texts:
I understand that when the human body loses weight, the vast majority of that weight is lost as $CO_2$ (and a small bit is lost as water). I expect the predominant way $CO_2$ exits the body is through exhaling.

So, let's take a human with no influx of carbon (they are not eating); I expect such a person is slowly losing weight, a near infinitesimal amount with each breath (correct me if I'm wrong).

If the person breathes faster (more breaths per minute), that causes an increase in the rate at which $CO_2$ is expelled, correct (more mass per minute)? Is this rate expected to decrease, i.e., as one breathes faster, less $CO_2$ is contained in each subsequent breath? Or, does perhaps the body mobilize and oxidize carbon fuels (carbohydrates first and eventually lipids) to generate $CO_2$ in an attempt to restore homeostatic equilibrium?

Could breathing quickly and heavily possibly cause an increase in the $CO_2$ content of exhaled breaths? That is, would voluntary hyperventilation cause an increase in heart rate (and thus increase in carbon catabolism)? How much $CO_2$ is in a typical exhalation during exercise?

I realize that without exercise, the amount of $CO_2$ being lost during normal breathing is nearly negligible. But perhaps laying down and breathing quickly could cause a measurable increase in the net rate at which mass leaves the body. What do you think?

Thank you for your time.


texts: Do mammals develop tolerance to anticholinergics?

texts: I know that first generation H1 antagonists, commonly known as antihistamines have anticholinergic effects. Their sedative side effects go away due to tolerance, but as for their anticholinergic side effects well that's something that is unknown to me at least. You might say use second generation H1 antagonists, but for this application the antiemetic effects that are unique to H1 antagonists that cross the BBB (i.e., first generation H1 antagonists) are desired.


texts: In glycolysis, what is the source of the electron that makes NAD+ into NADH instead of NADH+?

texts: I looked at the formula for the glycolysis reaction. The overall reaction seems balanced, however, I don't see anything on the left hand side of the equation that would provides the electron to convert NAD+ to NADH. Where does that electron come from?


texts: How much percent of image does our eyes focus at any instant?

texts:
I learned in highschool that even thought we have a wide view, we only observe a tiny fraction of that view through our eyes. So at any instant we are not really looking at all the objects infront of us, this is why we need to individually focus at each object at a time.
Question: What is the % of view that is in focus at any instant of time compared to the full view we observe thorough our eyes?


texts: How long can you keep sheep eyes in formaldehyde before dissecting?

texts: We're preparing for an experiment in our classroom and my teaching partner and I are at different points in the unit.  I am concerned that the experiment will be less successful because of the freshness of the eyes.  How long can they eyes be stored in the fridge before they have to be dissected and is freezing them an option?


texts: Does atrophy of the thymus not effect T-cell selection and tolerance?

texts:
The thymus atrophies as age progresses. Does the T cell selection (which happens in the thymus) continue to take place? This doubt came into my mind because in the cadaver we dissected, the thymus was hardly more than scanty fibrous tissue. This definitely should have some effect on immune tolerance right? Is this the reason why the elderly are more prone to autoimmune diseases?

Or is it that selection happens only in children? This line of thought would pose a problem since T-cells are short lived and they continuously need to be produced. Or is it that the site of selection is shifted to some other place?

P.S. I am asking these questions assuming that selection is necessary every time new T cells are made. Correct me if this primary assumption is wrong.


texts:
What sort of telomere elongation methods are there currently?

Would this stop aging? (edit: No, probably)

I couldn't turn up anything good on google. I was thinking that maybe you could sequence the telomeres, trim them all at a certain point, and then engineer a polymerase molecule to extend from that same point. Is this how it's done?


texts: In a strand of DNA, why does identifying the 3' side and the 5'side matter? Or the 3' --> 5' strand and the 5' --> 3' strand? Also, what is a single strand of DNA called, is it just a helix, or is the helix just the backbone?


texts: How does Trifluralin kill newly germinating seeds, with almost no effects on established ones?

texts:
Trifluralin (2,6-Dinitro-N,N-dipropyl-4-(trifluoromethyl)aniline) is a pre-emergent herbicide used in landscape beds before the application of mulch (my use for it, anyway). It kills the weeds as they germinate, while not harming most established plants.

From what I understand, the mode of action is as a mitotic inhibitor, which disrupts the microtubules that pull the cell apart when it divides (stops cell division).

How does this only affect germinating weeds, while not noticeably affecting weeds that have emerged from the soil (I have to hit those with another herbicide)?


texts: Does a cell deprived of growth factors undergo apoptosis or G0 stasis?

texts:
I can't seem to find a decisive answer on this topic in any of my textbooks. If a cell is deprived of growth factors does it:

Activate apoptosis
Go into the G0 phase but keep living?

Thanks.


texts: Can viruses be used to extract oil from algae?

texts:
I read that one hard step in algae oil extraction is to rupture (or fracture) the cell walls to get the contents inside. Some people use chemical methods; some use sonication or mechanical forces.

I wonder why nobody is talking about using viruses to accomplish this task? Viruses destroy the cells and release clones of itself. Some article states that there are plenty of unknown viruses in seawater. I'm sure a major part of it infects algae.


texts: What is this hairy, striped orange-black caterpillar?

texts:
There are so many these hairy, striped orange-black caterpillars in my backyard.

What are these caterpillars? Are these dangerous?


texts: Which X-Y chromosomes have the developmental genes for mammals?

texts:
I know that for a given mammal, half the chromosomes come from father and half from mother. This is typically denoted as x-y. I've recently read about "toolkit" genes that control how a cell develops into an embryo into an organism. I'm interested which set of chromosomes(x,y or both) contains these toolkit genes for development of an organism from a fertilized cell?

In other words, does an X chromosome know how to build a female and Y chromosome how to build a male, or is it some "overriding" of developmental instructions that Takes place when Y is present?


texts:
So, the HIV-1 jump to humans occurred as early as the 1920s, but the AIDS epidemic didn't start until the early 1980s.

Some things I don't understand about this:

Why the delay?
What is needed for a successful zoonosis transmission in the first place?
If Bushmeat practices (eating meat from non-domesticated animals, in this case HIV-infected fruit bats) have been the same for centuries, why has HIV only really spread in THIS century?


texts: Why are Barr Bodies usually seen along the edge of the nucleus under the light microscope?

texts:
We do a typical class exercise of aceto-orsein staining of buccal epithelial cells from female students to visualize Barr bodies under the light microscope. All the illustrations and pictures in the books depict a Barr body located on the edge of the nucleus, but that is not always the case in the students' samples. Given that the cell is a 3D structure, I couldn't explain why the Barr body would localize itself to the edge of the nucleus with respect to the viewer's 2D perspective.
In this article's introduction, a statement is found saying:

  "In interphase, the inactive X chromosome (Xi) is found as a condensed
  heterochromatic Barr body, usually positioned at the nuclear or
  nucleolar periphery (1-4)."

By "usually", does it mean that it is pure luck? Is there any explanation as to why we would have a tendency to see it localized to the edge from our perspective, exactly on the rim of the nucleus, and not just somewhere random?


texts: How correlated is the chirality of different molecules?

texts:
In astrobiology, a proposed way of testing whether life found on another world is alien or originates from Earth is to determine the chirality of its molecules. This is of course only useful when the biochemistry is similar enough that one may suspect contamination.
But this test has a weakness. While different chirality can confirm alien origin, similar chirality does not exclude alien origin.
To mend this, a plausible idea is to cross check the chirality of a wide range of compounds. A false positive suggesting Earth origin would then have an exponentially smaller chance to match every single compound tested.
...or so I hope.
The issue is that I fear various chiral compounds do not have statistically independent default chirality. For instance, common biochemical pathways may produce one compound from another, leading the chirality of the first molecule to directly determine the chirality of the second.
I'm looking for a high level perspective: Does the chirality of a single compound more or less determine the chirality of all other compounds in an entire biochemistry, or are there a great number of compounds that have an arbitrary default chirality compared to others?


texts: In CRISPR bacteria, how does viral genomes get integrated into the spacers of CRISPR? Also, in its use, where does Cas9 cut the DNA?

texts:
I've been out of Biology for about a year polishing my programming skills. I know CRISPR/Cas9 allows targeted 'cutting' of DNA via RNA-guidance. Few questions regarding this.

Regarding to its natural phenomenon, when a virus infects a microbe with CRISPR capabilities, how does the genome get integrated into the 'spacers' of CRISPR region versus elsewhere of the prokaryote genome so that when transcribed, the Cas enzymes know that it's a foreign DNA element to be targeted? My understanding of virus infections is a little cloudy too; I'm thinking random transpositions.
I'm looking into it now, so I may figure this out before someone answers, but when the target DNA is located via the guiding RNA, where does the Cas9 enzyme decide to 'cut' -- rendering it useless -- the DNA, and how does it identify the location?

-EDIT- Ah. The target sequence must also include a 'PAM' sequence downstream (Protospacer Adjacent Motif), which allows binding of the riboprotein complex(guiding RNA + Cas9), and biochemistry magic cuts it ~3-4 bases upstream of the PAM). citation: https://www.addgene.org/CRISPR/guide/

Just thought of another question, if the DNA is cut at the seemingly specific spot, is the DNA repair that ensues downstream totally random? I feel like it would be in the organism's best interest (anthropomorphogenic, oops), and evolution generally says it usually does, to have a mechanism to repair it to its original state.


texts: What is the relationship between W, X, Y and P, M retinal ganglion cells?

texts:
In Guyton and Hall Textbook of Medical Physiology (12e) the retinal ganglion cells (RGCs) are classified into W, X, and Y types. However, in Gray's Anatomy (40th ed.), RGS are subdivided into midget and parasol cells. What is the relationship between the W-X-Y versus midget-parasol classifications?

Summary of the WXY classification as in Medical Physiology:

About 40% ganglion cells are W cells. They are the smallest (<10 μm), and the slowest (8 m/s) to transmit signals, but they have the broadest receptive field. They receive signals from rods and detect directional movement.

About 55% are X cells. They have medium size (10~15 μm) and transmission speed (14 m/s). Their fields are small. They transmit color vision.

About 5% are Y cells. They are the largest (<35 μm) and the fastest (35 m/s) to transmit signals. They have broad fields. They respond to rapid changes in the vision.


texts: Ventral stream pathway and architecture proposed by Poggio's group

texts:
Please can you give me a very brief explanation about all functions in the ventral stream architecture summarized in this figure:

This figure is from Serre et al.'s A quantitative theory of immediate visual recognition. Prog Brain Res. 2007.

I read multiple articles about this model, but I still don't understand the basic aim, especially behind the two operations (Gaussian-like and max-like operations).. So please can someone explain to me in details the ventral stream pathway (from V1-V2-V4-IT-PFC) including the two operations in this model.

For example : I don't understand how the cells in S1 are constructed...


texts: Why can't we always create a vaccine against a virus when an ELISA test to detect it is possible?

texts:
Before precising my question, here are some facts that I presume to be true:

A vaccine works by injecting the antigens of a virus into the body to train the immune system to recognize the virus and to be prepared to fight it if it shows up.
The ELISA test indirectly recognize the presence of a virus into a blood sample by testing the presence of the antigens of the virus and the antibodies that fight against it.
One of the reasons there are still no vaccine against HIV is because this virus has a very high mutation rate.
The ELISA test is used to detect the presence of HIV.

I have the feeling these facts contradict themselves and I would like to know where I am misleading.

Indeed, if we have an ELISA test for HIV, we should be able to create a vaccine because we know the antigens of the virus and we can inject a harmless version of them into our body, right?
Apparently, the answer to this question is no because the HIV virus has a high mutation rate and the antibodies produced thanks to the vaccine won't be able to fight every mutation of the virus (that's the answer that gave me my former biology teacher in high school). But if the HIV has a high mutation rate, how can we be able to produce an ELISA test for it?


texts: What is the function of dendritic cell in immunity?

texts: I'm interested in how dendritic cells present antigens to  helper T-cells? I'm also interested in the molecular actions between a dendritic cell and a helper T-cell during the activation of the helper T-cell?  What function does the homing receptor on a T-cell have?


texts:
For my science fair project, I did an experiment on how paracetamol and ibuprofen affected the growth of bacteria. By day 5, however, parts of the paracetamol blackened (image below). I am wondering if E. Coli can metabolize paracetamol and if so, what operon in the K-12 genome is responsible for this.

EDIT: I realized it may be metabolizing other ingredients in the medicine I used. I am including a list of the ingredients in the medicine I used.

Acetaminophen 160 mg in each 5 mL (duh)

Other ingredients (33.015873 mL):

Anhydrous citric acid
FD&C red no. 40
glycerin
high fructose corn syrup
microcrystalline cellulose and carboxymethylcellulose sodium
purified water
sodium benzoate
sorbitol solution
sucralose
xanthan gum

I thought it might be the fructose, but is the byproduct really black? Still confused...


texts: Why the major gene model can be supported by finding de novo mutations in affected cases?

texts:
I found a sentence which I can't fully understand in a publication on the genetics of autism.

  The unified major gene model is supported by the significant increase
  in damaging de novo mutations found in subjects with ASD as compared
  to their unaffected siblings.

Is it saying under the major gene model, the de novo mutations comprise the majority of genetic risk?


texts: Lateral, axional and temporal resolutions for imaging in vivo

texts:
What are the spatial (lateral and axional), and temporal resolutions that one is expected to get with the following optical imaging techniques?

Optical Bioluminiscence Imaging (BLI)
Optical Fluorescence Imaging (FLI)
Multiphoton Microscopy (e.g. 2-photon microscopy)

Are they any better than the  others in providing higher resolutions?


texts: How do download a list of the gene length of all genes?

texts: I would like to get the gene length information of all the human genes. Is there a quick way to get this information? Thank you!


texts: Can Bioluminescence drive photosynthesis?

texts:
I'm trying to construct an anaerobic kitchen-waste digester at home.

The major output from the digester is methane - with a significant component of carbon dioxide. To scrub/reduce the CO2 I was thinking of passing the methane through a freshwater container charged with algae ... then it occurred to me to also think of introducing some bioluminescent algae to drive the photosynthesis & absorb some of the oxygen released by the other algae. Understandably this would be an unbalanced system.

But ... can bioluminescence drive photosynthesis?


texts: What is a good approximate functional form for an equation relating plant growth to sunlight?

texts:
Question is in the title.  I've got daily measurements of daily mean shortwave radiation at the surface, and annual measurements of plant growth (some measure, be it height or biomass or something).

I want to fit a statistical model

$$
growth = f(light) + \epsilon
$$

Assume that all other conditions are near-optimal, for simplicity.  What is a good first-order approximation for how to specify $f$?

For example, could it be:

Average daily light over the growing season?
$$
growth = \beta_0 + \beta_1\bar{light} + \epsilon
$$
Average daily light for each month?
$$
growth = \beta_0 + \displaystyle\sum_{months}\beta_m\bar{light_m} + \epsilon
$$
Maybe it's quadratic?

$$
growth = \beta_0 + \beta_1\bar{light} + \beta_2\bar{light}^2 + \epsilon
$$

Obviously something so simplified will never be perfect, but what's a good rule-of-thumb that'd cover most situations reasonably well?


texts: Why does UVA penetrate deeper than UVB, though it's weaker?

texts: Even though UVA radiation ranges in longer wavelengths (315–400 nm) than UVB (280–315 nm) and thus is less energetic, UVA is able to penetrate deeper into the skin and even reach the dermis. Why is there such a discrepancy?


texts: Identify this smooth-cocoon worm from Southern India

texts:
I couldn't identify which species these worms belong to. I believe they're insect larvae.
They measure approximately 5 to 10 mm in length, and are common in the southern states of India. They carry cocoons, open at both ends, which the worms can wriggle inside and alternate their direction of movement. These cocoons are perfectly smooth except for the openings.
Another post shows something similar, but the cocoon of that worm looks more woven, while this one doesn't.


texts: How plasma cells switches secreting different Ig classes?

texts: In Type 1 hypersensitivity how do B lymphocytes switch Ig classes, from synthesizing IgG to IgE? What is the mechanism? I studied multiple pathology books, it says the same as for IgG secreting pathway. So how does the body know how to change the Ig secretions in response to allergens?


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

texts:
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.


texts: Normal cell diffusion in normal organism?

texts:
We know, that cancer cell can travel across an organism.

Is this ABSOLUTELY impossible for NORMAL cells?

For example, is it EXACTLY ZERO probability to find some bone cells inside liver or some skin cells inside brain?

In non-living things and with molecules this is called "diffusion". Any two contacting things will penetrate inside each other after hundreds and thousands years.

Is something similar happening in living thing?

May be very slow?

Was this phenomenon searched for?

Are there some protection mechanisms against appearing wrong tissue cells inside another tissues?

I understand that cells appear in their places during grow, but in mature state I think it is not impossible for cells to travel.

UPDATE

I know that there are many cells that travel by nature, like blood cells.

The question is namely about "static" cells, those ones we normally regard as non-travelling.

Also, I understand that there are some mechanisms, making cells to prefer their normal places when they divide and grow.

But the question is what about all these mechanisms failed? And how often it happens?

For example, I am 40 y.o. So, how many bone cells from my legs are currently in my brains? Zero? One? Million?


texts:
I am studying biology by myself via distance-learning. I have been trying to solve the following problem for a while now and hoped you could help me. As this is "homework" I would appreciate hints rather than solutions.

Drosophila has a gene "yellow body", $y$, on the X chromosome. The other, dominant, allele is "grey body", $y^+$.
When crossing female grey bodies  with male grey bodies we get 50% grey females, 22% grey males and 28% yellow males.

What is the genotype of the parents?

My work so far:

The genotype must be $Xy^+X?$ for the female and $Xy^+Y$ for the male.
There are two cases to consider: $?=y^+$ or $?=y$.
In the former we get $\frac{3}{8}$ grey females and $\frac{1}{8}$ yellow females and $\frac{2}{8}$ grey and yellow males each; that seems correct except for the yellow females.
In the latter, we get twice as many yellow females.

Perhaps the XXyy (yellow females) genotype is lethal but this doesn't help in determining the parents' genotypes.

If $? = y$ then cross-over from $Xy^+\mathbf{Xy} \; x \; \mathbf{Xy^+}Y$ would not eliminate yellow females.

I don't know of other effects to take into account, so I am stuck.

$ $

If you'd like to suggest resources (websites, textbooks $\ldots$) pertaining to this subject or on biology at this level in general, I would very much appreciate it.

Thank you.

Edit: I'd like to add an image for anyone having a similar problem.


texts: Did modern alligators and caimans come from prehistoric crocodiles?

texts:
I know that crocodilians have been here since the time of the dinosaurs. I also know that crocodiles came first. But alligators have been here for a good 37 million years. Did alligators come from crocodiles when the crocs swam into freshwater areas?

And since the alligators and caimans are 2 groups in alligatoridae did they have a common ancestor?

And also if alligators came from crocodiles (which might or might not be true), why isn't it more like this:

Crocodylidae $\rightarrow$ Alligatoridae $\rightarrow$ Alligatorinae $\rightarrow$  Alligator

for alligators and

Crocodylidae $\rightarrow$ Crocodylus

for crocodiles?


texts:
everyone. I've just been introduced to the procedure of Western blotting from my reading, though I'm not entirely sure about some points. I'd appreciate it if someone could help me with this.

What exactly is the function of the blocking buffer?

Why does one need a secondary antibody?

When discussing nitrocellulose membranes, say of a 0.45 5m pore size, what does 5m refer to?


texts: Where does the energy required to turn ADP into ATP come from?

texts:
My teacher states that in order to convert ADP into ATP, energy from respiration is required.

However, I watched a video which states that energy from the son is used to turn ADP into ATP.

Which is correct?


texts:
I think i found very interesting lichen. I discoved it at 1.15 PM CET in Prague nature conservation area called Divoka Sarka.

I took this picture on the place of my discovery.

One piece of this specious had cca. 6 cm. And it look like a shrub.

And this is micro photograf with magnification about 200X.


texts: Can acid-fast M. tubercolosis obstruct alveoli?

texts:
I am not sure which word is the best here for colonisation of alveoli by acid fast-mycobacteria. I found this question, and I am getting confused by the term obstruction of alveoli because I tend to relate it to COPD which is not a case here:

Which of the following is the predominant pathogenic mechanism of tuberculosis?

a) cell-mediated hypersensitivity
b) obstruction of alveoli by large number of acid-fast mycobacteria

I think the right answer is "obstruction of alveoli by large number of acid-fast mycobacteria", but I am not sure if you can say that acid-fast mycobacteria obstruct alveoli.

Are acid-fast mycobacteria "obstructing" alveoli or just colonizing?


texts:
Can anyone please help identify this insect. It seems to be some sort of caterpillar but I'm stumped.

Location is in Suffolk, United Kingdom
Length is around 1cm, width is perhaps 4 or 5mm.

Image opens a video clip on YouTube.


texts: My feeling is that almost any observation can be explained by current evolutionary theory. Is there any example of someone developing a rigorous framework or mathematical model of how evolution works?


texts: I am writing an argumentative essay in which I claim that GMOs are safe. I know, it is not proved, but for the sake of my course I want to prove it. The counterargument that my professor said to me is that genetic modification is not like selective breeding. GM brings changes faster and most of the cases it is inevitable. We don’t know the consequences and they can be bad. On the other side selective breeding is changing the organism slowly and something bad can be prevented in the start of its development. What are disadvantages of selective breeding to compare with genetic modification? Can I use the mutagenesis as the example of selective breeding and use its cons?


texts: A little backstory, I was trying to get something that was in a little wooded bit at the back of my garden and stepped on a swarm of wasps was stung 3 times and got out of there but I brought 8 wasps inside and was wondering if they know if you've been stung and are attracted to it and also out of curiosity what would happen to a wasp if it was stung by another wasp


texts: Source of information on the evolution of aging/senescence

texts:
Do you know a good review (published peer-reviewed or an online course or whatever) that offers a good overview of all hypothesis explaining the various patterns linked with aging?

I'd like this review to make the following things clear; antagonist pleiotropy, Gompertz and Weibull models and what theoretical explanations are underlying these models, mutation accumulation, reliability theory, eventually group selection, age-specific efficiency of natural selection, telomere length, the definition of senescence, and all not-cited hypothesis to explain the patterns of aging/senescence.


texts:
I have a general question regarding which method would you recommend me to use if I would like to investigate the difference in the level of several proteins in tissue samples and compare different treatment groups. I could either do an LCMS/MS or a Western blot. Which one would you recommend and would you do both for validation? I am looking for time- and cost-effective techniques.
I'll appreciate any suggestions.
Thanks!


texts: I have coded an implementation of L-systems (Lindenmayer systems) and would like to use it to generate realistic looking trees. Is there a reference list that shows which rules are most appropriate for different types of trees? For instance, which rules are best for an oak tree, which are best for cherry trees, etc.?


texts: Is the regulation of lactose operon different between Gram + and Gram -?

texts: I know that in E. coli the lactose operon is shut down by CAP protein when binding cAMP. Is this true also for Gram positive bacteria?


texts:
On the website www.yourhormones.com it is written:

  "If there is insufficient thyroid hormone available for the brain, this will be detected by the hypothalamus and thyrotropin-releasing hormone will be released into the blood supplying the pituitary gland."

What allows the hypothalamus to detect a lack of thyroid hormones? Are there chemoreceptors in the bloodstream that send afferent signals to hypothalamus when the concentration of thyroid hormones is low (similarly to how chemoreceptors inform the cardiovascular center of the medulla oblongata in the brain stem when there is a lack of oxygen and/or excess of carbon dioxide)?


texts: Has any scientist elaborated on the "selfish neuron" hypothesis?

texts: Daniel Dennett references a talk by Sebastian Seung, where the latter speaks about "selfish neurons". I've been trying to learn more about this hypothesis, but cannot seem to find anyone who has elaborated on this line of thinking. Could someone point me to some resources, or this an idea whose time has not yet come?


texts: blastn: What substitution matrix is used?

texts:
I'm currently working aligning sequences, and I need to compute similarity between pairs of DNA 'words' of a particular length.

For amino acids I am able to use the substitution matrices in Biopython (Bio.SubsMat.MatrixInfo).

However, I haven't found anything similar for DNA, so I read up and found that most systems use a match/mismatch scoring system where each nucleotide match and mismatch is scored and then the scores are summed. This works fine as long as I am only dealing with A, G, C, and T, but I run into problems when I get a sequence containing N or M and the like (meaning nucleotide unknown).

Is there a standard way to handle the situation with unknowns? That is, how do I score A versus N or M versus N?

Thanks in advance.


texts: tetrads in meiosis are held together by what

texts:
This is from SAT subject biology test practice question. The answer it gave me was both chiasmata and centromeres. I can understand they are held by chiasmata but why also centromeres? I looked it up, I didn't find anywhere mentioned that they are held by centromeres also, only synaptonemal complex and chiasmata.

tetrads are truly held by spindle fibers on centromeres too, but isn't the question asking what hold them together? Even without spindle fibers, they can still be held by chiasmata I guess.


texts: Why do large neurotransmitters travel faster down the axon?

texts:
I understand that with large neurotransmitters, like neuropeptides, the precursor neurotransmitter and the enzymes are produced in the soma and quickly travel down the axon to be modified in the axon terminal.

With the small molecule transmitters, the enzymes are made in the soma and then transported slowly down the terminal to the terminal where they synthesize the small transmitters.

Why is it that the precursors and enzymes for large neurotransmitters travel fast down the axon, whereas the enzymes for the small transmitters travel slowly? Is there a specific reason?


texts: Can allelopathy succesfully be used against algal blooms?

texts:
Algal blooms caused by man (harmful algal blooms) are a major ecological problem. An excessive amount of algae causes hypoxia and logically, most marine wildlife can't be sustained in hypoxic conditions.

Can't we use allelopathic plants to reduce the amount of algae significantly?


texts:
I am not sure which project database to use UCSC or Ensembl for my asthma study about ADRB2 gene (Arg/Arg-16 genotype).

I am using the original Human Genome Project database at the moment.
However, I think Ensembl may be better suited for me.

Which genome database is good for Asthma research for Single Nucleotide Polymorphism (SNP variations)?
I am looking for something which has existing visualisation tools or one where you can easily write one yourself.


texts: Is there a relationship between Melatonin, Norepinephrine and depression in humans?

texts:
I'm reading a booklet on melatonin published in 1996, titled "Melatonin and the Biological Clock". This particular paragraph caught my attention and I would like to better understand what it means:

  The requirement of intact beta-receptor function for melatonin
  synthesis, and the stimulatory effect of norepinephrine on melatonin
  synthesis and release, point up a theoretic relationship of melatonin
  to depression.

I've been looking at the biosynthesis of norepinephrine  and tryptophan metabolism and do not see how the two cycles are connected. Is there a connection between the norepinephrine system and the melatonin synthesis in humans?


texts: Honeybee decision process: new food, new home, new threat

texts:
I have heard that honeybees send out scouts, then based on the scout reports more bees go then come back and report and so they are supposed to be efficient decision makers.

Can you give as complete as possible of a description of how honeybee decision making works with regard to:

finding new food/water sources for the hive
deciding where to place a new colony
how they determine if a big enough predator is around to merit a swarm

If you could point to published material that would also be appreciated.

Some links:

http://link.springer.com/article/10.1007%2Fs00265-011-1298-8?LI=true#page-1
http://cis.uws.ac.uk/research/journal/V9/V9N3/bees.pdf
http://www.igi-global.com/article/honey-bee-swarm-cognition/44981


texts: Mesophytic Climax community in succession?

texts:
My textbook says that in all cases of ecological succession (xerarch, hydrarch, etc.), the ultimate climax community, assuming constancy of environment, is a mesic community. Xeric or hydric pioneers are ultimately succeeded by mesic climax communities. Why is this so? In an environment under consideration, if for example water stress prevails (characteristic of xeric environments) shouldn't the final community be xeric and hence better adapted to the environment? Is my book wrong, or is there something I am missing in the understanding of the development of climax communities?

Moreover, I did find it written somewhere that mesic communities do depend on the climate of the place. But then doesn't the fact it is mesic contradict a few climatic conditions wherein ecological succession might occur?

Reference:-
Ecological Succession
Climax Community


texts: Dimethyltryptamine binding site on Sigma 1 type opioid receptor?

texts: I asked this question Dimethyltryptamine and Sigma 1-type opioid receptor interaction but it seems that I didn't express myself well. I was looking for the place on Sigma 1 type opioid receptor where dimethyltryptamine binds rather than the location of Sigma 1 type opioid receptor.


texts: Can the activity of a specific gene in a cell artficially be increased?

texts: While there are many gene regulation mechanisms from the cell itself, I was wondering whether it is possible to increase the gene activity in a living cell permanently (so that the protein that it codes for is produced in higher amounts) using methods of biotechnology (i.e. no external factors)? Are there any studies or experiments regarding this topic?


texts: What can pass through the intestinal membranes?

texts:
As I understand it, most substances need help to pass through the walls of the intestines.

For example, in hepatic recirculation (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781307/) bile salts are grabbed and transported across the intestinal membranes by particular polypeptides.

Is there a summary of the sorts of things that can be transported across intestinal membranes? For example, hormones, stearates, lipids, etc. What general classes of molecules can pass the membrane and what cannot?

I am not looking for an exact answer, but a general characterization of major classes of organic molecules and their ability to pass through intestinal membranes into the body.


texts: How much time does it take for the naive T Cell to get activated?

texts: Suppose a naive T cell comes in contact with an APC. How much time does it take for the T Cell to get activated and within how much time does the T cell move away from the APC due to incompatibility in their receptor structure? What is the probability that there will be activation of a naive T cell by an APC (I mean to ask that how many T cells should come in contact with APC before a T cell gets activated, some number like say 1 out of every 1000 t cell gets activated by an APC at a particular time)? Any resource you can provide that gives a quantitative value of the interaction of T cell with APC, please do if possible.


texts: Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?

texts:
Background

The standard definition of species refers to the concept of reproductive isolation. If two lineages are found to be reproductively isolated, then we consider these two lineages to belong to different species. My question concerns evolved reproductive isolation in Drosophila sp. following labs due to experimental evolution.

Question

Have we ever demonstrated that two Drosophila sp. lineages that could initially interbreed (in nature or in labs) evolved through artificial selection (and drift and mutations) in labs to finally not be able to interbreed anymore either due pre- or post- zygotic isolation (see wiki)? Or, in other words, have we ever demonstrated that two drosophila lineages evolved to become different species (reproductive isolation definition) in labs experiments?

If not, have we ever observed some partial reproductive isolation such as inbreeding depression for example?

Note: This question is motivated by @LotusBiology that could not receive the answers she/he was waiting for because he/she failed to ask questions that are possibly answerable! So I wanted to ask this question that somehow addresses this question he/she asked (now on-hold)

For more information about the concept of species, please have a look at How could humans have interbred with Neanderthals if we're a different species?


texts:
Ok, this question seems like it may be impossible to answer, but would be interesting to see if anyone has an idea.

Throughout the course of a human life, do we make more molecular bonds than we break, or vice versa?


texts: What does probe number and segmentation mean in copy number variation (CNV) data

texts:
In TCGA Copy number variation (CNV) data there is a column with title Num_Probes. What is the meaning of probe number with respect to the sample data below?

Chromosome  Start   End Num_Probes  Segment_Mean
1   61735   62152   4   1.1973
1   62920   12777697    6514    2.2882

According to wikipedia, probes are usually 100-1000 bases long. Then does it mean in the first row above that, it took 4 probes to identify the region(61735 - 62152). In that case what would be the meaning of Segment_Mean?


texts:
I would like to fully understand the phase shift in the grid cell in MEC. From my understanding, since there is a hexagonal (i.e. equilateral triangle) lattice, and hence there are 3 $\phi$'s, I have the following questions in regards to that:

1). If there are 3 $\phi$'s, how does the phase shift happen in (I guess) 3 phases, i.e. why are there 3 shifts? I am just very confused at a fundamental level: why does the phase shift happen, is it because of the phase resettling in neurons?

2). As Wikipedia defines it: "Phase shift is any change that occurs in the phase of one quantity, or in the phase difference between two or more quantities", so my question is, what is the "quantity" in the example with grid cells or what is "the phase difference between two or more quantities" here?

In other words, why there is the 1st shift, the 2nd and the 3rd? Why do the second and the third happen? Is it because the pattern of grid cells is an equilateral triangle and the 1st type of signal produces the 1st grid field (the blob) and the 2nd type of signal produces the 2nd blob, here I edited this picture to illustrate my thought:

and we can see, if we model it with cosine, since


texts: When glucose production is low, the brain begins using ketoacids as energy... how does that work?

texts: Can someone very generally describe how the brain consumes ketoacids/ketone bodies when blood glucose has been completely depleted?


texts: Mechanisms of extracellular stimulation of neurons

texts:
When stimulating a group of neurons with an electrode, let's say we put it in a region that contains axons, what is the mechanism by which the axons are stimulated?

I've been told electrodes (usually silver or gold) must be coated with ions, usually chloride, to allow the passing of the stimulus. So I'm not sure if the stimulus is based on changing the extracellular concentration of ions by injecting chloride, therefore changing the membrane potential with a depolarization (elevating the potential, possibly generating an action potential). Let's call this idea A.

The other idea, B, that seems possible would be having the ions in the extracellular fluid conduct the current to the nearby axons, thus changing the potential but not the intra or extracellular concentration of ions.


texts: Does a queen wasp sting also have poison?

texts:
Last night I got sting by a wasp and because of the time of the year I suppose it is a queen. But usually it swells and hurts for a day after it, but this time nothing happened only that I woke up of the sting which hurt a little for a short time, but in the morning I couldn't find any signs of the sting.

Now is this because of the poison is worked out because it could be a pretty 'old'  new wasp queen and her enzymes like histamines and aptoxine are got too old? Or do queen wasps not use/have poison or less? Or is it my body that just reacted different?


texts: What, if anything, would prevent flying fishes evolving to be capable of extended flight?

texts:
This extraordinary video documents a flying fish gliding above the surface of the sea for nearly two minutes. Occasionally it uses its tail for added impetus.

It is possible to imagine a fish gliding like this for longer and longer. However it would still be gliding. Is there any physiological reason that these animals couldn't evolve to flap their 'wings' and even learn to soar?

Another consideration is why this should happen. As I understand it, the behaviour is an adaption for escape from predators.  They do not fly in order to catch prey. What prey might they hunt in the air in the ocean?

Questions

Is there any physiological/anatomical dead-end that would prevent flapping/soaring from evolving?
Is there any adaptive reason that flapping/soaring should evolve?


texts: What is this red little cocoon like creature here?

texts:
I found this bug here outdoor on the wall of my backyard. I’m in California.
Red and looks like a cocoon, notice some tiny dots on its back. About 1cm.
Does anyone know what kind of insect is this? Seen it there for a few days now.
Thanks


texts: How much DNA of Albert Einstein is recoverable?

texts:
Since there seem to be five biological descendants of Albert Einstein, and the original chromosomes of him distributed among them ...

Is it possible to recover enough DNA of an individual from his progeny and proceed to clone him? Any information would be helpful


texts: How does human body keep track of its age?

texts:
How does the human body knows that it's time for a event that happens around a certain age like puberty or something that's periodic like menstruation or gestation time of 9 months?

Please note I'm NOT talking about day-night biological clock .


texts: Are there hyoid bones of Homo habilis in the fossil record?

texts:
Hyoid bones have been found for Homo erectus, Homo neanderthalensis, Australopithecus afarensis, and some more hominids. Have hyoid bones been found from Homo habilis?

References:

Capasso, L., E Michetti., & R, D'Anastasio. (2009). A Homo Erectus Hyoid Bone: Possible Implications for the Origin of the Human Capability for Speech. Coll. Antropo. 32(4), 1007–1011

Alemseged, Z., Spoor, F., Kimbel, W. H., Bobe, R., Geraads, D., Reed, D., & Wynn, J. G. (2006). A juvenile early hominin skeleton from Dikika, Ethiopia. Nature, 443(7109), 296-301.

Steele, J., Clegg, M., & Martelli, S. (2013). Comparative morphology of the hominin and african ape hyoid bone, a possible marker of the evolution of speech. Human biology, 85(5), 639-672.


texts: What is the acceleration profile of the greyhound?

texts: I'm interested in the acceleration curve over time that's typical of an adult greyhound prior to attaining this peak velocity. My curiosity is motivated by a desire to understand the biomechanical reason why land mammals run so fast.


texts: What magnification do I need to see blood cells?

texts: If I want to buy a microscope for my kids to be able to view single celled creatures and blood cells, about what magnification is required?  A Celestron Pentaview digital scope claims up to 600×. Is that going to be sufficient? I somehow get the impression that I'd need 2000× or better, but I'm having trouble verifying any information about magnifications via my good friend Google.


texts:
I researched about floral diagrams and this is what I found:-
This is floral diagram of Theobroma cacao. I managed to identify others but this part near the stamens was not found anywhere.
Also the floral diagram includes some circular parts which I have highlighted.
So what exactly are these parts called?
https://en.wikipedia.org/wiki/Floral_diagram


texts: Protein content in chemical composition of different phyla?

texts: The protein content in the human body is roughly 15%, what are the percentages for other organisms? Bacteria, plants, fungi, protozoa, etc.


texts: Is there a protein in the eye that gets kinked by photons and shipped down to the liver to get un-kinked?

texts:
My friend made the claim that there exists a protein in your eye responsible for vision. This protein is sensitive to different wavelengths of light, and when it gets hit by the right wavelength, it kinks. In order to be un-kinked, he claimed, it has to be shipped down to the liver, and then back up to the eye.

He teaches organic chemistry at UCLA, so I trust him a little bit. But I couldn't find this with a quick search. Anyone know if this is legit?


texts: It was found in the state of Virginia, on the east coast of the United States.


texts: When contracting a muscle will the muscle spindle stretch or contract?

texts: When you contract your muscle, will your muscle spindle stretch or contract? And why? I was always under the impression that it was contracting your muscle spindle, but now I am not sure.


texts: Why doesn't the cell membrane just...break apart?

texts: Forgive me if this is a silly question. I can't understand the basics. Why doesn't the cell membrane just break apart? What's keeping the layers in the phospholipid bilayer together? I know that the membrane is embedded with proteins and lipids, but I still can't wrap my head around the "why". Are the hydrophobic interactions in the middle "stronger" than the hydrophilic interactions on the outside? What's keeping the individual phosphate heads together instead of, say, one of them just drifting away due to a nearby water molecule?


texts: Can Naegleria fowleri enter through the eyes ( example rinsing/splashing eyes with water)

texts: I understand that it primarily enters the body through the nose by by "feeding on the olfactory neurons in the nose" as answered here in a different question. Would the nerve cells in the eyes present a similar entryway?


texts: Identity of strange bird with fish net tangled around one foot

texts:
This bird was photographed at a small beach in Rio de Janeiro, Brazil.

What kind of (ocean?) bird is this??


texts: What is the difference between spidroin-1 and spidroin-2?

texts: So I'm doing a research project for my school and I'm trying to decide on the exact nature of the project. My current plan is to try to genetically engineer E. coli or Yeast to produce spider silk protiens. However when trying to find an appropriate gene for my project I learned that the common house spider's silk has two different spidroin protiens. Just by a simple google search I can't tell the difference. So, what is the difference between spidroin-1 and spidroin-2


texts: Are there any alternatives to DNA as the hereditary material on Earth?

texts:
I wonder are there hereditary materials other than DNA  deoxyribonucleic acid (may be on different planets).

In addition, I learned in my high school that carbon and silicon are similar. Is it possible to have hereditary materials with silicon replacing carbon.

Why and why not?


texts: What is the highest number of genes expressed under one T7 promoter? Also, what is the longest polycistronic mRNA? I am interested in the context of heterologously expressing biosynthetic gene clusters in E. coli.


texts: Identification of a bug, Anobium punctatum?

texts:
At first I feared that our old building was attacked by Anobium punctatum. But now, I'm not so sure.
Each week we find 2-5 of them around our apartment. What are they? and should we worry?

The bugs were found in our apartment in Denmark.

UPDATE Added Picture of Antenna


texts: Are there two varities of dandelion leaves?

texts:
This is in India. I noticed a dandelion plant which had the familiar leaves.

Right next to it there was another plant which had similar flowers and white tufts, but the leaves were different.

Is the second plant also dandelion? I'm asking because I was considering feeding the leaves to my budgies, but needed to know if it is a dandelion, to avoid having the birds consume a toxic plant species.

Did a Google search, but all of them show the arrow-style leaves only as dandelion.


texts: Here are two lepidopterans I collected in Oregon (USA). The wingspan of the bigger one (on the left) is ~4 cm. I spent a lot of time browsing this website hoping to find a match, but I didn't have success.


texts: Why does rapid decompression make you lose useful conciousness so fast?

texts:
I was watching Smarter Every Day's episode on hypoxia, and it had an interesting chart that suggested that at 35kft, you have less than 10 seconds of useful consciousness.  This number seemed low, and I'd like to know why.

I have two pieces of evidence that make me question the chart (even though I know Destin from Smarter Every Day doesn't make mistakes lightly):

I can hold my breath after an exhale and function for well more than 10 seconds
It seems to me that the vacuum of space would be the ultimate test for how long you can sustain consciousness without oxygen, as the vacuum of space literally strips oxygenated blood as it passes through the lungs.  Wikipedia cites sources claiming you go unconscious in under 14 seconds, and a case of accidental vacuum exposure that resulted in a loss of consciousness in 15 seconds.

So why is it that the "useful consciousness" table seems to contradict these datapoints?


texts: Why do doctors use a new thread for each stitch?

texts: Why do doctors use a new thread of the same kind for each stitch instead of using a single thread for the entire stitch?


texts: I live in Moscow, Idaho and saw this guy early in the morning last week. It was about quarter sized if I recall. I've never seen one before and was in a hurry so I couldn't get a better picture, sorry.


texts:
Flies have a short lifespan, therefore evolution should technically happen over a shorter period of time (years).

Flies die all the time from getting hit by cars on the motorway.

Those flies that don't go near the motorways have a greater chance of reproducing.

If this was an advantage (motorway avoidance = not dying), shouldn't more and more flies be avoiding the motorway?

Cars have been around since, roughly ~1950. That's 60 years.

Why don't flies avoid the motorway?


texts: How to mimic / approach some animals/insects' anabolism?

texts:
This article states that some shelled animals - spiders, scorpions, crabs, worms and other creatures - have metal atoms in their claws, jaws and fangs.
I believe through anabolism, since they eat sand, soil and insects that are full of a mix of those.

For most human beings, it would seem silly to eat soil or sand, or even insects - and yet, I wonder if our bodies would be able to digest and create anabolic processes around, for example, metals, in such way that we would end up having stronger bones / teeth / hair / nails (or other things).

To a certain extent, I also wonder how anabolism isn't use to regenerate cells that become old or faulty in the body as we age or get sick (a special diet would help "regenerate" blood balance, feeble skin, brain cells, etc, if we knew what foods would turn into these cells the best by anabolic process).

This question is becoming a bit confused, so I'll end up rephrasing it: is there a document / research / map / experiences of all the foods & materials that the human body can not only digest (and in what quantities) but also how they transform into our cells (and a list of foods / materials that are NOT taken into account by anabolic processes). I.e., at what speeds they can become part of us, and how they can/could change and alter the body cells in a strengthening kind of way (not in a way that makes us sick or dead).

NOTE: I am not a scientist, just a writer, but I am fondly interested in the subject.


texts: Databases for gene regulatory network graphs?

texts: What databases are available for gene regulatory network graphs starting from a given gene? For example, starting from p53 gene, where can I find a gene regulatory network image that can be exported or embedded to another website?


texts: Simple question, how is it possible that there are people who appear to have 10 pack abdominal muscles while the human body has only eight?


texts: Chromosomal pair possible in metaphase - I

texts:
There is this question which was asked in my exam.

A diploid cell contain 6 chromosomes. How many possible random arrangement of homologous chromosomes could occur during metaphase-I?
 (consider that allele for only one character present on chromosome and they are in heterozygous condition.)

Options are :

i)4

ii)8

iii)16

iv)64

Answer given is : ii)8

But my answer is : i)4

My solution :

Aa       | Aa     | Aa     |  Aa

Bb       | Bb     | bB     |  bB

Cc       | cC     | Cc     | cC

Here,  1 column represents 1 possiblity.

These are the possible combinations according to me in metaphase-I.

Am i missing something?

Please tell me where am i wrong.

PS : i would have loaded the picture of my solution but it ain't getting loaded.
Sorry for any inconvenience.

Thank you. =)


texts: What are the structural characteristics of a protein-protein interaction network

texts: I am an researcher in computer science. I am interesting in the alignment problem of PPI networks of difference species. I know a PPI network is a graph in its nature. I want to know whether there are any structural characteristics or constraints of a protein-protein interaction network (such as, a certain kind of protein can only have certain kinds of interactions with other proteins, a certain kind of protein can appears in a PPI network at most certain times, and any thing like this). If a PPI network does't satisfy these structural characteristics or constraints, then people can know that this PPI network is not a valid one.


texts: In an open circulatory system, how is blood moved?

texts:
In the mollusks section, the powerpoint mentioned that gastropods and bivalves have an open circulatory system. According to the note, this means that the blood does not travel in vessels. How, then, does blood move? Does that mean that these organisms are simple enough to be able to survive by just pumping blood straight out into the body?

How does this type of circulatory system work?

Thanks!

evamvid


texts: Want to know about a creature which bite me

texts: I am Sachin from MP India. Few minutes back I have gotten bite by a creature. What is its name? Is it harmful if I got bitten by it? Feeling little pain there.


texts: Which kit provides the highest yield and purity of extracted DNA from FFPE tissue samples?

texts: I'm looking to extract DNA for sequencing from FFPE (Formalin fixed paraffin-embedded) tissue samples. I'd like to use a commercial kit that provides a high yield of good quality DNA.


texts:
What happens when my ears are popped?

I understand it increases the air inside there which makes my volume louder, what happens after that, do my ears gradually readjust back to the air pressure that they were before?

What causes ears to (need to) be pressurized/depressurized?


texts: Do we know of any "species ending bugs"?

texts:
Are we aware of a "bug" (virus, bacterium, prion, ...) that has completely exterminated an entire species? Either through direct observation or maybe some form of archeological evidence? If not, are there realistic scenarios where this could happen?

I am primarily interested in cases where the disease was the driving factor of extinction of an otherwise well established and healthy population, but examples of species that were in bad shape to begin with are welcome as well.

My understanding is that this is unlikely, since very deadly infections tend to burn out or evolve towards being less deadly. Killing your host is not conducive to your survival. But maybe it would be possible to reduce the number of individuals so much that reproduction became problematic. I imagine a species confined to an island or something might be susceptible.

I'm asking this because in an interview I saw, an epidemiologist said that his usual research interest are "bugs with species ending potential". The interview was on COVID-19 so he didn't elaborate on what he meant by that or give any examples.

For the special case of humans, I was able to find this article that claims such an event to be unlikely, but I suppose we are the best equipped species that has ever existed on this planet to deal with such a threat.


texts: Identifying Promoters in Non-homologous Sequences within the Same Organism

texts:
In this paper, the authors cloned a GPD promoter for use in driving a GFP gene from Lentinula edodes using a set of provided primers. The primers were derived from the following accession GQ457137.1 containing the GPD gene for this organism.
In fact, there are three accessions in GenBank containing gpd promoter sequences for Lentinula edodes, each of varied size and homology to the aforementioned sequence used in the paper.
I am working on defining a transformation protocol for Psilocybe cubensis (of which there are no published transformations) and I would like to design some primers as done in the paper above in order to clone the GPD promoter for this organism from its DNA; however, just as with L. edodes, there are multiple accessions of GPD in psilocybe cubensis: KM273235.1 and KT067727.1
In my case; however, there is no literature referencing either of these accessions and so I don't know which of these accession I could or should use to design my primers.
I have the following questions:

Why does the same promoter within the same organism have such varied sequences?
If the promoter sequence varies even within the same organism, the how can anyone extract the promoter with certainty since the organism may carry a different sequence for the promoter?
Generally, I'm trying to find the GPD promoter for P. cubensis (or any strong promoter) and clone it for use in my plasmid for transformation. I'm stuck as to how to go about finding a suitable candidate.

Thank you.


texts:
I am reading about the biology of depression and came across something I can't understand. Here is the thing:

Lesch K-P, et al. (1996) say that people with short alleles of 5-HTTLPR are more prone to anxiety and depression. Pezawas (2005) also say that short allele carriers have worse anterior cingulate cortex - amygdala connectivity, which is observed among MDD patients. This, however, doesn't make much sense to me, since I'd expect people with short allels to have underperforming serotonin transporter - and isn't it overperforming serotonin transporter that contributes to depression by preventing serotonin transmission by sending it back to the presynaptic neuron? So, wouldn't you expect people with long alleles then to be prone to depression more?

To complicate things further, Willeit et al. (2008) do say that enhanced 5-HTT is observed in Depression. And enhanced 5-HTT would be found in people with long 5-HTTLPR?

So my questions are:

Do I understand it right that Willeit's (2008) results contradict
Lesch (1996) and Pezawa's (2005) results?
To the best of today's knowledge, is it the people with short or
long allels who are more prone to Depression? If the answer is -
with short, could you please clear up my confusion about it (see 2d
paragraph)?

I hope my question makes sense.

References:

Lesch, K., et al.(1996). Association of Anxiety-Related Traits with
a Polymorphism in the Serotonin Transporter Gene Regulatory Region.
Science, 274, 1527-1531.
Pezawas, L., et al. (2005). 5-HTTLPR polymorphism impacts human
cingulate-amygdala interactions: A genetic susceptibility mechanism
for depression. Nature Neuroscience, 8(6), 828-834.
Willeit, M., et al. (2008) Enhanced serotonin transporter function
    during depression in seasonal affective disorder.
    Neuropsychopharmacology, (33), 1503-1513


texts:
Endosymbiosis was crucial to the development of complex life and it continues to happen to this day. The origin of mitochondria see bacterial guests in archaea hosts, some of which later took in cyanobacteria which became chloroplasts. Modern "eukaryotes" have varying ranges of ancestry from these two domains with animals being about 50-50. More recent endosymbiosis examples include bacterial or protist guests in eukaryotic hosts.
But are there any examples of a bacterial guest endosymbiosis in a bacterial host? Bdellovibrio bacteriovorus enters other bacteria but it destroys them much like the lytic phage cycle. Bacteria inside bacteria inside mealybug cells have been found. However, this isn't an example of a bacterial symbiosis of another free-living bacterium or even of an extracellular animal-associated bacterium. Are there any examples of bacterial endiosymbiosis of bacteria that aren't intimately associated with the intracellular machinery of a eukaryote?


texts: Is there a mechanism of timing or delaying the expression of gap genes?

texts:
Summary

  Gap genes are expressed in presence of the right combination and amount of
  transcription factors. But is there any additional mechanism of timing the expression of the gap genes to ensure that they are expressed at the right time?

Context and Detailed Question

Let's look at gap gene expression in Drosophila:

Firstly, bicoid and nanos are expressed and diffused from anterior and posterior ends respectively and form gradients;
Then, hunchback gets expressed, with bicoid acting as promoter and nanos acting as suppressor;
Then, Krüppel gets expressed, with
hunchback acting as both promoter and suppressor - meaning that there must be enough hunchback, but not too much.

(or a video: https://www.youtube.com/watch?v=uaedzlrnBGY)

Makes perfect sense, unless you look at it from dynamic, biochemical perspective:

Firstly, bicoid and nanos slowly build up in the embryo:

As soon as there's enough bicoid at the anterior region, hunchback immediately starts building up too: I mean, it can't just choose to wait for bicoid to establish its gradient or something - if there's a promoter for it, it should react accordingly.

And so it "chases" the bicoid gradient, in a manner of speaking, and will continue to chase it until it stumbles into nanos protein, which suppresses it.

All this makes sense so far.

The only problem is that at this point, there's just perfect amount of it for Krüppel at the anteriormost region, so Krüppel should start being expressed there:

Eventually, there'll  be too much hunchback at the anterior region, so Krüppel should cease to be produced - but some quantity of it should be expressed there nonetheless. The final gradient should look like this:

The only way to avoid it is if Krüppel kindly waited until the hunchback establishes its final gradient before even attempting to be expressed. But how is this possible? Is there some mechanism that prevents Krüppel from being expressed too early - and if so, then what releases it? Or maybe there's some mechanism of timing, that prevents genes from being expressed too early?

This Krüppel example is just one examples of several, when there must be some timing control in order for genes to be expressed properly.


texts: I observed this beautiful insect near a forest in northern Switzerland. What is it?


texts: Can someone help me analyze this article?

texts:
I need to read this article — "Beyond the rainbow" by
Marie-Claire Koschowitz et al., for an exam.

Following are some questions for which I could not figure the answer out after reading.

1) Why does this miniaturization necessitates insulation ? Following is quote from article: "For fast-growing, presumably warm- blooded animals , such miniaturization would only have been possible with sufficient body insulation. "

2) Dinosaurs suppose to have tetrachromacy. The article mentions "dinosaurs were endowed with the highly differentiated color vision of birds". Does this mean Dinosaur's "inherited" their tetrachromacy from birds ? Why does the article mention reptiles before that ? Are birds reptiles ?

3) The article starts talking about how mammals develop fur and lost their highly differentiated color vision because they gave up structural color signaling. What is the direct connection between mammals and the dinosaurs ? I don't see the parallel here....why bring the mammals into the discussion ?

4) What is the connection between pennaceous feather and planar feathers ?

Any or all questions answered is welcome ! Thanks !


texts: What traits make mountain goats so well adapted to mountain living?

texts:
I've never really understood how mountain goats manage to survive so well in mountainous regions. I've seen them scale almost sheer cliff faces with apparent ease, and they can almost sprint vertically downwards without losing their balance.

How do they manage to do this? I can't see any discernible characteristics that would make them able to achieve this particularly well. For example, snow leopards achieve similar feats, but they have incredibly long tails and large paws to help with balance and agility, yet the skinny legs and hooves of mountain goats seem largely unfit for this purpose.

What adaptations do mountain goats have that allow them to survive in mountainous regions, and how do they work?

I'm hoping mostly for information on how they perform such feats of agility as to move around on very precarious outcroppings and such, but am also interested to hear about any other qualities that they may have to deal with the other mountain conditions (altitude/ cold etc.).


texts: Accessing Expression Levels for Genes of Interest from GEO Experiments

texts:
I have a list of 100 lncRNAs (long non-coding RNAs). For each of these RNAs, I would like to query GEO to find any experiments that used a high throughput sequencing platform and detected expression levels of that RNA in FPKM. To filter further, I'd like to have those expression levels found in controls only. The last filter is to find experiments which found the specific RNA's expression in smooth muscle tissue.

Here are some example lncRNAs:

CDC37L1-AS1
LCMT1-AS1
FLJ21408
CDIPT-AS1
LINC00920
TAT-AS1
SUZ12P1

Is there any way to do any of this? Any help would be appreciated.

Thanks.


texts: Do all humans experience flatus regardless of their diet?

texts: Flatus frequency is affected by diet, so I was wondering if flatus production solely depends on the food eaten, meaning that some people never ever release flatus because they don't eat any flatus-producing food. I guess if they say they don't, they're probably in denial...


texts: Does Dorsal Raphe Nuclei firing pattern change in response to voluntary breathing?

texts:
I'm reading this paper, which discusses how Serotonin may be involved in motor functions of mammals: 5-HT and motor control: a hypothesis .

The paper includes the following diagram of the Dorsal Raphe Nuclei (DRN) firing pattern in a walking cat, and cat on a tredmill. Each step is associated with a distinct firing pattern. I'm wandering if the DRN firing pattern, in humans, changes in a similar way in response to voluntary breathing?

After searching wikipedia, I found a line that says:

  REM sleep is turned on by acetylcholine secretion and is inhibited by
  neurons that secrete serotonin. (Psysiology of sleep stages)

I'm interested in dreaming, and at times have practiced entering dreams consciously, from the waking state after laying in bed for a long time. One of the obstacles to entring a dream was seizing control of breathing and starting to breathe voluntarily. This prevented me from entering dreams on a number of occasions, and appears to support the idea that voluntary breathing would affect the DRN. But I'm looking for a more scientifically-validated answer.

Thank you for your input!


texts: The number of individuals constituting a population is called population size.  Over time population size does not remain constant, it fluctuates to different extent over generations because of several internal and external factors.  Populations with violent fluctuation in population size are called unstable and are more prone to extinction as they hit lower population sizes frequently.  And once a population in extinct, it is gone for ever.  Thus it would be interesting to investigate how population stability evolves.


texts: Where is a coacervate located in the levels of organization?

texts:
I'm confused about where to position in the hierarchy of the levels of organization of living things, the coacervate in the context of Oparin-Haldane's theory of the origin of life. In short, according to such levels of hierarchy, where should a coacervate be put into?.
According to the Wikipedia entry, a coacervate is an aqueous phase rich in macromolecules. Upon further reading the article mentions that there are membrane-less organelles which are biomolecular condensates.
But does this counts as to say it is situated in the supramolecular or in the organelle level?. The article doesn't say specifics other than forming droplets. Can it be considered at par with a virus?.
Can some help me to clear these definitions?. I'm confused because the word droplet implies that it doesn't have any other distinct or specialized function, it seems to imply that they are only held together by weak bonds and nothing else.
Is there a reference or something? Can someone help me here?


texts: How to design an experiment with scent triggered memory recall in humans?

texts:
I've recently learned that scents can trigger memory recall in humans, and am thinking about setting up an experiment where I would attempt to induce memory recall through exposure to scents.

In order to help reduce the amount of experimentation required to actually trigger recall, I'm interested in - What kinds or qualities of scents have been demonstrated to trigger memory recall in humans? Are they pleasant smells/unpleasant,  sharp or subtle?

Is there any information about how long of an exposure is needed to trigger such recall? Is it 2 seconds, 15 seconds, an hour?


texts: How is the carrying capacity of a logistic growth model calculated?

texts:
I am reading a book in epidemiology where the carrying capacity for a standard logistic growth rate is given by

K = (b - delta) / gamma

where:

K is the carrying capacity
b is the birth rate
delta is the death rate

but what is gamma?

Thank you


texts:
Hello,

I was wondering if i could get an explanation as to why the charge of this peptide is +2 and -2. How do you figure this out? What is it based on exactly?

Thank you


texts: why is DNA antiparallel? Can it be parallel?

texts: My biology textbook mentions that DNA is antiparallel and it got me wondering... Can DNA be parallel? What would happen if it was parallel? could DNA still replicate right?


texts: Molecular genetics textbook (free?) suggestion for first time

texts: I have never taken a molecular genetics course but want to prime myself for graduate school in the future. Does anyone have any suggestions or advice? A professor recommends "the molecular biology of the gene - latest edition" but I dont have too much money to spend on a text and simply prefer free/digital formats. ( less to carry)


texts: What is the evolutionary explanation for bat's echolocation

texts: The bat's ability for echolocation is amazing (so are other the abilities of other animals). I was wondering how all of it came to be.


texts:
Can the lipid-soluble hormones (like steroid hormones) go inside every cell, as their particular receptors are located in the cytoplasm or nucleus of the target cells? Is there anything special on the membrane of the target cells which enables the steroid hormone to know that it has to enter that particular type of cells and avoid others?

(Peptide hormones function through cognate receptors located on the cell membrane of the target cell.)


texts: What is this plant/creature in my freshwater aquarium?

texts:
I've been noticing these really small creatures (or plants, I'm unsure) in my tank recently. They measure less than 1cm in length and I've only seen them at the bottom of my tank; some attached to the gravel and some to the glass. They have tentacle-like appendages on the end of their stem(?) and seem to drift with the with the water movement rather than on their own accord.

My tank is a planted tropical freshwater.

What is this plant/creature in my tank?

Any additional information on whether or not these are harmful to my fish would be appreciated.


texts: Is there a chemical reaction that blocks two cysteines by reacting with a third molecule?

texts:
The idea is to block the two cysteines so they can't react in the future. We need the reaction to remove the -SH groups of the two cysteines, or modify them.
Also important, the reaction should not make cross-link between the two cysteines.

To explain briefly my motivation: I am a PhD student and I do optical tweezer experiments. We can hold and manipulate two micrometer beads in two optical traps. We have a process to tether one protein using two DNA linkers to the two beads. I need to block two of the three cysteines of my trimer to properly couple the protein to both beads.


texts: Identification of that red and black bug

texts:
Found in France countryside, few hours ago, on a bushlike plant in direct sun light.

There is dozens of individuals, by groups of 5-ish, everywhere on the plant, along aphids, maybe sucking the plant's sap.

Looks like a stink bug, with unexpected colors. Some of them were attached two-by-two by their bottom (mating, probably ?).

Sorry for the bad photo quality.


texts: Are there organisms with fewer than 1000 neurons?

texts:
I'm developing neural networks comprised of just 3 to 10 layers of virtual neurons and I'm curious to know if there are any insect brains out there with fewer than a thousand neurons?

Are there any tiny creatures with small numbers of neurons?
Do neuronal maps exist for those simple nervous systems?


texts: Can the spike protein created by the Covid mRNA vaccines be created independently of the human body, and is there a higher cost to that?

texts:
How different in principle is using the bodies own mRNA to create the coronavirus spike protein differ from other methods of using genes to manufacture other drugs or proteins and is there a cost benefit to it?
Take the scheme for instance that uses genetically modified genes in goats to manufacture spider silk, as shown in this link - The goats with spider genes and silk in their milk or Yeast cells genetically modified to create morphine-like pain killer
I understand that in the case of the Covid vaccines the human body's genes themselves are not modified, but it is the principle of using the body's own cells as a manufacturer of some desired protein that I'm inquiring about.
Even without any cost-cutting benefit does the way Covid mRNA vaccines work differ in principle from other gene based compound manufacture?


texts:
So I play soccer in evening at a nearby park. I noticed many times that after the game and even during it many mosquitoes hover over some of us. They sort of form a structure like a tornado.
The more the one is sweaty, the more the mosquitoes.
What can  be the possible reason?


texts: Are there any studies that show that heavy metals escaped from landfills can cause any harm to human health?

texts:
I'm not sure whether it's the right SE for this question, so please redirect me if it's not. Are there any studies that show that heavy metals, for example from e-waste, can leak from landfills, into the groundwater, eventually into the human body and cause any harm to human health? You can easily find information about dangers that, say, mercury vapors poses for human health. There are studies that show a high concentration of toxic metals in bodily fluids of people who engage in e-waste dismantling operations in developing countries (they burn imported e-waste to obtain metals). There were experiments on animals that were exposed to mercury and then suffered from something or died. But it seems impossible to link a certain condition with heavy metals that escaped a landfill and were digested through running water. And yet, some researchers raise this issue of landfilled e-waste and heavy metals. They might say [1], "Heavy metals may escape landfills" and in another place, "Heavy metals may cause brain damage and neurological disorders". The two may not be explicitly connected but it's implied that heavy metal-contaminated e-waste dumped in landfills is a health issue. Are there any grounds for that (given concentrations and everything)? Please cite academic publications, if any are available.
[1]: 'Electronic waste management approaches: An overview', Waste Management, no. 33.


texts: Salt Bridge for Microbial Fuel Cell: Full or Partly Full?

texts: I'm making a microbial fuel cell out of benthic mud and salt water in containers. My salt bridge will be made of agar and table salt solidified in PVC pipes. Does the salt bridge connecting the anode (benthic mud) and cathode (salt water) have to be full of the agar-salt solution, or can it be partly full?


texts: Use of amino-acid sequences versus use of nucleotide sequences in phylogenetic analysis

texts:
Reading a  paper about gene evolution, I see that they do phylogenetic analysis for bacteria using protein sequences. They take the method from another paper.

I can suspect that amino-acid sequences are more stable than nucleotide sequences, to the presence of synonymous substitutions.... but, is this stability required between closely related species? doesn't it make the analysis less powerful? does it make it more reliable? In other words, what's the advantage of using amino-acid sequences versus using nucleotide sequences for phylogenetic analysis?


texts: Insect identification: white spotted beetle

texts:
3 pairs of legs, a pair of antenna, wings absent, compound eye, 4-6 centimeter approx. in size.
I found this beetle at my door, in Pune, India.


texts: Will a vasectomy prevent genetic engineering of a child?

texts:
Making the assumption:

  Within 10 years, an adult will be able to genetically engineer (modify, enhance, clean, etc.) a child from their own DNA (and the DNA of a non-related partner).

then would getting a vasectomy today preclude this?


texts: How compelling is the hypothesis that dinosaurs were killed by toxic plants?

texts: A friend of mine has recently told me that dinosaurs were "killed by flowers". I was a bit surprised and so I googled. And I did find a lot of recent articles in popular media on this topic, probably based on this. To me it doesn't sound convincing at all, but I'm an outsider. Does anyone think that there's more to that than just a usual journalistic overhype?


texts: What effect does vortexing have on a fluid sample that simple mechanical shaking does not?

texts:
Some protocols call for fluid samples to be mixed with a "vortexer" on the high setting.  What effect does the vortexing have on fluid samples that mechanical shaking does not?  Does it shear long molecules like DNA, for instance?

A friend is setting up a new lab and asked if vortexers were strictly necessary.  I am aware they are often called for in various protocols, but I actually don't know what specific effect the vortexing has that makes it better than manual shaking.  What do you think?


texts: What causes spontaneous muscle twitches?

texts:
Sometimes a small region of my body starts shaking, without any reason and then stops abruptly. Apparently this is a common phenomenon (source: NIH).  I researched its cause for a bit and came to know that it is because of nerve excitation.

Why do those nerves get spontaneously excited in the first place, without any conscious, voluntary, internal stimulus being presented?


texts: What are the differences and similarities between fimbriae and adhesins in microbes adherence factor?

texts:
Adherence factors in microbes is to attach to a host cell or to an extracellular matrix.
So what is the difference and similarities between fimbriae and adhesins?


texts: What is the relationship between induction of cell differentiation and DNA methylation status?

texts:
This may sound like a broad question to ask, but I am working on interpreting a review article for my epigenetics course and I'm having trouble reconciling two seemingly contradictory things this review is saying.

Ehrlich, M., & Lacey, M. (2013). DNA methylation and differentiation: Silencing, upregulation and modulation of gene expression. Epigenomics, 5(5), 553-568. doi:10.2217/epi.13.43

On page 554,

  Constantinides
  et al. found that treatment of an embryonic
  fibroblast cell line with 5-azacytidine (5azaCR),
  an inhibitor of DNA methylation, induces the
  formation of [myotubes] [35].

and

  Treatment with DNA demethylating agents
  can not only convert non-myogenic progenitor cells to Mt, but also can induce other cell-
  type interconversions in progenitor cells. For
  example, with 5azaCR treatment, the C2C12
  Mb cell line can be induced to express genes for
  key osteogenic transcription factors as well as
  adipocyte markers [40]. The outcome of DNA
  demethylation treatment is dependent upon the
  cell type as well as the treatment and growth
  conditions [41].

and

  The conversion of a multipotent adult stem
  cell to dissimilar differentiation products by
  treatment with DNA demethylating agents
  can be explained by the hypothesis that some
  genomic methylation restricts the differentiation
  potential of progenitor cells [40].

These three quotes, all on the same page, seem to indicate that at the very least, induction of differentiation is contingent on demethylation. More specifically, DNA methylation restricts the possible differentiation activity that a progenitor cell can undergo. However, just a little further down,

  Terminal
  differentiation predominantly led to increases
  in DNA methylation and both increases and
  decreases in H3K27me3, depending on the
  gene involved.

and

  [...] to
  hypothesize that changing the DNA methylation status of pluripotency genes in vivo is critical to their function [43]. DNA methylation is
  considered a more stable repressive mark than
  repression-associated histone modifications [42].
  The association of differentiation and the loss of
  pluripotency with DNA methylation at previously unmethylated sites (de novo methylation)is consistent with the inability of ESCs to differentiate when Dnmt1, the most abundantly
  expressed DNA methyltransferase gene, is
  homozygously knocked out [44].

I'm working on a presentation on DNA methylation and gene silencing, and I want to make an accurate portrayal of the role of DNA methylation in cell differentiation, and this is only a portion of the whole presentation, so I am not including a lot of data on this topic. However, I want whatever I do present to be self-consistent and accurate. How do I reconcile these two phenomena? From what I can tell, there is no explanation in the intervening text between these passages about how these two phenomena are similar but distinct. Am I accurate in determining that this is a difference between induction of differentiation and terminal methylation status? If so, how is it that ESCs can be differentiated with demethylating agents, but also ESCs have trouble differentiating when Dmnt1, which promotes methylation, is knocked out?


texts: Hamilton's derivation of direct fitness from his 1970 paper

texts:
In his 1970 paper "Selfish and Spiteful Behaviour in an Evolutionary Model", Hamilton uses Price's equation to derive his well-known rule $rb -c >0$. My question is about one of the steps in his derivation.

Hamilton considers a population of $n$ individuals. Let $s_{ij}$ be the effect of individual $i$ on the fitness of $j$. The fitness of an individual $j$ is defined as $w_j = 1 + \sum_i s_{ij}$, $w=1/n \sum_j w_j$ is the mean fitness in the population, and $q=1/n \sum_j q_j$ is the average frequency of a certain allele. Using Price's equation, we get

$w \Delta q = Cov (q_j, \sum_i s_{ij})$.

So far so good. But Hamilton then says that this equation can be rewritten as

$w\Delta q = \sum_i 1/n \sum_j (q_j - q)s_{ij}$

Based on the definition of covariance (i.e., $Cov (X,Y) = E((X-E(X))(Y-E(Y)))$, this seems to only be the case if $E(\sum_i s_{ij}) = 1/n \sum_j \sum_i s_{ij} = 0$. But this would imply that the average fitness wouldn't change over time, which sounds odd for me. In sum, I don't understand this step in Hamilton's paper. What am I missing?


texts: Will plants accumulate toxins from soil contaminated by toxic substances like paint thinner/lead paint?

texts:
After my grandfather died, demolition crews dumped garbage from the house onto his huge vegetable garden, including lead-painted windows, aluminum, asbestos tiles and more.  Much of it got burned in a few bonfires, which I assume released the toxins into the soil.

I've cleaned out every object I can see from that pile, but I'm wondering if the vegetables grown in that soil will be toxic?  It's been about three years since the demolition.

Also, to avoid the possible toxins from that area, we created a raised container garden using soil from a different location.  Yesterday, 3 Tablespoons of paint thinner mixed with water was dumped accidentally on one of the plants. We hosed it down, and it's still alive, but I'm thinking that the squash it will eventually produce is now toxic too, right?

Thanks in advance. We're new to gardening and really want to understand how this works.


texts: How do CD 8+ Tc cells reach the site of tumors?

texts:
In normal humoral immunity, dendritic cells present antigens to the Th cells by arriving at the Lymph node. This is fine. But consider a tumor cell. How does the Tc cell sitting in the lymph node know that there is problem out there? Consider there is a single cell which has undergone mutations and is expressing altered proteins. This wouldn't cause much inflammation to attract the Tc cell there.

So, is there continuous surveillance by the Tc cells? Where exactly do the Tc cells reside? Do they roam around like Th cells? How about the NK cells? do they too roam around in the tissues?

Cases of viral and intracellular pathogens, there may be some inflammation which draws the Tc cells there. Maybe. This can not be in tumors. So how do the Tc cells reach there?


texts: why does water go from high to low osmotic pressure to decrease the size of the nucleus?

texts:
I am reading this paper "Volume regulation and shape bifurcation in the cell nucleus" (linked below)
https://jcs.biologists.org/content/joces/128/18/3375.full.pdf
I am confused by this sentence "During cell detachment, because the cytoplasmic osmotic pressure decreases dramatically, water flows out of the nucleus and the nuclear volume shrinks."
Since water flows from low to high osmotic pressure, I would have thought that this decrease in osmotic pressure of the cytoplasm would cause water to flow into the nucleus, not out of it. Why does the opposite happen here?
The article also states that the volume of the cytoplasm will decrease. So is this something to do with the extracellular space?


texts:
Here is the chemical equation of photosynthesis

$$CO_2 + H_{2}O \longrightarrow C_{6}H_{12}O_{6} + O_2 $$

We see that the water is in reactant side of the equation. By the way, It ought to be catabolic reaction. However, It seems anabolic reaction on my textbook.

What should we think for this reaction?
How do we get If energy turned out in product side of the equation?
Why isn't photosynthesis catabolic reaction?


texts:
I am confused as to how I was meant to know E for a X^2 test in the following question:

2.i and 2.ii give no more information.

Not knowing what to do I used E as 0 for the first row and 40 (3+37) for the second row, but that was just a guess. It was wrong and the correct answer for E is 20.

I suspect this has something to do with the 20 fields but I can't beleive that I'm just meant to know they expect one butterfly per field...

How was I meant to know E?


texts: Are genes associated with obesity selected for?

texts:
I've read that there are several SNPs associated with increased risk of clinical or morbid obesity. I was wondering if there is any evidence that these are under positive selection. Would you expect them to be so?

I guess I'm interested to know if they would previously offered a selective advantage and only recently, say in the post-war period in the West morbid obesity become a problem due to differences in the diet.

Related question:
How many, and how severe, are known single gene polymorphisms for obesity?


texts: How can my sister have dark brown eyes, while my parents have blue eyes?

texts: Both my father and mother have blue eyes, just like me. But my sister has dark brown eyes, contrary to what I've read about the dominance of brown eye genes and recessive blue eye genes. What happened (apart from the possibility that my mother dated a brown eyed guy from which she was born, which for sure didn't happen because we both look like our father and mother; though you never know with those Italians...) that gave her those dark eyes?


texts: What are reciprocal inhibitory synapses?

texts:
Quoting Kandel's Principles of Neural Science, 2013,

  Amacrine cells generally receive excitatory signals from bipolar cells at glutamatergic synapses. Some amacrine cells feed back directly to the presynaptic bipolar cell at a reciprocal inhibitory synapse. Some amacrine cells are electrically coupled to others of the same
  type, forming an electrical network much like that of the horizontal cells.

(Page 593)

I tried searching for what a reciprocal inhibitory synapse is but could not find any relevant information.


texts:
It looks like it might be an emerald moth but its hard to tell from the discoloration in the wings and it is too high up for me to get a better look.

When: July 23rd 2018

Where: Central Illinois


texts: Do octopuses have better eyes than humans?

texts:
I've read that unlike humans, octopuses have eyes "designed" the "right way", i.e. with the nerve fibers behind the retina, thus getting rid of the blind spot we humans have as well as theoretically improving eyesight.

Have there been tests to compare octopus sight with that of humans, and do they indeed have better vision than us?


texts: Are there any auto-immune diseases caused by T cells not detaching from antigen presenting cells (APCs)?

texts: By not detaching I'm referring to after they have formed an immunological synapse, if they don't ever detach.


texts: Action potential frequency presynaptic neuron comared with in post-synaptic neuron/ muscle cells

texts:
I am a physicist interested in knowing how the action potential frequency in a presynaptic neuron compares with that in

a) a post-synaptic neuron and

b) membrane depolarisation of muslce cells, and

c) how the membrane depolarisation of muscle cells quantititavely relates to muscle contraction.

From the reading I have done so far, it seems that the theory of c) is standard, and goes by the name is 'excitation-contraction coupling'. I would think that the actual relationship between the frequency of muscle cell membrane depolarisation and degree of muscle contraction- however it is quantitifed- would differ for muscle type, depletion of Ca2+ stores from the sarcoplasmic reticulum, etc. In any case, some theory is covered here for instance, although I haven't seen much mathematical modelling and quanitative comparison here.

In any case, I am then still wondering regarding a) and b). I would think that there isn't a straightforward answer; the sequence of events is action potential -> neurotransmitter release into synaptic cleft -> neurotransmitter binding -> membrane depolarisation -> hopefully an action potential.

I already see some potential sources of non-linear behaviour in the final step, and the neurotransmitter binding ->depolarisation step would prbably also be dependent on the recptor kinetics. Since we are talking on the behaviour on a temporal scale, we would have to consider the degredation rate of the neurotransmitter within the synaptic cleft, and no doubt several pathologies arise because of some dysfunction in changes in neurotransmitter degredation/re-uptake rate... Come to think of it now actually, I think differences in the extent of binding (say due to differences in the number of receptors on post-synaptic neuron membrane) are the basis- or at least one factor- in neuroplasticity. So of course they would differ. But still the question remains as to what extent. I am not sure whether for some circuits, say those in the motor system, there is little deviation between responses in people.

To give some context to my question, I am interested in technologies which actively stimulate, or disrupt stimulation, of neurons in a controlled manner, so as to achieve a desired output effect. There are several technologies and lab techniques being developed with this in mind- optogenetics on the single-neuron level, DBS and epidural stimulation for stimulating large groups of neurons for some non-specific duration of time. I would think that these techniques could be much more powerful and potent, if we knew the temporal relationship between consecutive neural firing rates on stimulation.


texts: What are these needle-like plants growing in the ground?

texts:
I was outside and noticed some strange, needle-like plants growing on the ground. I managed to search for "needlegrass" but couldn't find it.
Here is the photo taken on April 20, 2021 in Long Beach, California; these red circles point at what the strange plants look like:


texts: How do you go from virus infection to disease?

texts:
I heard on the radio a few days ago1 a discussion on viruses and diseases (go figure why :)).

The guest was very precise in how the virus enters a cell, how its RNA merges with the cell's one and how it turns the cell into a "virus factory" (roughly speaking).

The question which was not accurately answered was "and so what? how does this makes someone actually sick?"

One of the points vaguely confirmed by the virologist (following a question from the journalist) was that the immune response of the body (notably the raised temperature) was what we perceived as the disease.

Since their time was short, there were no more deliberations on that interesting point.

My question: what happens that turns the "virus replication" activity into disease? I understand that the raised temperature is a direct effect of the immune system fighting these foreign bodies (the virus) but there are other effects such as headache, cough, etc.

Are all of these a consequence of the immune system fighting back? Or is the virus changing the way the cells function, and therefore they fail at their intended activity?

1 French radio France Culture, the guest was Olivier Schwartz, director of the Dept of Virus and Immunology of the Institut Pasteur, link to the podcast (in French, obviously)


texts: Phenotypic Variation of cattle - looking for academic sources

texts:
Can someone please point me in the direction of a good academic article on the following:

What are possible sources of phenotypic variation of different 400 day weights of cattle?

Furthermore how much variation is likely to be due to each contributing source?

I have tried the following searches in google scholar:

Phenotypic, genetic, environmental cattle weight
Phenotypic variation cattle weight
Phenotypic variation
Phenotypic variation, genetic
genetic variation, dam, sire


texts: Why most small organisms seem not to be interested in any organic matter which has all moisture removed?

texts:
On the first glance, it seems that most small organisms do not exhibit any interest in consuming any live or dead organic matter if it is completely dehydrated. Regardless if the food consists of protein, fats or carbohydrates, or any mixture of them, it appears to me that removing water makes bacteria, mould or even insects not consider it food.
Here I consider organic matter which can last for years without being subject to decay by small live organisms:

ghee, made from butter by boiling off all water, lasts for a year or more
freeze-dried food, which still can have 0.5% to 3% moisture, but can last 20 years
honey, supposedly can last forever

While the humble homo sapiens will happily put freeze dried milk in his mouth, most small organisms seem not to have any interest in organic matter with ultra-low moisture:

bacteria
mould
and to a certain extent even insects

For example I noticed ants will quickly gather around any drop of fat used in cooking, which has moisture and other impurities, but will ignore clean, dry ghee.
Why is moisture removal such an universal protection against small organisms and where exactly is the boundary between organisms which can't consume dry matter and the ones which can? Are there any known microorganisms which will consume completely dry organic matter?


texts: Is it possible that the DNA of an individual changes significantly over a period?

texts: Is it possible that the DNA of an individual changes significantly over a period ?