text:
Could multiplexed CRISPR disable the mitotic and meiotic genes of cancerous cells?
Although I believe there is a good reason -- or reasons -- why this theory, that CRISPR could disable the genes for division in cancerous cells, is incorrect, I haven't been able to find them.
In short, the theory is that multiplexed CRISPR could knock out the genes responsible for cellular division (mitotic and meiotic genes) and thereby prevent the uncontrolled division of the cancer cells.
I understand that off-site edits, multiple mitotic and meiotic pathways, and the resiliency of cancer are difficulties, but in theory the idea makes sense.
Obviously, if the theory would work, probably someone would have done it already, so there must be a good reason why this won't work. Please could someone explain it to me? Please let me express my gratitude for your consideration in advance!

As with all cancer therapeutics one of the biggest problems is how you get the therapeutic to kill cancer cells without also killing so many healthy cells that the therapy kills the patient.
For CRISPR to work you have to get the CRISPR components into the target cells. Right now this is done using relatively harmless viruses like adenoviruses. The viruses "smuggle" the CRISPR components into the cells as they infect them. Nanoparticle containers are being researched as an alternative to viruses. The problem with your proposed therapy is that there is no way to target the viruses only at the cancer cells. You'd end up shutting down the cell division genes in healthy tissues too. Turning off cell division of a bunch of your healthy tissues is likely to kill you. There is also no way to ensure that all of the cancer cells would pick up the CRISPR components. You leave a few cells behind and the cancer quickly comes back.
Currently the most promising CRISPR cancer therapies are aimed at enhancing immune therapies. You take blood/bone marrow from the patient, sort out the immune T-cells, edit their genome using CRISPR to enhance their ability to identify and kill cancer cells, then inject them back into the patient. The result is hopefully a robust, ongoing immune attack on the cancer cells.

Thanks for the clear and detailed answer, Charles!

@ColinPace do not forget to upvote answer and accept it - if you like it.

@AlexanderChervov thank you for the note about etiquette. I believe I have already accepted the answer (clicking the green check mark), and I tried to upvote the answer, but I do not yet have enough experience points.

Bezeljak (2022) discusses recent advances in targeting cancerous cells with viral vectors: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8884858/


text:
Whats the difference between the term "open" growth and inderterminate growth in plants?
My textbook has a paragraph whose heading itself is

"Plant Growth Generally is Indeterminate"

and in that paragraph it says

The cells of such meristems
have the capacity to divide and self-perpetuate. The product, however,
soon loses the capacity to divide and such cells make up the plant body.
This form of growth wherein new cells are always being added to the
plant body by the activity of the meristem is called the open form of growth

and thats it! in the entire chapter it doesent bother to speak about these terms....so would be great if anyone helped...

Which text book is this?

I think 'open growth' and 'indeterminate growth' are synonymous in this context. The opposite of 'indeterminate growth' is 'determinate growth'. 'Determinate growth' refers to when a plant ceases growth after reaching a certain size or number of cells, and 'indeterminate growth' is when a plant could continue to grow indefinitely until in runs into resource/space/physiological constraints.

i dont know how to reply to a comment but @-M_ this is a school textbook in India called the NCERT https://ncert.nic.in/textbook/pdf/kebo113.pdf a link to this particular chapter its on 2nd page. and @Eonema thanks for the help

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
Why isn't bacterial colony a monolayer?
I am an engineer entering the field of microbiology. I was watching bacterial colonies (lab strain E. coli to be specific) being grown on agar plates. I was surprised that the bacterial colony was not a monolayer (i.e. a single layer of cells), but a mound with bacteria piled on top of each other (except may be at the edge of the colony). Why doesn't bacteria spread out in a monolayer over the entire agar surface? And, how do bacteria in the pile which are not in direct contact with the agar survive? Is it that nutrients are passed upwards by those cells which are in direct contact with the agar surface?

I like your question. :) You can start by learning about the bacterial extracellular matrix. If you still have a question, or don't understand something you read, edit your question or ask a new one with link and quote. On this site, people need to to show evidence of trying to answer the question when they post. Not doing so is both a down vote reason and a close vote reason (not my rules, just informing you.) We actually like to help people who are willing to learn on their own as well. Good luck in your new endeavors!

@anongoodnurse Thanks for the reference. After reading it I believe that the answer to my question is that only bacteria in direct contact with the agar surface are metabolically active, while those away are inactive (though not dead). This arrangement is necessary to protect the colony from external insults. So, may be under the right conditions you can coax the colony to spread out in a monolayer.

Close! All bacteria produce an extracellular matrix through which nutrients pass. the nutrients in the agar diffuse both passively and actively through the matrix feeding all the cells (within limits, meaning that a colony does not grow indefinitely. The bacteria also share between each other. Some bacteria become specialized, if you will, and unable to form a colony on their own. Having read the paper once (which was not an "easy" paper, nor too technical), try it once more and see if you can get more out of it.

As suggested by your conversation in the comments with anon, the bacterial colony is the outcome of a mechanistic growth model in which nutrient diffusion occurs from below to above.
For an explicit mathematical model of this process (which also incorporates mechanical forces), you can see this paper (Warren et al. 2019). Notably, this mounding occurs even in the absence of an extracellular matrix, and is proposed to be related to cell orientations within the colony. I reproduce Figure 4 which shows some of the relevant results:

The cross-sectional anatomy of a simulated colony.
(A) Snapshot of cross-sectional view of the colony at t=20h
. Cyan represents horizontally oriented cells (≥45o
with z-axis); Yellow represents vertically oriented cells (≤45o
with z-axis). (B) Fraction of vertically oriented cells averaged over z
vs radius. (C) A side view of the azimuthally averaged director field, indicating the orientation of the rod-like cells. (D) A side view of the azimuthally averaged velocity field. (E) Vertical component of velocity, Vz
, at various values of z
along the center of the colony. Increase in vertical speed is seen only for the bottom 10 µm (F) A cross-sectional view of the colony, color representing the time since last division. Purple and blue represent cells that have not divided for the past 10 h, and red represents the actively dividing cells. (G) A cross-sectional view of the local growth rate in the colony, with the color bar showing the values of local growth rate. A disc-shaped 'growth zone' is revealed by the red color at the bottom of the colony.
Other similar models describe "verticalization" of bacterial colonies as an explicitly mechanical process (Beroz et al 2018), without regard for nutrient flow. However, differences in these models lead to qualitatively different results for how tall colonies get.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Open databases for copy number variations similar to TCGA
The Cancer Genome Atlas(TCGA) has open data for copy number variation(CNV) from at least 10k different cancer patients. They offer two types of data, CNV data from tumor and CNV data from normal tissue samples. Is there any other open databases that offer CNV data from at least one cancer type?

The ICGC has CNV data for many different cancer types. It has many both restricted and open data sets. The DCC releases page will let you hunt through them - those that are public are easily downloaded. They also have matched expression, SNV, DNA methylation, and structural mutation data for many samples.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
I read that the average cell will divide between 50-70 times before cell death. How, then, can human cells be constantly dividing?
Aren't those 2 statements contradicting each other?
See https://en.wikipedia.org/wiki/Hayflick_limit and e.g. http://book.bionumbers.org/how-quickly-do-different-cells-in-the-body-replace-themselves/.
Take stomach cells. If they divide every 2-9 days, doesn't that mean the stomach cells will all die in about a year (5 days x 70 division)?

What brings you to the idea that human cells are constantly dividing? And why should this contradict the Hayflick limit?

Clarified question.

Has something to do with progenitors I think? I don't exactly know how stomach cells divide, but I would imagine that there is a lining of undifferentiated cells that consistently differentiate towards the inner lining of the stomach. It's differentiated cells that are constricted to the hayflick limit.

I think your problem might be with a misunderstanding of the meaning of "average".  That doesn't mean that every cell type divides that many times, e.g. neurons seldom if ever divide.

The answer may simply be yes, as the parent cells are dead, but no since the daughter cells are still alive and kicking.

You have to consider telomere length, rate of proliferation and the presence of stem cells.

@Bob that makes sense. Can you write the answer? This brings another question: why is hayflick limit associated with ageing if it doesn't apply to stem/progenitor cells and thus body repair?

@jamesqf I'm not convinced. Average means average - in case of stomach cells, if I randomly pick one stomach cell, on average it will divide in 2-9 days. Some cells (neurons like you mentioned) might be different but most cells do.

@AliceD Are you saying that if I have a cell that can divide 50 times, after 1 division the daughter cell can still divide 50 times, but the parent can only divide 49 times now? That doesn't make sense.

YuZhou, I do not think that I know enough about the subject to formulate a proper answer. But, I think doing some research on what I have commented, and on what @CMosychuk has commented, you will be able to find a reasonable answer to both your first question, and your new question. Maybe afterwards you could share your findings in the form of an answer for anyone else who ever asks a similar question?

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Cell dye in red fluorescence spectrum
There are some cell dyes available for stianing cells intracellularly / membrane. I am aware of other channels (CFSE \ PKH26). But I want to stain cells for flow cytometry with a 'red' dye.
I have looked at a few options from Thermo but did not find sufficient data on either.
Specifically I am planning to stain a single cell population with two different dyes, treat each stained population somewhat different in between, and then culture them together and distinguish read-outs later. Antibody-staining for a surface marker would be possible with Fab fragments (the antibodies itself may interfere with cell activation during culturing). Therefore I would rather use a red-spectrum dye like CFSE or PKH26 as this may be cheaper and possible for secondary use with other cell lines.
I have multiple cytometers available and the specific emittance doesn't matter as we can pick what is generally possible (LSR/Fortessa).
Thus, I am looking for a dye with emittance in the red fluorescence spectrum which has staining protocols available that can be adapted for my purposes.
Is anybody willing to share their experiences?
Edit

Clarified that I needed a 'no-antibody-staining'
Clarified question with regard to biological question and FACS

What is your question? Are you looking for a product recommendation?

So you're doing a dye dilution proliferation experiment? Please explain what you're doing! Especially what cytometer you plan to use in case the stock filter set up is ill-suited to certain spectra.

I've used the ThermoFisher brand of CellTrace dyes. Specifically, I co-cultured two populations of cells, one with CellTrace Far Red in the APC channel and another with CellTrace Yellow in the PE channel. My choice was in part guided by a product review by another lab touting the relatively low cytotoxicity of these products.
The protocol is quite straight forward. It's also available in CFSE and Violet, though I haven't tested those. These dyes are also optimized for lymphocytes, and so I'd recommend titrating if you're staining anything else.
The dyes are quite bright, and so there were issues with costaining APC-Cy7, for example. I ended up leaving my CellTrace dyes as the only markers on their respective lasers and stacking my phenotyping on the 355nm and 405nm lasers.
For compensation, you might just stick with cells, but in the product manual for CellTrace, however, it says:
"The CellTrace™ reagents readily diffuse into cells and bind covalently
to intracellular amines, resulting in stable, well-retained fluorescent staining that can
be fixed with aldehyde fixatives."
So if you use the ArC amine-reactive comp beads for LIVE/DEAD kits, you might be able to just make comp beads with those. I'll verify this when I'm back at work if need be, as I haven't done it myself, but it's a nice thought!

There is a number of different dyes possible, as you can see in this figure (from here):

A good overview can be found in the "Selecting Reagents for
Multicolor Flow Cytometry" application note publication from BD (in reference 1) and also the Fluorochrome Specifications from BD (reference 2).
References:

Selecting Reagents for  Multicolor Flow Cytometry
BD Life Sciences Fluorochrome Specifications

Thanks for your answer, Chris. I realize that I was a bit vague about my question, and have edited it above.


text:
Human Fat Adipose Tissue: Maximum Energy Transferred out per Day?
The article "A limit on the energy transfer rate from the human fat store in hypophagia" states that subjects with moderate activity levels are found to have a limit on maximum energy transfer rate from human fat stores of 290 kJ / kgd. This results in 31 kcal / lbs.
Question: Does anyone know (possibly with access to the full article) if above numbers are kJ/(kg body fat) or kJ/(kg body weight)?  Optional, the article mentions moderate activity, what happens in the case of high activity?
I asked because if its kJ/(body fat), then this limits a 185 lbs male with 27 lbs body fat to 837 kcal/day metabolized from fat adipose tissue into energy, limiting his weight loss to about 2 lbs/week.  If it's kJ/(body weight), then a 185 lbs male can transfer 5723 kcal/day from fat adipose to energy and lose about 13 lbs / week.  Rough calculations made where 3500 kcal deficit = 1 lbs weight loss.
I have information that suggests a person without any food, only water, performing moderate exercise of 6 miles walking per day, for three weeks, loses about 4.3 lbs/wk (accounting for the loss of 11 lbs material in colon). This data suggests:
They either:

This examples uses energy from breaking down muscle tissue over the 837 kcal/day limit (fat store max) suggesting this article calculates using kJ/(body fat weight).
This examples uses energy over 837 kcal/day, which was 2344 kcal/day from the fat store, not including muscle tissue, suggesting that this article calculates using kJ/(body weight).

If I understand correctly, what you actually want and need is the access to the full article. There are various ways to do this: either contact your library, a friend working at the university, directly request it from the authors, or ... well, there are also other ways which should not be publicly promoted, but are available online.

I have full access now and my suspicion is that the result is a max of 837 kcal/day/lbs body fat can be transferred from fat adipose tissue per day.  This suggests that maximum weight loss of adipose tissue before using energy from free fat mass (skeletal muscle) is about 1.6 - 2 lbs/wk.  I suspect people dieting should know this..

Paper
From the conclusion: "The main thesis of this paper is that the FM is able to transfer energy to the FFM up to a maximum rate of (290±25) kJ/kg d."
Where FM is fat mass and FFM is fat-free mass.
So (290±25) kJ/kg d or (31±3) cal/lbs d is the maximum rate of energy transfer possible from FM to FFM where the kg or lbs in question are that of FM.
Example
I weigh 175 lbs and my body fat percentage is 10%. That means I have 17.5 lbs of FM. My theoretical limit of energy transfer from FM to FFM is anywhere from 17.5 * 28 = 490 calories per day to 17.5 * 34 = 595 calories per day.
That's:

Min: 490 cals * 7 days = 3,430 cals per week
Max: 595 cals * 7 days = 4,165 cals per week

So if we take 1 fat lb at 3,500 calories it's 0.98 lbs to 1.19 lbs maximum fat loss per week.
Dr. Alpert Later Remarks
Here's the thing though, the late Dr. Alpert went on to later state he miscalculated the numbers in the paper and it was more like 20 cal/lbs d to 25 cal/lbs d. Unfortunately he didn't republish the paper though.
Personal Experiments
I highly recommend performing your own experiments as the paper was done for a somewhat esoteric sample which was very small. A friend and I ran two personal experiments that might be of interest using DEXA scans to see how our results add up to those in the paper.
I followed a progressively restrictive deficit until I started experiencing muscle loss. I collected 7 intervals of scans. For me the maximum amount of fat loss was in fact 21 cal/lbs.
Interestingly enough once I experienced muscle loss my body started upregulating how much muscle it utilized and preserved fat which caused my fat utilization to drop all the way to 9 cal/lbs. I theorize this is some sort of evolutionary switch as I am very muscular. The body probably senses an "emergency" and starts preserving fat while utilizing muscle. Given muscle consumes more energy to maintain than fat, this seems like it would kill two birds with one stone for increasing the chances of survival.
My friend did a more extreme test where he fasted for 7 days and measured the FM change. He was able to hit 23 cal/lbs d of fat loss so it matched the paper very closely as well. His FFM was all over the place during the experiment but it's tough to tell what was water, carbohydrate, glycogen, etc. loss so we only looked at how much fat he lost.


text:
Human Body's rate of conversion of carbs, protein and fat into energy?
I understanding there are some complicated processes, but I'm interested in generally how fast the body converts certain chemicals into energy and the period of time this conversion occurs.  I'm specifically interested in carbohydrates, protein and fat (perhaps distinguishing saturated from unsaturated).
I have the following notes where glucose is energy, do they appear correct?

Carbohydrates convert to glucose over a 2 hour period after a meal.  The peak glucose/blood levels are 30 - 45 minutes after a meal.  Conversion starts about 15 minutes after a meal.  1 g of carbohydrate / 1 g of glucose conversion.
Protein converts to glucose over 3 - 5 hours after a meal with a 70% conversion of protein into glucose.  I also read that protein converts to glucose at a rate of 3 - 12 g protein / hour.  1.3 g protein / 1 g of glucose conversion.
Fat converts to glucose over 4 - 6 hours after a meal.  Only about 5-6% of the fat triglycerides are converted into glucose.  I also read that 2.5 g of fat / 1 g of glucose conversion, which seems to differ then the 5-6% number.

This question seems to be based on the false assumption that proteins and fats are necessarily converted to glucose. It is possible for certain amino acids in protein to be converted to glucose by gluconeogenesis, but not others. However they may also be used for protein biosynthesis, metabolized oxidatively as different intermediates or even converted to fat. As regards fat itself, only the glycerol moiety can be converted to glucose, but whether this happens or the glycerol is metabolized differently depends on the nutritional state of the individual.

It is quite complicated, the speed of conversion of carbohydrates, protein and fat in to energy is definitely not linear and dependent on what the body is doing.
You should be close to right in carbohydrates. Since digestion starts in the mouth with the release of amylases to chop down starch and since the absorption of glucose is quite fast in the early stages of digestion in the intestines, your numbers should not be far off if you consider a non-branch form of starch. That will change depending on the type of carbohydrate, and some form of carbohydrates are even impossible for the body to digest and are either digested by bacteria in the gut or simply excreted in the feces.
Regarding protein, this is where your assumptions start to be off. The primary purpose of protein is not for energy production, but to supplement the cells with aminoacids to build other proteins. So, although it is possible to convert protein into glucose, it is not done in digestive system. Also, each aminoacid is converted into a precursor that will generate some energy eventually, not glucose. And depending on the aminoacid, the amount of energy differs, which makes it more complicated to give an estimation.
As for fat, they cannot be converted into glucose by the human body. As you mentioned, this is the slowest macromolecule to be absorbed by the body but it is also the most energy dense. Although 1 g glucose generates about 3 cal, 1 g of fat generates around 9 cal (protein is around the same as glucose).
Regarding on how fast macromolecules can be converted into actually energy, some cyclists can burn up to 120 g glucose per hour during a race.

The poster mentioned triglycerides in relation to fat, rather than fatty acids. The glycerol portion of triglycerides can be converted to glucose in the liver. I imagine that is where the 5–6% figure comes from.

@David yes, the 5-6% of the triglyceride conversion to glucose figure is confusing.  I read that body fat, which I understand is made of of triglycerides, is only 85% usable energy per unit weight.  Much different than the former number.  Any idea if these numbers are correct?

@Vilut you mention that fat cannot be converted into glucose by the human body.  You mention that 1 g of fat generations ~9 kcal of energy.  Therefore ingestion of fat resulting in energy availability to the body.  Its now my understanding that fats are converted into fatty acids and glycerol. These fatty acid chains are converted into energy via a process called beta-oxidation (electron transfer), which generates acetyl-CoA entering the citric acid cycle, yielding ATP.  Is this correct?  How long does the process take vs others like carbs?

@Nick, yes, fatty acids are converted into Acetyl-CoA through beta-oxidation, which then enters the citric acid cycle to result in ATP that the cells can use.
As for the length of the processes, I don't know. What I know is that, in athletes, glucose is used primarily in big and speedy efforts (100 m), while fatty acids are primarily used in long efforts (marathon and ultra marathon). Which means that glucose can be used to produce ATP fairly quickly relatively to fatty acids. Of course, other factors should be taken into account for more precise values.


text:
Optic Nerve: neurons/area and bit rate?
Does anyone know the number of neurons adjoining a cross sectional area of the optic nerve and the theoretical bit rate of the nerve?
I read that the ON cross sectional radius is 3-5 mm and the diameter of a neuron is .004 - .1 mm. Area of cross section: (5 mm)^2 * pi = 75 mm. 75 mm / .004 = 18,750 neurons/cross section. The average action potential of a neuron is 1 ms in duration, making maximum signal rate of 1,000 Hz.  The action potential is both a frequency (on/off/unk) and amplitude (intensity).
I read that light at min intensity signals at 0-1 Hz and max at 30 Hz. At 30 Hz that’s 18,750 * 30 Hz = 562,500 bits/sec or 562 kB/sec or .5 mB/sec.  at 15 frames per second that’s 37.5kB/frame.  Now I think something is wrong because this is very slow considering all three cones and rods must signal over this slow bandwidth.
They are also orders of magnitude off from the 576 MB image calculated for the human eye. I read that the nerves are really signaling contrast changes, but it seems like a large amount of bits just for contrast.

Neurons are not encoding a digital signal in the sense of computers, so it may not make any sense to think about it that way. Neurons can't fire at 1000 Hz, even if an AP is 1 ms wide. Like I've suggested elsewhere, start by just learning about neuroscience. Read a whole undergraduate-level neuroscience textbook. Purves' "Neuroscience" or Kandel's "Principles of Neural Science" are good options. I know, it seems like a lot of work, but it will save you a ton of time wasted.

Well, upon some simplification, we're talking digital vs. analog information. An 8-bit digital image can distinguish between 256 tonal values. The exact amplitude of a neuron action potential along an axon is continuous ("analog"), and perhaps more importantly, the summation/integration of electrical information along any point in the neuronal soma and dendritic regions, before the axon hillock, is entirely continuous, and as such is theoretically "infinite-bit" in "infinite locations", digitally speaking. So bandwidth is infinity. That's what you get when you compare digital and analog.

@SPr It seems you are implying the amplitude of the signal has infinite states.  That makes sense.  I think in OP I confused intensity and amplitude.  Am I correct saying the signal amplitude is intensity and the frequency is on/off/unknown?  Or is it the other way around?

Start with basic neuroscientific principles such as action potentials as suggested above. An action potential is a signal propagated through an axon of a neuron, that's the most basic idea to grasp as to how neurons send information down the 'wire'. Here, the exact amplitude doesn't correspond to intensity, either there's a signal propagating or not, so it's binary in that sense; usually signal intensity is coded for in part by frequency of action potentials and is limited by its input (stimulus) and other things like their refractory period.


text:
Organism-specific Kegg Pathway: Must all boxes be high-lighted/present for a reaction to occur?
I'm new to using Kegg and not sure how to interpret the position of the pathway enzymes in the pathway that I'm looking at. More specifically: If all boxes (of KOs) must be present/colored green or not for a reaction to occur.
I'm looking at this pathway: http://www.kegg.jp/kegg-bin/show_pathway?ooe00010
Looking at the 'help' for Kegg indicates that the KOs represent a protein complex, because the boxes are 'stacked' against each other. Is this correct?
Specific reactions that I've been looking at: alpha-D-glucose-6P to beta-D-glucose-6P (One box is there, the other is missing).
Or the route from Glyceraldehyde-3P to pyruvate. I'm thinking that these pathways must be present, but in the very first reaction only 1 of 2 boxes are colored. I suppose it's also a possibility that Kegg's database is simply incomplete?

Also note that green boxes indicate that the enzyme was found present in the organism you are looking at, however White boxes do not mean that the enzyme is not present, it only means that there is no evidence (or not yet) found that the enzyme is present in the organism. (Probably in some cases it's found that the enzyme is not present, but in general it means that there is simply no evidence)

Your interpretation of the pathway map is incorrect.
The boxes do not represent KOs (Kegg Orthologues) and they do not represent a protein complex. They are Enzyme Commission (EC) numbers and where there is more than one box this means that there is more than one enzyme that can catalyse the reaction.
In the case you cite the two enzymes are EC 5.3.1.9, glucose-6-phosphate isomerase, as you can see by clicking the box, and EC 5.1.3.15, glucose-6-phosphate 1-epimerase. Only one is needed to catalyse the reaction.


text:
At what point is a picked flower considered dead?
Let a flower be picked from the ground such that its stem is cut and the flower is separated from the root system (as in figure).

Questions:
1a. At what point is it considered dead?

Does the flower and attached bit of stem continue to live for some time before dying?

Is this like asking when an limb that has been chopped off an animal dies - should we considered not the flower, but the root system?

1b. How does one define death for an organism without a nervous system?

In medicine, people have problems defining at what point a human is considered dead. Here we do not have consciousness (that we would know off), so I guess the flower is considered dead as soon as it is cut. It lost its ability to regenerate. The plant from which the flower was cut in most cases is still alive.

Thank you for your interest. The flower can still "live" for some time if placed in water/nutrients, correct? If the root system had a single flower before the plucking, could the root system still regenerate the flower?

Regenerate the same flower? No. Grow a new one if it is not an annual plant or it is at least early in the season, yes. The cells of the flower would still be alive for a while, but how you would decide that for the flower is more of a philosophical question.

i don't know about the flower in your picture, but a lot of plants will not die at all, but grow roots and become a new individual plant if you put a piece of it in water. about the bigger question, wikipedia has a list of things characterising "life" of all forms: https://en.wikipedia.org/wiki/Life#Definitions (but as with humans, i guess it's not always that easy to tell)

I've voted to close this since it seems to be both unfocused (there are at least two separate questions — one about the definition of death and another about how that applies to a cut flower) and unclear (how are you defining alive? — the answer you accepted makes it clear that this is somewhat arbitrary). Since you are taking the time to edit, please consider fixing these problems. Thanks!

This is very much analogous to your "limb" suggestion, or, since the flower is a reproductive organ, one can ask,

At exactly what point is the uterus considered dead after a hysterectomy?

or,

At exactly what point are the testicles considered dead after a male dog is castrated?

The organism (woman and dog respectively) does not die. Tissue dies. Tissue dies all the time. Red Blood cells die after about 120 days, give or take. Skin cells die faster than that.
It depends on the definition of death. If one of the requirements for "life" is the ability to reproduce, are both the woman and the dog now dead? Of course not. They had the potential, or perhaps they already reproduced.
If one of the requirements for "life" is the ability to grow, well, the uterus and the testicles are dead immediately upon removal. But we stop "growing", and we don't die.
If one of the requirements for "life" is the ability to respond to its environment, the uterus and the testicles are not dead. They are "alive" for a time, though the environment is toxic to them if thrown away. If placed in nutritious media, they will "live" a bit longer.
Common sense, which often isn't reliable in science, would dictate that the flower dies when it can no longer maintain cell turgor, i.e. can no longer absorb fluids. But the argument can be made that it is only "dying" at that point.
Basically your question depends entirely on the definition of life. And that has not been agreed upon.

Consider also that at some point the flower will be "dead" even if it is not removed from its plant.  The petals will wither and drop off, and if fertilized the ovary will develop into a seed capsule, which will in turn wither and die after  releasing seeds.  Then the stem which it was attached to may in turn wither and die back.  In extreme cases, such as bulbs, the entire above-ground part of the plant and much of the root system will also die, only to re-grow next year.

For a time, a cut flower with a stem, when placed in water can still absorb water. If other nutrients are placed in the water (such as sugar) the flower can continue to absorb those nutrients. If the stem is cut just below the node, and the water is changed, some cut flowers can stay alive for a few weeks.  They are alive in that they continue to absorb nutrients through the stem (including water) and some types of cut flowers will visibly grow for a time. However, at a certain point, growth will stop and the flower will begin to wither. The process is more gradual than in an animal, so the moment of 'death' would not be observable.
That said there are some flowers that will grow new roots from the stem, such as geranium. In that case, the cutting can be considered part of a process of regeneration or reproduction.

Welcome to Biology.SE! This could be a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— Thank you for taking the [tour], but please also consult the [help] pages for additional advice on [Answer] effectively on this site. In particular, the question should be ignored as it is off-topic (unclear & unfocused). Thank you!


text:
What kind of fish is this white blue-stained fish?

This fish has been spotted at the Great Barrier Reef near Cairns (Queensland).
I put a big effort to find it via Google but never could encounter anything similar.
I have also made an attempt to find this fish here with no luck.

I don't know whether this helps, but that looks like a parrot fish.  I had a look online and also didn't find anything with that distinctive pattern. The closest I could find was Scarus ghobban (common names include blue-barred and blue-trim parrotfish), which is highly variable but the blue edges on the fins seem constant.
According to the sources linked above this fish can be seen in areas with sandy bottoms, so that seems consistent with your photograph.
Reference pictures:


text:
Validity of comparing gene expression levels between alive and <24h postmortem cohort
There is a recent paper about assessment of a suicidal risk in psychotic patients https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759104/
One of the important points is that the authors compare gene expression levels between alive patients and post-mortem suicidal completers (RNA extracted from blood <24h post-mortem).
In result, they identify suicide-specific blood biomarkers that also have "biological roles in immune and inflammatory response, growth factor regulation, mTOR signaling, stress, and overall the switch between cell survival and proliferation vs apoptosis".
Do you think that one may really perform this type analysis if we know that post-mortem biochemistry is very different? Plus they killed themselves via different means (gunshot, hanging, electrocution, slit wrist etc.)


text:
What physiological pathways lie behind inhalants hallucinogenic effect?
I searched through the web and surprisingly I found pretty much nothing on the physiology of hallucinogenic effects of inhalants. Any idea how people get high with inhalants (household and industrial chemicals) and what physiological pathway lies behind this mechanism?

Interesting question, although I'm not an expert on inhalants. But part of the many reasons of its psychoactivity may be of the less oxygen-saturated blood going to your brain (i.e. your body not having enough oxygen due to inhaling some gas).


text:
Estimating Weight of Human Skeletal Muscle?
Is there a way to measure the weight of skeletal muscle?  I understand body fat and lean body mass can be measured by: skin fold calipers, electrical impedance, table lookup based on formula of weight, age, and height.  I have not seen a method to determine skeletal muscle.  I asked an endocrinologist and they were not aware of a method.
I suspect subtracting the weight of the skeletal bones, skin tissue and organs from the lean body mass weight could determine weight of skeletal muscle.  It seems this number could vary greatly be the person unless perhaps people who handle deceased people have accurate measurements of the above for age, weight, height, etc...
It would be useful to know the weight of skeletal muscle because it could be used to determine body energy expenditure, as lean muscle uses more calories than fat.

You probably know that evidence of prior research is required on this site. It's a good question. Editing what you've found so far would make it better. :)

Updated with research references.  Are my categories ok for this?

Did you search "how to determine skeletal muscle mass"?

I did and the calculations are for Lean Body Mass (LBM) = Total Weight – Fat Mass which includes Organs, Skin, Bones, Body Water, Muscle Mass.  I think I'm looking for Muscle Mass, which will allow me to multiply it by 6 kcal/lbs and fat, 2 kcal/lbs to get a more accurate calculation of BMR.  I don't think the 6 kcal/lbs is supposed to include organs, skin, bones and body water... I suspect this factor is for muscle tissue only.

Hmm, I see that you're correct that the first few hits do refer to lean body weight, but on the first page of hits (for me) is a good article specifically on skeletal muscle estimation, which discusses the method with which I'm most familiar.

What link are you referring to?  I see https://www.healthline.com/health/muscle-mass-percentage, which uses a estimated chart and the numbers don't add up to the correct BMR.  There are some formulas here, but again it is rough estimate and don't measure if a person has lifted lots of weights https://www.frontiersin.org/files/Articles/505707/fendo-11-00031-HTML/image_m/fendo-11-00031-t001.jpg.  There is suggestion of using an MRI, water displacement.  There is a formula using impedance https://journals.physiology.org/doi/full/10.1152/jappl.2000.89.2.465.

Also, Creatine ( methyl-d3) dilution in urine for estimation of total body skeletal muscle mass.  The only problem here is if a body builder is taking creatine supplement, it will throw off the results.  Are you referring to this?

This was the article I saw towards the bottom of the first page of hits. It compares two methods of estimating skeletal muscle mass. The method I'm familiar with is that using a DXA scan, although I'm passingly familiar that one can use MRI, but have not ever bothered becoming knowledgeable about it, because DXA scans are so easy and so much less expensive. Good research on your part, btw.


text:
How is the biggest animal ever existed measured?
Blue whales are considered the biggest animal ever lived with maximum confirmed length nearing 30 meters. While some titanosaurs reportedly were somewhat longer (up to 40 meters for Argentinosaurus and up to 37 meters for Patagotitan).
It's obvious that size constitutes not just length, but I don't quite understand how one can be certain that the said sauropods were smaller provided that they are about 1.5 ~1.33 times longer?

Just look at the body structure of a blue whale vs a sauropod. Whales are round/elliptical in cross-section, and their width is larger proportional to their length than sauropods. Put simply, they just have more volume, even though they may be somewhat shorter. BTW, 40:30 is not 1.5x.

@MattDMo you are right, but I believe there should be more precise way to say that than just raw approximation based on the body structure

We'd also be forgetting about the largest animal ever recorded which is a syphonophore at 46 meters, a spagetti jellyfish.
A blue whale can weigh 196 tons. Argentinosaurus could weigh in at 77 tons:
Initial estimates placed it at 40 meters (131 feet) long with a weight of 77 tons. This makes it comparable to the next largest titanosaur, Puertasaurus (which has been estimated at 73-83 tons by some studies), and thus one of the largest land animals in Earth's history.
People can confuse voluminous, massive, largest, and longest. Scientists will generally not agree about the best way to measure he largest animal, whether it is the syphonophore or the whale.


text:
Calculate radius of curvature of DNA
I am using this article to calculate the radius of curvature of DNA. I know that

150bp segment of DNA length wraps itself 1.7 times around a histone core.
There are 0.34nm/bp
DNA's persistence length l is 53 nm.

How can I use this data to calculate the radius of curvature of DNA?
According to the article, $l = \frac{B}{k_BT}$ ($B$ is bending modulus, $k_B$ is Boltzmann's constant, and $T$ is temperature). However, the only way the units cancel correctly is if $l = \frac{k_BT}{B}$. Which is the correct formula?
Assuming I know $T, k_B, l$, I can calculate $B$. Since DNA is a homogeneous isotropic rod, $B$ is equivalent to Young's modulus $E$. Is there a way I can use $E$ to calculate the radius of curvature? Or am I doing this completely wrong?

According to the article E= Bl/2R^2. Does that help?

Yes, but I am then confused how to get E/I.

I'm no mathematician by any stretch of the imagination, but it seems from the paper that E~kbT, and l~B/kbT thus by substitution l~B/E and therefore E~B/l for a given temperature and if R=l. I get units for l as N.mm^-2.J^-1, but it should be just distance (nm in DNA's case) correct?

I don't think DNA has a particular radius of curvature any more than it has a particular length. It will depend on the situation. In the case of DNA wrapped around a histone, the radius will be half the diameter of the histone + half the diameter of the DNA.


text:
Aging and Hormone Levels
Hormone levels in humans decrease with age. The effects are especially detrimental for women after menopause.
Biologists state that turtles do not exhibit most of the phenomena related to aging. For example telemore shortening does not happen in certain turtle species.
Here is my question:
Do turtle hormone levels decrease with age as in humans?

Your first sentence does not make sense, as men do not undergo menopause.


text:
Why Is Gray Matter Gray?
When I researched I found  different reason for this, the  popular
ones are
1) white matter is mylinated .this reason was given in reference books and   this website
while others say
2)cell body concentration causes grayish appearance ,as in brain the cell body is concentrated outside. As mentioned in this .i.e cell body orientation.
also my teacher agrees with 2nd one, that the nissls granules contribute to the grayish appearance.orientation causes the effect of gray matter and white matter
I feel 1st reason to be more appropriate as there are billions of it couldn't be arranged as depicted in the second reason.
kindly help  me out to choose the accurate one, with appropriate reason of-course!

so whats is your question ? :) Just teasing you but kindly i higly doubt you will get anything more than just comment on it.

why is that true  ?

man i just say that this type of question is rather fit to the chat room rather posted like that. In my opinion SE its about sharing information not discuss like that. Still i hope that somebody try give you proper answer not jus opinion.

@L.Diago the question is clear and definitely answerable, you just might not be familiar with it if you haven't worked with gross specimens.

You are right that was the reason of my special interest to this question so thank you man. :)

The terms gray and white matter relate to their color in gross specimens (i.e., not microscopic specimens) that have been formalin fixed. Nissl granules describe a microscopic structure, the rough endoplasmic reticulum, and aren't directly related to the color of gross specimens. Here's an example of a frontal cross section from a University of Utah slide set:

You'll see it's generally a tannish-yellow (at least on my monitor, this image is a pretty good representation of what it looks like in person), but there are lighter "white" parts in the white matter areas, and darker "gray" parts in the cortex.
A live, or a recently deceased and not formalin fixed brain has different qualities, including color and consistency.
The color of the formalin fixed tissue is an artifact of the process of fixing, so it's not necessarily accurate to describe the gray color as something inherent to the cells in the gray matter, but generally yes, the whiter color in the white matter of formalin fixed brain is because of the high lipid concentration. The grayer color of the gray matter is because of the lower lipid concentration. This lovely old JBC article from 1929 discusses some of these issues, mostly regarding white matter in response to staining after fixation, but also gray and white matter before staining.

Nice answer but i still dont see that answer to question what exacly makes gray matter gray ? :)

@L.Diago "the grayer color of the gray matter is because of the lower lipid concentration."

I know, actually i am trying to give you constructiv criticism. But the other part was about the fact what makes gray matter gray (i am not telling that your answer is bad but he put on tabel something about nissle substance )

@L.Diago can you please clarify your suggestion? I'm not sure what you're getting at.

I think the criticism is a bit nitpicky. It's not like there is a "gray chemical compound" in gray matter. This answer provides the correct one: gray is the color of formalin-fixed brain tissue that contains less lipids than white matter. Unfixed brain tissue is not gray.

@BryanKrause I just tried to get him inculed something about the nissle substance. You know only to makes the answer perfect, but i know doesnt need to be included. But still i think he wanted oppinion about the nissle substance. Still wrote that i just teased him.

@L.Diago Nissl granules don't have much to do with it, but I've added it to the answer to clarify that.

@DeNovo I am sorry for that, but you know  this type of question can be usefull for anybody new in neurosciences so i wanted that to be perfect answer.

The grayer color of the gray matter is because of the lower lipid concentration. Is it known, why the lipid concentration differs between the inner outer parts of the brain?

@Marzipanherz myelin

so you are saying first answer is correct right? i.e white matter is mylinated , inturn mylin is made up of lipids. but the problem with that is mylin sheath is formed in between shwaan cell and axon how could you see the color of middle layer

@sudhanvab plasma membranes are not opaque. The intracellular contents of a tissue are typically what give that tissue a characteristic color.


text:
What controls specific gene silencing during cell differentiation?
I am intrigued by the fact that all cells of our body use the same DNA. How do the cells differentiate during the post fertilisation divisions?
I read about gene silencing, which can be an answer to this. But still I do not understand how the cells decide which gene it is supposed to silence, by making the micro RNA.
Consider a zygote that is beginning to divide. I would assume that the chemical and physical context of each daughter cells would be more or less similar in beginning. Then how can there be a differentiation? Is there some supervising authority present in the zygote that decides what to make out of each daughter cell?

Possible duplicate of which exact mechanism triggers the first cell differentiation after n divisions?

The cells differentiation during post fertilization period is govern by a set of regulatory genes called Homeotic genes.These are genes that "select" the identity of entire segments or structures in the bodies of developing organisms.
These gene encodes a transcription factor that is expressed in a specific region of the organism starting in its early development i.e. embryo stage. The transcription factors change the expression of target genes to enact the genetic “program” that's right for each segment.

The homeotic transcription factors shown in the diagram above[homology between Hox genes in mice and humans] contain a DNA-binding protein region called the homeodomain, which is encoded by a segment of DNA, called the homeobox.The animal genes containing homeobox sequences are specifically referred to as Hox genes. This family of genes is responsible for determining the general body plan, such as the number of body segments of an animal, the number and placement of appendages, and animal head-tail directionality.
In addition to this genes, the early developmental cascade include the following genes:

Maternal effects genes:These are genes whose mRNAs are placed in the egg cell by the mother before fertilization. Some of the mRNAs are “tied” to the head or tail end of the embryo and are responsible for setting up the head-tail polarity. The maternal effects genes encode regulators of transcription or translation that control each other as well as other genes.
Gap genes: They are activated through interactions between the protein products of the maternal effects genes, and they also regulate each other. They're responsible for defining large, multi-segment regions in many organisms.
Pair-rule genes: These are turned on by interactions between gap genes, and their expression patterns are refined by interactions with one another. They appear in multiple “stripes” along the embryo, similar in pattern to the segments of the adult organism.When a pair-rule gene is missing due to mutation, there is a loss of structures in the segment regions where the gene is normally expressed.

For further information you can refer this link:
-  Click here 1
- Click here 2
-  Click here 3

Hox, pair-rule and gap genes are all expressed well after the first differentiations.

Activation and deactivation of different genes commands the process of cell differentiation. Gene expression responsible for cell differentiation is  controlled by intrinsic and extrinsic signals. This regulated signalling from inside and outside the cell is responsible for embryonic development.
Environment around the cell, such as small molecules, proteins, temperature and oxygen control the gene expression.  Cellular communication takes places to decide the fate of particular cell by interplay of signals between the proteins synthesized around the cell. These proteins can be morphogens, growth factors or cytokines. This extrinsic signalling sets off intercellular signalling that stimulates expression of genes. Alteration in gene expression by turning gene on or off, regulates the production of gene product.
Gene expression is regulated intrinsically by modifying DNA. DNA and chromatin are altered chemically. Change in chromatin effects gene expression by controlling the binding  of genes to transcription factors. These epigenetic  chemical modifications are known as DNA methylation and histone modification. Chromatin modification plays important role in gene expression during cell development.  For example, proteins responsible for chromatin modification  play important role in muscle cell differentiation. Transcription factors MyoD and MEF regulate enzymes responsible for chromatin modification, such as histone acetyltransferases and deacetylases.
Via:  https://www.nature.com/scitable/topicpage/gene-expression-regulates-cell-differentiation-931/#
Chromatin modification helps in continuous gene expression which is required during cell differentiation. The gene silencing involved in embryogenesis, promotes cell development into mature cell types. This silencing of gene is done by making gene inaccessible to transcription machinery, and when genes are needed again in adult cell type the chromatin modification opens DNA and make it available for transcription.
Embryonic cell types have particular regions for chromatin modification that regulate gene expression required for embryonic development. These regions can modify gene expression by activating or silencing genes.
Via: (https://www.ncbi.nlm.nih.gov/pubmed/16630819)


text:
Can/have bacteria been engineered to express ACE 2 receptors?
In light of SARS-COV-2 binding to the ACE 2 protein in human cells, I was wondering if any bacteria exist or could exist that possess this membrane protein. If not, do you believe that an ACE 2 like protein https://www.jstage.jst.go.jp/article/jpssuppl/92/0/92_2-YIA-09/_pdf expressed by a bacteria could allow  the COVID-19 virus to successfully attach and be fused into the bacterium?

Could you edit your question so that it is clear whether you ask about expressing a functional membrane attached ACE2 receptor allowing for SARSCOV2 infection, or about simply producing ACE2 receptors with engineered bacteria.

Short answer is no, because the ACE2 receptor is only a trigger (and anchoring point) for endocytosis.
The endocytosis requires many enzymes/proteins which are (as far as I know) specific to eukaryotes. You'd need to express those too in your bacterium and the lack of adequate eukaryote-like transport protein in your bacterium will likely forbid the whole from functioning.

That makes perfect sense, thank you. Do you know of any attempts to get a eukaryote targeting virus to infect a prokaryote?

@user91617 It is not exactly my domain of expertise. If not for pure curiosity, I fail to see why such an attempt would be made. I also noticed I failed to answer the title question : can a bacteria express the receptor : yes, see http://www.ndsl.kr/ndsl/search/detail/article/articleSearchResultDetail.do?cn=NART51710590.

Thank you for the link. As you inferred, my ultimate question would be whether it is possible for the COVID-19 virus to infect a prokaryote such as E. coli (engineered or otherwise).


text:
Australian Tree Identification - maybe pine?
Can you help identify this species?

(Link to imgur album with all images)
It was growing next to the Yarra River (maybe 10 meters from the bank) in Melbourne. At first I thought it was a type of pine however this page says Australian pines at not actually true pines. It does look much like some of the images of Australian Pine Casuarina equisetifolia
However the Wikipedia page for Casuarina equisetifolia says there are 2 subspecies, equisetifolia and incana. Equisetifolia is only found in Southeast Asia & northern Australia so that rules that one out. Incana is found on the east coast of Australia (eastern Queensland, New South Wales) - could it also be found as far down south as Melbourne?
I've also compared it against all the pines on this site as it specifically shows Australian species.
From there I thought it looks a bit like a Port Jackson Cypress Pine Callitris rhomboidea but the needles look longer and narrower.
I think it also looks a little like a Narrow Leaved Wattle Acacia linearifolia if you ignore the yellow flowers.
I'm carving a spoon out of some of it's wood so would like to know for sure what species it actually is. Any help greatly appreciated.
UPDATE:
I went back to the tree to get some more photos but the whole tree had fallen in the river!

I did get a branch off it however to get a close up of the nodes / internodes but I could not find any seeds or cones.

FINAL UPDATE:
I've tried to get a close up of the apical portion (the top bit right?). My twig sample has started to dry up a bit so this is the best I could get.

ONE MORE UPDATE
Due to my last pictures being rather fuzzy I got out the DSLR and the tripod. These photos are very high res and around 8mb each so may take a while to load...

I'll go back to the tree to get more close up pictures

After more research I now think it is Casuarina obesa - Swamp Sheoak but will still get some more close up pictures (when it is not raining)

Those are great photos!

@AlwaysConfused - I've added a close up of the nodes / internodes - but a shame the whole tree has fallen in the river!

My tree was just a bit off that map. Yes, I do have a twig sample. I'll photograph some more tonight.

Native cherry, Cherry ballart or Cypress cherryn belongs to the sandalwood family of plants.
http://en.wikipedia.org/wiki/Exocarpos_cupressiformis

I think your right. All the pictures on this page of Exocarpos cupressiformis match all my photos

I did some research following the latest answer on species of Exocarpos. I believe it is Exocarpus cupressiformis as well.
You can refer to this Australian website for a key to determine the actual species of Exocarpos : http://plantnet.rbgsyd.nsw.gov.au/cgi-bin/NSWfl.pl?page=nswfl&lvl=gn&name=Exocarpos#4
Also, as I researched, I found other Exocarpos species to mismatch with your images, except for two; Exocarpos cupressiformis and Exocarpos strictus. One mismatch of E. strictus was with the way flowers were arranged in your last few pictures.
Find below the pictures of flowers of E. cupressiformis (First) and E. strictus:

You can see that E. strcitus has the flowers blooming on stem edges and not at all on tips. In contrast, your images show flowers clustering at tips just like E.cupressiformis.

You are most welcome.


text:
Why we utilize dextro glucose and levo amino acids?
Our body only digest dextro(Right handed) glucose and levo(Left handed) proteins and can't digest Levo glucose and dextro proteins. Why?
Our body synthesis levo proteins. What is the reason?

Because of different proteins taking care of each.

Great question - AliceD is correct that our enzymes exhibit stereospecificity for each, but there is also another vital reason why humans utilize D-glucose and L-amino acids... will post as an answer

I am not clear what your question is. Are you asking why only one stereoisomer is used in each case, or are you asking why it is D-sugars and L-amino acids (rather than D-amino acids)?

Our body digests only certain type of enantiomers like L amino acid and D sugars because enzymes are specific for their substrates stereochemistry meaning they will only recognize a particular enantiomer.So I hope this answers to your first question.
Now, why we only see L amino acids and D sugars, there is some interesting hypothesis listed in this article.Here is the link
http://guava.physics.uiuc.edu/~nigel/courses/569/Essays_Fall2006/files/Rajan.pdf
I am adding some answers I found from research gate here, which includes
1)I think the prevalence of L-amino acids in biological systems is a quirk of our evolutionary history; there's no reason D-amino acids wouldn't work chemically, but once early life forms started building proteins out of L-amino acids, L-amino acids became abundant an it became selectively advantageous to use L-amino acids because then you could use the amino acids you obtained by eating someone else. It's a matter of compatibility; if you use D-amino acids, you have to build them all from scratch, because you're not going to find them in your environment. As long as you use L-amino acids, you don't even need to maintain the de novo synthetic pathways; you can just eat something that has those pathways (hence the 'essential' dietary amino acids).
2)There are a couple of reasons for biological homochirality.
One, our galaxy has a chiral spin and a magnetic orientation, which causes cosmic dust particles to polarize starlight as circularly polarized in one direction only. This circularly polarized light degrades D enantiomers of amino acids more than L enantiomers, and this effect is clear when analyzing the amino acids found on comets and meteors. This explains why, at least in the milky way, L enantiomers are preferred.
Two, although gravity, electromagnetism, and the strong nuclear force are achiral, the weak nuclear force (radioactive decay) is chiral. During beta decay, the emitted electrons preferentially favor one kind of spin. That's right, the parity of the universe is not conserved in nuclear decay. These chiral electrons once again preferentially degrade D amino acids vs. L amino acids.
Thus due to the chirality of sunlight and the chirality of nuclear radiation, L amino acids are the more stable enantiomers and therefore are favored for abiogenesis.
3) Morozov, L. 1979. Mirror symmetry breaking in biochemical evolution. Origins Life Evol Biosphere 9: 187-217
But I think we have D amino acids also, as this paper says https://www.hindawi.com/journals/scientifica/2016/6494621/
Hope this helps!


text:
Influence of carbon dioxide concentration on the rate of photosynthesis
The experiment to prove that carbon dioxide concentration influences the rate of photosynthesis:
Click here to see the image
The experiment is repeated after adding some sodium hydrogencarbonate (which dissolves in water to produce carbon dioxide) to the water. It is observed that more oxygen bubbles are produced, and thus this shows the increased photosynthesis rate.
My question: The equation for the dissolution of sodium hydrogencarbonate is NaHCO₃ (s) ⟶ NaOH (aq) + CO₂ (aq). But won't the sodium hydroxide turn the solution basic and also influence the rate of photosynthesis?
Thanks in advance,
Ramana

@ bpedit. One of my friends (who is a biologist) said that when hydrogencarbonate dissolves, it forms carbonic acid which turns the solution acidic. But how? He says that the hydrogencarbonate combines with the hydrogen ions in solution to form carbonic acid......

Unimaginable that this question passes unanswered for over three years. It is very important to understand the advantages of increased carbon dioxide levels.


text:
Do pregnancy and breast feeding increase basal metabolic rate?
Since pregnant or breastfeeding women have extra nutritional needs, does that mean they have a higher BMR?
Why I thought the conclusion would be sensible: Since BMR is the energy needed to perform body functions (breathing, respiration, homeostasis, digestion, etc), pregnant woman or breastfeeding women, because of their extra 'activity' (due to the presence of the fetus) will have a higher BMR.

Basal metabolic rate for a particular organism is determined by the amount of calories that the organism needs for basal metabolic processes (i.e. basal energy demands). Since pregnant and breastfeeding women have increased caloric requirements (i.e. increased energy demands), then that means by definition their basal metabolic rate is increased.

A pregnant woman’s total energy expenditure during pregnancy is mainly because of a raised basal metabolic rate, or BMR. The energy necessity of basal metabolism is influenced by nutrition prior to pregnancy and the size of the fetus. According to a 1990 study, “Energy cost of physical activity throughout pregnancy and the first year postpartum in Dutch women with sedentary lifestyles” by Joop MA van Raaij, et al, “BMR is increasing throughout pregnancy mainly because of fetal demands.” BMR will decrease to preserve energy if maternal energy stores are too low when a woman becomes pregnant. Also, women having larger babies tend to have greater increases in their BMR and greater decreases in the rate of their energy stores than pregnant women having normal-weight or underweight babies.

could you add active links that users could click to go directly to these sources? it would greatly strengthen your answer. thanks for your contribution.


text:
What are Expressed Sequence Tags (EST)?
I read in an article that ESTs are partial or sub-sequences of cDNA. What are ESTs exactly? Which part of cDNA is cut in order to make ESTs? Why are they so instrumental in genomic research?

The question does not cite the source of the poster’s information, but it might well be the Wikipedia article on ESTs. I suspect the reason that does not answer the first question (“What are ESTs”) is the confusion in how ESTs are generated from cDNAs implicit in the second question “Which part of cDNA is cut…”. I therefore start by dealing with the source of the confusion.
Clarification 1: A Sequence need not have been Sequenced
One source of confusion lies in the word ‘sequence’. One meaning of this (noun only) is “a specific linear contiguous fragment or region of nucleic acid”. When used in this way there is no implication that even the length of this is accurately known, never mind the identity and linear arrangement of the nucleotides. The second use of the word sequence (noun) is the identity and order of nucleotides in a (linear) nucleic acid, with the corresponding verb meaning to determine this. Because today it is so cheap and quick to determine the sequence of a nucleic acid fragment, the student may not realize what a relatively slow and expensive undertaking it was in the last century. I shall use DNA fragment or region instead of the first use of ‘sequence’ in the rest of this answer.
Clarification 2: There are cDNAs and then there are cDNA clones
The second source of confusion seems to be with the cDNA clones. The question does not use the word ‘clone’, but asks “which part of cDNA is cut…”. This implies the poster is thinking in terms of individual cDNA clones in which the inserted cDNA fragment has been characterized — restriction mapped, perhaps sequenced and the protein product even identified. This is the approach adopted when the scientific problem is to identify the mRNA or gene encoding a particular protein — actin, beta-globin, etc. This is not the case with ESTs. Here the only characterization performed on a cDNA clone is a single DNA sequence determined (historically by the Sanger method) from a primer position in the cloning vector. This is because the focus is on producing a bulk library of DNA sequences.
So, what are ESTs and how are they generated?
As an alternative to the standard definition, one might say:

An EST is a single DNA sequence read derived from only part of a mRNA. Despite its uncharacterized nature, possible redundancy, limited size (perhaps 100-200 nt) and likelihood of errors it is useful in combination with many others from the same tissue as providing a reference to genes that are expressed in that tissue.

So, to reiterate, the answer to “what part of the cDNA is cut…” is “none”. One (presumably) just isolated total DNA from the recombinants in the M13 plaques and ran a single sequence determination from the primer site. And this was because one did not know which EST would be useful, but a collection or library of ESTs would likely contain some that would be useful.
The word ‘tag’ expresses the fact that they act as a handle or reference to the gene or mRNA, rather than being complete in themselves.
Why are/were ESTs important/useful?
The words the poster used originally were “Why are they so instrumental in genomic research?”, but I think that certainly exaggerates their current — if not their past — utility, so I have rephrased the question. Examples of the use of ESTs are given in the Wikipedia article already quoted, so I shall quote from Peter Goodfellow, writing in Nature in 1995.

Only 3 per cent of the human genome codes for proteins… the most important
  part of the genome is the protein coding genes and that sequencing these
  will give the largest return of biological information…

After pointing out his own scepticism towards the approach he briefly mentioned one important historical issue:

Given these disincentives, why have tens of millions
  of dollars been spent on ESTs? After a brief exploratory phase… a major driving force was the hope and the fear that ESTs could be used to patent any gene that had been tagged. Attempts to patent genes via ESTs raised the spectre of an international trade war and the echoes are still reverberating around courts in the United States.

No longer, I hope. Goodfellow then turned to the science:

It was hoped that large-scale EST projects would define the broad limits
  on the number of genes and the types of genes in the genome and provide a
  snapshot of their expression patterns. It was also expected that enough sequence
  information would be generated to be able to recognize new members of gene
  families of biological and commercial interest.

Coda: Yesterday and Today
Currently the method most used to investigate expression of genes as mRNA is, of course, RNAseq, which is faster, cheaper and, unlike ESTs, comprehensive.


text:
Which programming language is beneficial for a cell biologist who does extensive confocal microscopy and image analysis? Python or MATLAB?
I'm currently learning to acquire images using confocal microscopy and subsequently analyze the images using the Fiji software. I want to know how and where exactly Python or MATLAB is used by practising cell biologists and microscopists for image analysis and learning which language might be beneficial.
Thanks in advance!

Fiji is Java based, it is a modified version of the NIH ImageJ...so Java...

This is really not a question about a problem in biology. You might try SE Bioinformatics, but cut the stuff about prerequisites for learning different programming languages, which is certainly a separate question (and one I would judge to be off-topic).

I agree that the first part of this question is off-topic here, and the second part is probably off-topic on most Stack Exchange sites. That being said, speaking from experience as a Python programmer, that language is not only pretty straight-forward to learn (never used Matlab, so can't speak to that), but it also has tons of 3rd party modules available for image processing, recognition, and analysis, both for general use and some specifically for working with microscopy data. Python also benefits from having a huge developer and user base, and it's open-source, which Matlab is not.

@MattDMo — Please do not make statements like "Python is very easy to learn". That is completely subjective, and depends on whether you have already learned programming in some other language. That is one of the reasons why, as you acknowledge, the question is off-topic.

@David Please don't take what I said out of context, and please accurately represent what I said. I purposely did not say that "Python is very easy to learn" because it isn't, necessarily, especially if you've never programmed before or if you're coming from a completely different paradigm. I said "speaking from experience as a Python programmer, that language is [...] pretty straight-forward to learn". The language is clean and straight-forward, as computer languages go, in that it isn't overly convoluted or cryptic.

I can't speak for MATLAB, but:
Why it's good to know Python:
Python Ecosystem
There is a lot of support for scientific image analysis in Python, as attested by such powerful and heavily maintained packages as scikit-image and opencv.
Both are used extensively in biology and other scientific areas.
And the vast majority of libraries in Python are free (not so for MATLAB).
Also, there's a huge amount of material freely available online, like tutorials, Q&A's, and more than a few different free IDEs to choose from, for pretty much any operating system you'd like.
Python AI Support
More importantly, most of what's happening in AI these days is image processing, and most of what's happening in AI image processing these days is implemented in Python (at least at the top level).
So, whenever you think machine learning might be a good fit for your application, most likely Python will be as well.
Yes, it is true that there are bindings for a lot of other languages, including MATLAB (and Java, and R...), but those aren't typically native to the ecosystems and they won't be as well supported.
Python General Purpose Programming
I believe the most important argument for Python and against MATLAB and R is that Python is a general-purpose programming language.
It has excellent support for image analysis and statistics (arguably not worse than MATLAB and R), but it also makes it easy to do what is needed to actually use your solutions in practice, like file system operations, data base access,  user interfaces, and microscope control:
It's not enough to have a great algorithm for finding nuclei in an image, you also want to be able to apply that algorithm to a slew of images you download from somewhere on the fly or acquire using an automated microscope or camera.
Oh, and you'll be much more likely to apply your programming skills in Python than in MATLAB outside of research.
Where is Python Used?
Python is used wherever the above arguments are important.
That means that Python is used in biology wherever:

image analysis is important, but
the job is more than just plain image analysis, and especially
wherever AI/machine learning is a good fit.

I would even go as far as saying that Python is simply more modern than MATLAB, and wherever people are free to choose, they tend to go for Python.
(That said, MATLAB and R have a long track record and a huge following in all the sciences and they're still very well used.)

I would not really compare MATLAB and R. The main knock against matlab is that it's proprietary subscription software, and a costly subscription at that. As such, many academics avoid it (I'm one of the ones who doesn't and uses MATLAB extensively). R is the premier language for statistical software at the research level; almost everything available in Python was first available in R until someone ported it there. I also use R extensively. They do very different jobs.

I agree that MATLAB and R have a different focus. But they're often (ab)used for the same purposes. You can do image analysis in R, although that's not necessarily one of its strengths, and you can do statistics in MATLAB, although R has much better support for that. The choice of tool is very often determined by what people and their communities are used to rather than the specific strengths of the tools. And as an arrogant Python developer, I'd argue that there isn't much nowadays that MATLAB or R have that Python doesn't.


text:
HAR1 speedy mutation
From wiki:

Human accelerated region 1 (HAR1) is a segment of the human genome found on the long arm of chromosome 20. It is a Human accelerated region. [..] These 49 regions represent parts of the human genome that differ significantly from highly conserved regions of our closest [living relatives, the chimpanzees] in terms of evolution.

What could explain those differences?
A back of the envelope computation shows that in the course of 8mio years, at a rate of 64 mutations per generation, one can expect 1% of mutated basepairs. Indeed, the HAR1 of length 106 bp has 1.08 substitutions in the chimp. But humans have 13.93. (Data: see the table in this article.)

Can you please show how you computed the 1%? When you state the HAR1 of length 106 bp has 1.08 substitutions in the chimp, you mean substitution compared to what species? But humans have 13.93 substitutions compared to chimps I suspect? Or maybe you made an attempt at reconstructing the hypothetical sequence of the ancestor and compared to it? Or maybe you referred to some paper who sequenced a fossilized genome?

@Remi.b: yes, I was wondering also, but I think both numbers refer to the most recent common ancestor. At 64 mutations per generation over 400'000 generations, that's roughly 25mio mutations among 3bn bp, or roughly 1%.

But where did you get these numbers from? For example, I can't see the number 13.93 in the linked wikipedia articles.

Substitution rate at neutral sequences
The rate of substitutions at neutral sequences is given by the mutation rate. It si a very simple and classic result. It is because the probability of each new neutral mutation to fix is $\frac{1}{2N}$ (which you can calulate from a Moran branching process as well as from a simple Wright-Fisher model of genetic drift) and there are $2N\mu$, new mutations at each generation (where $N$ is the population size and $\mu$ the haploid mutation rate), resulting in a substitution rate of $2N\mu\frac{1}{2N} = \mu$.
Substitution rate at non-neutral sequences
A beneficial mutation has a probability higher than $\frac{1}{2N}$ to fix, while a deleterious mutation has a probability lower than $\frac{1}{2N}$ to fix. Therefore, the more beneficial mutations there are, the higher is the substitution rate. There are a number of approximations to the fixation probability of a non-neutral mutation. For example, using diffusion equations, one can approximate the probability of fixation of a deleterious mutation with selection coefficient $s$ by $\frac{1-e^{-\frac{4s}{N}} }{1-e^{-4Ns}}$ from some Kimura paper.
This rate of substitution therefore depends upon the selection scenario. It is lower than $\mu$ in conserved sequences and it is high than $\mu$ in sequences that undergo positive selection. So, the reason for such fast evolving sequences is just that they are under positive selection.
How about HAR1?
Without looking for more accurate statement form the scientific literature, the same wikipedia article you cite says

HAR1A is active in the developing human brain between the 7th and 18th gestational weeks. It is found in the dorsal telencephalon in fetuses. In adult humans, it is found throughout the cerebellum and forebrain; it is also found in the testes.[1] There is evidence that HAR1 is repressed by REST in individuals with Huntington's disease, perhaps contributing to the neurodegeneration associated with the disease

It already gives you a vague idea of potential selection pressures on those sequences in the human genome.

The rate is higher in sequences that undergo positive selection is a non-explanation to me. What is the mechanism? Is the mutation rate under "neutral selection" actually dampened (namely 13-fold?)?

I am not sure I understand what is unclear to you but let's try to make our way through it. A beneficial mutation has a probability higher than $\frac{1}{2N}$ to fix, while a deleterious mutation has a probability lower than $\frac{1}{2N}$ to fix. Therefore, the more beneficial mutations there are, the higher is the substitution rate. Does that clear things up?

Ok, so the "mechanism" is statistical: mutations do not easily result in substitutions because, being diluted in the population, they are weeded out. So in absence of selection pressure, the substitution rate is lower than the mutation rate. Yes? Maybe I'm not using the terminology correctly.

The exact number of substitutions is definitely is stochastic process. In absence of selection, the substitution rate is $\mu$. If mutations are often beneficial, then the substitution rate is higher than $\mu$. If mutations are deleterious, then the substitution rate is lower than $\mu$. You said So in absence of selection pressure, the substitution rate is lower than the mutation rate.. Well it depends upon whether selection is purifying or positive.

Ok, thank you. I upvote for potentially useful pointers, but cannot accept the current answer due to lack of clarity.


text:
Is this Poison Hemlock?
There is a lot of this growing in standing water near a drainage route and spring. It looks similar to water or poison hemlock.

This is most likely water cress (Nasturtium officinale), which is in the cabbage family (Brassicaceae).
This is a water dwelling species that has white flowers and leaves in a pinnately compound form and flowers in clusters.
In contrast, hemlock (Conium maculatum) has its flowers in distinct umbels (umbrella shape), and the leaves are also pinnate, but deeply divided and lacy in appearance as opposed to the intact and lightly toothed edges on watercress.
Here's a picture of hemlock leaf from Iowa State University, contrast it to the ones in your question:

Thanks! It looked similar but is missing distinguishing features like umbels, 5 petals, reddish stem, protruding stamen, etc.

@noshery no problem, it is certainly good to get clarification around these sorts of things. Water cress is very edible and tasty, though rather peppery when raw - tastes like radish or mustard. If you are certain that the water source is clean (i.e. not polluted or have human/animal waste in it), then harvesting and eating is a possibility, but could need cooking if in doubt as to the water.


text:
Percentage of nervous energy used by human eyes
I am reading a book 'How to stop worrying and start living' by Dale Carnegie. I stumbled across this statement below and I couldn't find any research article to backing this claim. Does anyone know if this claim is reasonable or not? Following is the claim:

The reason the eyes are so important in relieving nervous tension is that they burn one fourth of all nervous energies consumed by the body.

"Nervous energy" might seem not to refer to refer to calories as much as fidgeting and muscular tension. Could you clarify the disjunct between the question title and the image text. We discourage text images, as those using a text reader for reasons of accessibility are less likely to be able to read it, if you can use the quote function and type the text in, that would be preferable.

Thanks for editing in the quoted text, but as I indicated, the phrase "nervous energies" is idiomatic, it doesn't refer to Joules or calories, it refers to muscular tension and restless fidgeting. Could you make the title agree with the body of the question. We also require that you show your prior research, once you've worked-out what question you're asking that is.

I couldn't find any information about this topic while doing my research that is why I thought I could ask in this forum

This seems very...non-rigourous. To be honest, I've heard what I can only refer to as quacks speak in a similar manner.

But the question is very unclear, the title being different from the body of the question - please begin by editing so that it's making sense.

Could you do it, I don't know how to frame it better

There is no metric known to me that fits the description "nervous energies". It's the sort of unchallengeable rhetoric that self-help gurus come up with that gives the impression that it's in some way scientific, but the meaning is more intuitive than quantifiable by science. If you can find a metric for "nervous energy" then I'd be surprised if it had a sound methodological underpinning. Don't let that stop you trying though.


text:
Why is my tissue sample coagulating during centrifugation? How can I prevent this?
I am working on extracting water-soluble compounds from a biological tissue sample. A problem I am encountering is that the sample is too cloudy with debris/large tissue pieces to filter into HPLC vials for analysis. So my hypothesized solution is to centrifuge the samples and try filtering the supernatant instead.
When I tried this (centrifuging 5mL at 12000rpm for 5 minutes) the resulting sample was gelatinized/coagulated and even more resistant to filtration. Any ideas on why this is happening, centrifugation parameters to try instead?

What tissue are you working with, and how are you prepping it? If coagulation is an issue, adding heparin into your sample preparation procedure should inhibit it.

Welcome to the site, please take a [tour] and visit the [help] for information on what makes a good question and answers. To answer your question, as @MattDMo asked, we would need specifics on the tissue, reagents and procedures you are using in your preparation.  Also, besides centrifugation, what else have you attempted and how do others in your lab overcome this problem?

Your question and self-answer don't seem to make sense. You write about "platelet" in the question, but then say you were using plant-based samples in you answer. There is no point in posting publicly unless you are clear enough that someone else can learn from what you've posted. Consequently, I've voted to close this as "Needs details or clarity". Please follow the above advice and then either [edit] or delete these posts according to what you've learned (and whether you are willing to put the work in to improve your posts).

Answering my own question: I was using plant-based food samples that were extracted at medium/low temperatures. This denatured the proteins into absorbing more water. The samples were also starch-containing and gelatinized during centrifugation. I am only unsure why centrifuging initiates starch gelatinization like when cooking.


text:
Has an artificial symbiotic relationship ever been created?
Have 2 organisms ever been introduced to create a symbiotic relationship that doesn't occur in their natural environment?

Can you please give your definition of symbiotic relationship? No everybody uses the same definition. Some use it as an equivalent to mutualism. Some uses to describe any kind of relationship and I've heard people using it as "obligate mutualism or commensalism".
What kind of barrier to their relationship existed in their natural environment? If you consider a symbiotic relationship to be any relationship and you accept any barrier preventing their interaction in nature, then almost any example of introduced species would answer your question.

@Remi.b I've been thinking on this, and it's a good question, but I'm not sure how to answer it. I was just thinking of pairs that don't normally interact in nature, but were introduced (with or without genetic alteration) in an artificial setting to induce a cooperative or symbiotic relationship with benefits that either replicate their symbiotic relationships with other organisms, or else create a new beneficial relationship.

does domestication count?

Here are some examples:

symbiosis between genetic modified yeast cell populations (Shou W et al. 2007)
symbiosis between green algae and embryonic chick connective tissue (Buchsbaum R et al. 1934)
symbiosis between EcoBot II and microbial fuel cells (Ieropoulos, Ioannis, et al. 2005)

Do not forget domesticated animals that we now keep as pets. It's not unreasonable to argue that the relationship between dogs/cats and humans has a symbiotic character. The pet gets foodand shelter whereas the owner benefits in other ways, e.g. companionship, deterrence of enemies, herding,...

I thought of that initially, but the mutual benefit varies wildly when considering abusive/neglectful pet owners, and like my cat for example, she offers nothing in return. She overeats and ensuingly throws up on the regular, stands in my way wherever I'm trying to go, and deters very few enemies...very few indeed.

So if your cat actually offers nothing, why do you still own her? What I want to say by that: the pure presence of a cat often suffices to make their owner more comfortable. If a cat would not have nothing to offer, no one would have one as a pet...
Anyway, you would certainly agree that at least dogs perform useful tasks in some cases.

well I do enjoy giving her smooches on the whiskers, so I suppose there is some benefit.  I'm not sure if that qualifies as a symbiotic relationship, but maybe a re-defining of the word is in order to include the aforementioned smooches.


text:
Questions regarding the four pollination mechanisms of papilionaceous flowers
I want to understand the four mechanisms of pollination in papilionaceous flowers: pump/piston, explosive, valvular and brush.
The topic is lightly touched upon in this part of a Wikipedia article, but I find the explanations somewhat shallow and incomplete.
This study from the journal Plant Systematics and Evolution about the explosive mechanism mentions all mechanisms but only deals with the explosive. Regarding the explosive mechanism it mentions that the androecium and gynoecium are subjected to pressure from the keel. My interpretation is that when a pollinator presses upon the keel the reproductive column "snaps" up due to the released pressure. Taxa which I know utilize this mechanism are: C. scoparius, Medicago sativa and the three Desmodium species studied in aforementioned publication (D. incanum, D. subsericium and D. uncinatum) but due to my location I have not been able to study the explosive mechanism in the field. If my interpretation is correct, then how is the pollination transferred to the pollinator after the column is released? In the previously mentioned Wikipedia article it is said that the column hits the banner (standard), but it does not tell whether this "collision" with the banner is what causes the pollen to be released. Does the collision with the banner release the pollen in a "cloud" which envelops the pollinator? Or does the reproductive column hit the pollinator along the trajectory it travels from keel to banner?
The pump/piston mechanism I have on the other hand been able to study quite easily due to the great amount of Lupinus polyphyllus growing in my area which inhibit this technique of pollination.
This study published in The Scientific World Journal explains the valvular mechanism as follows:

In the valvular mechanism, the upper rim of the keel is unsealed; it opens along its total length when the keel is moved downwards by the pollinator and closes when the insect leaves the flower. In this case pollen can be released repeatedly to numerous visitors.

and the brush mechanism in this way:

In the brush mechanism, as the pistil is longer than the stamens, the stigma extends beyond the anthers, avoiding self-pollination; the upper part of the style develops erect trichomes acting as a pollen brush. When sufficient pressure is exerted on the standard and wing petals, the pistil protrudes from the keel tip: the stigma comes first into contact with the insect receiving (if present) external pollen and the style brushes the pollen on the visitor. When pressure is released, style and stigma return to their former position inside the keel.

As for this last explanation of the brush mechanism I do not entirely understand how the spread of pollen occurs. The publication says that the stigma extends further than the anthers and that the "style brushes the pollen on the [pollinator]". What do they mean by this? Does it have to do with the trichomes on the style? If so, how do they play into the transfer of pollen?

The formulation of this question suggests that it is homework of some sort, which would definitely require you to show the research you had done to solve it yourself (a general expectation in any case). Furthermore it seems to ask several questions or a general review, whereas this site exists to answer specific questions. Please re-read the [Tour] and the Help on Asking Good Questions.


text:
New earliest life found, what are the implications?
So a couple of days ago it was announced that new fossils of microorganisms were possibly discovered around former hydrothermal vents. According to the paper these fossils "are at least 3,770 million and possibly 4,280 million years old" making them the earliest instance of life found so far. If the upper estimate is correct that would mean these organisms existed "only" ~250 million years after the formation of Earth.
Does this discovery shake up any of our previous ideas and/or provide new insights about the earliest life?

One can make a comparison between dating of extremely old fossils but IMO, no one can really answer to the question there new insights to be gained? as this very much depend on your specific interest. In other word, IMO, this part of the question is to broad.

I don't have access to Dodd et al. 2017 that you cite but I suspect they made comparisons with other recent discoveries. As you cite the abstract, you might have not read the paper. You should probably just try to read it.

@Remi.b I don't have access to the paper either :). I mean insights about earliest life/abiogenesis but yes I'll edit the sentence. I'm not so much looking for a copying of the article's discussion but more the scientific consensus on the importance of this find but I'm not sure if that exists yet.

Not a lot, the sample is not conclusively biotic in origin nor is it necessarily much older than known fossils, 3.7 billion vs 3.5 billion. The sample is a few simple hematite filaments, complex hematite filaments do form as a byproduct of oxygen using (aerobic) bacteria, they can also be formed by metamorphic processes. Subscribing these filaments to life and proposing oxygen must have been present far earlier than any evidence supports based on this is wishful thinking at best.
If it were correctly identified and as old as possible it would have only a small effect, it would make finding life on other planets more likely becasue it would mean life forms basically as soon as you have persistent liquid water. It might indicate oxygen earlier than suspected but that seems unlikely.

As I have not read the paper, could you please develop on the sample is not conclusively biotic to include a discussion of their sampling technic? Also, when you say is it necessarily much older than known fossils can you please provide referenced examples to allow a reader to make a comparison?

The OP's own linked articles discuss it. But I will expand.

Nice answer. However, could you add a reference on the different ways these filaments can be formed?

The effect of this hypothetical discovery (because I haven't seen the dating of the rocks yet) is almost non-existent. It just reinforces an idea already present in the origins of Life community for a lot of time-you discover life as soon as you discover solid rocks capable of creating fossils, so Life must have originated immediately after the cooling of the Earth's surface or possibly it simply originated elsewhere in the Solar system and was transported here by meteorites (there is solid evidence for this hypothesis in the ability of bacteria to survive extreme environments). What is important however is the reinforcing of the idea there is some "missing link" in the history of the transition of chemistry to biology which is definitely not in the fossil record!
The fact we can't discover some intermediary complex molecules between the primeval Earth and the bacteria means for most of the scientists that either Life simply "hitched a ride" on some comet or meteorite to come here from some other place in the Solar system it originated (possibly Mars) which in turn would imply that the entire Solar system gave rise to a single "type" of Life and therefore even if we find Life outside Earth it will probably be based on DNA and the central dogma and be too much like our own or that the emergence of Life was so fast it simply can not be by chance! I think the implications of the second case are greater but the first one can make a lot of "noise", too I guess (especially if they find bacteria on Mars and they turn out to be just like those here). I myself, however, am a little bit of an "heretic" here and believe the continuous occurrence of the same fossils everywhere in the ancient geological record (and in meteorites from Mars, too) may indicate a little bit different view of what Life can be defined as. What we are looking here are not evidence of cells, but rather evidence of metabolic products which we (not they by themselves) contribute to cells! Because modern cells can produce such products we assume they are produced by cells! But we don't have cells we can look at under the microscope in those rocks. We have thin bands of material we think comes from cells (it is the same with the Martian meteorites-science in a way becomes a "point of view" which you should consider isn't very "scientific"). But what if these bands were the result of metabolism, but is was not cellular! I myself think this is entirely possible, but most of my colleagues do not even consider this idea. This can easily explain the rise of products of metabolism early on but at the same time give enough time for the complexity of the modern cells to form under the influence of great competition among metabolic pathways themselves, rather than living cells-for which we seem to have direct evidence at a much later period. This hypothesis can also explain why are all the basic metabolic pathways in Life today so conservative (unlike the genes themselves which determine them-what is really more conservative-the gene or its role?) while the proteins coding for them can be coded under different genomic organization-e.g. different structure of the genome in different domains. The place of the gene can change, even to a certain extent its sequence, but what remains the same is their relationship to each other, e.g. their topology to respect of each other in the general graph of metabolism. Why? What if metabolism was more ancient than cells, but the evidence of this "metabolism evolution" was lost in the age before the cell(because there were no cells, no structures, no anything to leave fossils of the metabolism evolution, excepts its waste products (in a way its "coprolites"). I would like to think this evidence supports such hypothesis but again it is just an opinion.
I hope you like this answer.

Your answer is rather hard to follow, are you saying metabolism started inorganically?

Not exactly, actually I am saying what we perceive today as metabolism was the way the first form of life evolved in the beginning of its history. Actually, I (and not only me, of course) put forward the idea of gradual metabolic evolution whose waste products formed what we today find as the oldest fossils of living organisms. I think we don't have enough data to call them results of cellular activity, so they could well be the results of metabolic activity before the rise of cells. If metabolism evolved first, then its fossils can exist even if there weren't cells during that time.