a mesh that slows your macromolecules down. So, after running a gel for a certain amount of time, molecules of different sizes will have traveled different distances. This can be visualized by different methods (ethidium bromide for DNA and antibodies for proteins, commonly) after further preparation.
So, the amino acids in question should not be dissolved in buffer, as this would result in loss of sample.
Edit:
Regarding the last point: when loading samples on a gel, they must first be dissolved in some loading buffer that will help the sample settle into the well and not diffuse out. I took your mention of "buffer" in the original question to be the running buffer for electrophoresis, which you should not dissolve your sample in. I am also unfamiliar with analyzing amino acids by electrophoresis, and I do not know if there is a specialized loading buffer that kind of analysis would require. A quick look didn't uncover anything, but you might be in a better position to answer the loading buffer issue.

I'll take this point by point: i) thanks for pointing that out, it's been a couple of years since I've had to think about conformational changes during electrophoresis. ii) Antibody staining would indeed require a Western, I should have been more precise there. iii) My last sentence was an attempt to tie the answer back to OP's question, where they were assuming that the amino acids should be dissolved in buffer. I assumed they meant the running buffer for the electrophoresis process, but they could easily be referring to loading buffer, too. I'll edit my answer to reflect this.


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Is a fatty acid a polymer?
From my understanding, polymers are long chain molecules containing repeating units of monomers.
For example, proteins are polymers called polypeptides with repeating units of (different) amino acids. Therefore, a fatty acid, saturated or unsaturated, would classify as a polymer as they are long chain molecules with repeating units of alkyl monomers?

You are wasting your energy on a semantic question of no biological importance or interest . This is not unusual for people with chemical backgrounds. For the record you will seldom read the word polymer in biochemistry books. But if you know the structure of these molecules that is sufficient — focus on what the functions of these molecules are and how it relates to structure.

From a chemistry perspective they would be considered oligomers rather than polymers, since they generally have quite a short and specific length. (P.S. don't let anyone tell you that chemistry is not important in biology, nor that nomenclature is not important in chemistry!)

In the IUPAC Gold Book, IUPAC defines a polymer as follows:

A molecule of high relative molecular mass, the structure of which essentially comprises the multiple repetition of units derived, actually or conceptually, from molecules of low relative molecular mass

Fatty acids are relatively high in molecular mass compared to the monomer (which is essentially a carbon atom), although they're quite low in mass compared to all other biological polymers. Since we consider proteins polypeptides, as you rightly note, the monomers clearly don't have to be chemically identical, so the variations around a simple carbon that are present in various fatty acids should be fine.
The definition states nothing regarding typical numbers of repetitions or minimal numbers of repetition.
The IUPAC definition also mentions that for most (but not all) polymers, the specific number of repetition has little impact on the molecular properties of the polymer. Fatty acids do generally work more or less the same regardless of their specific length.
Sounds like fatty acids are carbon polymers to me, even if indeed we don't usually think of them like that.

The monomer for fatty acids is ethane, not methane.  Most of the biochemical reactions that handle fatty acids work on pairs of carbon atoms.

It is interesting that polyketides have a similar biosythetic pathway (and the enzyme complexes too) as fatty acids but the former are still labelled if not considered as polymers but not the latter.

Fatty acids are usually not considered polymers.
From a biological viewpoint this is simply because there is only a very limited set of chain lengths that exists in nature (~2-20 or so) and also even numbered chains are much more common than uneven numbered ones. In contrast to this 'true' polymers can have an arbitrary length of chain length (of course there is still a limit in biology, but not a super strict one) and no specific lengths are favoured.
From a chemical viewpoint fatty acids are also not really a polymer: you can't just take a bunch of alkyl monomers and fuse them to one long fatty acid  chain, because simple alkyl monomers don't have chemical groups that allow this reaction to take place (making C-C bonds is chemically not the easiest thing to do).

I'm not sure about your last paragraph; after all, the same could be said of polyethylene, which is certainly a polymer. (The name "polyethylene" is a hint to how it's made, but its actual structure is just a long chain of single-bonded carbon atoms with hydrogen atoms attached where appropriate.)

@ruakh : That reaction takes places at high pressure and temperature.

I've never heard of anyone consider fatty acid to be a polymer.
I'm not a biologist, but all of my research is on polymers-specifically paints and coatings.  Fatty acids are often used in the coatings industry as one of the building blocks to make an alkyd coating.  In my eyes, fatty acids would be seen more as a monomer or oligomer.  Like you've observed, fatty acids do have repeat units; but many would opt to use other words to describe the molecule


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Why is there a layer of moist lining the inner walls of alveoli?
I'm taught that the walls of the alveoli are moist, so gaseous oxygen molecules can dissolve into this water. This then allows the dissolved oxygen (liquid state) to diffuse faster from the alveoli into the bloodstream through the basement membrane.
However, why is it faster for gaseous oxygen to first dissolve in water (transitioning into liquid state) then diffuse through the basement membrane and dissolve into the blood stream than for gaseous oxygen to directly diffuse through the basement membrane and then dissolving into the blood stream?
The second mechanism would eliminate the need for the moist layer lining the alveoli wall.
Is there some physical or chemical explanations to this phenomenon?

The fluid in the alveoli contains phospholipoproteins that act as pulmonary surfactant, which keeps the alveoli open during breathing.


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Why is xylem a tissue and not an organ?
My textbook "CGP AS-Level Biology Exam Board: Edexcel Complete Revision & Practice" says xylem is a tissue.
Then I read from this website that "[Xylem's] major components include xylem parenchyma, xylem fibers, tracheids, and xylem vessels." Therefore, from my understanding, xylem is made up of multiple tissues including xylem parenchyma tissues, xylem vessel tissues and etc to carry out the functions of transporting water and nutrients in plants? Therefore that would make xylem an organ instead of a tissue?

In plants, there are three types of tissue: meristematic, simple, and complex.
Meristematic (embryonic and totipotent)
Simple (composed of only one type of cell), such as

parenchyma
collenchyma
sclerenchyma

Complex (composed of more than one type of cell), such as

dermal (protective covering)
vascular (conducting tissue)
xylem (conducts water and dissolved minerals)
phloem (conducts water and dissolved organics)
ground (bulk of the body; primarily parenchyma, collenchyma &
sclerenchyma)

With this information in mind, let's take a look at what the source you provided says that makes up Xylem tissue.

"[Xylem's] major components include xylem parenchyma, xylem fibers, tracheids, and xylem vessels

Here are the roles of said cells in Xylem:

Xylem parenchyma are cells specific to storage and short distance transport.
Sclerenchyma Cells (xylem fibers) are specific to support and protection.
Vessel Members (which are conducting cells) are specific to water, mineral transport, and support mostly in advanced angiosperms.
Tracheids (which are also conducting cells) are specific to water, mineral transport, and support mostly in gymnosperms and lower angiosperms.

I hope this information helped you understand why Xylem is not an organ, but rather a complex tissue of plant.
References:
http://facweb.furman.edu/~lthompson/bgy34/plantanatomy/plant_cells.htm
http://www.bio.miami.edu/dana/226/226F09_5.html

Thank you very much for the detailed answer. May I then ask what is the fine line that distinguishes complex tissue and organ? (i.e. at what point can we say something is an organ and not a complex tissue?)

Ok, so just disregard the accessory word 'complex' for a moment and think about just tissue. A tissue is the combination of cells. Xylem is made up of a collective of specialized cells in order to perform its tasks. An organ is made up of a collective of tissues. The reason xylem is a complex tissue is because different cells make it up, whereas in a simple tissue is made up of the same cells. Hope this helped!

Thanks again. But I'm still not sure at what point can we say something is an organ and not a tissue. In the case of xylem, your argument is that it is a tissue since it is made up of different cells to perform its tasks. But can't I also say, xylem is made up of different tissues to perform its task e.g. xylem parenchyma tissue, sclerenchyma tissue, vessel members tissue and tracheids tissue - since tissue is simply a combination of cells. Thereby, making xylem an organ?


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No genes' ID in peak annotations during ChiP-Seq with ChIPpeakAnno R package
I am trying to perfom Chip-Seq Analysis which is greatly described in that conversation: introduction to Chip Seq . The same as autor of mentioned question I am a student of Applied Mathematics and I am doing my best to enter bioinformatics fields.
I am basically at the moment where I would like to annotate peaks with genes' IDs. To do this I am using ChIPpeakAnno R package from Bioconductor. I used below  code to annotate my reads (outputs from MACS) with genes' ID's
> library(ChIPpeakAnno)
> # data(package = "ChIPpeakAnno")$results[,3]
> macsOutput <- toGRanges(data="example_peaks.bed",
+                                               format = "MACS")

> data(TSS.human.GRCh37)
> macs.anno <- annotatePeakInBatch(macsOutput,
+                                                                AnnotationData=TSS.human.GRCh37,
+                                                                output="overlapping", maxgap=5000L)
> library(org.Hs.eg.db)
> macs.anno <- addGeneIDs(annotatedPeak=macs.anno,
+                                               orgAnn="org.Hs.eg.db",
+                                               IDs2Add="symbol")
>
> # no annotations for some genes
> as.character(head(as.data.frame(macs.anno)$symbol))
[1] "PTCHD2" "PTCHD2" "PTGER3" NA       "HFM1"   NA

but there occures that there are no genes' annotations for some peaks. Can anyone tell me why this might happen? And how to avoid this? Does this refer to the maxgap=5000L parameter? When creating output from MACS I set a parameter for length to be 10 000.

I had the same problem.
This how I solved it, I found the solution somewhere here, I don't remember where, and it worked for me.
macs.anno <- annotatePeakInBatch(gr_broadPeak, AnnotationData=TSS.human.GRCh38,
                                     output="both", maxgap=5000L)
 macs.annoL=addGeneIDs(macs.anno,"org.Hs.eg.db",c("symbol", "genename","entrez_id"))
 macs.annoDF=as.data.frame(macs.annoL)
   result=macs.annoDF[which(macs.annoDF$symbol!="NA"),]

I'm on vacations.

I'll check your solution soon and then, if it will work, I accept it :)