texts: What is the function of the polar bodies produced during oogenesis?

texts:
Why are polar bodies produced during oogenesis in human females?

I read that polar bodies are produced during meiosis so that the oogonium (or gamete mother cell) can be converted into a haploid female gamete or ovum by getting rid of the extra genetic material.

So, it is pretty clear that one follicle (containing one gamete mother cell) produces only one ovum.

So what is the point of producing polar bodies? Isn't it just a better mechanism over all for the meiotic devision of the oogonium to result in equal distribution of the cytoplasmic content to both daughter cells? That way, one oogonium can produce four ova, not just one. Th entire process of DNA replication during the synthesis phase (S phase) of the meiotic cell cycle seems like such a waste if 75% of the total genetic material produced is going to be expelled as polar bodies.

There is also the argument that since the ovum is non-motile and always within the female body, it need not be produced in large numbers as it is in a safe and protected environment. But, in that case, would it not be a better system is fewer follicles were produced, but each follicle divided to give four ova? This mechanism would end up producing the same amount of ova, but with lesser labour (such as DNA replication) going waste.

So, taking these arguments into consideration, what exactly is the function of the polar bodies produced?


texts: Are there animals that usually sneeze with their eyes open?

texts:
As per title. I believe that most animals tend to sneeze with their eyes closed, but wonder if any normally keep their eyes open.
Is it the case?


texts: Why are ammonium ions reabsorbed in the thick ascending limb during acid secretion?

texts:
In order to produce HCO3- from glutamine and to subsequently reabsorb it,
H+ ions need to be secreted. The kidney does this by via ammonium ions
in the PCT. But why are the ammonium ions then reabsorbed in the TAL before
being put back into the collecting duct? Wouldn't it be more efficient if
they were just left in the tubule fluid where they would reach the
collecting duct eventually? The first method seems to be a longer way of
achieving the same result.


texts:
I refer to J.H. Jones' Notes on R0.

Preliminaries
The standard SIR model consists of a system of three differential equations
$$ds/dt = -\beta  s  i$$
$$di/dt = \beta s  i - \nu i$$
$$dr/dt = \nu   i$$
for the fractions $s, i, r$ of susceptible, infected, and recovered (removed) individuals, $dt$ = 1 day.
$\beta$ is the infection rate, i.e. the number of individuals an infected indiviual infects per day, $\nu$ is the removal rate, being defined as the reciprocal of the duration of infectiousness $d_i$ (measured in days), i.e. $\nu = 1/d_i$. The reproduction number $R$ is the product of infection rate and duration of infectiousness, i.e.
$$R = \beta \cdot d_i$$
To reduce the growth of spreading of a disease, mitigation measures typically target at the infection rate, at least when a reduction of the duration of infectiousness is not at sight.
To estimate the impact of a mitigation measure on the infection rate, it is worth to consider it as the product of several factors, which may be influenced separately and more specifically.
One common approach is to consider the infection rate as the procuct of

transmissibility per contact $\tau_c$, i.e. the probability of getting infected when being in one contact with an infected person and

mean rate of contact $c$, i.e. the number of single contacts an average individual has per day, i.e.

$$\beta = \tau_c \cdot c$$
Let alone that it is not so easy to define what a contact is, other factorizations are conceivable when considering these candidates:

transmissibility per hour $\tau_h$, i.e. the probability of getting infected when being in contact with an infected person for one hour

mean duration of contact $h_c$ (measured in hours)

Let "being in contact" specifically mean "closer than 1.5 m in the average".
We then have
$$\beta = \tau_h \cdot h_c \cdot c$$
We can group factors:
$$\beta = \tau_c \cdot c$$
with $\tau_c = \tau_h \cdot h_c$, and
$$\beta = \tau_h \cdot h_d$$
with $h_d = h_c \cdot c$ the number of hours per day an individual is in contact with other persons.
Question
I am looking for references where such factorizations of the infection rate are considered, especially in the context of Covid 19.


texts: Are human fetuses more likely to be male?

texts:
Question: From a physiological point of view, when sex is determined in a human fetus, is it equally likely to be male or female?

Studies in this area typically measure age at birth, where the data would have already been biased.  There's a slight imbalance in the human sex ratio, in that there's an overall tendency towards males.  However, this could be accounted for in numerous ways, such as abortion.

Fisher's principle suggests there would be an evolutionary tendency towards 50:50 chance.


texts: What causes the human body to “jump” when we get a shock?

texts:
At a Remembrance parade today, a cannon was set off to mark the beginning of a two minute silence. As it went off, the crowds quite comically jumped in sync, from the shock it gave them. I’ve seen very similar reactions in other scenarios, such as a jump-scare in a horror film.

Seeing the in-sync crowd jump today made me wonder.. what is it, in the human body, that make us jump when we get a shock?


texts: Parameters for Fitzhugh-Nagumo model of Action Potential

texts:
I'm a high school student who's currently in AP Biology, so my background in biology is quite limited. I'm interested in mathematically modelling action potentials.

Doing a quick google search, I discovered the Fitzhugh-Nagumo model, a simplified case modelling the voltage of the cell during an action potential as a second order differential equation $ C \frac{d^2V}{dt^2} + \epsilon(V^2-1) + \frac{V}{L} = 0$. I want to solve this equation numerically, but I can't find the numerical values of $\epsilon$, $L$, or $C$ online. What are some reasonable parameters for this model for a human neuron?


texts: Can SIRS occur without Sepsis from Infection?

texts:
I am thinking this figure

It suggests me that there has to be Sepsis that infection can lead to SIRS.

I am thinking particularly the pathogenesis of Cryptococcus neoformans where

respiratory tract $\to$ pulmonary infection $\to$

asymptomatic and nonspecific pulmonary signs in normal patients
progressive systemic disease in immunocompromised patients

and the last row.

Can SIRS occur without preceding or simultaneous Sepsis?


texts: When a banana fall on the floor or get a certain impact, the impact location gets darker (it bruises) after a certain amount of time. The darkening affects the peel as well as the fruit itself. Why does this happen?


texts: Are the cichlid fish in Africa an example of divergent or convergent evolution? On the one hand they have evolved similar features to each other indicating convergent evolution, but on the other, they formed as a result of an adaptive radiation which indicates divergent evolution.


texts: Why don't we breathe nitrogen when it makes up most of the air?

texts:
Why don't we breathe nitrogen while it makes most of the air?

Why do we always tend to breathe oxygen, not hydrogen and nitrogen?


texts:
“Before taking lactulose, tell your doctor and pharmacist what prescription and nonprescription medications you are taking, especially antacids, antibiotics including neomycin (Mycifradin), and other laxatives.” (Quote from here)

Why do antacids have a special importance when taking lactulose?


texts: How many animals inhabit the United States?

texts:
How many animals inhabit the United States and its waters? Not the number of species, but the number of individual animals. And since animals are diverse, maybe we can limit the estimate to just vertebrates - domesticated and wild. I totally get that nobody knows the answer to this, but I'm wondering if anyone has made an estimate, or if there are sources from which I could piecemeal an estimate.

Thank you!


texts: I wonder what is its function and if it can be the genetic material for a living organism. If not, why?


texts:
Here are some pictures of human iPS cells in culture. After several passages, some cells look really weird, can you help me understand what is going on? What am I looking at? What are those blastocyst-like structures? (bluish picture) and what about that cell full of vacuole-like thing?

P.S. do not pay attention to the scale bar, it's incorrect.

Extra info:

I did not induce them, I got them already dedifferentiated so I can't be specific on that part of the protocol. However, I am growing them in Essential 8 Flex Medium (with supplements as specified from the kit protocol), I add rock inhibitor 4h before passaging them. Passages are done by dissociating colonies using EDTA only (no enzymes). Most of the expanded cultures look normal, some showed the formation of embryonic bodies (the last picture added) but the blastocysts are very different and not really expected.


texts:
First of all, I am unclear as to whether the answer to this question is a matter of fact or of opinion.
Nevertheless, I hope to find the answer.

In the image below, is the green beat considered ectopic?


texts: How is the growth of benign tumors suppressed?

texts: A benign tumor  has an outer layer of cancerous cells beyond which are regular cells (I Think).  The Tumor must have some kind of boundary layer like a wall where somehow the cancerous cells can't affect any more normal cells outside the wall. A Benign Tumor I think can be inactive for many months; it might never grow anymore. Might it be that the cancer cells at this Benign Tumor Wall are inhibited from affecting any more cells? Could there be an Apoptosis shut-off inhibitor or a cell-death pathway shutting-off inhibitor in this case?


texts: How does the body differentiate between sources of good and bad cholesterol?

texts:
I keep hearing "good cholesterol, bad cholesterol" everywhere, and how certain food sources of cholesterol raise LDL and certain other raise HDL.

I don't understand how any food can increase specifically HDL or LDL. I just don't understand the mechanism. Cholesterol is cholesterol, regardless of whether it ends up in LDL or HDL, or whether it came from eggs or or dairy. Somebody please explain to me how specific sources of cholesterol raise HDL and why others raise LDL; how does the body differentiate between the source.

As far as I know, all cholesterol and fat digested from the intestines, regardless of the source, are packaged in chylomicrons as 1) phospholipids, 2) triglycerides, 3) cholesteryl esters, and enter circulation from the lymphatic vessels, then deposited as a chylomicron remnant (CR) in the liver.

How does the liver know whether the 3 particles in the CR came from a good source or bad source? And how does this trigger HDL vs LDL synthesis?
[Btw, if im not mistaken, the liver only makes HDL and VLDL, not LDL]

I'm looking for the biochemical pathways behind these claims. I just cannot picture the mechanism.


texts: Why is squeezing not recommended after a needle prick?

texts:
I've read some interesting things about the risk of infection after a needle prick (30% - hepatitis B, 1.8% - hepatitis C and 0.3% - HIV), but I've also saw that the local squeezing is not recommended.

It's true that I've also found some articles that considered that there is no difference if you squeeze or not, but most of the articles I've read (in my native language) specified "Do not squeeze!!!". By squeezing I mean an act of extracting the blood by pushing the skin near the needle-prick.

Why?


texts: Importance of Double Helix DNA Structure

texts: Gene expression involves transcribing only one strand of DNA molecule. So i was wondering what are some biological advantages of the double stranded DNA?


texts: Has anybody used Evrogen's DSN-normalization protocol for cDNA normalization?

texts:
I found the link to a commercial product by Evrogen to normalise cDNA samples for gene discovery projects here:
http://www.evrogen.com/technologies/normalization.shtml

The most up-to-date reference seems to be this Curr Protoc Mol Biol. paper by Bogdanova et al.:
http://www.ncbi.nlm.nih.gov/pubmed/20373503

They claim their method is compatible with nextgen sequencing platforms:

  cDNA normalization using duplex-specific nuclease (DSN) is a highly
  efficient approach that can be applied for normalization of
  full-length-enriched cDNA (Zhulidov et al., 2004; Zhulidov et al.,
  2005). The resulting cDNA contains equalized abundance of different
  transcripts and can be used for construction of cDNA libraries and for
  direct sequencing, including high-throughput sequencing on the next
  generation sequencing platforms (Roche/454, ABI/SOLiD or
  Illumina/Solexa).

Has anybody successfully used it for next-gen gene discovery projects?


texts: Can someone who is color blind recover color vision by surgical means?

texts: I am currently studying color blindness, and there is no medicine that can help it. Is it possible nonetheless for someone who is color blind to have their eyes restored to normal color vision by replacing the patient's eyes with donor eyes? Please explain any answer. Thanks!


texts: How does the ATPase stain for muscles revert on changing the pH?

texts:
Muscle sections are stained with ATPase to differentiate between types of fibres and to display the ckecerboard pattern. But it is done at two different pH. The staining is reversed at acidic/basic pH.

To quote this site

  Acid preincubations inhibit the myosin ATPase activity in fast (mammalian type 2A, 2X, and 2B) fiber types, but not slow (mammalian type 1, see Figure 1A). Conversely, basic preincubations inhibit myosin ATPase in slow fiber types only (Figure 1B).

Why is this so? Isn't the ATPase same in both the fibres?


texts: Why isn't acetyl-coA an entry point for gluconeogenesis?

texts:
The process of gluconeogenesis starts from various possible precursors - plausible entry points like, Pyruvate, OAA, Fumarate, Propionate (as succinate) and alpha-KG. It is important to note that, acetyl-coA is not an entry point for Gluconeogenesis.

Entry points shown as blue circles.

The most common reason cited for this is the irreversibility of the enzyme, pyruvate dehydrogenase. Since it is irreversible, Acetyl coA can't get back to pyruvate to go on forming glucose.

But, Acetyl CoA naturally enters the Krebs cycle, so why can't it go ahead and form glucose via gluconeogenesis using one of the Krebs intermediates?

I have had this doubt for very long and tried to come up with an explanation to satisfy myself but I still don't know if it is valid.

So here it goes. All the entry points to gluconeogenesis (mentioned before) are an addition to the Krebs cycle. They get on the boat, sail along, get off at oxaloacetate and leave. They don't bother the boat in any other way. Even Pyruvate, forms oxaloacetate via pyruvate carboxylase and then gets on the boat for gluconeogenesis.

On the other hand, Acetyl coA would be a part of the Krebs cycle itself. It is not adding anything to it (2 carbons that are added are lost as CO2). So an Acetyl CoA added, can't leave as OAA. It would be analogous not sailing on the boat but eating it down itself. Slowly, it would lead to a decay and loss of the intermediates Krebs cycle and it would come to a standstill (?)

Is this explanation right? Are there any other ways to explain why irreversibility of PDH results in this?

Although acetyl-coA can enter gluconeogenesis via pathways like glyoxylate cycle (not in humans) and pathways to make pyruvate from acetone (not economical) to form glucose, the question is why it can not do so directly via the Krebs cycle.

Image: Harper's Biochemistry, 29th Edition.


texts:
The Wikipedia article about adaptation states:

  Adaptation differs from flexibility, acclimatization, and learning.

What is a more general term than adaptation? For example, is there an umbrella term for adaptation and learning (and optionally other phenomena)?

Edit: Some examples of possible definitions of terms that I'm looking for:

mechanisms that change/improve fitness over time [over lifetime (learning) or generations (adaptation)] by matching the environment
how the phenotype changes [over lifetime (learning) or over generations (adaptation)] to match the environment
properties of anything that is alive that change [for example in the gene pool (adaptation) or in the brain (learning)] to improve chances of survival


texts: What is the largest perennial herbaceous plant? My guess would be some kind of banana or bamboo.


texts: Do macrophages in the dermis consume any foreign invader to the body, or simply pathogens and cellular debris?  For example, would macrophages consume vitamins or medications injected into the dermal layer of the skin?  Thank you


texts:
I have been having trouble with what should be a fairly simple ligation. I had a plasmid that I needed to cut part out of, so I designed a couple PCR primers to do that. The plasmid already had a BamHI site on 1 side of the region I wanted to remove, so I made the other PCR primer with a BamHI site on its 5' end with 3 extra Cs so the restriction enzyme would bind better. Here is a crude diagram of what I tried to do:

So I did the PCR and BamHI digest, it looked good on gel, so I purified it from the gel, got the concentration on the Nanodrop, and set up a ligation.

However, I keep getting zero colonies. I have tried a 24 hour reaction at 4 degrees, and 10 minute reaction at room temp. I am currently trying a reaction where I supplement the buffer with fresh ATP, because the buffers are a little old. If that works, problem solved, if not, I am asking how to troubleshoot this.

This seems like it should be relatively simple, because I have no insert, just trying to close an empty vector, which seems to happen on its own when I don't want it to and dephosphorylate the vector.

UPDATE:

The reaction with extra ATP did not produce colonies. I will keep trying. One idea I had was to do the PCR and then try blunt end ligation, since the Pfu polymerase should make blunt ends. Also got a new sample of ligase.


texts: How to edit/insert new gene after cutting with CRISPR/cas9

texts:
I'm a student started who has started learning about CRISPR/Cas9. As I understand it, CRISPR/Cas9 is an enzyme that is used to cut a gene at a specific sequence.  I would like to know how scientist do the next step to insert/edit a genome.

For example, say I have an original sequence ...AAATTT... Is it possible for me to insert a new sequence into the middle so it becomes like this: ...AAAGCGCGCTTT... ? Or is it possible for me to edit a single nucleotide of the sequence like this : ...AACTTT... ?

How is a new sequence inserted at the cut region? Is there any enzyme required to make them join each other?  How is it ensured that the sequence is not inserted or joined at the wrong position ?


texts:
I have a couple of new pictures of insects which I am really curious about. This is one of them. I found this fly near my cottage in Prague, Czech Republic.

It is fluffy with very long proboscis (almost half of an inch in length).


texts: Best methodology to compare computed phylogeny tree with taxonomy?

texts:
I have computed a phylogenetic tree using an alignement of sequences, and I would like to :

Compare it to the "known" taxonomy (uniprot/ncbi which I know is not
the most up to date one) and extract a metric of how "divergent" it
is.
[Optional] Visualize the differences (I can probably come up with a
solution for that one, but if someone knows of a nice tool to do so
?)

What are the best metrics / tools / methodologies to do such a comparison ?

Thanks !


texts: Which parts of the cerebral cortex don't belong to the neocortex?

texts:
In the Wikipedia article on the cerebral cortex one reads:

  »Most of the cerebral cortex consists of the six-layered neocortex.«

Accordingly, in the Wikipedia list of regions in the human brain, one finds "cerebral cortex" and "neocortex" as almost synonyms.

But assuming that they are not perfect synonyms – but that there are some parts of the cerebral cortex that are not part of the neocortex – I wonder which parts this might specifically be.

To make my question specific, I list here all parts of the cerebral cortex as listed at Wikipedia:

Cerebral cortex (neocortex)
Frontal lobe
    Primary motor cortex
    Supplementary motor cortex
    Premotor cortex
    Prefrontal cortex
    Orbitofrontal cortex
    Dorsolateral prefrontal cortex
    Superior frontal gyrus
    Middle frontal gyrus
    Inf. frontal gyrus
    Brodmann areas
Parietal lobe
    Primary somatosensory cortex (S1)
    Secondary somatosensory cortex (S2)
    Posterior parietal cortex
    Postcentral gyrus (Primary somesthetic area)
    Precuneus
    Brodmann areas
Occipital lobe
    Primary visual cortex (V1)
    V2
    V3
    V4
    V5/MT
    Lateral occipital gyrus
    Cuneus
    Brodmann areas
Temporal lobe
    Primary auditory cortex (A1)
    secondary auditory cortex (A2)
    Inf. temporal cortex
    Posterior Inf. temporal cortex
    Superior temporal gyrus
    Middle temporal gyrus
    Inf. temporal gyrus
    Entorhinal cortex
    Perirhinal cortex
    Parahippocampal gyrus
    Fusiform gyrus
    Brodmann areas
    Medial superior temporal area (MST)
Insular cortex
Cingulate cortex
    Anterior cingulate
    Posterior cingulate
    Retrosplenial cortex
    Indusium griseum
    Subgenual area 25
    Brodmann areas

If there are parts of the cerebral cortex missing here, a hint would be welcome!


texts:
What type of flower is this?
Location : India


texts: Many black people I've met have bigger lips than white people, why?

texts:
I noticed that many black-ish people I've met have bigger lips than the white-ish people I've met. However, not all black-ish people have big lips.

Is there any explanations in terms of natural selection, geographic localisation, common ancestors, or something else that could explain why a subset of dark skin people have bigger lips on average than pale skin people?

Edit: This question is different from the other one because the answer talks about the nose and its function (air temperature) linked to the environmental factors. I don't see how this applies to lips.


texts: Is the eukaryotic nucleus composed of a single or double membrane?

texts:
I know that it is usually considered a double membrane like those surrounding mitochondria and chloroplasts, but I read a review that stated "according to topological details it is actually a single lipid bilayer; this distinction is important"1.

Could anyone please explain how this is true and why the distinction is important? And why this topological analysis wouldn't apply to other membranous structures in the cell?


texts: How valid is the theory of human's chimp-pig origin?

texts:
Edit: I have also asked the question on skeptics.stackexchange.com and it has been answered there. Here is the link.

There is a person called Dr. Eugene McCarthy who has a theory that the origin of humans come from pig-chimp hybridization (online article about his theory). How acceptable is his theory in comparison to the other common theories?


texts: Is setting high mismatch and gap penalties sufficient to distinguish perfectly mapping reads?

texts:
I have a fat pile of 125bp whole genome shotgun reads that have undergone quality control, and I would like to pull out just those reads that do not map perfectly to the genome. When I set extremely high penalties for mismatches and gap opens/extensions (with bwa mem -B 1000 -O [1000,1000] -E [1000,1000]), it looks like the alignments for perfectly mapping reads are shown, and the rest of the reads are reported as unmapped. If this is true, I could then pull out the unmapped reads with samtools -f 4.

Are there any holes in my reasoning here, or will it work to discard all of the reads that map perfectly to the genome?


texts:
It's a famous fact that bones begin as cartilage and later become bone, but I never was clear how exactly
 this changeover occurs. Could someone please explain this to me?


texts:
I found a vertical mud tube about the thickness of a pencil in my garden with a series of metallic green insects coming out of it. They came out when I pulled a weed but stopped when I stopped, as if the vibrations were scaring them out. I think they were bees, wasps, or flies. They were 1/2" long or a little longer and thin. Head, thorax, and abdomen were all shiny green, wings transparent. What are they?

I live near Philadelphia and it was in the upper 60s F today.


texts:
Does anybody know what kind of mite this is?

It is living in my pepper plants' pots.
My region is south of Germany. (Baden-Württemberg)

I will try to take another picture including some size measurement today.

Update:

As suggested by @theforestecologist, I added pictures including a size bar.

Thanks to @tyersome, I managed to merge my two accounts now.


texts: Amino acid substitutions near the receptor binding site HA protein in type A H3N2 influenza strains?

texts:
I have read the scientific paper, "Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution" by Björn F. Koel et al (http://science.sciencemag.org/content/342/6161/976).

In the paper, important positions to influenza antigenic drift include positions 109-301, with special emphasis on sites 133, 144, 145, 155, 156, 158, 159, 189, 193.

However, nowhere in the paper does it specifically mention which positions are part of the receptor binding site and which are close to it.

The range (109-301) is a bit broad since it includes amino acid positions that are unimportant to antigenicity. I would like a list of all very important AA substitutions (that are near the receptor binding site) to involve in a bioinformatics project. The special emphasis amino acid sites list does not include all amino acids that are near the binding site.

To convey a sense of the problem, if position 155 is important, does that mean position 156 is also important?

I don't know if position 156 is considered "near" the receptor binding site.

Any help is appreciated.


texts: What is the most basic organism to respond to Classical conditioning (capable of learning)?

texts:
I have been doing some reading of Classical conditioning which is considered to be an indication of animal's ability to learn...

Before this I considered insects to be machine like - devoid of any sort of 'thinking' just doing things that evolution 'made' them to do to survive...

However I have found that cockroaches and even fruit flies could be conditionally trained...

Which made me wonder What would be the least complex species that respond to classical conditioning?

I have also read this question about single-celled organisms capable of learning and I don't think that this 'cuts it'... this is nothing more than chemical response... however classical conditioning is different and in my opinion certainly does indicate ability to learn...


texts: Why are multiple copies of the 35S enhancer used for overexpression in plants?

texts:
I know that the CaMV 35S promoter is widely used for transgenic plants, and I also know that it can be used as an enhancer element for overexpression.

I noticed that it is always used as a multimerized enhancer with 4 copies. Why 4 copies? Why not 1, 2, 3, 5, or 10?


texts: Are the cpli and ctli tests time senstive(i.e. is it needed to test right away in order to get accurate results)?

texts:
I'm sending the blood samples to a lab and this takes some time until the actual testing.

Some information on the tests.

TLI : http://www.vcahospitals.com/main/pet-health-information/article/animal-health/trypsin-like-immunoreactivity/405

CPLI : https://www.vetstream.com/canis/Content/Lab_test/lab00522


texts:
I'm trying to study how age as a confounder may affect the relationship between commute mode and BMI (and design a research proposal).
To explain age as a potential confounder, I compared age to commute mode and then age to BMI. I found a weak association between age and BMI in my data.
In the literature does anyone know if BMI is expected to change with age? Is there a linear/ other relationship form? Please could someone attach any papers/ links for help.
Also, does anyone know what a clinically meaningful BMI is too? Would a change of 1-2 be important?


texts: Background correction when reading ELISA with TMB substrate

texts:
I'm doing some ELISA development, and I'd like some justification/best practices for background correction. I'm using a horseradish-peroxidase (HRP) detection system along with a TMB substrate and an acid-based stop solution, which is quite common. When TMB is cleaved by HRP, it produces a blue (maximum absorbance (Amax) of 650 nm) product. The addition of the acid not only stops the reaction for endpoint detection, but it amplifies the signal two- to three-fold, and turns the solution yellow, so that it should be read at its Amax of 450 nm. The acid itself supposedly has an Amax of 540 nm, which is why you should use that wavelength for background correction, subtracting it from the A450. Other sources claim the A540 reading is supposed to correct for "optical imperfections" in the plate.

Using either of these explanations, one would assume that the A540 would be relatively uniform across the plate, independent of the A450 of the same well. However, in my experience, that is not the case at all. My blanks and negative controls are averaging about 0.041 absorbance units (AU) at 540 nm, with an average A450 of about 0.065. However, an A450 of 0.9 gives an A540 of 0.051, 1.4 gives 0.6, 2.0 gives 0.73, and 3.5 gives about 0.14. The absorbance spectrum (Fig. 2) of the substrate appears to be quite minimal at 540 nm, so why am I seeing this dose-dependent increase as the A450 increases?

More practically, how should I do background correction? Currently, I'm subtracting each individual well's A540 from its A450. Should I continue this practice, or should I determine an average plate background at 540 nm using my blanks and negative controls, and subtract that value from each individual A450?


texts: What do the variants on the PolyT sequence mean?

texts:
My son has been diagnosed with Cystic Fibrosis.  I am not looking for medical advice regarding his condition, but I am very interested in understanding the genetic causes of his condition.

In addition to the common CF mutation Delta F508, my son's genetic testing revealed both 6T and 9T variants of the PolyT sequence.

If I understand it correctly, it seems that the variants (I have found repeated reference to 5T, 7T, and 9T variants, but almost nothing on 6T) are tied to errors in the RNA transcription of the CFTR protein, but I don't understand how, or what the difference between these variants are.

What does "variant of the PolyT sequence" mean in this context, what are the difference between 5T, 6T, 7T, and 9T, and how do they impact the production of the CFTR protein?


texts: Have there been any experiments that duplicate chromosome copies from 23*2 to 23*3 or 23*4?

texts:
Deinococcus radiodurans is an amazing bacterium with a fantastic survival rate. It can survive to high doses of radiation, in a complete vacuum and in hydrochloric acid.

How does this bacterium manage to restore damaged chromosome?
It is polyploid with 4 to 10 copies of the genome which are packed in a highly ordered manner.

Does this imply that creating multiple copies of the genome or inceasing DNA base repair activity would increase life span?
Is that even conceivable on bigger life forms?


texts:
Wikipedia writes:

  In human anatomy, and in mammals in general, the mons pubis (also known simply as the mons, and known specifically in females as the mons Venus or mons veneris), is a rounded mass of fatty tissue found over the pubic symphysis of the pubic bones. In human females, the mons pubis forms the anterior portion of the vulva. It divides into the labia majora (literally "larger lips"), on either side of the furrow known as the pudendal cleft, that surrounds the labia minora, clitoris, urethra, vaginal opening, and other structures of the vulval vestibule.

The Foundational Model of Anatomy suggests that the feature also exist in the non-gender specific pelvis concept. Does it?


texts: How does extra chromosome 21 in Down's syndrome cause all the characteristic developmental errors?

texts:
How does the presence of an extra chromosome 21 result in the characteristic craniofacial findings, developmental errors and other health issues?

I'd like to have an exact answer, because I can't seem to find a precise answer anywhere online, it seems all they mention is the fact that nondisjunction occurred during meiosis I. But I would like to know is why this extra chromosome creating so much complications?

It wouldn't make sense to talk about the position effect, so then I'd hypothesize that all the genes on chromosome 21 are over-expressed. How does this cause all the symptoms of Down's syndrome?

Thank you very much!


texts: How did the "serendipitous rediscovery" of Sulfasalazine as an antirheumatic agent after 30 years happen?

texts:
This excellent answer describes the history of the ~50 year old drug Sulfasalazine, and it's worthwhile to take a moment and read through the answer now.
Roughly speaking the drug is an antibiotic molecule linked to a molecule of aspirin, developed at a time when rheumatoid arthritis inflammation was assumed to be caused by an infection. Ironically the drug is now widely used as a treatment for RA, but its mechanism of action does not seem to be related to the way that it was originally designed to work.
Sulfasalazine is on the World Health Organization's Model List of Essential Medicines. See section 17.3, Anti-inflammatory medicines.
Within one of the block quotes in that answer from a publication by the Department of Medicine at Princeton can be found:

[...] Early therapeutic results were encouraging, but the drug was discarded as an antirheumatic agent for 30 years, until its serendipitous rediscovery (emphasis added).

Pubmed shows this to be Pinals R.S., J Rheumatol Suppl. 1988 Sep;16:1-4., PMID: 2903922, but I can't find access to the Journal of Rheumatology Supplements that far back in time.
Can somebody track this down and relate the "serendipitous rediscovery" story here? Or perhaps find a link to another author's version of the story I can read? What was the serendipitous biological evidence that led to rediscovery of Sulfasalazine as a disease-modifying anti-rheumatic drug? (DMARD, see also arthritis.org)


texts: me and my partner had itchy patches that looked like bites so we were scared we might have bed bugs and we found a bunch of these creatures behind the bed in between the frame and a concrete wall as well as behind the sofa. Would they be baby 1st stage bed bugs? We’re obviously panicking... on the pic you can see them trapped in an ikea glass. They seem to jump a little but they dont seem able to jump over 0.5 to absolutely max 1 cm.


texts: meaning of "usually greater than 200 base pairs"

texts:
From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese:

  Homologous recombination. All cellular organisms have molecular functions dedicated to recognizing and recombining DNA molecules that have extensive sequence similarity at the region of cross-over, usually greater than 200 base pairs. The principle molecule involved in homologous recombination belongs to the family of RecA/Rad51 DNA binding enzymes that catalyse post-replicative strand exchange during meiotic/mitotic recombination or repair of DNA double-strand breaks. These enzymes show some sequence preferences (Raja et al., 2006) and require minimally efficient processing segments of 20–30 base pairs to initiate strand exchange (Majewski and Cohan, 1999).

I'm not sure of the meaning of "greater than 200 base pairs". Does that relate to "sequence similarity"? Is similarity somehow measured in base pairs?

Or does that relate to "the region of cross-over"? Is the meaning "the region of cross-over is usually greater than 200 base pairs"?


texts: A disease which is characterised by polycythemia and thrombocytopenia at the same time

texts: I've read that polycythemia vera is associated with increased levels of RBC, WBC and/or platelets, but is there a disease associated with high levels of RBC and low levels of platelets?


texts: What do firebugs do when they "connect" by their rear?

texts:
See this image for example.

What are they doing? What is the name of this process?


texts: I'm trying to get into Biology, reading introductory texts. A discussion on E.Coli estimates the mass of the cell from $$density =1g/mL=1g/cm^3$$ and $$volume=1µm^3$$ From this I get $$ mass=density × volume = \frac {10^{-6} g}{10^{-2}}=10^{-4} g$$ which is wrong since the answer is supposed to be $1pg$. What am I doing wrong? Thanks!


texts:
A vast majority of humans get at least some grey hair as they age. As far as I know this applies to both genders and all races. Presumably this means that at least some grey haired humans have noticeable reproductive advantage, or maybe they had it in the recent past.

Theoretically, because this feature is so prevalent, there must be a strong evolutionary pressure to keep it. Am I right? If so, what is it?


texts: Why is it possible to make yoghourt with lactose-free milk?

texts:
The function of the Lactobacillus bulgaricus and Streptococcus thermophilus  cultures is to ferment lactose to produce lactic acid. The increase in lactic acid decreases pH and causes the milk to clot, or form the soft gel that is characteristic of yogurt.

In lactose-free milk, all the lactose was transformed in glucose and galactose using lactase. Is it possible for those bacteria to ferment glucose and galactose instead of lactose? Or is this based on other biological reactions?


texts: what is meta-sympathetic nervous system?

texts: I always knew about the sympathetic and para-sympathetic nervous systems, and today I was told about the meta-sympathetic nervous system, but I didn't understand well the man who told me about it and I didn't find enough or reliable information about this system, and if it's accepted in the scientific world or it's arguable.


texts: I plan to measure the effects of Tenofovir a Nucleotide analog reverse-transcriptase inhibitors useing qrt-pcr with HIV-RT as the rt enzyme. Tenofovir causes early termination of the reverse transcriptase by binding to reads preventing the continuation of the chain process rather than stopping the action all together. How will qrt-pcr quantify the low molecular weight short incomplete fragments? I think since the areas complementary to the forward and reverse primers will rarely be on the same continuous double stranded dna expression will be decreased uniformly. Is this correct? Will I need to use absolute qrt-pcr since the changes will be the same for all genes?


texts: Why is competitive inhibition reversible?

texts: My Biochemistry book mentions that 'competitive inhibition' is a reversible form of inhibition. But given that the inhibitor is blocking the active site and prevents an enzyme-substrate complex to be formed, how can it be reversible?


texts: In induced pluripotency experiments, what happens to the cells that do not become pluripotent?

texts: I am new to this topic, so forgive me if my question is naïve. In an induced pluripotency experiment a few transcription factors are overexpressed in somatic cells and as a result a small portion of the cells become pluripotent (fully or partially), but the vast majority of the cells do not. My question is this: what does happen to these cells (the ones that do not become pluripotent) in terms of gene expression levels? Do gene expression profiles of these cells remain unchanged (the same before and after overexpression of the pluripotency factors)? Or do they change and become something that is different from both pluripotent cells and the original somatic cells?


texts:
When scientists choose viruses for the influenza vaccine based on biological and clinical data, what indicates that a certain strain will circulate and likely be dominant in a certain season?

Does a low HI titer (meaning antigenic novelty) for a virus antigen relative to an antiserum of a virus that is currently prevalent mean that the new virus will likely dominate in the next season? OR is a high HI titer a better choice for the vaccine since it means the virus in question is very similar to currently circulating viruses?


texts: How do developing neurons become tuned to fire only on receiving specific inputs?

texts:
Research has uncovered neurons that seem to "listen" for specific inputs and fire only when these inputs are received. For example, neurons in the visual cortex may fire at a higher rate when visual stimuli of a particular orientation is presented, and may not fire for stimuli of other orientations.

Are there any good models on how neurons develop this tuning for specific inputs? Could anyone provide links to good papers or other resources?


texts: Is there an evolutionary purpose to armpit perspiration?

texts:
Given that most Americans seem to do fine using anti-perspirant, it got me wondering: is there an evolutionary purpose to underarm perspiration?  I can't imagine it acts to attract the opposite sex.

Or is it just likely an unfortunate side effect of whole-body evaporative cooling via sweat?


texts: What does it mean to have square brackets around a genus name?


texts: Are archaeological DNA samples (bone fragment) stabilized and isolated the same ways as living saliva samples?

texts: I've been studying how saliva DNA samples are suspended in a stabilization fluid then isolated using magnetic beads. Are old archaeological DNA samples of deteriorating bones put through this same process? If not, how are those  stabilized and isolated?


texts: How can CI repressor both activate and repress $P_{RM}$ promoter found in $\lambda$ phage?

texts:
I'm reading a paper where the authors constructed a toggle switch that uses bidirectional $P_R/P_{RM}$ promoter found in the $\lambda$ phage. There are 3 binding sites - $O_{R1}$, $O_{R2}$, $O_{R3}$ - located between the two promoters. CI is expressed by $P_{RM}$ and CI dimers bind to these binding sites:

What I don't get is that CI seems to function as both an activator and a repressor of $P_{RM}$.
First, my understanding was that $P_{RM}$ is an inducible promoter activated by CI which also represses a constitutive promoter $P_R$:

CI is a transcriptional activator of $P_{RM}$, thus producing positive feedback.
CI preferentially binds to $O_{R1}$ and $O_{R2}$, repressing the constitutive promoter, $P_R$.

However, it is also stated:

In high concentrations, CI binds to $O_{R3}$ and acts as a repressor to $P_{RM}$.

This seems to suggest that the CI can function either as an activator or as a repressor depending on the binding site bound; specifically, CI dimer binding to $O_{R1}$ and $O_{R2}$ will repress $P_R$ and at the same time activate $P_{RM}$, while CI dimer binding to $O_{R3}$ will repress $P_{RM}$. Is this correct?
I (a computer scientist by training) was always given the impression that a transcription factor is either inherently a repressor or an activator of a promoter, but this doesn't seem to be the case here. I would expect that e.g. CI would act as a repressor to $P_R$ and an activator to $P_{RM}$ regardless of the binding site. So why does CI binding to $O_{R2}$ (and $O_{R1}$ as well?) activate $P_{RM}$, while binding to $O_{R3}$ represses it - why the inconsistency? Note that I'm primarily interested in this from the modeling perspective.
What I also don't understand is whether or not $P_{RM}$ promoter is inducible or constitutive (e.g. in the absence of bound transcription factors, how leaky is it)?


texts: What would happen if there were no SOX9 in an XY human?

texts: Would testes be produced? If SRY is functional, can it produce other proteins that can direct the production of testes, which may or may not be sterile?


texts: Why are Arabidopsis plant seeds being sent to the moon and not other seeds?

texts:
The latest Chang'e-4 rover brings an entire ecosystem with it, including Arabidopsis plant seeds and silkworms.

My question is: why Arabidopsis? Is this question conclusive without having to ask Chinese sources, such as just by having an educated guess as regards to the plant's own qualities?


texts:
I know. This is going to be extremely difficult without a picture. But bear with me here, because I haven't seen it afterwards. I hope somebody can give me a list of possibles.

I was taking a stroll down the street when I saw this creature. Maybe two feet long. It was black, with a tail about the size of the tail of a cat. It had catlike paws, which were not that big. Its face was pointy, with a reddish nose and brown eyes, with a whitish area of fur above the eyes. Ears were small and curved at the end. It was hiding in a bush, and did not seem to run away when I checked it out. When I got up, it made a sharp screech and ran away.

I'm from Kerala, South India. Thanks in advance.


texts:
I am struggling to set up a project proposal for validation of a known treatment for metastatic colorectal cancer in mouse models.
I want to see how SNPs in patients contribute to their drug resistance and/or toxicity. For the validation of these SNPs as predictive biomarkers, I will use cell lines and mouse models. But, how am I supposed to "induce" these specific SNPs in the mice? CRISPR/Cas9 can be used for the alteration of bigger parts.
Any idea is a useful idea!


texts:
If you inhale to your maximum capacity and hold your breath for an extended period of time, it begins to feel uncomfortable; slowly releasing your breath at this point seems to provide relief from this discomfort.

Is there a biological reason why this is so, or is this something psychological?


texts: how long do chaperone proteins take to fold a protein?


texts:
Leena is a molecular biology student. She purifies two fragments of DNA, 800 and 300 base pairs long. These were obtained from a plasmid after digesting it with HindIII. Each of these fragments has a single EcoRI recognition site.
Leena wants to join these two fragments to get a 1.1kb gene as shown in Figure 7.1. She suspects that this gene has a unique protein-coding sequence.

She, therefore, mixes the two fragments in the presence of excess DNA ligase in an appropriate buffer and incubates the mixture. She removes an aliquot (a small part of the reaction mixture) after 30 minutes and loads it on an agarose gel to check the results. She is surprised to find many bands along with the expected 1.1kb band  in the gel.

FIG 7.1

Leena is interested in the 1.1kb fragment shown in Figure 7.1. Hence, she elutes the 1.1kb fragment from the gel shown in Figure 7.2 and subjects part of this sample to HindIII digestion. She obtains the expected pattern with two bands, 800 and 300 base pairs long. To confirm its restriction map, she subjects the remaining sample to complete EcoRI digestion. Which pattern of bands would she obtain?

The answer given is this and I understand why this is the answer and other options given in the question(not posted here) are definitely not the answer but I do not understand why there are no 0.4kb fragments, 1.1kb fragments here.


texts: How does the brain regulate its temperature?

texts:
I recently ran into a bio-physical paradox while trying to solve an engineering problem, using nature's way as a guide; namely the brain.

I'm working on designing a totally new system of liquid/gas cooling for a project. In Normal systems, the coolant is first cooled at a point, then sent along to the target areas; however, the coolant gets too hot along the way and cannot meet my target at one of the end components. Additional external cooling fins along the path still do not compensate.

I took biology classes in college and recall some mechanisms of the brain and pictures too (usually depicting the brain as all white internally). So, I theorized that maybe the coolant (blood) was not in direct contact with the brain in a substantial volume; however that was debunked: Why is the brain white?

From what I gather from the major answer, the brain's way of achieving homeostasis might present the answer to my problems. There is a lot of blood in the brain. This blood comes from the carotid arteries, which means it comes from the main circulation, and is hence at body temperature {considering homeostasis of all the body organs i.e. the lungs in this case}. By connotation, the brain should be the hottest organ in the body!

Considering the volume of blood in the brain, how does it regulate its temperature?


texts: These are the two caterpillar I found at Taipei, Taiwan. Can anybody help me identify the species. The first caterpillar is about 6-7 cm long and the other one 10-12 cm. Thanks in advance!


texts: Why aren't drugs tested on sick patients proactively?

texts:
I read an article about a new drug which may stop neurodegenerative activity in the brain and this triggered a question I had for some time already.

Why such novel drugs are not tested on seriously/terminally ill patients, to check whether they are not dangerous, and maybe useful?

I completely understand the need for double - blind trials which can assess that the drug works or not. This requires a lot of tests beforehand to make sure that the drug is reasonably safe for humans.

On the other hand I am sure that seriously or terminally ill patients would take the risk to, maybe, have a chance with the new drug, with the risk of complications (all in reasonable boundaries). I know I would.

Beside some indication that the drug works or not (again, I understand the  implications of a lack of double-blind trial but if the result is 100% success or failure, it is at least one data point) it could be an indication of its lack of safety. If all patients develop an unrelated organ failure (as it was the case in the article I linked), it would help research which otherwise relies on similarities between animals and humans.

Is it just an ethical concern or are there scientific reasons not to use these opportunities?


texts: How, on a physical level, does ATP confer energy?

texts:
When ATP is used as the energy currency to make, say, reaction X + Y → Z happen, is what happens on a physical level down at the molecular scale that during the reaction

ATP + H2O → ADP + Pi       ΔG˚ = −30.5 kJ/mol (−7.3 kcal/mol)

that 30.5 kJ/ mol is conferred by ATP molecules physically bumping around the reactants X and Y, the kinetic energy of the above reaction being what does it?

I mean, is the energy coin of ATP conferred to reactions by molecular collisions, or is it an electric field effect in the spatial geometry the way the ATP molecule tends to break apart?


texts: Can we make any judgements about sleep or readiness to sleep from a heart rate metric and/or pulse oxymetry?

texts:
I'm looking at inexpensive and un-intrusive ways to quantify the state of human body/mind . One of these is Actigraphy, which is a study of human motion over time. This can be done with an iPhone mounted on a wrist. There are algorithms that correlate actigraphy measurements to sleep and allow to calculate sleep onset latency, sleep efficiency, etc. I'm looking for additional metrics that may be added to actigraphy.

Recently, there has been a new iPhone app called "heart rate" which uses a camera to shine light through a finger, capture a series of images of the finger and count the heart rate based on the blood flowing in and out of a finger, changing the color of camera images. This is similar to pulse-oximetry derived heart rate, and maybe the technology would evolve sufficiently to give information about the blood oxygen content as well.

As a sleep researcher, I'm wandering if there are any known algorithms or studies that relate heart rate (as beats per minute) and/or pulse oximetry to sleep or human's ability to fall asleep?

It appears to me that with a device like an iPhone measuring pulse at the same time of the day, it should be possible to create a history of heart rate, while accounting for the diurnal variation of heart rate. I'm wandering if there's anything biologically or medically relevant that can be glimpsed from such history of heart rate metric.


texts:
I try to understand details of the Needleman–Wunsch algorithm and use an example from the book [Nello Cristianini, Matthew W. Hahn. Introduction to Computational Genomics. A Case Studies Approach, www.computational-genomics.net].

To my opinion, the algorithm is described not very neatly, so the question arises.

Consider two sequences:

I: VIVALASVEGAS

II: VIVADAVIS

The first step is clear:

Also, the calculation of the score for diagonal neighbor is also clear,

because this is an alignment without a gap:

I: V

II: V

Unclear moment is the alignment for left (or above) neighbor. Say, the left  neighbor

corresponds to this

I: V

II: -

or this

I: -

II: V

alignment?


texts:
I was reading an article on MIT Technology review about superpatients for low cholesterol that got me thinking whether such patients exist for cancer.

The article is

http://www.technologyreview.com/featuredstory/532421/the-search-for-exceptional-genomes/

I had also previously read an article on naked mole rats and the hyaluronan in the ECM.

http://www.wired.com/2013/06/naked-mole-rat-cancer/

Therefore, I am wondering whether there are any current studies, that is trying to discover the genetic outliers for cancers. Ie, humans that have hyaluronan in their ECM that is almost naked mole rat like. Since I understand that with a genetic pool of 7+ billion there has to be at least one outlier.

Thanks


texts: Reason behind formation of positive supercoils during DNA replication/ transcription

texts:
When a twist is unwound without cutting the DNA strands or is removed by cutting the strand(s) and resealing, negative supercoils are introduced in the DNA.

From Cell and Molecular Biology -Karp

But strangely enough unwinding of DNA by helicase cause the DNA ahead of the primosome to form positive supercoils. Why is it so?

From: Molecular cell biology -Lodish

My speculations: Underwinding cause the adjacent DNA to overwind and as the DNA overwinds the associated stress developed cause the DNA to form positive supercoils (which would have happened naturally had new twists been introduced in the DNA (Time:1:54) ).

I think removal of twist creates negative supercoils initially but when the unwinding causes too much overwinding of adjacent DNA, the strain developed cause the already negatively supercoiled DNA to form positive supercoils.


texts: How is it possible for phosphate to form two ester bonds in DNA replication?

texts:
I understand that in phosphodiester bond formation, two hydroxl groups on the phosphate molecule bind to the 3' and 5' OH groups on two independent pentose sugars. This is a condensation reaction, so two molecules of water are released.

I am just confused about the hydroxl groups on the phosphate. From what I know, the phosphate molecule looks like this.

How is phosphate able to do a condensation reaction with two pentose sugars if it has no hydroxide groups?

Thanks a  lot


texts: I found a bug on my bedroom floor. Is this a bedbug?

texts:
I found this insect on my bedroom floor. I'm worried. I hope this is not a bed bug.

Size: 3-4 mm


texts:
Problem:

A certain species has somatic cells with ploidy 3n (the organism inherits
three sets of homologous chromosomes from each of three parents). At a certain locus, there are three possible alleles A 1 , A 2 , A 3 , which are
completely dominant in the order A 1 > A 2 > A 3 . The proportion of organisms
exhibiting traits A 1 , A 2 , and A 3 are respectively 0.614, 0.306, and 0.08. In
addition, the proportion of organisms that are completely heterozygous
(genotype A 1 A 2 A 3 ) is 0.18. Which of the following are allele frequencies of A 1 , A 2 , and A 3 , respectively?

Answer Choices:

A. f(A 1 ) = 0.5, f(A 2 ) = 0.3, f(A 3 ) = 0.2

B. f(A 1 ) = 0.3, f(A 2 ) = 0.5, f(A 3 ) = 0.2

C. f(A 1 ) = 0.3, f(A 2 ) = 0.4, f(A 3 ) = 0.3

D. f(A 1 ) = 0.6, f(A 2 ) = 0.2, f(A 3 ) = 0.2

E. f(A 1 ) = 0.7, f(A 2 ) = 0.2, f(A 3 ) = 0.1

Correct Answer:

A

Solution:

No clue. I'd guess that the solution follows a hardy-weinberg model for polyploids. For simplicity, I will refer to A1, A2, and A3 as x, y, and z, respectively.

(x + y + z)^3 = x^3 + 3x^2y + 3xy^2 + y^3 + 3x^2z + 6xyz + 3y^2z + 3xz^2 + 3yz^2 + z^3

Given that z^3 = 0.08, shouldn't z (A3) equal the cube root of 0.08 = 0.43?

That doesn't match any of the answer choices, so I will assume that my steps were incorrect.

Any suggestions?


texts: Can stem cells from male convert to cells of female-only organs, and vice versa?

texts: As we know, stem cells can convert to different cells of other organs, can male use their own stem cells to convert it into cells of female-only organs(and vice versa)?


texts: Is there a name for dominant-intraspecific competition?

texts:
Some ecological competition dynamics have particular names (e.g.: scramble competition, contest competition, ...). I wonder if there's such a name for competition dynamics where the interspecific interaction is weaker than the intraspecific one.

By weaker I mean that the non-diagonal elements of the community matrix are lower than the diagonal ones.


texts: Characteristics of radius of blood vessel

texts:
Which properties do determine the radius of blood vessel?

I have these thoughts

distension,
elasticity,
contractility and
cross-sectional area of the walls.

Is there any other properties?


texts: Is there any functional difference between Occipital lobe ( in mammals) and Optic lobe (vertebrates other than mammals)?

texts:
Visual processing centre in mammals and lower-vertebrates, are known to be different.

In mammals, such as human, it is the Occipital Lobe of 2 hemispheres of cerebral cortex; which is a part of forebrain. But in more lower groups of vertebrates, it is the Optic lobe, which is a part of midbrain.

(https://en.wikipedia.org/wiki/Optic_lobe, https://en.wikipedia.org/wiki/Midbrain#Corpora_quadrigemina)

Image: Placement of optic lobe, Source: http://understanding-vertebrates.weebly.com/nervous-system.html, URL: http://understanding-vertebrates.weebly.com/uploads/3/8/6/8/38682649/8113431_orig.jpg

Now, does this difference cause a difference in how the visual information is processed in their mind? such as which-features of the image extracted, how they are recalled, how they are correlated , joined  etc?


texts:
To start off: I'm not a biology student, but a computer science major

It has always been my understanding that humans have 2 eyes so that we can have 3D vision: the left eye see more of the left side of an object than the right eye and vice versa, this helps us to estimate depth among other things.

Now when I close one eye, I still am able to perceive depth: I assume this is because my brain fills in the blanks? For how long does this work? Do people eventually lose the depth perception (or at least is diminishes significantly) when they lose a single eye?

If so, how low does it take? If not, clearly we are capable of perceiving everything with one eye: why do we then have two (besides redundancy and a larger field of view? What is considering the evolution of man better in having 2 eyes as opposed to 1 or 3,4,..?


texts: Best colour for a dog to track an object against green background

texts: As dogs have limited colour perception, what colour would appear with most contrast against a green background for a dog? I understand that red and green are very close in a dog's colour perception, so would blue offer better contrast?


texts:
The DNA molecules contain phosphate groups involved in $3'\rightarrow 5'$phosphodiester linkages. These groups, in the bonded state with deoxyribose, contain 1 negative charges ($\ce{3'-PO4^{-}-5'}$). This means that the two strands are very highly negatively charged. What than stabilizes the double helix, preventing the natural electrostatic repulsion between the two strands?

[I am assuming that the phosphate groups are dissociated under physiological pH, correct me if I am wrong.]


texts: Does common PCR amplify genes regardless of what cells / barriers they are in?

texts:
I have some understanding of how PCR testing works. What I have always been wondering: how can we be sure that a primer reacts with the targeted gene(s) regardless of where¹ the genes are inside a sample?

¹: Specifically with "where" I mean what cells or other barriers they are inside. In other terms my question is: how can we be sure primers reach every possible target?

In more detail: when targeting a gene that is part of the host organism's own genome things might be quite clear, we can have strong assumptions of "where" the gene is. But when targeting genes that are part of organisms that have a parasitic relationship with the host, a very complex system of  interactions (mostly called "immune system") should govern the (co)existence of host and parasite. These complex interactions might lead to situations in which the parasitic organism is present in a very special, isolated manner / place in the host. To give one example: micro organisms in the cell walls of macrophages that are about to undergo lysis. Can we be sure that common PCR would detect genes of such micro organisms? Why?

EDIT: as pointed out in the comments the perhaps most correct phrasing is, how do the DNA isolation techniques employed guarantee that primers reach every possible target?


texts:
I remember reading this in a biology textbook, and decided to do a little digging. Redheads have a lower sensitivity to some pain and a higher sensitivity to other compared to people of other colored hair.

Sciencenordic.com and webmd.com note that redheads have a higher sensitivity of pain when it comes to dentistry, yet can tolerate more pain subcutaneously. According to the Journal of the American Dental Association, redheads require more anesthesia due to some mutation in the MC1R gene. What mutation could account for this difference, could this be a point mutation or nonsense mutation?

Source: http://www.webmd.com/pain-management/features/whats-your-pain-tolerance?page=2
http://sciencenordic.com/redheads-feel-different-kind-pain


texts: At any given moment, how much energy is stored in the human body as ATP?

texts:
At any given moment, approximately how much energy is stored in the human body as ATP in the ADP-P-bond?

This of course depends on what type of cell it is and the activity of the individual in question. The calculation should be fairly simple, as we know that ATP hydrolysis release about 30 kJ/mol. Hence, the question could actually be re-phrased to $"$At any given moment, how much ATP does the human body have?$"$


texts: What is the amount of mRNA transported by exosomes?

texts:
I would like to better understand, if possible, what kind of RNA molecules exosomes transport in human cells.
The experiment behind this general question is our goal to do a combination of mRNA-Seq and miRNA-Seq. We would like to be able to prepare libraries for sequencing from the same samples to reduce possible bias as good as it gets. For that we would like to extract both RNA and miRNA from the exosomes, if possible in one run.
Is there a way to approximate the ratio of how much small RNA molecules compared to MRNA is transported by exosomes?
How much of the small molecules transported by the vesicles are truly just fragmented mRNA and not real small RNA (e.g. miRNA, snRNA etc.)?
If anyone is aware of a paper/research regarding this direction, I would appreciate the citing.
thanks
Assa


texts:
Also, what is the definition of polar in this case? (9th Grade)

Does it have to do with the bonds it makes?


texts: Why do we use cRNA instead of initial extracted RNA in the microarray technique?

texts:
I am recapping for the exam in transcriptomics and stumbled into a question about microarray. So, our regular workflow is to

extract RNA from cells
generate cDNA from the initial RNA using reverse transcription
transcribe cRNA from cDNA
label cRNA with biotin
fragment biotin labeled cRNA
hybridize to a plate, scan and quantitate

So the question is - since we use RNA for the further quntification steps why should we perform reverse transcription+transcription to produce cRNA while we could just use the initial RNA?

Is the cRNA more stable than RNA? Or we already make labeled cRNA using labeled nucleotides?


texts: Does drinking spoiled milk that has been boiled upset the GI tract?

texts:
With water, boiling will kill harmful pathogens. Does this also hold true for milk ? If it does not, what in the milk will continue to cause gatrointestinal distress ? Shouldn't boiling kill the harmful bacteria ?

I'd rather not get into a discussion whether animal milk should be consumed by humans. I am asking about a typical person who is not lactose intolerant and does not have any milk allergies.


texts: Are viruses ever manufactured directly from viral DNA embedded in the genome?

texts:
Some viruses can cause their genetic material to be pemanently stored in the human genome -- even getting passed on to offspring.

Endogenous Retroviruses, for example are thought to make up between 5~8% of the human genome.

Does stored viral DNA present in an otherwise uninfected human being's (a newborn baby for example) genome ever get used to spontaneously manufacture new virus bodies, thus infecting the host, and causing them to suddenly become contagious without ever having encountered an actual virus?

Put differently, is it possible that a human being harboring viral DNA and quarantined in a sterile enclosed environment (bubble, etc) preventing any contact with external contaminants (viruses), could ever spontaneously become infected with a virus, due to the stored viral DNA getting expressed?


texts: Which factors dictate the mineral composition in plants\vegetables?

texts: Here's a table of vegetables mineral composition (one of many), just as an example. Each vegetable contains different amounts of minerals, and my question is why is that, or in other words: Which factors dictate the mineral composition of different vegetables, since the diffusion process by which the minerals are absorbed from the ground into the root is essentially the same for all plants\vegetables?


texts: Understanding Research Paper Differences

texts:
I'm doing a high-level research which led me to the following paper - https://www.researchgate.net/publication/280389511_Quality_of_life_of_patients_with_chronic_lymphocytic_leukaemia_in_the_Netherlands_results_of_a_longitudinal_multicentre_study

As it's mentioned there are many groups of testing and comparison in the research, which are: the general population, total patient group and three groups of CLL patients.

I'm a bit confused about the definitions' differences between "the total general population" and "the total patient group".

I appreciate every advice / help.


texts: How does Cro protein expressed by lambda phage kill its host?

texts:
I read that the DNA segment of lambda phage integrated in host DNA could switch between lysogenic state where cI represses the expression of Cro and lytic state where Cro expression takes over and self produces more.

But how exactly does the high production of Cro kill its host?
The virus has a DNA segment shielded with a protein coat. While entering host it gets attached to host membrane and releases DNA inside without damaging host. Then how does host get killed when virus goes outside it which happens during lytic phase and doesn't happen when it got inside?
And if the virus has to go outside host, it needs protein coating. How is that produced? Is it produced only during lytic phase or also during lysogenic phase?


texts: ECT or shock treatment is used to treat psychological disorders. How much voltage,  current and duration is used for this? Wikipedia mentions a treatment of 0.8 Ampere for 5 seconds.


texts: I photographed this group of trees a couple of years ago at the northern tip of Prudence Island in Narragansett Bay. Any idea what species these are?


texts: Were there any marine/aquatic dinosaurs?

texts:
Most dinosaurs were terrestrial, but there were a couple of groups of arboreal and flying dinosaurs (microraptors, birds etc).

I have read that the theory that Brachiosaurids were aquatic has been largely discredited1, but that Spinosaurids were probably semi-aquatic2.

Excluding modern marine birds (e.g. penguins etc.), were there any other marine/aquatic dinosaurs?

Note: I am aware that the marine reptiles mesosaurs, phytosaurs, mosasaurs, dolichosaurs, Icthyosaurs, thalattosaurs, Sauropterygia (placodonts, nososaurs, plesiosaurs etc), Choristodera were not part of Dinosauria.

1.

 • Three new sauropod dinosaurs from the Upper Jurassic of Colorado, Great Basin Naturalist.
 • The Physiology of Dinosaurs: Circulatory and Respiratory Function in the Largest Animals Ever to Walk the Earth, Respiratory Care
 • A note on the habits of sauropods, Annals and Magazine of Natural History
 • Tipsy punters: sauropod dinosaur pneumaticity, buoyancy and aquatic habits, Proceedings of the Royal Society of London

2.

 • Oxygen isotope evidence for semi-aquatic habits among spinosaurid theropods, Geology
 • Semiaquatic adaptations in a giant predatory dinosaur, Science
 • Convergent evolution of jaws between spinosaurid dinosaurs and pike conger eels, Acta Palaeontologica Polonica
 • Functional Morphology of Spinosaur ‘crocodile-Mimic’ Dinosaurs, Journal of Vertebrate Paleontology


texts: Do single oligo sgRNAs for CRISPR require a modified CAS9?

texts: I am attempting to use CRISPR to insert a tag into a gene. The way we have done this in the past is to use separate crRNA (with a sequence to interact with the tracr) and the universal Tracr sequence seperately. This is then injected with an isolated Cas-9 protein and repair template. My question is can one use a single oligo sgRNA (crRNA+entire Tracr) interchangeably, or do you need a modified Cas9 to accept the single oligo version gRNA.


texts: Can catecholamines degrade back into tyrosine, or, is synthesis irreversible? (in human body)

texts: Catecholamines like dopamine, noradrenaline and adrenaline are broken down with enzymes that catalyze the reaction. Can they degrade back into tyrosine (a conditionally essential amino acid), or is the synthesis of catecholamines like adrenaline irreversible? (in context human body, but, broadest possible phylogenetic or biochemical context welcome in answer.. )


texts: Breathing becomes harder in certain wind conditions

texts:
I'm not sure if this is the right site to ask this, but it seemed like the best option.

I've observed on myself that, if I stand on a train platform and a cargo train drives by, creating strong, short gusts of wind, it becomes harder to breathe for me during the gusts, almost like fighting my body into breathing.

A commenton parenting.se leads me to believe this is due to the mammalian diving reflex.

1) is this assumption correct? 2) what causes the change in breathing?


texts:
Can we half-close our eyes such that they don't vibrate?

If not, then why we are unable to half-close our eyes properly?

Alternatively, why isn't it possible to keep the upper eyelid close to the lower eyelid without it vibrating?


texts: Do you know what type of insect this is?

texts: I found these in my appartment (we live in a half basement). It's been three so far and I can't find the thing anywhere in insect lists, etc. Could you tell me what type of insect this is?


texts: Why denatured proteins can't fold back in their native form

texts:
I was wondering why a denatured protein isn't able to fold back into it's native form again.
Because a polypeptide before it's folded has a enthalphy and entropy drive to do so. What does the denaturation process do whith this favouring force to fold into the native structure.
In my opinion I can't see the differences between the unfolded protein (direct after translation) and the denaturated protein.


texts: Please help me identify these fish. I looked around but wasn't able to determine its species.


texts: Oculus rift (or, what do other eye placements see?)

texts:
I could be WAY out of line in the placement of this question, but here goes:

Everyone I'm sure has heard of the Oculus Rift or any of the several other VR headsets making their way around.

It reminded me of a friend who, when in art school, said, "Dali's eyes were crooked [whatever the opposite of crossed is], and it may have helped him develop a different sense of perspective, and we have been taught to practice letting our eyes go relaxed to recreate similar effects."

I don't know if he did it, and I never saw a representation. But now I am interested...

If an Oculus used a model with eyes pointing different directions...or on the "sides of the head" with a wider field of view like many non-predatory animals...

What would we see?

(And maybe if it's an interesting answer... a VR Dali or VR cow simulator might be in order...)


texts: How does the drug, modafinil (Provigil), exert its eugeroic (wakefulness-promoting) effects? I've read that it works by increasing dopamine and histamine concentrations in the CNS and by serving as a partial agonist at the dopamine D2 receptor. Perhaps by interfering with the function of orexin?


texts: Sunlight is used by green plants in photosynthesis, but it is also used by animals in the synthesis of Vitamin D. Are there any similarities between the two processes and how is the light energy actually used?


texts: How can a ligand be an integral membrane protein?

texts: My background is in mathematics, and not biology, so please bear with me. I am currently working on a project involving the effects of Epidermal growth factor treatment (EGF) on cell migration. I am reading a review of EGF signaling (Epidermal growth factor receptor targeting in cancer: A review of trends and strategies by Chetan Yewale, et. al.), and it states that "Various ligands can activate EGFR ... These ligands are expressed as integral membrane proteins." This statement makes absolutely no sense to me, and makes me question my understanding of signal transduction. I think of ligands as freely floating molecules that may eventually come into contact with the cell membrane and attach to some receptor. But a ligand expressed as an integral membrane protein? This seems contradictory to my understanding of ligands, which (I thought) are released from the cell in order to signal with cells (be it the same, neighbor, or distant cells). Integral membrane protein ligands would only be useful for autocrine signaling, which I don't think is true of EGF.


texts: What are the total number of action potentials in the human brain?

texts: Is there an approximate figure of the total number of action potentials in the human brain? It's my understanding that there are ~ 60 billion neurons in the brain with ~ 100 trillion connections between them. Plus there are graded responses between those connections. Is there an estimated figure for what the total might be?


texts: Regarding secondary growth in dicotyledonous angiosperms

texts:
I had read that (and as this image shows) the secondary and primary phloem eventually get crushed due to the repeated division of cells forming the secondary xylem, during secondary growth in dicotyledonous stems. While the primary xylem remains intact, the secondary and primary phloem are crushed.
My question: Is the phloem crushed to such an extent that it is not usable by the plant to conduct organic solutes? Then how does it compensate for this? Does the xylem take over the functions of the phloem?


texts: Why do bumble bees run repeatedly into walls?

texts:
I have noticed on dozens of occasions that bumble bees will run repeatedly into a wall. Usually between 1 - 5 times before clearing the obstacle or flying away.

 Credit: Spine Films

This source suggests that this might be due to "unpredictable, unsteady airflow ... [that results in them being] buffeted back and forth by wind."

However, I've seen this occur in very clear, calm weather.

Further, I do not see other genera of bees colliding into things with anywhere near the frequency of bumble bees.

So what's going on here?

(FYI: their eyes, though primitive, are not likely the reason. Nor is their intelligence).


texts:
I'm looking through the literature on the topic. It seems like hydrophilic PVDF membranes are ideal for low-protein binding but it also sounds like Regenerated Cellulose is an appropriate substitution.

Looking at one resource (http://www.zellnet.com/elispotplatescolumn/)

  When PVDF filter plates were introduced, some investigators chose to use PVDF plates and some continued to use NC.  The reasons for choosing one plate (membrane) over the other are highly varied and won’t be addressed in detail here.  The fact that some laboratories and individual researchers feel strongly that one membrane is superior to the other runs contrary to the large body of Western blotting experience:  Despite some clear-cut differences in how each of the membranes can be used, there is essentially no reported difference in terms of detection sensitivity or signal to noise on NC versus PVDF in the Western Blotting application.  This having been said, it is clear is that the two membranes and their properties are quite different.

The assay that I am looking at in particular is protein/nanoparticle binding to mammalian cells. I am looking for a balance that will enable me to remove free protein without fouling the membrane and/or killing my cells.


texts: Can more than one antibody bind the same antigen

texts:
I'd like to clear something up about antibodies that I'm not sure I've understood in the articles I've read. Looking at concepts such as "affinity maturation", "monovalent antigens" and "polyvalent antigens" it seems as if there are multiple antibodies which can bind to the same antigen. (Although I think I'm right in saying that individual antibodies can only bind to one antigen?) However, when I read sentences like "It has been estimated that humans generate about 10 billion different antibodies, each capable of binding a distinct epitope of an antigen" on the Wikipedia page (for antibody) it does make it sound like it's one antibody per antigen? Is this the case? Or is it one antibody per epitope. Either way, to put this question in a nutshell:

Is it true to say that the same substance could bind with (and, therefore, be recognised by) more than one antibody, or not?

Also, if the answer is no, does that mean that antibodies with different binding affinities are classed as the same antibody or not?


texts: Which sex is homogametic in side-blotched lizards?

texts: I'm just trying to find out whether the male side-blotched lizard is the hetero- or homogametic sex in side-blotched lizards (Uta stansburiana) - some reptiles are ZW system (female heterogamete) and some are XY (male heterogamete).


texts:
I have been getting very low yield from islet isolations from rats.

My procedure is as follows:

Inject the pancreas with 5mL Liberase (1 wunch unit/ml) in HBSS + HEPES through the CBD (decent inflation, atleast of the frontal part of the pancreas) and excise it to an Erlenmeyer flask with 5mL Liberase in HBSS + HEPES on ice (takes ~10 minutes).

Once all animals have been processed, I incubate for 21 minutes at 37C.

After incubation, I shake for 5 seconds and stop digestion using HBSS + 10% FBS. I sediment for 20 minutes and homegenize again using a wide-tipped pipette.

The tissue is pelleted and dissolved in 20mL Histopaque gradient. Spun at 380g for 20min at RT.

Wash twice in culture media and handpick islets.

Can anyone flaw my procedure or give me some clues as to what might cause very low yields in general? I've read somewhere that blood and fat tissues might inhibit digestion. Does anyone have any experience with this?

My current concern is that the islets are over digested.

Thanks in advance.

Jesper


texts: How do I interpret this graph regarding introduced genes and virus-infected cells?

texts:
This graph appeared in a practice test for the MCAT. I am trying to interpret it, but it confuses me a bit. On the x-axis we have some introduced genes, and on the y-axis we have % of cells infected. What I don't get is what the top part represents. How do the "Culture cell genotypes" relate to the rest of the graph. I would also like to know what -/- and +/+ mean. By the way, information in the passage lists CatB and CatL as mammalian proteases, and their inhibitors reduce the infectivity of viruses with the EGP glycoprotein (found in Ebola virus).

Here are some questions based on the graph:

Based on the passage, does optimal VSV-EGP infection in vitro require CatB, CatL, or both?

Based on the passage, is CatL expression sufficient for VSV-EGP infection of the mouse cell lines presented in Figure 1?


texts: How Would I Isolate and Amplify a Viral Enzyme?

texts:
what procedures would I use to isolate and amplify integrase? If I am trying to study the integrase enzyme which is found in HIV how would I
1) destroy the viral capsule to release its contents.
2) separate Integrase from other enzymes and the viral DNA.
3) make copies of the enzyme for testing.
Any help would be greatly appreciated!!


texts:
I'm from Pennsylvania and I used to get this kale all the time at the grocery store, but I moved to the West Coast recently and can't find it anywhere! It looks exactly like this photo:

Image source: http://www.specialtyproduce.com/produce/Kale_Purple_764.php.

I've seen this referred to as purple kale, salad savoy, and flowering kale, but I don't think any of those are 100% accurate. The purple kale I've found here is tougher and more bitter, with spikier leaves and a more reddish color, and it doesn't come as a bunch like this but as individual stems. Does anyone know exactly what this variety is called?


texts:
Im trying to find a proper and general file with chromosomal coordinates for meiotic recombination hotspots.

I know that ucsc hgtables, has a table with recombination regions and their recombination rate. However these regions are all 1Mb, and several articles states that these hotspots regions are more local with a regional length of 2Kb.

https://genome.ucsc.edu/cgi-bin/hgTables?hgsid=782680683_Cxp9zzjwgsql7P0T81FFyATyTNOl&clade=mammal&org=&db=hg19&hgta_group=map&hgta_track=recombRate&hgta_table=recombRate&hgta_regionType=range&position=&hgta_outputType=primaryTable&hgta_outFileName=

Do any of you know of a file or database containing the chromosome coordinates for humans which have been identified as a recombination hotspots?

Thanks a lot for your time and help.


texts: Is there a way to get white blood cells to move while on a microscope slide? I want to try to get some microscope images of them moving, but so far I have only found them stationary.


texts:
A Finnish firm Valkee sells light-ear-plugs against thing such as jetlag. I asked a researcher in Aalto university how do they really work and he responded "why would evolution have lead to photoreceptive cells in ears?" -No direct answer. I asked a well-respected professor who said she did not know this area well enough. Now Valkee guided me to the publications such as Penetration of light into the brain of mammals (1963) and Spectral characteristics of visible radiation penetrating into the brain and stimulating extraretinal photoreceptors (1979). Related to the first one, I found this (1980) from the references:

  "It  is  now  fully  accepted that  the  perception  of  light  by  extraocular  photoreceptors  plays  a  significant  role  in  synchronizing  endogenous  rhythms  with  the  environmental  light-dark cycle  in  non-mammalian  vertebrates"

Things such as certain birds and lizards apparently have extraretinal photoreception aka photosensitive cells not in eyes (this is how I understand it). Now the publication continues

  "The  limited  number  of mammalian  species  tested  to
  date  and  the  near  exclusive  reliance  on  nocturnal  animals  leaves  open  the  possibility  of  extraocular  photoreception  in  some  adult  mammals  (Rusak  &  Zucker, 1975;  1979)."

Now according to a skeptical researcher in my university, there is only one paper supporting photosensitivity in mammals' brains: Wade et al (PNAS 85 (1988) 9322-9326 with rats. My professor in system sciences was extremely scornful when I even asked this question on a seminar course about brain -- he did not specify his reasons and pretty much labelled my thinking as inexperience. Now I am not sure whether researchers are even speaking about the same issues: too large disparities between opposing and proposing teams for the assumed effect apparently through the mechanism called "extraretinal photoreception in mammals". I am very curious.

Helper questions

  What are the mechanisms by which a led in ear would affect a mammal such as a homo sapiens? You don't get D vitamin because of no UV light. You get very-very light heat because of tosslink connection. So it cannot sense the heat as antidote against things such as SAD and jetlag. Other mechanism?
  Is the "extraretinal photoreception in mammals" just placebo or does there exist scientific proofs for it particularly with large mammals about the size of homo sapiens?
  Why would evolution have lead to extraretinal photoreception in mammals?
  Do the terms "extraretinal photoreception" and "non-eye photosensitive cells" mean the same thing? Other terms for the same thing?
  Now eyes are developed very late in cell-division with mammals. Do born-blind mammals and later-blinded mammals experience extraretinal photoreception differently? If led-light (non-UV light) has an effect on large mammals, then I expect this may be possible to see by analyzing results of mammals with different-developed visual-cortexes.
  Does this statement "Light penetrates deep brain areas, eye's receptors have developed from receptors of old CNS." by Humancharger justify the extraretinal photorecetpion?

P.s. I presupposed in this question that extraretinal photoreception is the effective mechanism by which light-in-ear would affect a mammal. It is also possible that there are other mechanisms -- I am not an expert with the terminology here, anatomically and physiologically challenging.


texts: In ketogenesis, why is acetacetyl-CoA not directly hydrolized to acetoacetate in ketogenesis?

texts: Ketogenesis pathway maps show acetoacetyl-CoA converted to HMG-CoA and only then to the first ketone body acetoacetate. Why this detour instead of directly hydrolyzing off the CoA to get there in a single step? Is it possible that some ketone bodies are made by direct conversion? The enzyme acetoacetyl-CoA hydrolase to do this job exists and can be found in rats.


texts: Why are peas in mendelian genetics different?

texts:
In mendelian experiment, yellow seeds were seen to be dominant over green seeds. The peas I've seen are generally green and not yellow. Did he use a different variety of pea plant ?
The other trait that was seen was white or grey seed coat where grey is dominant over white.
Why are these results not consistent with the peas found in pea pods ?


texts: What is the largest species of polychaete?

texts:
My Google searches seemed to avail no results. My question is: What is the largest living species in the class Polychaeta?

That's about it. I understand that there will be few accessible weights for these worms so length will suffice.


texts: Large Alpine Hymenopteran Seen in the White Mountains

texts:
I was hiking in the White Mountains in New Hampshire, USA, and at the peak of Mount Eisenhower saw a number of large bee-like insects. They appeared to be nesting in a rock cairn, and were strikingly large---length was about 1.5" (~40mm). Weather was clear, sunny, about 65 degrees Fahrenheit. Time of year was early July. Environment was alpine tundra, a few hundred feet above the treeline. Besides the habitat and large size, they seemed like fairly typical bees (I'm saying bees because they were almost certainly hymenopterans, but didn't have the typical "narrow waist" of wasps). The abdomen was the longest part of the body. Behavior-wise, they flew in and out of the cairn, and often rested on the ground (or on backpacks, water bottles, etc). Does anyone know what species this may have been?
(I'm sorry I don't have any photos; even if species is impossible to determine without them I'd be happy for any information on possible family or genus)


texts: Reading and Understanding profile bands in DNA Fingerprinting

texts:
I have very limited knowledge when it comes to DNA fingerprinting. I know about the technique gel electrophoresis and how everything is carried out. But I don't know how to read the result or understand that. Can anyone please explain me how to read the result  [profile of bands]?

Because of my lack of knowledge, I can't solve problems like this one.
Please explain me using this one so that I can get a clear idea about DNA profiling. This seems like home-work problem but the thing is I want to understand the technique of restriction mapping by reading the result of restriction digestion on electrophoresis and my intention is to understand the topic. Please Help.

And I can't describe how I tried to solve this question because I don't have any kind of knowledge about this technique [Restriction Mapping] so my efforts are very silly to mention and I have improper way of approach to this as I don't know how to do the Restriction Mapping.

But I am given the answer which I tried to make sense by working on it but I just couldn't help it. It seems easy after seeing the Map but I don't get the relation between the profile of bands and the Map so if I am given a different problem I will fail to come up with a reasonable answer.

What I am trying to say is, by seeing this map and working on it I get to agree that this is the correct mapping for the data given but I have some doubts, like, why we keep 3Kb distance between BamHI and EcoRI sites. Working out in some another way will end up with wrong answer. How these inticacies are understood? By reading the profile of bands [data given] right? So that's what I am asking for you to explain to me. I don't know anything about it.

Thank you always.


texts: How can I simulate heart electrical activity in a 2D plane?

texts:
I am not a biologist/medical student, I study software engineering. But I really like when medicine and engineering hold their hands together to achieve great things.
As a side/toy project, I was looking at creating a basic app that allows the simulation of the electrical conductivity of the heart (eg in the Left Atria), and to simulate some rotor drivers and fibrosis.

I got inspired by this Android App.
This app almost does what I want. Ideally I would like to extend this app to allow a more accurate model, allow fibrosis, allow pacing (i.e. manual intervalled stimulation of one point on tissue and see if it reveals rotors), and of course, allow manual ablation.
Unfortunately, this app has 2 issues for me:

I didn't find the source code of it, and I would not want to reverse engineer it and use it, even if just for fun, without any kind of consent. As a matter of principle, and I believe that all these kind of research should be open to the public by default, that's how Humanity evolves.

I don't know if this app is "too simplistic" in this simulation, I would like to use a more accurate model if possible (and still have this real-time simulation). I have seen tools such as OpenCARP, but they seem too heavy for a lightweight app, and I could not find a single tutorial showing how to make a 2D simulation of this kind of electrical activity, much less to do it in real-time and with user interaction. You can see that this app's rotors are not very accurate, as they do not depend on the tissue they conduct on, you can see as the simulation progresses, rotors are always generated at different spots, while in the real world rotors have a fixed location that corresponds to their core (which does not move constantly!), as depicted bellow:

So, it all boils down to: I will create my own app, inspired by that one, I will make its code publicly available, extend a few features and try to design it in a modular way such that other people can then easily extend it.
My ultimate question here regards the electrical physiology part of these simulators. And I need your suggestion: What is a good model for the electrical propagation, that I can use, that accounts for "fibrotic" obstacles, multiple rotors, etc.?
From a paper I have read regarding this topic, I found out they were using this model and obtaining some satisfactory results. Paper from that model.
I am still reading their paper, but their model seems complex to implement and probably will not result in any kind of real-time simulation (it seems it can take hours to simulate a single second of electrical activity).
So I would like to ask you what is the best model I could use for my app, that allows for a more real-time (not necessarily real, but at least allowing some 10fps, similar to the app), dynamic features (like different conductivity in different cells, fibrosis, manual pacing, rotors, etc.), being more accurate than what this app looks like?
Thank you!


texts: What are the 2 general systems to understand the whole natural world?

texts:
In Graham Bell's book Selection, it's written:

  To some it may be a cause of regret that the natural world cannot be understood in terms of a single set of rules and laws, but at least, so far as we know, the whole of the natural world can be understood in terms of just two general systems, and no more. This book is an account of one of these, in the context of biological systems. It is an account of the Second Science

The first system or process is Selection. What is the second?


texts: What percentage of genome do slugs and scallops have in common?

texts: We can know genetic distance of thousands of species. The OTT tree of life gives genetic distance for nearly all species. Is there a resource to compare the genomes of any sequenced animals to know the percentage of DNA they have in common? I wanted to know for slugs and scallops.


texts: Why marker and control are loaded in the beginning or ending lane of the gel?

texts: I have seen gel images in several literature. Almost in all, markers and controls are loaded in the  extreme lanes (before 1st sample or after last sample) of the gel. I am just curious, is there any reason or logic to do so? Is there any problem if I load it in the middle lanes, in between my samples


texts: Is there a physiological difference between love and infatuation?

texts: I find that people generally distinguish between love and infatuation. Is there a physiological difference between the two? Or are they biologically identical, and the difference is circumstantial?


texts: Relationship between toxicity of drugs and negative effects on brain

texts:
Are psychoactive drugs with lower lethal doses more neurotoxic (more damaging to the brain)? For example, tetrahydrocannabinol (one of the active components of cannabis) has a much higher lethal dose than benzoylmethylecgonine (cocaine), so could we deduce that cocaine is more damaging to the brain?
Moreover, is a mathematical relationship between neurotoxicity and lethal doses known?


texts: What does it mean to "map the human genome"

texts:
I know some elementary chemistry and biology. I also think I know what a gene is (it's a sequence of DNA which encodes a particular protein). I also know that on a chromosome there are sections of DNA which are kind of junk and do nothing. But being armed with this information, doesn't seem enough for me to understand what it means to "map the human genome".

Some possibilities:

a. It tells me the entire sequences of nucleotides that make up a particular human's chromosomes (it could not possibly do this for humans in general because of course the sequence is different from one human to another).

b. It tells me the entire sequences of nucleotides that make up a human's chromosomes... with some annotations along the lines of "at this point in the molecule, we could optionally have nucleotides A, B or C".
It tells me the start and stop points for each of the genes along the chromosome.
It tells me the function of every gene.
Something completely different!


texts:
I'm an art student in need of a little help. I'm looking for microscopic pictures of camel's red blood cells, I need their shape for an art project.

The pictures I find on Google seem a little sketchy as in "is it reeeeeally camel blood or is it from some other animal?" kind of sketchy.

I have tried looking further on the net and in books, but without any luck so far. I hope there is someone out there who can help, thanks for reading anyway!


texts: What are the biological processes of ingesting radioactive particles?

texts:
As someone who has basic understanding/education in physics and how radiation works, there is something that is confusing me and which I would like to shed some light on (I posted about this previously, but the discussion diverted to the risk of radiation in North America from the Fukushima incident, rather than the biological processes of ingesting radioactive particles).

With background radiation, and even relatively high levels of surrounding radiation, I understand that the risk is non-existant to very minimal. However, it seems that lately, people and officials are saying that food near and even in Fukushima is completely safe to eat.

In the case of surrounding radiation, sitting next to something that reads 3000 μSv/h is completely different to eating food that also emits 3000 μSv/h of radiation. In the former situation, once you walk off, the exposure stops. In the latter, radiation is constantly emitted inside your body.

Even more, the amount of radiation is not absorbed by the body equally, but it is usually very concentrated in a particular area of the body, as the particles lodge somewhere and sometimes bioaccumulate. From my understanding, the exposure to the surrounding cells is therefore more intense and prolonged.

To what degree is ingesting radioactive particles in food considered safe (or if at all), such as those in food near Fukushima, when taking into consideration that a concentrated and continuous source of radiation is different from an external one?