texts: What could cause hairs to gray at the tips but not the roots?

texts:
I have noticed that some of my sporadic gray hairs are gray at the tip side but oddly, not near the roots.  Some are even only gray in the middle.  I find all of this very counter intuitive, and I assure you nobody is secretly dying my hair.

How does the graying process work, and how is it that this can be happening?


texts: Can predator-prey relationship be an example of negative feedback?

texts:
Predators eat their prey, prey population decreases. This results in the predator population to decrease, so less prey are consumed which causes the prey population to increase.

Therefore, if the reduction in prey population results in its increase then can this be described as negative feedback?


texts: What are the appendeges behind a crane fly's wings?

texts:
I noticed that crane flies have strange appendages behind their wings. The appendages look like a pair of antenna or a pair of vestigial wings. In the following picture I marked these appendages with arrows.

The specimen in the picture sat on my window this morning. I looked through the genera on Wikipedia, that is, on the images if there were any. All crane fly species seem to have these appendages.

While the appendages are clearly visible in most images I couldn't find a description of them. I've never seen anything like them and would like to know:

What's the name of these appendages?
What are they good for? Are they vestigial wings, antenna, or some sort of counter weight to stabilize the flight?


texts: What Conditions must Drugs satisfy for them to be Deliverable via the Transdermal route? I assume a high $\log{P}$ (lipophilicity) would be one, are there any others?


texts: Common ancestry of our cells to the first unicellular cell

texts:
If we start the chapter of life with low fidelity self replicating RNAs forming exactly identical copies of themselves,  which then later evolved to form the first primordial basic cells which further reproduced, and formed identical daughter cells and so on ... besides mutation and other factors that might affect gene expression, our genome must still be derived from the very first RNA strand.
So is it too far fetched to say that in our bodies, our cells are the primordial cells themselves, as reproduction happens either by mitosis and meiosis (which keep the integrity of the first cell genome besides factors like mutation, etc.)?


texts:
Like snakes or lizards, did any dinosaur molt ?

if yes, have we any proof of it ?


texts:
My house (in Israel) has a concrete structure, with a decorative veneer of Jerusalem Stone at least an inch thick. Yesterday I came out to discover a little hole in the wall - and a pair of bees coming in and out of it! (See video)

This wall is no more than 5-6 years old, and I have never drilled anything there; they're not reusing a human-made hole. I must conclude that the bees somehow dug that hole.

Is that possible? What kind of bee could do this?

Update: As interesting as these bees are I didn't want them living in my wall, so I filled up the hole with a silicone-type glue. A few hours later, they had dug through that, too.


texts: What kinds of cells does human saliva contain?

texts: I have heard that our saliva contains cells. What cell types can be found in human saliva?


texts: Is the golden ratio of anatomic measurements universally beneficial for sexual reproduction?

texts:
It is often claimed, in popular media, that the golden ratio (Fibonacci series) in for example some face measurements is aesthetically (and hence reproductively) attractive with respect to the humans. I wonder if this is particular for today's (maybe since 10,000's of years or so) human anatomy and aesthetics. As in an after-the-fact acquired taste which was culturally psychologically emerged from the actual human ratios of anatomy as it has happened to evolve for whatever practical reasons, way out of intuitive comprehension for human consciousness. Or if it is deeply biological and evolutionary across all lifeforms.

Is the golden ratio as verifiable (if at all) also for the primates who came before us? Some examples are easy to find, but how statistically significant is the golden ratio as an advantage for sexual evolution for non-humans?


texts: The cloned sheep, Dolly, was said to have died very soon because the cells used to create it were taken from an adult sheep with an aged telomere. Why doesn't this happen with humans? Why aren't we born with 25 years less lifespan?


texts: If you are 30 degrees, and touch something that is 50 degrees, do you only feel 20?

texts:
First off, I don't know if this is the correct site to post this question as it could possibly fit into others? If so, please flag it to be moved as I would appreciate that very much.

Now, if my body was at a temperature of 30 degrees (celcius), I would feel somewhat warm. However if I then dipped my hand into a bowl of water at 50 degrees, would I begin to feel 20 degrees difference?

This seems likely as when I come out of a freezer (at work, don't stress), and wash my hands to "warm myself up", the water feels boiling hot and painful to touch but indeed is only maybe 30-35 degrees. Until it gradually becomes more bearable.

Or you come out of a spa, into a colder pool and you feel freezing cold?

To add some depth to this question, may I ask why this happens, and how your body actually reacts in this situation?


texts: RNA seq: Should non-infected units be used for RNA-seq?

texts: I am designing a RNA-seq experiment to study transcriptomic profile changes upon parasite exposure. Some papers I read, mostly extract RNA from the entire treatment group (organisms exposed to parasite), without (seemingly) bothering if all the organisms were indeed affected. Doesn't this practice bias results? Are there any studies on how this could affect results?


texts: Breakdown of energy expenditure at the level of a single cell

texts:
The metabolic rate measures how much energy an organism expends over a unit of time. Its breakdown for the human body in terms of its functions is well documented : so much for the heart, for the brain, etc.

In West et al, 2002 I have found an estimate for the metabolic rate of a single cell. But how does this breakdown in terms of elementary functions in the cell?

E.g., how much of the energy made available from nutrients is used in the process of replicating genome, of expressing proteins, of trafficking...?

Following Jeremy Kemball's link suggestions, I find in this paper the fraction of ATP consumption for the following processes:

Protein synthesis    0.34
Na+/K+ ATPase        0.16
Ca2+ ATPase          0.17
RNA/DNA synthesis    0.25
Unidentified         0.09

(which adds up to 1.01 rather than 1 for spurious reasons). Their measurement is indirect, based on $O_2$ consumption for an assumed steady-state regeneration of ATP. I wonder how GTP-based processes are accounted for? Or are they negligible compared to ATP ones?

This is for a specific cell type, rat thymocyte, is there a reason to expect that this will be hugely different for say a fibroblast? Also, they stimulate their thymocyte with concanavalin A. I understood they are not getting RNA/DNA consumption signal without Con-A, but didn't get why it would be so.

Finally, what would be in the remaining 9% ? One candidate for ATP consumption suggested by Jeremy Kemball is actin turnover, I guess it fits only in the "unidentified" line. Tubulin turnover is a GTP process, not sure about intermediate filaments (do they turnover?). All ATP-molecular motors (myosin, kinesin, dynein at least?) have to be there too.  What else?

I am particularly interested in the total amount of ATP energy that goes to myosin.


texts:
I saw some documents which were trying to say that they can prove via sweat smell selected by women that humans are developed to find a partner with similar genes. At the first glance, I refused it as absurd for many examples of organisms behaving in reverse but then I realized that I don't know any satisfying evolutionary explanation for this (and more: I could even explain the contrary: If less developed and more developed human had a baby, the better genes could be maybe annulled by the worse genes, on the contrary two very developed partners would have not only a lot of descendants, but their descendants would have also lot of descendants and so on.)

And more thing: if genetic diversity is truly evolutionary practical, could for example even people with genetically transmitted disease help our gene pool?

Thanks a lot.


texts: Why don't mosquitoes evolve towards muting themselves?

texts:
Quite certainly, muted mosquitoes would be much more effective as far as their blood-sucking pursuits are concerned, since mosquito sound is predominantly responsible for sealing their fate (between the two palms of the hand). Muting themselves would certainly reduce the chances of being caught in the act. For instance, unless you notice by looking, leeches go undetected for long periods because there isn't any obvious sound emanating from them.

Thus, reasoning says - this should be favorable from the point of view of evolution, unless there is a some indispensable purpose served by this sound, which can not be otherwise served. This page seems to suggest that this is so from the point of view of mating. In fact, quoting verbatim:

  Since female mosquitoes are larger, they flap their wings slower, and males know it. They use the distinctive pitch of the females' buzz to recognize them. Louis M. Roth, who studied yellow fever mosquitoes for the U.S. Army during World War II, noticed that males ignored females whenever the females were quietly resting, but whenever the females were flying, and therefore buzzing, the males wanted to mate with them. The males even wanted to mate with recordings of female mosquitoes or tuning forks that vibrated at the same pitch.

But mating signals could also be of other forms, like some chemicals secreted (I envisage something like pheremones). Why is making sound so important? Why can't this noise be either less intense, or lie outside the audio range for humans (their targets)?


texts: Are the controls for RT-PCR the same as those for RT-qPCR?

texts:
I am searching for negative and positive controls for RT-PCR but all the results seem to point towards RT-qPCR. Are the controls the same for both?
I have found

-RT control
No template control
exogenous control
endogenous control
no amplification control

Do they apply for both or just RT-qPCR?


texts: What happens when the brain is no longer capable of co-ordinating or regulating the heart and breathing rates?

texts:
Does the heart no longer function? Does it go into ventricular fibrillation?

What happens?


texts: What is the difference between muscle tension and muscle tightness?

texts:
Is there any difference between muscle tension and muscle tightness?

I want to study the relation between forearm muscles tightness/tension and tendinopathy (specifically, medial and lateral epicondylopathy) in humans. In that context, I wanted to understand whether muscle tension and muscle tightness are synonymous, and if not what the difference is.


texts: How to use swiss-mod to predict the secondary structure and 3D structure of a protein?

texts:
I'm trying to predict the protein secondary and 3-D structure for the sequence [Q1NN20] and need some help getting the ball rolling.

I'm getting confused with how and when to use Jpred, swiss-mod, and PDB. So far, I got the sequence from scanprosite, put it into swiss-mod, but what next? When does jpred come in?


texts: If primers weren't present in PCR at what temperature would DNA re-anneal? I am wondering how primers manage to bind on DNA strands before DNA manages to anneal back together.


texts:
I recently got a light microscope to start exploring microscopic features of fungi (and to explore microscopy in general).

What are some of the most common and easily available stains used when preparing microscope slides for fungi? Which situations are they each best for?


texts: Are acid-fast bacteria Gram-positive or Gram-negative?

texts:
Both procedures involve using a stain, decolorising agent, and then a second stain. I am tempted to conclude that acid-fast bacteria, which resist decolorisation (eg. by strong carbol fuchsin), also resist decolorisation in the Gram staining test (eg. by gentian violet) and are thus Gram-positive.
After all, there are much fewer acid-fast bacteria than Gram-positive bacteria.

Is this line of thinking incorrect?

Image URL: http://www.scienceprofonline.com/images/science-image-library/microbiology/staining/differential-bacterial-stain-controls-diagram.JPG


texts: Why isn't hearing the same as tasting? How do we feel and differentiate external stimuli?

texts:
When I was at school, I learned that:

Skin, tongue, ears, and other sensory organs have sensors/convertors that turn external environment stimuli into "electric" signals.
Neurons send information as electric propagation of K+ / Na+ along their axon. Hence, the real nature of the stimuli is definitely lost in translation.
Each region of the brain is a cortex specialized for vision, sound, smell, and other sensations yet they all are made of the same neurons.

So:

Then how do we feel? How are "electric" signals turned into taste or smell?
Why does the brain not feel the same way about these different stimuli, rather than only differentiating amplitude and frequency of the signal?
Why do we even feel pleasure or pain at all? A machine would just transfer the information.

That part was never explained to me. Is it quantum (entanglement?) physics-related? Or even metaphysical? Does anyone really know?

Philosophically speaking, I am not even sure I taste things or feel music the same way other people do.


texts: Why are monarch butterflies attracted to particular flowers but not others?

texts:
I have a "Purple Emperor Butterfly Bush" (Buddleia davidii 'Purple Emperor') and sure enough it does attract butterflies.
I have seen monarch butterflies using it, which confuses me, because I thought that monarch butterflies only fed from milkweed.
What makes this type of bush a substitute for the milk weed, but not other flowers?


texts: What happens when you take a deciduous tree and place it in a climate controlled greenhouse?

texts:
The greenhouse would have stable level of light, (matched with day/night wavelength brightness changes like outside the greenhouse), humidity and temperature.

Do certain processes in the tree not trigger?
Does this harm the organism, and are there changes in life expectancy?


texts:
I am trying to get standard ECG by using PhysioNet's ATM with parameters

but I get

It should be something like

How can you get complete standard 12-lead ECG out of Physionet database?


texts: I was thinking, as I know, sometimes the process of producing DNA did not work well(correct me if I'm wrong), so it gives us some changes in the object we gonna have(for example: increasing or decreasing a part, enabling  or disabling  a part), could human brain grow more that it is now?


texts:
I was studying about conjugation in bacteria, I have a doubt. In conjugation F- cell transforms into F+ cell when there is a formation of sex pilli in between the two. The doubt is if the F- cells convert into F+ cells how can F- cells form again...?

If all the F- cells convert into F+ can we expect F- cells to form again?


texts: What are the functions and differences between axons and dendrites?

texts: My textbook doesn't do a very good job of pointing out what the differences between the two are. It basically mentions axons only in the same breath as the synapse (that synapses are the endings/tips of axons).


texts: Does conjugation support gene selection?

texts:
I have already posted this on chat but haven't got any response. A recent question on group selection stimulated me to ask this here.

QUESTIONS: Why should bacteria conjugate? If we consider that a bacterium is another bacterium's rival (in terms of obtaining resources) why should a bacterium "share" it's antibiotic resistance gene, for example, with another bacterium? I can think of 2 reasons. One is group selection, and the other is "Gene Selection". Group selection has been highly criticized in recent years, and individual selection has dominated thinking, but here my support goes for gene selection rather than individual selection.

Gene selection seems to me the easier explanation over individual selection. Even if we consider the fact that a colony is made from divisions of single cells and the cells are extremely similar and also that conjugation is more probable between cells of a colony, we should also consider that conjugation can happen between very different bacterial species.


texts: How to quantify the "stability" of a protein complex?

texts:
From experiment we've identified a subset of known mammalian protein complexes as interesting (approximately 50 CORUM complexes). We'd like to do an enrichment-style analysis to know more about them. One question I have is whether these complexes are particularly stable, since stable complexes should be biased towards detection. However, I don't have a chemistry or molecular biology background, so I don't know how to approach finding the stability of a protein complex.

Given a list of proteins in a complex, are there any conventional, in silico ways to estimate the stability of that protein complex? If not, have people published numbers for the stability of well-known complexes?

Edit: I'm okay being vague about the definition of "stability" since I'll be satisfied with an answer that uses any definition of it.

Edit: This question is answered on biostars.


texts: What is the normal water volume per 1 L of blood, and how much deviation from that norm causes dehydration or hyponatremia?


texts: Why does IUCN classify pistachio as a "Near Threatened" species?

texts:
When reading the Wikipedia entry on pistachio, I noticed that IUCN has classified the plant under "Near Threatened". On looking up its entry at IUCN, I see that its population is trending downwards, and it is "threatened by fruit collection, livestock grazing and cutting". The treat seems to have nothing to do with the often reported fungus. Looking up the yearly yields at Administrative Committee for Pistachios, I see that 2010 and 2012 were bumper years, but otherwise, I see no real trend of a decrease. Quite the contrary, I get the impression that the yearly yield is increasing. It's not as if the tree is difficult to grow, and we rely on trees growing in the wild; these trees are grown in orchards.

So, what's going on? Why would IUCN say that pistachio is Near Threatened?


texts: Is SCNT possible with only the nucleus of a somatic cell (rather than a whole somatic cell)?

texts:
The following figure from Life: The Science of Biology (11th edition) explains how SCNT (somatic cell nuclear transfer) was used in the cloning of Dolly:

(The original paper about cloning Dolly - Viable offspring derived from fetal and adult mammalian cells)

Note that an enucleated oocyte and a whole somatic cell were fused, i.e., the nucleus of the somatic cell wasn't isolated from the somatic cell.

Another example in which SCNT was used successfully is the cloning of the monkeys Zhong Zhong and Hua Hua. In this case, fetal fibroblasts were fused with enucleated oocytes, as explained in the paper Cloning of Macaque Monkeys by Somatic Cell Nuclear Transfer.

However, one can find various explanations and figures on the internet that explain that in SCNT, only the nucleus is transferred into an enucleated oocyte.

For example, the following figure is used in Wikipedia's SCNT page:

Though it is noted alongside the figure:

  The diagram depicts the removal of the donor nucleus for schematic purposes; in practice the whole donor cell is transferred.

So my question is:
Has anyone ever successfully used SCNT while using only the nucleus of a somatic cell, without the whole somatic cell?

(My guess is "no, the nucleus alone won't do", basically because of the importance of the centrosome, along with the following quotes from the paper From Zero to Many: Control of Centriole Number in Development and Disease:

  Centrioles are essential for the formation of microtubule‐derived structures, including cilia, flagella and centrosomes. [...]

  Notably, oocytes and spermatozoa lose parts of the centrosome in a complementary manner. Centrioles, but not centrosome proteins, are lost in the oocyte. On the other hand, in sperm, the PCM material is lost, but not the centriole/basal body, which is necessary for flagella formation. Fertilization brings together the basal body from the sperm, which becomes a centriole within the zygote, and the PCM from the egg.

)


texts: AS internet  tells is it is thigh bone which is strongest, but why, it carry only upper part of body, does not heel or any foot bones should be strongest in body as they carry full body weight ?


texts: Can skeletal morphology change in adults?

texts:
I'm just a curious layman, so be gentle. I read around that things like the cranial1 and pelvic2 morphology change with age, but I also read seemingly contradictory information that bones are 'completely ossified' around age 25 (can't post a third link for reference) and that's often cited as meaning "done changing."

Wikipedia (my trusty friend) also describes 'bone remodeling' as a lifelong process, yet also describes ossification (not a lifelong process) as a key component.

So I'm confused. What actually changes in terms of bone morphology throughout an adult's life? Does bone tissue continue to form in adults? Do bones "bend" and flatten ever so slightly into new forms? Additional reading would be appreciated as well.

Thanks


texts: Does the string "...CATCAT..." appear in the DNA of Felis catus?

texts:
In Hofstadter's Gödel, Escher, Bach: An Eternal Golden Braid (GEB), the following claim appears:

...in the species Felis catus, deep probing has revealed that it is indeed possible to read the phenotype directly off the genotype. The reader will perhaps better appreciate this remarkable fact after directly examining the following typical section of the DNA of Felis catus:
...CATCATCATCATCATCATCAT...(OP note: truncated because, you get it)

Is this true? A cursory search for the DNA of Felis catus gives me this 1996 paper by Lopez, Cevario, and O'Brien and the given sequence does not appear – there are some instances of "CAT" but not repeated enough to make it as remarkable as claimed in GEB.
I don't know enough Biology to judge the veracity of this claim. Some points I am considering are:

GEB is full of wordplays. However, the tone of this part of the text does not sound like one to me.
GEB was written/published around 1978. The paper I linked to – which was cited by some 236 others according to Google – was published in 1996, way after GEB's time. If my impression that Lopez et al.'s work is significant because it is the first time Felis catus has been sequenced, then there is no way Hofstadter could've known of it when he wrote GEB. Then again, I don't know enough Biology that there might be some nuance to Lopez et al.'s paper that I'm missing (i.e., the results of the paper might not be mutually exclusive to the claim made in GEB).
GEB has reference notes and bibliography and there is no reference cited to back this claim. However, GEB does not attempt to be a rigorous academic thesis and the references is only called upon more when Hofstadter quotes other works directly while the bibliography is a list of readings which the reader may want to check out, regarding the main thesis of the book.

So are cats recursions with no base cases?


texts: Evolutionary reasoning behind redundancy of CST and RuST

texts: According to my neuro-anatomy class, both the Corsticospinal Tract (CST) and the Rubrospinal Tract (RuST) control upper limb movement. What the evolutionary reasoning behind this redundancy and the fact that the RuST is much more important in non-human primates when compared to humans?


texts: I have googled  for the structure of cnidocyte but images of google is unclear or complex .so please draw a simple understandable structure of cnidocyte .I know that cnidocyte works by osmosis but I don't know how exactly osmosis make cnidocyte to function .so please explain the mechanism of cnidocyte.


texts: Could higher carbon dioxide levels be beneficial to plants?

texts:
C4 plants take ATP-expensive routes to ensure photorespiration does not occur.
They minimise oxygen concentration in cells where the Krebs cycle occurs and cart carbon dioxide into these same cells. To over-simplify, they increase the carbon dioxide concentration and decrease the oxygen concentration in these cells.

Despite the ATP this costs them they are enormously successful (in hot areas at least).

Considering this, would human-caused carbon dioxide emissions, i.e. increased concentration in environmental carbon dioxide, be beneficial to plants?

Considering @Cell's comment: I mean beneficial from the 'plant's point of view', i.e. the plant can grow faster-reproduce sooner or less photorespiration occurs; due to the higher level of carbon dioxide. I think we can disregard ocean acidification for now, climate change is relavent but perhaps it could be disregarded initially? Especially as climate change effects different areas differently.

Please note: I am not encouraging or supporting human caused carbon emissions; this is a genuine question asked out of curiosity.


texts:
Since a human woman is born with a set number of eggs, and meiosis is the process by which sex cells are produced, would meiosis in a woman happen before she is born or soon after she was born?

If meiosis creates sex cells and women are born with a set number of sex cells, when in the development of a woman are her sex cells created?


texts: Often, pieces of feces have a clearly-defined shape and size — both length and width (that is, cross-sectional diameter, or caliber). But that width seems to vary quite a bit, even among pieces of feces from the same person. Why? What determines the width? Why is it wide when it's wide, and why is it narrow when it's narrow?


texts: How to detect specific mRNA dsRNA by Northern analysis?

texts:
I silenced a gene by RNAi method, for that i chose the gene and the size of the gene is 1.5kb and my insert size is 500nts. i did the transfection and i want to confirm the silencing by northern analysis. when i did i got the ribosomal RNA instead of my specific mRNA reduction and dsRNA accumulation.
Total RNA was prepared with TRIzol reagent (Sigma), and 20 μg/lane was fractionated on a 1.2% agarose, 2.2 M formaldehyde gel. The RNA was visualized with ethidium bromide. The RNA was transferred to a nylon membrane (Hybond; Amersham Biosciences) for 14 hrs and probed with [α-32P] UTP-labeled used SSC for transfer and Prehybridization at 55 for 2hrs incubation, in the probe for 10hrs and Washing at 60 for 2X SSC 20 mins two times.

In this image you can the samples TET induced and uninduced RNA. but the result was confusing and am getting such a strong ribosomal RNA (2.2 Kb) contamination.


texts: How do we know that mild forms of rabies are nonexistent?

texts:
Wikipedia's rabies article says: "Death usually occurs 2 to 10 days after first symptoms. Survival is almost unknown once symptoms have presented, even with the administration of proper and intensive care."

I am wondering why we exclude the possibility of bite victims developing a mild form of rabies, in the same way that influenza can be mild or asymptomatic depending on the individual and the season. I noticed that rabies vaccines use an inactivated (killed) virus, while influenza vaccines can be attenuated, for example cold-adapted, so that a live virus may be used causing minimal symptoms. Clearly, for these vaccines to work, influenza infection must be able to proceed without symptoms. Similarly, the bubonic plague bacillus Yersinia pestis is endemic in many regions and presumably spread through asymptomatic carriers. Rabies vaccines are made from viruses whose infectivity upon intracranial injection is titrated according to a method of serial dilutions, suggesting that a harmless live vaccine would also be feasible at some level of dilution (barring, perhaps, the infeasibility of intracranial administration of such a vaccine).

What evidence do we have to suggest that rabies is different from influenza or plague, i.e. that it is not possible to have an infectious case of rabies with no or with mild symptoms?


texts: Why do animals have more heavy nitrogen and carbon than plants?

texts:
There are two stable Isotopes of nitrogen N14 and N15. The ratio of
  15N/14N tends to increase with trophic level, such that herbivores
  have higher nitrogen isotope values than plants, and carnivores have
  higher nitrogen isotope values than herbivores. Depending on the
  tissue being examined, there tends to be an increase of 3-4‰ at each
  trophic level.

  The tissues and hair of vegans therefore contain significantly lower
  percentage of 15N than the bodies of people who eat mostly meat.
  Isotopic analysis of hair is an important source of information for
  archaeologists, providing clues about the ancient diets.

https://en.wikipedia.org/wiki/Isotopic_signature#Nitrogen_isotopes

But how does N14 'disappear' from plant to animal?


texts: What is the mechanism responsible for the 'delay' in delayed rectifier potassium channels?

texts:
I've been trying to find a comprehensive explanation concerning the nature of the 'delay' in neurons' delayed rectifier potassium channels. As it's written in my intro to neuroscience textbook, these channels are voltage gated and become activated when the typical neuronal membrane reaches an electrical potential of approx. -40mV. While the channel is activated at this point, it only opens up after a delayed period of approx 1ms.

I'm mostly trying to clarify that this isn't an confusion in wording and that delayed rectifiers aren't actually activated when the inner membrane reaches a charge of approx +40mV which would be correlated (at least in textbook examples) with the '1ms delay', but caused by the actually typical charge observed at approx 1 ms of delay during an action potential.

Thanks so much. Let me know if I can clarify something. I know this wasn't necessarily so well asked


texts:
18th century Feodor Vassilyev is said to have had children by two wives, each of whom only ever had twins, triplets or quadruplets. His first wife has 16 sets of twins, 7 of triplets and 4 of quads; his second had 6 sets of twins and 2 of triplets. Is there any known plausible biological explanation for this, or do we have to dismiss it as a fabrication?

I could understand a woman's body being unusually susceptible to multiple births. I can't find information on whether these women tended to have monozygotic or polyzygotic offspring, but neither option seems unviable to me. However, since it's unlikely two of Feodor's sexual partners would share such a trait, one would think to attribute it to him. Presumably there would have to be a mechanism by which paternal DNA can trigger embryo fissions, in which case I imagine the offspring would be polyzygotic.


texts: What's the name for this kind of pointy/raised texture in animals?

texts:
I was in a store and I saw a jackfruit, seen here https://livenaturallymagazine.com/all-about-jackfruit/ with this sort of...scaly yet round and also pointy texture.

Then, I could have sworn I saw some kind of texture like this on animals, so I tracked down a couple images, like the back of a bearded dragon https://shannonwild.photoshelter.com/image/I0000Wf4WI2Vn.V0 and the pads of an owl
https://i.pinimg.com/originals/a1/94/07/a19407eff53e0fd06c48144c4541e3d8.jpg

What is the name for this semi-spiky texture, and what is the practical use of its topology?


texts: Which immunosuppression caused by long-term usage of these antibiotics in untreated celiac disease?

texts:
These antibiotics include

amoxicillin + acidum clavulanicum (beta-lactam, inhibit cell wall synthesis, broad specturm, 3rd gen aminopenicillin) / last part preventing the resistance
ceftriaxone (3rd gen cephalosporine, inhibit cell wall synthesis, broad spectrum)
clarithromycin (macrolide, inhibit protein synthesis by binding to ribosomal subunit S50)

used regularly for cyclic middle ear infections for years during the childhood - ages 2-10 for a patient with untreated celiac disease.

I am thinking what kind of immunosuppression can this lead to.
I think it mostly conquered by suppression of adaptive immune system.
Little lowered innate immunity lowered too.

I am especially interested in the antigen-presenting cells (mostly dendritic cells) and their function in an immunosuppressed patients of the antibiotics.

There may be other factors which I have not mentioned related to this kind of immunosuppression.
Feel, free to propose.

How can dendritic cells work in an immunosuppressed patients?

You can assume any combination of cases for the three antibiotics: 8 possible cases.
For instance,

(1) and (2) high antibiotic resistance, and only susceptible to (3)
High antibiotic resistance to (1)-(3)
...

Possible cases which reminds

this immunosuppression can remind this one: immune reconstitution syndrome like in HIV but milder


texts: How does flow rate of Ion channels depend on the length of the selectivity filter?

texts:
The length of the selectivity filter of ion channels such as the potassium channel commonly is only half of the thickness of the membrane. Some book such as MBoC says this can benefit the transfer, so I wonder how will the flow rate of the channel depend on the length of the selectivity filter.
Intuitively, the longer it is, the lower the flow rate will be. But consider the following factor this may not be true:
There is no "resistance" in the selectivity filter. The ions in the channel are basically in thermal balance with the selectivity filter wall and bounce forth and back randomly all the time. The driving force of the flow is not kinetic energy, but the ion density difference at both side just as normal diffusion process. From this point of view, the flow rate should not be depend on the length of the selectivity filter, at least not very much.
If so, then the fact that the length of the selectivity filter is only half of the thickness of the membrane maybe only a coincidence in evolution history and doesn't bring much benefits.
Considering most ion channel have very similar selectivity filter length and synthesis of new ion channel proteins with longer selectivity filter is not possible with today's techs, this can't be decided by experiments. Is there some molecular dynamnics simulation about how the flow rate depend on the length of the selectivity filter?


texts: Movement of few ion during changes in membrane potential

texts:
My question is very simple: why is it sufficient for a very few ions (such as 1 in 100000 K+) to move across the membrane to generate a remarkable variation in the membrane potential (like a change of 100mV) ??

I took the examples from my university textbook, which, though, doesn't explain the reason behind this statement. Is it because during this event the permeability changes so dramatically that the number of ions doesn't have to be so big?

Can someone help me? Thank you!


texts: I find this graph incredibly confusing. Is it saying that when there is a decreased affinity (of hemoglobin to oxygen, I think?), the partial pressure of oxygen increases with the same percent saturation of hemoglobin? What does that even mean if that's the case?


texts: Name for fluid that leaks out of phyllid (non-vascular) plants?

texts:
As Wikipedia says (https://en.wikipedia.org/wiki/Non-vascular_plant):

  Consequently, phyllids are unable to control the rate of water loss from their tissues and are said to be poikilohydric.

And indeed, if you've touched these types of plants, they can feel wet and sometimes even slimy. Sometimes the liquid leaking out can look like dew drops, too.

Is there a proper term for this fluid? I thought sap at first, but it seems that term is reserved for vascular plants.


texts: Does depolymerisation take place at the minus end of microtubule?

texts:
Wikipedia says that

  Dynamic instability refers to the coexistence of assembly and disassembly at the 'ends' of a microtubule.

but Karp's Cell Biology, 7th edition says

  Dynamic instability is an inherent property of microtubule itself, more specifically, of the plus end of the microtubule.

I was of the opinion that the GTP bound to the minus end does not hydrolyse and so no depolymerisation take place at the minus end.

But again from The Cell: A Molecular Approach. 2nd edition I found that

  treadmilling is a dynamic behavior in which tubulin molecules bound to GDP are continually lost from the minus end and replaced by the addition of tubulin molecules bound to GTP to the plus end of the same microtubule.

The concept I have developed so far is completely shattered by this treadmilling thing. Can somebody explain,

i) Whether GTP remains attached to the minus end?

ii) Whether depolymerisation occurs at the minus end?

iii) If depolymerisation does not occur, then is treadmilling a special condition?


texts: I can't think of any reason why plants wouldn't be able to get cancer, but I've never heard of a plant growing a tumor. I've also never seen a plant with a noticeable abnormal growth. Can plants get cancer?


texts: What happens when two sperm fertilize an egg?  This can be either naturally or by experiment.


texts:
After Gram Staining,
We use counter staining to find out that is there any gram(-) bacteria present on the prepared slide.

My question is-

What component in the cell wall of gram(-) bacteria is responsible for the retention of Safranin dye?
Like the Techoic Acid is responsible for the retention of CVI complex in gram (+) bacteria.

As I have just studied the staining process,any additional useful information is appreciated.

Thanks!


texts: Does blood typing still provide a use for ancient tissue analysis?

texts:
Modern techniques.

In recent years, DNA sequencing has become extremely cheap. This, compounded by the ability to PCR miniscule samples to viable samples for analysis, means that aDNA can be extracted and analysed from ancient tissue samples that 20 years ago would have been impossible to sequence.

Pre sequencing techniques.

However ancient biochemical analysis was around before the human genome project revolutionised sequencing technology.

Although blood typing was fiddly, grossly time consuming, and expensive, people were able to define historical lineages.

Question.

How does the "old-school" approach of blood-typing compare in terms of cost, accuracy, sample required, and speed against the modern aDNA analysis? Do those sort of experiments still have a place in a modern ancient tissue lab?


texts: What brain regions consume the most energy?

texts:
It's well known that the human brain consumes roughly 20% of the body's energy, and that grey matter is much more energy-intensive than white matter.

Beyond this basic information, it seems difficult to search for the total energy consumption of the brain broken down by lobe, or ideally further. For instance, how much power is consumed by the typical hippocampus, averaged over a typical human lifespan?


texts: Has kin selection enabled the evolution of interspecial communication?

texts:
I know animals often imitate specific behaviour (like when they show their teeth to evoke "danger!" in the reciever) as a form of communication. Although, for a fully-fledged language where we can express anything we can think of to develop, we need more complicated signals.

And for that, we need both the reciever and the signaler to understand the same signalling system. And since for a language as complex, the animals need to share a lot of similar "associations" with similar signals - it's good when the communicating animals orientate a similar environment - such as siblings.

Is this a possible explanation of the evolution of language?

I know the signalling theory is a biological branch on its own, however I seem not to be able to come up with an alternative explanation. Also, I know that this kind of group selection is sometimes used to explain the evolution of altruism. So is this how the evolution of communication happens?


texts: I read today in the news that villagers in Borneo were attacking refugee Orangutans. Why would they do this?


texts: Why do morning people have shorter biological clocks?

texts:
First of all, we all have a circadian clock than is run endogenously by differential gene expression and controls our change in awakeness, temperature, hormone levels, etc.. Circadian clocks are not exactly 24 h and they vary among people: some people have shorter clocks and other have longer ones. Apparently, people who have shorter circadian rhythms are morning people, and those that have longer one, are night owls.
How is this possible? In the following article "https://www.futurity.org/biological-clocks-sleep-disorders-protein-mutations-2289312-2/" it says that a 20-hour biological clock will make a person fall asleep earlier because they will get tired earlier and they will get awake also earlier. But for me, that would only be possible the first period or two if both cycles start at the same point time. Afterward, the cycles will get out of phase and that will not be true any longer.


texts: Evolutionary selection pressure for human hair patterns?

texts:
Are there hypotheses or conjectures that postulate any selection pressures or benefits that account for the patterns of non-pubic human hair?  Particularly:

Humans do not grow notable (i.e., non-vellus) body hair until puberty.
Terminal body hair growth in adults is not only sexually dimorphic but also peculiar in its patterning:

Source
As with any trait: it is quite possible that the evolution of human hair patterns had no selective significance.  It could also have been the result of a sexually-selective feedback loop, and therefore are an arbitrary sex trait.
I am looking for hypotheses or conjectures that suggest some objective benefit to terminal body hair.  I struggle to imagine one particularly because of the sexual dimorphism in adult hair patterns:  E.g., if facial hair provides some benefit to men, why would it not provide the same one to women?
If we stipulate that the pattern is only fully expressed in males then it is still peculiar: For example, I can't see any functional characteristic that would make hair on the front torso beneficial while not conferring a benefit if present on the shoulders or top of the torso.


texts: Looking for Kelly Chibale's paper on Malaria cure

texts:
From National Geographic, there has been a lot of hype on Kelly Chibale's work from University of Cape Town on the aminopyridine MMV390048. Unfortunately, this was from an announcement from an internal meeting so there is very little literature on the compound.

So I ask, does anyone have good literature on the compound?


texts: How to drop a grid of points in DICOM images of a CT scan (imageJ? Horos?)

texts:
I have a series of DICOM images from a CT scan of a bucket of rocks. I want to systematically measure the size of the interstitial spaces. The reason I'm doing this is to compare it to a simulation I've made to check that my simulation is giving accurate data.

In order for the measurements to be comparable to data from my simulation, I want the method for measuring the gaps to be as follows: define a 3D grid of points within the rocks (say, every 5 mm). At each point that falls within a gap (not in the centre of a rock), measure the gap width from that point in the X, Y, and Z directions.

I've tried messing around with both Horos and ImageJ but I can't work out how to define points (ROIs?) in a systematic way, or to have them show up in all three directional slices of the scan (I'll need to measure two dimensions from one 2D image e.g. X,Y and then switch to the X,Z image to get the third measurement, but use the same defined point).

Ideally once I know how to drop points and understand how they work, I could program the software to automatically do these measurements. Can anyone point me in the right direction?

Thanks!


texts: Are tuna fish present in the Baltic sea?

texts:
Yesterday my grandmother ate fresh tuna at a friend's party. She swears it was fresh and bought at a local fishmonger. The problem is, that we live in Gdańsk, by the south-eastern side of the Baltic sea and I have never heard of tuna in the Baltic. I told her that the fish couldn't have been local and therefore couldn't have been fresh but frozen and thawed. But the thought still bothers me, maybe tuna fish can reach the Baltic?

I did search a bit and found that tuna may be sometimes found in the Northern sea, so maybe it actually can travel so far east as to reach the Baltic? But the water in the Baltic is hardly saltwater (6-8‰), so would it be able to survive?


texts:
I have some questions about the IBD-value and IBD-fraction for two of the condensed identity states, $S_1$ and $S_7$.

My questions:

1) Is the IBD-value for the individuals i and j two (2) in $S_1$ and 2 in $S_7$ as well? (We can form the pairs aa aa in $S_1$ and the pairs aa and AA in $S_7$. The number of alleles in $S_1$ (and similarly for $S_7$) for individual i that are IBD with alleles of individual j is therefore 2)

2) Is the IBD-fraction ( or coefficient of relationship) 1 in $S_1$ and 1 in $S_7$ ? (We have the fraction 2/2 in each case since both alleles of each individual are IBD with the alleles of the other individual as described in 1) )

Picture source: http://openi.nlm.nih.gov/imgs/512/114/3579841/3579841_pone.0057003.g001.png

Edit: Comments about the figure: The dots represent alleles for one particular locus. When two alleles are IBD they are connected with a line. We look at two individuals i and j and consider the SAME locus in both individuals. There are only two persons in each of the states. In state $S_5$ individual j is homosygous and it's alleles are also IBD. One of the alleles of i is also IBD with the alleles of individual j. We therefore get the three lines between the alleles.

Definitions used:

IBD-value: "An Identical-By-Descent (IBD) value is the number of alleles which are the same because of descent from a common ancestor. Since each (diploid) individual has two alleles for a given (autosomal) gene, the number of them that are IBD with another individual can only be 0, 1, or 2."

Source:
IBD-value in pedigree with inbreeding

Coefficient of relationship: "..is the fraction of genes in two individuals that are identical by descent,..."

Source:
https://books.google.no/books?id=Q9ofvKZAmpEC&pg=PA35&lpg=PA35&dq=identicAL+BY+DESCENT+FRACTION&source=bl&ots=oOc4-PBzZg&sig=jJgJarUg36b4DbyT7sphDD6j_7c&hl=en&sa=X&redir_esc=y#v=onepage&q=identicAL%20BY%20DESCENT%20FRACTION&f=false


texts: Role of drift in evolution of sexually dimorphic traits

texts:
Is there a model for predicting how drift can affect the evolution of a sexually dimorphic (SD) trait? I've been trying wrap my mind around this paradoxical question; sexually dimorphic traits evolve due to sex-specific selection. So how can drift affect SD traits?

I've found the quantitative genetic equations (eq 1) in Lande 1980 very helpful for thinking about the parameters and how sexual dimorphism evolves.
Can this model be applied to a population bottleneck? Or comparing the degree of SD in a trait of two divergent populations (assuming s, Ne and other parameters remains constant).
$$
\begin {pmatrix}
\Delta z\\
\Delta y\\
\end{pmatrix}
= {1 \over 2}
\begin{pmatrix}
G_m B \\
B^{T} G_f\\
\end{pmatrix}
\begin{pmatrix}
P_m^{-1} s_m\\
P_f^{-1} s_f\\
\end{pmatrix}
$$

Edit: I've added the equation from Lande 1980, which models the phenotypic response for sexually dimorphic traits. I'm wondering how aspects of drift (Ne and fixation probabilities) can be merged with an equation such as this. From my understanding drift may affect the G, B and P matrices (that is the Genotype variance covariance, intersex (B) variance covariance and Phenotype matrices. One of the assumptions of this equation is that these matrices remain constant.


texts: What is the difference between DNA vs RNA Editing in the context of gene therapy?

texts:
As a someone with beginner knowledge on biology, I have come across the terms "RNA editing".

Take this paper for example : RNA Editing with CRISPR-Cas13

From my understanding, DNA -> RNA -> Proteins

If we use a vector for delivering a gene to a cell in-vivo, does it mean that corrections aren't permanent for RNA edits?


texts: What does "local folding" means in secondary structure?

texts:
I'm new to biology field, so I'm learning all kinds of biochemistry knowledge for a bioinformatics project. I've found a few definitions of secondary structure online. For example, I found this brief definition here:

  A structure of a biological molecule characterized by the local
  folding within the biopolymer as a result of hydrogen bonding (within
  the biopolymer).

What does "local folding" mean here? More specifically, what does "local" in this context refer to? Thanks in advanced.


texts: If an organ was to start failing, not total failure, such as the thyroid gland, is it possible that the fault may not lie in the failure of the organ but in the nerve signals coming from the brain?


texts: Why do red blood cells maintain Iron in the Haem group in the +2 (ferrous) oxidation state?

texts:
A lot of sources tell me that RBCs contain a number of enzymes, and that these serve multiple functions from maintaining the structure and elasticity of the corpuscle wall, to preventing the oxidation of iron (ferrous) in Haemoglobin to the +3 Ferric state.

But what none of them say, is what problems (if any) arise when the iron is oxidised. Hence the question, why avoid the Ferric state?

I'm still a high-schooler and from what I've learnt, is that the higher the oxidation state of the cation, the higher its polarising power (Fajan's Rules) hence stronger the bond. So wouldn't iron in the Ferric state be able to bind with oxygen better, and isn't that desirable? ( Or is oxygen release to tissues going to be problematic? )

If the Ferric state is desirable, then why do RBCs have mechanisms (the enzymes mentioned earlier) in place to prevent the oxidation of the Ferrous to the Ferric state?

Thanks!


texts: why dead mouse doesn't bleed when we cut their skin?

texts:
When we are pricked by a needle, we bleed nevertheless it's so small wound.
But when we do mouse anatomy, it doesn't bleed even if we cut their whole abdominal skin.
Other student asked about that, professor didn't know exactly but just guessed that mouse skin has no blood vessel. But I think it's wrong. that makes no sense.
As my guessing it's because mouse is dead when we do anatomy so there is no enough blood pressure.
Mouse have to bleed like ourselve. is this wrong?


texts: Is it possible for a substance to be absorbed by the hair or the scalp?

texts:
I've heard that the aplication of Monovin A in the hair would allow it to grow faster. Monovin A seems to be only A vitamin, according to the first website.

Could the application of A vitamin in the hair make it grow?

I'm thinking it's not very probable that applying it to the hair and the scalp would affect the hair growth. References will also be useful.


texts: What is the chemical composition / empirical formula of Herpes Simplex 1?

texts:
Viruses such as polio are so well documented that a search for "empirical formula polio" gives you something like

 C332,652
 H492,388
 N98,245
 O131,196
 P7,501
 S2,340

We know that the virus consists of 70% protein, 22% phospholipid, 6.5% DNA, 1.5% carbohydrate (from the book Herpes Simplex and Pseudorabies Viruses by Kaplan)

Is there any information on the actual chemical composition of HSV1 and varieties?

Thanks!


texts: How does current delivered by a neural stimulator propagate in the brain?

texts:
I have been trying to find good literature on how a stimulus current propagates through a medium that contains both gray and white matter (like the brain). Is it safe to assume that a current will spread through grey matter more easily than white matter, because of all the insulation provided by the myelin? Is it then safe to assume that, if you stimulated tissue which has white matter on one side of the electrode and grey matter on the other, the current would preferentially flow through the grey matter?

As an example I tried to sketch something that would represent a deep brain stimulation electrode in the subthalamic nucleus (STN) sending pulses through its bottom electrode (let's assume the return electrode is the implant case and far away from the target structure). As the STN is close to the internal capsule, I'm wondering if any assumptions can be made about the tissue activation region. More specifically I'm wondering if the current would spread more easily through the STN and have more trouble getting past the internal capsule (exciting the fibres there if the current is strong enough but maybe not getting past those fibres because of all the myelin?). So could we imagine the activating region of the stimulus pulses to be biased toward the STN rather than the white matter tracts?
Hope this clears things up.


texts: Did the capacity to be "knocked out" arise because it conferred an evolutionary advantage?

texts:
From first principles, it seems surprising that a blow to the head would cause unconsciousness rather than just impaired function.

I've heard a lot of analogies to computers -- "Your brain has to reboot." But computers reboot when there is an error because they are explicitly designed to do so, in order to recover and prevent further damage.

So, did we evolve the capacity to get knocked out for similar reasons -- because it helped us recover or prevent further damage? Or is the capacity to get knocked out just an "accident" or an inevitable consequence of the way our brains are designed, without a good evolutionary explanation?

(I realize the answer might be: "we don't know". In that case, I'd wonder what the prevailing opinions are and what if anything we've ruled out).


texts: Why are beta-galactosidase proteins overexpressed in senescent cells?

texts:
Wikipedia explains that it's a hypothetical hydrolase enzyme that catalyzes the hydrolysis of β-galactosides into monosaccharides only in senescent cells.

I'm just wondering - what causes it to be overexpressed in senescent cells - to the point that it often becomes a biomarker of senescence? And what exactly happens to the particular cell when you catalyze the hydrolysis of more β-galactosides (like lactose) into monosaccharides?


texts: Carcinisation is described succinctly in a Wikipedia entry. The entry references few scientific publications regarding the subject. But are there any popular scientific articles describing and giving examples of carcinisation in the layman's terms?


texts: Electricity generated by the body and its applications?

texts:
I recently came across this article from Nature. In it, it states that the snails have "tiny biofuel cells that extract electrical power from the glucose and oxygen in the snail’s blood", and that the power obtained is dependent on "how quickly sugar and oxygen can be taken from the creatures' blood". They go on to say that the power obtained decreases over time, and that these implants could power future pacemakers in humans.

Would this application in humans require that a patient eats more and "breathes more" than average? Why does the power output decrease over time, and couldn't that potentially lead to the malfunctioning of a pacemaker?

References

Van Noorden, Richard. “Cyborg Snails Power Up.” Nature (March 12, 2012). http://www.nature.com/doifinder/10.1038/nature.2012.10210.


texts: What is the reproductive success of a biting mosquito?

texts:
Female mosquito can lay ~50-100 eggs in each batch. It takes some time between the hatch and until the time the female mosquito bits. During this time many of them will die.

What is the average percentage of the eggs that mature (in other words, if a female mosquito lays one hundred eggs, how many of them will become grown females that bite)?


texts: when does an erythrocyte start carrying oxygen molecules and what is the binding capacity

texts:
As it is in the title, I am just wondering when does an erythrocyte (especially Reticulocyte) start carrying oxygen molecules and what is the binding capacity for oxygen.
That is, Under normal conditions, reticulocytes are the youngest erythrocytes released from the bone marrow into circulating blood. They mature for 1-3 days within the bone marrow and circulate for 1-2 days before becoming mature erythrocytes. How much oxygen molecule a reticulocytes can carry ?

I mean, I need an approximation of the number of O2 molecules bound to hemoglobin per reticulocyte


texts: Proteins with alpha helices alone and beta sheets alone?

texts: I would like to see some examples of proteins with PDB ID so that I can download and see them in VMD software. I need some proteins with alpha helix only and proteins with beta sheets alone.


texts: Do transcription factors block transcription entirely?

texts: Transcription factors bind to the DNA to block the transcription of a certain gene, right? But while they are bound to the DNA, do they completely block any transcription of this gene for as long as they stay there or can they also partially block transcription?


texts: What are some of the known fungi with heat resistant spores

texts: Are there any fungi whose spores can survive 100+ degrees for 15 minutes and grow in a sugar-deprived medium?


texts:
What is the energetic costs in KJ/g NH3 for nitrogenase fixation.
I want to compare Haber-Bosch vs nitrogenase.
How would I force the biological stochiometry of 8e- electrons into an energy quantity.
$N_2 + 8e^- + 8H^+ + 16ATP + 16H_2O → 2NH_3 + H_2 + 16ADP + 16P_i$


texts: What could cause individual false positives in ELISAs, while the rest of the plate looks fine?

texts:
I run indirect ELISAs for COVID antibodies. That's my whole job right now as a research technician. I coat the plates with a pure RBD, then detect antibodies in serum. Recently it's come to light that I've run plates with false positives. Running those same serum samples again gives VERY different (negative) results. If entire plates were giving false positives we could figure out what mistakes I'm making, but for the most part the duplicates look good, the standard is good, the dilutions are good... The person who wrote this protocol hasn't included a negative control because there have been occasions during the development of the protocol where pooled serum from 2018 or earlier was used as a negative, but those pooled serum controls were somehow consistently more positive than that of several confirmed, post-recovery COVID patients. Obviously that lack of negative control has predictably come back to bite us.
Originally we thought it was a plate washer malfunction, but it turns out these smatterings of false positives predates the plate washer acting up.
The short of the long is that some of my plates have very clear, obvious negatives, some borderline positives, and some clear, obvious positives. The issue is that some of those positives are false positives and neither I nor my supervisor can for the life of us figure out why.
Ideas would be awesome. ELISAs are my entire job right now, and the PI is understandably not thrilled with me.
Additional details:
Plates are washed by an automatic plate washer after the incubation of sample dilutions, and after the incubation of the secondary antibody/HRP. The plates are blocked before sample addition with a fractionated bovine serum/gelatin/tween20 blocking buffer. Dilutions are made in that same blocking buffer, and the secondary antibody is also diluted in blocking buffer. We're using Immulon 4HBX plates. The plates are developed with ABTS in McIlvain's plus H2o2.
Ask my anything else that might help figure this out. I'll answer what I can.


texts:
Why is it said that , warmth facilitates assembly and cold facilitates disassembly of microtubule?
But till now what I  had learnt is that as temperature increases so the kinetic energy of molecules increases so does the order decreases.
So what is the reason behind the above phenomenon?


texts: What will be the deficits when left half of the brain is removed in adults?

texts: Hemispherectomy is a surgical procedure to remove half of the brain. It is typically done on children with severe epilepsy. What will be the deficits when left half is removed in adults? Is aphasia a certain outcome in case of left hemispherectomy in adults?


texts:
There have been demonstrations of ecomorphs in different taxa, where each morphology type is associated to a single environment. I know that it happens because special morphological characters increase the fitness and therefore will be positive selected.

My question is; if we find similar places (talking about natural pressures and climatic conditions) on earth and given enough time, can we expect to see more or less the same ecomorphs living in different places? Also, assuming that, could evolution be a regarded a non-stochastic process?


texts: Deduce length order of 4 decapeptides based on the Ramachandran plot

texts:
I have stumbled upon the following past exam question:

  4 decapeptides A, B, C, D, made only of glycine residues, have
  different conformations, and the phi and psi angles of individual
  peptides are indicated on the Ramachandran plot (unfortunately I
  cannot provide a specific plot). Order these peptides by decreasing
  length.

How should I solve this, what information useful in solving this problem can I deduce from the Ramachandran plot?


texts: Why would growth hormone (somatotropin) cause both lipid AND glucose release?

texts:
GH increases lipolysis (lipid breakdown) and the release of fatty
  acids from adipocytes into the blood. Fatty acids then can be used as
  energy sources to drive chemical reactions, including anabolic
  reactions, by other cells. GH also increases glucose synthesis by the
  liver, which releases glucose into the blood. The increased use of
  lipids as an energy source accompanies a decrease in glucose usage.
  Overall, GH activates the use of lipids to promote growth and protein
  synthesis.

(From Seeley’s Anatomy and Physiology, 10th edition.)

That passage has gotten me confused. So more lipids are used by cells instead of glucose, yet the body releases more glucose into the blood in response to GH. What would be the point, or benefit, of this occurring?


texts: Why does a stronger heart cause blood pressure go down

texts:
Intuitively, why does a stronger heart cause blood pressure to go down? The answers I've found from a cursory google search seem to indicate that it has to "work less hard" to pump the blood and that it "beats more slowly," but I do not immediately understand the implications of this.

Furthermore, if it is due to a slower heart beat in a stronger heart that blood pressure is lower, then how does (/is it true that) blood pressure remains lower in those with a stronger heart during exercise? Wouldn't a stronger heart beating just as fast as a weaker heart lead to higher blood pressure?

Thanks for any help. :)


texts: How do membrane proteins find their target locations?

texts:
The question might be asked for any kind of "bound" proteins, but I'd like to restrict it to membrane proteins.

Assuming membrane proteins (or their main parts) don't (or aren't) build in situ but at some distance of the membrane, I wonder by which mechanisms they travel from their generation site to their final destination inside the membrane (inner or outer).

Proteins that are distributed roughly evenly (or randomly) over the membrane don't pose a big conceptual problem: they could have gone their just by diffusion, possibly from many generation sites, distributed roughly evenly (or randomly) inside the cell.

But what about uneven distributions, where some proteins are more densely and non-randomly packed (significant and functional) at some sites of the membrane than at others, e.g.

receptors at postsynaptic densities
Na+ channels at action potential initiation sites like the axon hillock or the axon initial segment
Na+ channels at nodes of Ranvier?

By which mechanisms (forces, signals or structures) are these proteins led to
 their targets?

Maybe it depends, and there are different mechanisms. These I came up with (by contemplating first principles):

uneven distribution of generation sites inside the cell (due to what?)
uneven distribution of origins of attracting signals inside the membrane (due to what?)
some "self-attracting" forces or signals (leading to accumulation by positive feedback)
microtubules

Which mechanism is — possibly — predominant?

Related questions:

Life cycle of proteins
Pathways of ligand-gated ion channels
Distribution of synapses of CA1 neurons
Distribution of dendritic spike generating ion channels on the dendritic tree
Visual maps of the neuronal membrane
Distribution of sodium–potassium pumps


texts:
I wonder why (especially human) sex lasts longer than just a few seconds?

My thought is that the shorter it takes a man to ejaculate, the lesser is the risk that he gets interrupted by a rival or a predator. Therefore, men who ejaculate quickly get an evolutionary advantage in the long-term.

But, as human sex lasts several minutes, I'm obvioulsy wrong with my argument. Anybody knows why?


texts: Why is sheep erythrocyte lysis considered as classical complement activation pathway, and rabbit as alternative one?


texts: Is the mutation rate in organisms in general consistent over the genome?

texts:
Coming from computer science with an interest in genetic programming (a process emulating evolution) I'm curious about whether the rate of mutation is homogeneous across the whole genome, or if some parts of the genome differ in the rate of mutation.

For example we could imagine, without going to into details that could invalidate the example, that parts of the genome associated with the immune system could have a relatively higher mutation rate, because this would allow for a quicker adaptation to quickly evolving pathogens.

Is there any empirical support for that different part of a genome of some species have different mutation rates, that would give us empirical support for the possibility that some species under evolution have the ability to adjust (by NS itself or even epigenetics) the mutation rate of specific parts of the genome?

Clarification

I'm only interested in the mutations happening in the scope of the lifetime of a individual organism, I'm not interested in whether the mutations persisted under NS are equally distributed over the genome.


texts: Influence of temperature on transcription, protein binding and decay rates

texts:
I am the kind of biologist who doesn't know much about molecular genetics and about the dynamic of biochemical reactions.

Question

My question concerns the influence of temperature on the dynamic of molecular genetic processes. Typically, I'd like to know how (quantitatively speaking, looking for the $Q_{10}$ for example) the following parameters get modified with temperature.

rate of transcription

UPDATE See How is the rate of transcription influenced by temperature?

protein binding to a DNA-binding-motif

UPDATE see influence of temperature on protein binding and decay rates

rate of protein decay

UPDATE see influence of temperature on protein binding and decay rates

rate of mRNA decay

UPDATE answered by @Chris below

Why do I ask this question?

In order to know what kind of default parameters values I should enter for modeling purposes in evolutionary biology. While our scope is large we decided we would consider parameters values that are observed in yeast.


texts: Mechanism of Decorticate & Decerebrate Posturing? Also why is only Decorticate Rigidity a misnomer?

texts:
I read these two from various books, and got confused. The confusion is -

Reticulospinal tracts control gamma motor neurons. Gamma motor neurons control tone of muscle.
In decerebrate rigidity, the reticulospinal tracts are cut, so the gamma motor neurons start firing excessively, and SPASTICITY develops. I understood this part and why Decerebrate Rigidity is a misnomer as it is actually spasticity.

Question is, in decorticate rigidity, the cerebral cortex is damaged. The basal ganglia are intact. One explanation I found is that the basal ganglia keep the reticulospinal tract activated so gamma motor neuron is under control. But if basal ganglia have no direct communication with brainstem or spinal cord, and their efferents pass through cerebral cortex, then even in decorticate rigidity, the reticulospinal tract should not be working, and thus the gamma motor neurons should fire excessively, in which case the decorticate rigidity also becomes a spasticity.

Am I missing anything? I am keeping red nucleus and vesticular nuclei out of this just to make matter simple. My question is about activity of gamma motor neurons in these two conditions. I hope you got the question. Thank you.


texts: Pathogenesis of Group B Streptococci and C5a

texts:
I am thinking the pathogenesis of the C5a in GBS.
I think the pathogenesis happens like

  C5a-peptidase in acid environment (Sialic acid, capsule) $\to$ cleaves C'-derived Neu chemoattractant C5a $\to \downarrow$ alternative pathway of Complement.

However, this part cleaves C'-derived Neu chemoattractant C5a is not clear to me.
I think this means that C5a-peptidase cleaves Neu C5a from the previous complement reaction that inhibits the next coming alternative pathway of complement.

How does this pathogenesis of GBS happen?


texts: Do animals have different taste preferences within the same species?

texts: Humans (especially children...) seem to dislike certain foods or drinks, that other humans seem to like. Common examples are coffee, french cheeses, olives, milk, fish and cabbage. Are there examples of animals either wild or in captivity that show the same behaviour? For example a group of primates that eat something except one or two members of the group? And if so, any clues to the evolutionary aspects of such preferences?


texts: Detecting a Fasting State in the Body via Lasers

texts: I was just wondering wether it would be possible to detect if the body is in a "fasting" state, via lasers attached to the body. If it is possible, what sort of laser would be needed?


texts: Sex differences in response to food deprivation

texts:
This question was inspired by a casual conversation with friends the other night. Some of us had noted that women tend to eat smaller meals more often (snacks, fruits etc) while men eat larger portions more infrequently. Also, several of the women said to be sensitive to food withdrawal, getting very hungry after a few hours and experiencing low blood sugar symptoms (even fainting in one case) if not eating regularly, for example if skipping lunch. Men (including myself) seemed to be less affected, often skipping meals without noticing.

This was a highly unscientific investigation with a tiny sample size :)  just based on our personal stories and friends we know. It could, of course, reflect attitude/perception/habits rather than actual biological differences. It should also be said that not everybody agreed -- some men also stated that they felt sensitive to food withdrawal. But there are of course known differences in metabolism between the sexes, so it doesn't seem entirely implausible. It might also be related to different body mass, muscle mass, etc.

So my question: is there any scientific evidence that women and men react differently to short-term food withdrawal? Here short-term would be, say, up to 24 hours, as when skipping breakfast and/or lunch. Are there any data on differences in blood glucose levels after food withdrawal, for example?


texts:
I have a question about cancer cure statistics. Many of the cancer literature or databases I have come across speak about 5 year or 10 year survival rates. In this case survival means that the patient with cancer is still alive 5 or 10 years after diagnosis. I am in need of references about the statistics which explain what is the percentage of people in these groups who are in progression-free survival group and disease-free survival group. That is for instance among the cancer patients which survive for some X years, who are completely cured of cancer (which means that the cancer is completely cured and has not reoccured with in this X years).

Update: USA data is preferred

Thanks


texts: Simple computational biology project for AP Biology class. Ideas?

texts:
Our teacher assigned us a project to do with an extremely open-ended prompt and it should be completed within a month.
I was planning on doing something related to computation and evolution in terms of biology although I'm not really sure where to start. I say simple because I'm not a professional programmer, rather, extremely interested in the field and I hope to use this as an opportunity to stretch by skills.
Any ideas on a project or where to start would be greatly appreciated.


texts: Does the cell have a mechanism to determine DNA sequence from protein?


texts: Will two Type IIS restriction sites cut if they are directly back-to-back?

texts:
I want to put two BbsI (or BsaI) restriction sites right next to each other, facing out, like this:

       \/ |BbsI||BbsI|  \/
CTCAAATGCGGTCTTCGAAGACGTTTTAGAG
   /\                      /\

Should I expect this to cut, or are the two restriction enzymes going to block each other?


texts:
I formally come from a physics/physical chemistry background, but I have begun to specialize in the area of the biomedical sciences and biomedical engineering. I found myself reading an article which talks about using leukocytes as carriers for targeted cancer drug delivery. One of the frequent adhesion molecules that comes up in the paper is E-selectin, whose wikipedia page I looked up to learn more about the molecule.

On that wikipedia page, it says that E-selectin is encoded by the SELE gene. Now, I can see that the gene is called "SELE" as it abbreviates "Selectin E", but my question is: how did this become the "official" name for the gene? Why doesn't the official name reveal anything about the actual nucleotide sequence of the gene? If someone had never heard of E-selectin before, how is he/she supposed to learn anything about the gene just from the name "SELE" ?

Sorry if this is a very nit-picky question. It's just that most of the substances talked about in chemistry have official names that reveal information about the structure, even if there is a more commonly used "nickname."


texts:
From WIKI:

Modern humans and Neanderthals share 99.7% of their DNA

and

1–4% of the DNA of living non-African humans are found by the Max
Planck Institute to likely come from Neanderthals, a result confirmed
in 2012, and refined to 1.5–2.1% in 2014

What do they mean? If it is similar for 99.7, how it could be that 1.5%-2% is unique genes from Neanderthals?
The Africans do not have them, so African different from European in 1.5-2% ? But that's not true.


texts: What is the name of this plant with mango type leaves?

texts:
Location: South India

Leaves: Mango Type

Indoor/Outdoor/Wild: Indoor

Month: May


texts:
I got this question and don't really understand the difference between the answers.

Diffusion is (in cell membrane):

a) passive by nature, no metabolic energy is needed

b) driven process by pressure or voltage


texts: Why are childhood cancers less frequent than infant or adult?

texts:
According to data provided by Cancer Research UK, the lowest rate of cancer incidence by age occurs between 5 and 15 years.  Infants have a higher rate, and the odds of an adult developing cancer increase over time, especially during old age; until the odds plateau around age 85.

I understand that an accumulation of DNA damage over time increases likelihood of cancer with age.  But what explains the almost flatline rate of cancer amongst those aged 5-15?  Surely it makes more sense for the rate of cancer to increase uniformly every year from infancy?


texts:
So obviously, viruses are nonliving. But when my teacher was teaching viruses in the video (we're doing "flip" learning this semester), the way he described it, it seemed like the viruses responded to their environment in that they moved around until they found a cell of the right type, and then they latched on and hijacked it.

I had always thought of it more like that they were just kind of floating around, carried by the host system (blood in animals for example), until they "bumped into" the right kind of cells and both sets of membrane proteins "docked". But my theory/idea doesn't really make sense because it doesn't account for how viruses would be able to infect bacteria.

But, the idea that viruses propel themselves doesn't make much sense either, because viruses are nonliving, and one of the characteristics of life that they do not meet is that living things acquire and use energy.

In summary my question is, how are viruses propelled? Do they move themselves, or are they moved by external forces?


texts: What is the "male gender rudiment" that women allegedly have?

texts:
In The Man without Qualities Robert Musil wrote (my emphasis):

  "But the nature," he thought, "gives the man nipples and the woman
  a male gender rudiment. We cannot conclude from this, however,
  that our ancestors were hermaphrodites."

What male gender rudiment does he mean? It must be some "useless" body part in female body (like man's nipples).

Original German text:

  "Aber die Natur" dachte er "gibt dem Mann Saugwarzen und der Frau
  ein männliches Geschlectsrudiment, ohne dass daraus zu
  schliessen wäre, unsere Vorfahren seien Hermaphroditen gewesen.


texts: Why does alcohol cause the hemolysis of RBC in a large proportion?

texts:
I had today an experiment that we put 95% alcohol to the blood which made it completely transparent so hemolysis must have occurred.
I started to think about the reasons.

I think that this is because alcohol dissolved the lipid membrane of cells outside of the cell.
Alcohol molecule is also very small.
I think that I can go through the bilayer too.
So I started to think that the other possible reason was that alcohol went inside the cell so caused

dissolution of the membrane from the inner side
increase in the volume of the cell so bursting

What are the main reasons why Alcohol cause hemolysis to the red blood cell?


texts: What is the current thinking on the typicality (or otherwise) of fossils as representatives of their species?

texts:
Since fossil records represent a tiny percentage of species populations, how do paleontologists determine how typical those specimens are?

Is there any research or analysis to determine how the distribution of fossil specimens within a species corresponds to the distribution of specimens of the species population as a whole?


texts: how to find accurately the closest species to my plant species?

texts: I'm working on some bioinformatic analysis of a non-model woody plant within the family with least information. So, I'm looking for a closest species to my plant. Any suggestion would be highly appreciated. Also, It will be great if I have know about the divergence time (? million year) between two species. Is there any documents or website to address this issue? Thanks


texts: How can I avoid digesting protein-bound DNA?

texts:
I'm interested in sequencing and analyzing the bound DNA, and minimizing the amount of unbound DNA that gets sequenced through digestion.

When digesting protein-bound DNA, is all of the unbound DNA digested? Is there a way to maximize the amount of unbound DNA that is digested?


texts: How can a virus be determined to cause a disease?  From other posts I have read here, humans carry hundreds of different strains of viruses.  How is a study structured and carried out to determine that one virus is the cause of a disease, and not any of the other viruses present?  Any examples of studies are greatly appreciated as well.


texts: Is poison venomous and is venom poisonous?

texts:
I know the difference between poison and venom AND poisonous and venomous.
But I just want to know if an ingested venom would do harm to humans and if an injected poison would do harm to humans.
I really think that poison is both poisonous and venomous AND venom is both venomous and poisonous.


texts:
When a farsighted person looks at a distant object and sees it clearly, what is the state of their eye lens? Is it relaxed?

Rationale:

It is something we read about in class that is confusing.I know a person with 20/20 vision would have a relaxed lens when looking at a distant object. I think a farsighted person would have a relaxed lens when looking at far objects since they can see distant objects, but since they have trouble seeing close objects the lens would not be relaxed when looking at close objects. Those that are nearsighted would have a relaxed lens when looking at close objects, but not when looking at distant objects. So, a relaxed lens just means the eye does not need to strain when looking at something?


texts: What is this insect that has invaded my home in Texas?

texts:
After the recent floods in central Texas this past weekend I noticed my that bedroom has suddenly been infested with these small insects that have climbed in through the window. Previously, the hole in the window was used by ladybugs who hatched larvae in the room (they didn't survive long).

However, these insects have been here for 3 days now. They seem to disappear at odd times during the day (haven't nailed down a pattern yet) and return a bit later. There are roughly 20-30 of them in my room at a given time. They don't do much and seem very uninterested and passive, mostly just flying around or meandering across the walls on and off. Some of them have wings and others do not (that or the wings are hidden and they just aren't using them).

I would like to identify what this insect is so I can find a way to get rid of them. A picture is linked below. Note in the picture that the white-ish segments on the leg are actually closer to yellow in color.


texts: What's the best wat to combine biological replicates in qPCR gene expression analysis? (2^(-∆∆Ct) method; one-way anova, turkey's test)

texts:
I am measuring the levels of gene x after transfection of cells with a plasmid and I want to compare them to the levels in mock-transfected cells. I did three different transfection experiments, in different days (three biological replicates). I then quantify expression through RT-qPCR.

How can I combine the data from the three biological replicates?
I was applying the ∆∆Ct method to each biological replicate separately, and then combining and analyzing the final fold change of the three replicates in a one-way anova, with turkey's test for significance calculation.

My supervisor suggested a different strategy: calculate the ∆Ct values (Ct mutant - Ct housekeeping) of the three biological replicates, then calculate the difference (∆∆Ct) of each ∆Ct with the average ∆Ct of the mock-transfected cells (∆Ct(transfected cells; replicate nr. x) - ∆Ct(mock; average of replicates)). Then, calculate the 2^(-∆∆Ct) of each ∆∆Ct obtained.

In both ways, at the end three fold change values are obtained (one for each biological replicate). However, the variance is much greater in the second method and, for example, there's no significative difference (one-way anova, turkey's test), while the significance is reached with the first method.

My question is: which method is the best? And, possibly, why?

p.s. I really hope I made myself clear, it's not easy to explain with words what I mean. Please tell me if you cannot understend some parts of the question.


texts: gene mutation occurs on two strands of DNA or just one strand?

texts:
Suppose we have one strand with 3'-AAA-5' and the other strand is 5'-TTT-3'.
So when point mutation occurs, does it happen to two strands at the same time? e.g. 3'-AAA-5' becomes 3'-AGA-5' and 5'-TTT-3' becomes 5'-TCT-3'?
Or the mutation can occur with only one strand? e.g. only 3'-AAA-5' becomes 3'-AGA-5'? but in this case, A would pair up with G.
When transcription starts, the 3'-5' strand is transcribed, if the mutation does no occur in this strand, does it mean this mutation wouldn't affect any downstream products?
Is it same for indel?


texts: I've always been told that most electronic devices such as WiFi/phones/laptops and such emit a non-ionizing radiation which is completely fine as it does not damage human DNA. I've been googling and i see people arguing about it but there seems to be no evidence to back up the fact that it's not damaging. I'm just curious is what I'm saying correct? or can it damage the human body as i see people mention it can lead to pretty serious health problems.


texts: Can qPCR primer with several mismatch works?

texts:
I am designing primers for qPCR from conserved regions of a few different fish species.This is because gene sequence for my fish species are yet unavailable in NCBI database.

Is it OK (can the primer anneal to the target sequence) if the primers have several mismatch at the interior and towards it 5’ end? At the 3’ end, I can only design primer with maximum 5 conserved bases.

Thank you.


texts:
Inbreeding depression may be reduced by selection against deleterious alleles, which eliminates, or purges, them from the population. I have two questions:

Is genetic purging based on random shuffling of the genes of an individual or is it more intentional way of removing deleterious recessive alleles?
Do the individuals/couple with deleterious alleles that breed together, pass down the purged genes EACH AND EVERY TIME they produce offspring? Does it happen every time they mate or just some times?


texts: 0.1 M sodium citrate in 10% ethanol and DNA solubility

texts:
I understand how DNA precipitation works in the presence of salt (such as 0.3 M sodium acetate or 0.2 M sodium chloride) and alcohol (30 ~ 50 % isopropanol or 60 ~ 75% ethanol)

However, in the Trizol kit manual, DNA could be washed and precipitated in 0.1 M sodium citrate in 10% ethanol

At only 10% ethanol and 0.1 M sodium ion, how can DNA be in a "compact/insoluble" form so it can be precipitated by a low speed centrifugation (2000 x g for 5 mins)?


texts:
I need to run gels that are of not the "most" importance. So I do not want to waste alot of money on step ladder. How do I dilute DNA step ladder? Is there a general procedure, for I have tried googling for one, but I get varying answers, such as a 1:4  dilution, and so on.

This is the information on the Step ladder, by Promega, posted as an image, since copy and pasting would mess up readability.

EDIT:

Even though I awarded the bounty because it gave me the same concept; what I had actually did was to assume I would use $60ul$ of ladder combined with $1$x dye.

Therefore since I started with $1ml$ of $6$x loading dye, $100ul$ of DNA step ladder, and available nuclease free $\ce{H2O}$, and I desired a 5:1 ratio of solution(dye and $\ce{H2O}$)  to ladder.

I would then use $12ul$ of stock to the $60ul$ total.

To make the dye $1$x, I would add $10ul$ of the $6$x dye to make the final concenetration of dye $1$x.

Then I would add up to $38ul$ with nuclease free $\ce{H2O}$.

So, sorry if this was worded redundantly, but It helps me to read, therefore in summary:

$$  +10ul  \text{ of 6x dye}$$
$$  +12ul \text{ of stock 100bp DNA step Ladder}$$
$$+ 38ul  \text{ Nuclease Free } \ce{H2O} $$
$$ \text{__________________________________}$$

$$\sum{60ul} \text{ of ladder & dye} (1 \text{x}) $$

of which total I can aliquot out to my hearts desire.

EDIT2:
The ladder turned out successful.


texts: Why do pigeons kill their chicks when touched by a human?

texts:
I used to have many pigeons around the house. If by chance one of the chicks fell out of the nest, we used to put it back using gloves.

Usually, if we would touch the chicks with our bare hands, however, the other pigeons would usually kill the chick. I want to know why they do that?


texts:
In 'E.coil in Motion' Howard Berg says that

  'If it [a cell] is to go far enough to find out whether life is
  getting better or worse, it must outrun diffusion.'

I am confused about the exact meaning of this expression and can't seem to find an explanation. What is meant by 'life is getting better or worse' and why can't a cell just wait for things to come to it by diffusion?


texts:
I have a VCF file and wish to calculate a few indices of population divergence over a sliding window.

I consider using pypgen but the documentation is currently very limited. Can you please give me an example (for Jost'D for example) of a code that would work?


texts:
What is the meaning of the num_tol_term attribute in a PeptideProphet (pep.xml) search_hit?

<search_hit hit_rank="1" peptide="DATDDFEDVGHSTTAR" peptide_prev_aa="K" peptide_next_aa="A" protein="Traes_5AL_64120ED6B.1"
    num_tot_proteins="4" num_matched_ions="9" tot_num_ions="30" calc_neutral_pep_mass="1735.7364" massdiff="-0.0269"
    num_tol_term="2" num_missed_cleavages="0" is_rejected="0" protein_descr="| AT2G32720.1 | member of Cytochromes b5">


texts: if sperm contains only 50% of someone's DNA how can it be used to identify someone?

texts: Is DNA so unique that 50% of it is enough to identify a single person?


texts: Why is cancer more lethal than (hypothetical)infections?

texts:
I am a computer science student and I'm interested in algorithmic aspects of cancer! Once I heard that there exist more bacteria in human body than our own cells, I wondered that why bacteria, which divide faster than cell bodies, do not cause something like cancer in body? Isn't it evolutionary more probable for bacteria to gain aggressive properties and invade human tissues? Or maybe is it the case that bacteria really produce some lethal colonies like cancers in the body?

One difficulty with cancers is that cancer is a very complex disease  because of it's intra-tumor and inter-tumor heterogeneity. Isn't it more probable for bacteria to cause extremely heterogenous infections with regard to existing simple evolutionary models which are used to describe cancer?


texts: Identify brain junk - What are all the known intracellular and extracellular substances which build up with age and clog the brain?

texts:
What are the known junk substances which the body is unable to dispose of and which build up in the brain with age to eventually causes age related problems?

Starting with the most obvious ones:

Amyloid beta - https://en.wikipedia.org/wiki/Amyloid_beta

Lipofuscin - https://en.wikipedia.org/wiki/Lipofuscin


texts: I found this animal, which I suspect it's an insect, on the floor of a kitchen in Spain some days ago. It's about 8-10 mm long. I don't think I've ever seen it before. What is it?


texts: Differentiating molecules based on peptide sequence? How to annotate?

texts:
I want to differentiate between classical class I and non classical class I MHC molecules in a model organism using well conserved structural features within classical MHC I molecules (eg intradomain disulfide bridges within class I a1 domain). To do this I need to align the peptide sequences of transcripts of that model organism with transcripts of classical MHC I human genes and see which genes from those transcripts have those structural features. So I am looking for a tool to align and annotate those structural features in a replicable manner
Additionally if you have any other bioinformatic ideas /computational analyses on how to find classical MHC Class I molecules on an organism which is poorly annotated that would highly appreciated!


texts: Why cannot machines use energy stored in a way similar to biological systems' energy storage?

texts:
Owing to the generality of the question I am interested merely in key problems so that I could do further reading.

As I understand man-made energy storages are significantly less efficient than biological ones. I would like to focus on quickly available energy for small systems (human scale or smaller) - after all we can say that hoards of coal are a pretty nice energy reservoir.

For example, a robotic bee:

https://www.youtube.com/watch?v=lJCMIsLuGpg

What can we see here? A wire - and I think we cannot expect to have a long lasting independent robotic bee with the current technology due to inefficiency of our energy storage.

How do biological systems store the energy then? https://en.wikiversity.org/wiki/Energy_Storage_in_Biological_Systems

  Living organisms use two major types of energy storage. Energy-rich
  molecules such as glycogen and triglycerides store energy in the form
  of covalent chemical bonds. Cells synthesize such molecules and store
  them for later release of the energy. The second major form of
  biological energy storage is electrochemical and takes the form of
  gradients of charged ions across cell membranes. This learning project
  allows participants to explore some of the details of energy storage
  molecules and biological energy storage that involves ion gradients
  across cell membranes.

To be more specific let me give an example: why cannot we have a machine that would have an input for carbohydrates, a converter to say glucose and then ATP which would finally break down and release the needed energy?

Why is it not viable? Do we lack technology to do this? Which step is problematic? Are we far from having biological-like storages?


texts: Lack of A/B-antigen equivalent to Rhesus disease

texts:
Rhesus disease occurs when an Rh- mother is exposed to Rh antigens (often due to blood contact with an Rh+ child during delivery) and mounts an immune response which eventually results in the production of IgG Rh antibodies. In subsequent pregnancies, these antibodies cross the placenta. When the foetus is Rh+, these antibodies can bind to the corresponding antigens on the foetal erythrocytes and cause haemolysis, which can result in anaemia or even, in serious cases, stillbirth.

Given all of this, why does the same principle not apply to A and B antibodies? In other words, what is special about Rhesus antigens or antibodies that does not apply to other erythrocytic antigens or their corresponding antibodies?

I'm specifically wondering about Rhesus disease and its effects on the foetus, and why similar effects do not occur on the foetus in the case of an ABO type mismatch between mother and foetus.


texts: How can I make a protein interaction/protein-complex network?

texts:
Let's say I have a list of proteins ID. I would like to know whether I can find any complex based on that list. Any example, explanation is appreciated.

An example input is what you see below. What can I do with the following list of protein IDs? These IDs are from human.

P41182,P56524, P41182,Q9UQL6, P41182,Q8WUI4,Q92793,Q09472,Q9Y6Q9,Q92831


texts: How can I extract ligand with neighboring protein atoms from PDB with complex?

texts:
I'm not familiar with biology and coming from Data Science field, so please excuse me for the lack of knowledge. What I want is to create 3D voxel representation of ligand atoms with neighboring part of the protein (looks like it is called pocket) from PDB file which contains complex.
For example, let it be 10gs from RCSB (https://files.rcsb.org/download/10GS.pdb). For other example, it can be 4xit or 4wkc.
What I planned, was identify both protein and ligand atoms, compute the geometric center of the ligand, and then calculate proximity for each atom and fill some 3D surrounding cube.
When I open PDB for this complex (10gs) I see what I understand as two possible binding sites for ligand VWW, and another two - for MES:
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE VWW A 210
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC2
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE VWW B 210
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC3
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE MES A 211
REMARK 800
REMARK 800 SITE_IDENTIFIER: AC4
REMARK 800 EVIDENCE_CODE: SOFTWARE
REMARK 800 SITE_DESCRIPTION: BINDING SITE FOR RESIDUE MES B 211

How can I proceed from this point? Does this PDB contain atoms for ligand VWW, properly oriented, and how can I identify them along with neighboring ones of target protein?
Or my formulation of the problem is totally wrong?


texts:
I am reading about scorpion venoms and toxins for my bio class and they appear to have a variety of potassium channel blockers. My professor asked "What effect would this have on a neuron?" and naturally two things came to mind

Potassium channels are necessary for repolarization
Potassium channels participate in controlling the concentration gradient of the cell.

I have found evidence in articles supporting the first claim, but I don't know much about the second.

Do potassium channel blockers affect the resting membrane potential?  Would they significantly alter the concentration gradient?


texts: 0.9% Saline or Ringer's Solution for in vivo work

texts:
A few of the labs where I currently work routinely use 0.9% saline for in vivo work (washing out debris during surgery, diluting substances for IP/IV/SC injections, etc.)

A few years ago I worked in a lab where the standard was to use Ringer's Solution. Obviously, in both labs the choice was based on an organizatorical/historical reasons. But I was wondering: Does either of these solutions perform any "better" (i.e. causes less physiological disturbances) than the other?

My guess would be Ringer's is better, since it is also suitable for keeping cells alive in vitro - and there is also this paper that calls 0.9% Saline into question altogether. But I could not really find any good comparison tests.


texts: How many ancestral generations do I have?

texts:
Following on from this question: How many humans have been in my lineage? Is it almost the same for every human currently living?

How many generations back do my ancestors go? Not just human ancestors, but all ancestors, right back to the first lifeform.

I recognise that there are some impossible unknowns here, so I’m looking for some kind of Fermi estimate.


texts: Why insects are so energy-efficient while flying?

texts: Why are insects so energy-efficient while flying? Is it because of their light weight and aerodynamics or due to very efficient biochemical transformations (food->energy)?


texts: Although blue foods exist, they're rare enough compared to other foods for food preparers to use blue plasters as a convention. The natural colour of a given food is due to pigments that have some biological origin. Is there any evolutionary reason why these are rarely blue?