What sections of the brain can be removed without causing instant death? Years ago I've read about a young man you had lost a large section of his brain (frontal lobe) in an accident but surprisingly he survived it and continued his normal life. You may have read about that.

Now let's break down the question into 3 steps. Which parts of the brain can we remove without:

Affecting the normal life. This means, still being able to see, talk, understand, and more. Just like a normal person.
Losing conscious. This includes just being able to maintain conscious, being able to think and understand.
Dying. Which means only having the crucial organs such as heart and lungs running.

UPDATE

I'm neither looking for a list of every part of brain's million sections, nor it's possible to cover them all in a single answer. I'm merely looking for a list of widely-known largely-scaled sectioned, such as the below image.

Image credits goes to Mid Brain Power.

Many areas of the cerebral cortex aren't essential to life/consciousness, damaging/removing them will only destroy the function associated with that area, e.g. visual cortex in the occipital lobe, auditory cortex in the temporal lobe etc. The Corpus Callosum can sometimes be bissected without any major detrimental effects to the "patient/victim".

Edit: The point here is that what appears to be a major link between the hemispheres of the cerebral cortex can be destroyed without necessarily killing the patient. Whether it falls under the same surgical category as a frontal lobotomy or not, I don't know.

Generally the "lower" portions of the brain, midbrain and brainstem are more important as regulatory centres. However these are each made up of multiple smaller regions, each involved in multiple functions, e.g. the Pons, medulla, thalamus. Removing any of these could have wide-ranging consequences, e.g. the thalamus is important for integrating multisensory information.

So, broadly speaking, cortex damage is OK, midbrain/brainstem, probably not unless you only removed very small regions (e.g. removing the cochlear nuclei from the Pons would probably only affect hearing).

If you use the added image, you can predict what removing each brain area would affect, removing the brainstem would remove respiratory centres, certain death. Removing visual areas would lead to blindness, but probably not death.

Fully answering your question would probably require an entire book to list all of the known brain regions and the implications of removing them.


Are there tools for automatically parsing glycan names into tree structures? My colleague and I are working on a project involving data produced at a glycan microarray facility. The array data that came back to us were a list of glycan names (in IUPAC condensed format). We would like to parse the list of 610 names into the graphical representation of the glycan.

To clarify, I wanted to take a list of glycans, written in the IUPAC condensed nomenclature, and return an image for each glycan. Here, each image would be the "graph" representation (nodes + edges). Ideally, I would like to be able to write a Python script to get this done, so we wouldn't have to do this by hand.

Is this possible? If so, what tools are available to get this done?

Thank you!

Edit: C# Functions used in our system, slightly paired down for to simplfy

using Microsoft.VisualBasic;
using System;
using System.Collections;
using System.Collections.Generic;
using System.Data;
using System.Diagnostics;
using System.Web;
using System.Net;
using System.IO;
using System.Text.RegularExpressions;

public class KEGGCaller
{
    public object ReturnKEGGgif(string GlycanMonoCode, System.Web.HttpServerUtility HTTPUtilityHolder)
    {

        string CallURL = "http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords=";
        string GlycanURL = HTTPUtilityHolder.HtmlEncode(GlycanMonoCode);
        WebClient wc = new WebClient();
        System.Drawing.Image GlycanGif = default(System.Drawing.Image);
        CallURL += GlycanURL + "&mode=bfind&max_hit=1";
        StreamReader reader = new StreamReader(wc.OpenRead(CallURL));
        string Gcode = FetchGcode(reader.ReadToEnd());
        if (Gcode == "Failed") {
            return 0;
        } else {
            System.Net.HttpWebRequest Request = default(System.Net.HttpWebRequest);
            System.Net.HttpWebResponse Response = default(System.Net.HttpWebResponse);
            Request = System.Net.WebRequest.Create("http://www.genome.jp/dbget-bin/www_bget?gl:" + Gcode + ".gif");
            Response = (System.Net.WebResponse)Request.GetResponse;
            if (Request.HaveResponse) {
                if (Response.StatusCode == HttpStatusCode.OK) {
                    GlycanGif = System.Drawing.Image.FromStream(Response.GetResponseStream);
                    return GlycanGif;
                } else {
                    return 2;
                }
            } else {
                return 1;
            }

        }

    }
    public object FetchGcode(string PageBlock)
    {
        string MatchURLString = "?gl:G\d\d\d\d\d";
        Match URLMatch = Regex.Match(PageBlock, MatchURLString);
        if (URLMatch.Success) {
            return Strings.Right(URLMatch.Value, 6);
        } else {
            return "Failed";
        }
    }

}

Remainder of the Answer

Biomodels.Net is a great resource to begin with and familiarize yourself with the field and get ideas of how to tackle your qualification needs.  We used it when we were doing drug screens.

More specifically for glycans, you're going to be looking at KEGG.  Then use KEGG draw for your visual application.  If you actually just want to parse them, here is the table on the monosaccharides used (most places).

Here's a better link right to the download in case you didn't find it.  The script we wrote was pretty simple, here is the basic logic.

Start with the monosaccharide code.

Call a single return of DBGET to GenomeNet pulling from KEGG Glycan.  For example:
(GlcNAc)6 (Man)3 (Asn)1
would be called:

 http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords=%28GlcNAc%296+%28Man%293+%28Asn%291&mode=bfind&max_hit=1

Where http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords= and &mode=bfind&max_hit=1 are going to be constant and the middle part is going to be your search.

You need to change your monosaccharide to standard URL ASCII Reference, concatenating each monosaccharide with a "+".  Thus (GlcNAc)6 (Man)3 (Asn)1 becomes %28GlcNAc%296+%28Man%293+%28Asn%291.

That will give you one hit with the link to your exact match if there is one.  There will be one link on the returned page in the format of http://www.genome.jp/dbget-bin/www_bget?gl:G#####, where G##### is your glycan number (in our example G00021).

Once you have the glycan number you're good to go.  All of the structure images can be found at:
http://www.genome.jp/Fig/glycan/G#####.gif

And then you just download your GIF.  The way we did our batches was to do each step for all the hits then move to the next step.

Hope that helps more.


Is there any evidence that humans have faced extinction before? Have we as a species faced extinction in the past? Resulting in a 'population bottleneck'?  If so, what genetic evidence is there of this occurring?

There is ample genetic evidence for a population bottleneck following the out-of-Africa migration. This would account for the reduced genetic diversity found in non-African populations.

There is further evidence for an earlier major bottleneck that reduced the human population to around 10,000 individuals.

These kinds of studies are typically done now via Coalescent theory using whole-genome sequences.

I just found this nice blog post summarizing the Nature paper I linked to.


Is kissing a natural human activity? The word natural here is meant in contrast to it being a sociological construct.

  Is kissing in all its forms something natural for humans? Is it instinctively erotic? Or is it just a conventional form to show trust and intimicy, i.e. the association besically just comes via a social means?

Because the only other advantage of this mouth to mouth contact I could see is maybe for the immune system.

Wikipedia actually has a note on the evolution of kissing.  They point out that there are grooming behaviors such as licking and social behaviors like dogs touching noses in many species even insects.  They note that it is not decided at all whether kissing is learned or from some sort of instinct.  They also mention that its reminiscent of feeding behavior common in birds (and other animals) where food is pushed down the throats of young.  (try thinking about that next time!)

I seem to remember though that there are some culture which do not kiss. with their lips at least. This would favor kissing as a learned behavior, but these cases are very rare and isolated peoples and it might be simply a taboo to talk about kissing with researchers or at all, which is a hazard of that sort of work.  In addition, bonobos, one our our closest primate cousins, do kiss frequently with the lips, as a social and intimate gesture and the parallels with most human cultures are difficult to ignore.


How far can a mosquito fly over the sea? My question is: how far can a mosquito fly over the sea? I am interested to know, because from this, I could possibly deduce on which islands there either might not be mosquitoes or on which it would be achievable to eradicate all mosquitoes until somebody brings another larva.

If we ignore the weather effects mentioned by Count Iblis we can do a fairly simple calculation.

The lifespan of a male mosquito is about 10 days whereas females live to about 50 days.

Their flying speed is generally about 1.2mph.

So if we assume that they can fly whilst asleep and maintain a constant velocity for their entire lifespan (obviously ridiculous because of the need to eat etc), their maximum ranges would be:

Male: 1.2 * 24 * 10 = 288 miles.

Female: 1.2 * 24 * 50 = 1440 miles.

It should be noted that these are absolute theoretical maximums. I would suspect real life values to be somewhere in the region of 10%-20% of these. However, once wind is taken into account they can easily spread globally.


How does a tree trunk sprout and grow after being cut? After I cut trees into logs and remove the branches in winter, they start growing. They sprout out and grow completely normal looking stems and leaves and maintain them all summer. The sprouts mostly appear around the cut branches.  Sometimes they last all winter and grow for another year. How does it find the energy and water necessary to maintain and grow these stems without ground connection and a water source?

This is basically the same that happens after pruning and involves a basic hormonal regulation mechanism in the plants.

What happens is that the cut piece of the wood forms a new meristem which allows the growth of new organs. What’s important is that there is no other growth happening nearby, since that would hormonally inhibit any further growth. This is why such growths happen once you’ve cut the wood, not before (on the healthy stem). This inhibitory effect is known as apical dominance, which has now been disabled.

As to where the energy and water comes from, to some extent it is stored within the branches themselves. That’s why you need to dry them before being able to use them in a fire. However, this growth is pretty limited. Further water is probably collected by condensation of water vapour in the air.


In Japan, the official average body temperature is 36.0 °C. Why so different from that of Europe? The Japanese Wikipedia states that the average human body temperature is 36.0 °C (here,"ヒト").
The statement references the data from the Japanese government.

Actually all of my Japanese friends think the same.
A body temperature of 37.5 °C is considered a serious illness in Japan, justifying absence from work.

Most other countries' sources cite 37.0 °C as an average.
Is there a biological explanation for this apparent discrepancy?

Factors that can lower body temperature:

low environment temperature
low metabolic rate
hypothyroidism

I couldn't find any relevant study addressing the Japanese people situation, but:

  There is significant variation in metabolic rate in humans, independent of differences in body size, body composition, age, and gender. Although it has been generally held that the normal human "set-point" body temperature is 37 degrees C, these interindividual variations in metabolic rate also suggest possible variations in body temperature [1].

And here's a factor that increases body temperature:

  The present experiment investigated the effects of skin pressure by foundation garments (girdle and brassiere) on the circadian rhythms of core temperature and salivary melatonin. [...] The results suggest that skin pressure by clothing could markedly suppress the nocturnal elevation of salivary melatonin, resulting in an increase of rectal temperature [2].

Whether there are differences between Japanese and other people in metabolic rate and /or clothing behavior remains unclear.

References:

Rising R, Keys A, Ravussin E, Bogardus C. Concomitant interindividual variation in body temperature and metabolic rate. Am. J. Physiol. 1992 Oct;263(4 Pt 1):E730-4. PubMed PMID: 1415692.
Lee YA, Hyun KJ, Tokura H. The effects of skin pressure by clothing on circadian rhythms of core temperature and salivary melatonin. Chronobiol. Int. 2000 Nov;17(6):783-93. PubMed PMID: 11128295.


It's right to say coding sequence is part of exon sequence? Some basic ambiguities making me confused. I downloaded 5'UTR, CDS, 3'UTR, and exon sequences, separately from Biomart for a gene P4HA2 (Homo sapiens) and found some simple sequence repeat (SSR) on them. While there is a repeat x on the exon sequence, it was not located on the 5'UTR, 3'UTR, and coding sequence (or CDS) of gene. As I remember, exon sequences is the same with coding sequence, except for the first and last exon, which are parts of 5'UTR and 3'UTR, respectively, am I right?. Could you please help me out to find how the mentioned event is possible?
Thanks

As I remember, exon sequences is the same with coding sequence, except
  for the first and last exon, which are parts of 5'UTR and 3'UTR,
  respectively, am I right?

Not necessarily. The UTRs can be composed of multiple exons and there can be an exon that spans both sides of the start codon i.e it is both a part of the 5'UTR and CDS. Similarly, an exon can span both sides of the stop codon.

A reason for why you are not able to map your repeat to any of the regions of the mRNA could be that your repeat falls in an exon that spans the start/stop codon. The repeat itself might span these sites. You need to provide additional details such as the location of the repeat, size of the repeat and which exon it maps to. Also mention which reference genome file are you using.


Gene pool simulation this simulation, you sampled the gene pool without replaceing beads in the beakerafter you drew each one. Thus, f(A) and f(a) in the gene pool changed slightly after each bead was drawn. For example, if you begin with 50 light and 50 dark beads, the probability of drawing a dark bead the first time is 50/100 = 0.5. THe beaker would then contain 49 dark beads and 50 light beads, so the probability of drawing a second dark bead becomes 49/99 = 0.495. Does this make your simulation slightly less realistic? In small natural populations, does one mating change the gene pool available for the next mating, or not? What biological factors must be considered in answering this question?

I am not sure I'm answering your question but I hope this will help.

There are two main models of genetic drift in biology: Moran model and Wright-Fisher model.

The Wright-Fisher model implies picking $N$ beads (where $N$ is the population size) with replacement in order to form the new population. Therefore, the change in allele frequency (due to genetic drift) follows a Poisson distribution.

$$\frac{2N!\cdot p^kq^{2N-k}}{k!(2N-k)!}$$

The Moran model consists of the following: At each time step you draw two beads. One disappear from the population and the other replicate in order to keep a stable population size.

The two models yield to similar results. Moran model runs twice as fast as Wright-Fisher model.

I don't fully understand your model. You say that in your model you pick one bead at a time. What do you do with this bead? How do you construct your population at the next time step? Do you allow changes in population size? Can you please try to develop how you defined your model. If it is a computer simulation you might paste the important part of your code, that might help.

Haldane and Kimura both worked a lot on these models of genetic drift. For example, they provide different ways of calculating the mean time to fixation of a given allele given their selection coefficient $s$ starting from a given initial frequency $p_0$. Also some work has been done on genetic drift in population where the population size changes over time. Some work have been performed considering more or less complex probability density function for the number of offspring per individual. This kind of literature is very interesting but sometimes ask for quite good knowledge in mathematics (especially for Kimura's articles).

I once asked this question concerning the different models of genetic drift and their assumptions but I didn't get an answer yet.


What causes this acorn disease? This year, many acorns in our area (Germany, Schartzwald) fell prematurely, plagued by some kind of warts or gall-nuts which I see for the first time:

Some of the acorns are covered by two or three warts at a time, so that the actual nut itself is practically non-existent.

Judging by the hole present in all the warts, I'm guessing those were houses for some insects or larvae. Unfortunately, warts on acorns available for inspection (those which already fell) are already abandoned by their hosts.

Does anyone know who those guys are and how they look like?

The structure on the oak nut is a knopper gall.

  It is a distortion of growing acorns on pedunculate oak (Quercus robur L.) trees, caused by gall wasps(Andricus quercuscalicis), which lay eggs in buds with their ovipositor.

An Andricus quercuscalicis larva in an open gall of an acorn:
Link

Here's a video by BBC on the same you may find it interesting.


Why is the thyroid gland in the neck? The neck seems like an odd place for it. All other neck anatomy must interface between the head and abdomen (trachea, esophagus, circulation, spine etc).

Surprisingly I have not been able to find any explanation for the thyroid’s location.

Almost certainly not the pituitary proximity hypothesis. Simple counter-examples include the adrenal gland (ACTH-cortisol axis), liver (GH-IGF1 axis) and  the gonads (LH/FSH axis).


Why is SOC medium recommended for transformations? In pretty much every transformation protocol I've seen SOC medium is used to grow the bacteria for a short while after the tranformation and before plating.

I've usually substituted LB medium for this step for easy retransformations, but I gather that the SOC medium is supposed to make some difference in efficiency, or else the simpler LB medium would be recommended in the protocols.

Why is SOC medium used for transformations? What difference does substituting with LB medium cause for the transformation efficiency?

To summarize from Hanahan's paper (see below for reference), he carried out a systematic review of conditions necessary to improve transfection efficiency. Among the conditions tested were the presence of various cations (Ca2+, Cs+, Mn2+, K+, Mg2+), DMSO, and growth temperatures (and a few other conditions not so commonly used these days). He worked with a strain that he subsequently isolated a derivative of, called DH1, which is now available commercially as DH1-alpha and other strain derivatives.

He defined transformation efficiency to be the number of transformed colonies on a plate, a measurement still used today. He found when the transforming media contained: certain cations, specifcally Mn2+, Ca2+, Rb+; as well as DTT, hexamine cobalt (III) and DMSO; greatly improved the transfection efficiency compared to the standard Ca2+ treatment. He also found that sucrose and K+ were useful, though not strictly necessary for his experimental strain. It was stated in this paper, though not explained, that sucrose acted as a stabilizer, possibly to guard against his initial use of 0°C incubation and/or freeze/thaw cycling. For the rest of his work, he did not use sucrose.

Among his conclusions, he states that DTT is necessary, as well as di-valent and mono-valent cations, but that they seem to be nonspecific. In other words, there is no strict requirement for having Ca2+, since Mg2+ and Mn2+ perform equally well, nor is there a requirement for K+, though it's admittedly easier to use than Rb+.

There are today a number of "rich" media broths that are available: SOB, SOC (SOB + MgCl2 and sucrose), 2xYT, NZY+, TB, etc. All of these are superior to LB for transformation purposes because of the refined salt balance and in particular the inclusion of these di-valent and mono-valent cations. Sucrose seems to be included for the ease of metabolism and stability of the heat shock process (though I can't find a paper explicitly explaining why it is used, other than tradition).

The two most common ways to transform bacteria are to have them chemically compentent (E. coli already in a rich media broth) or to electrically transform them (electroporation). The purpose of both of these is to induce holes into to cell membrane of the E. coli (chemical transformation relies on the heat shock process for this). Once these holes are made, DNA is free to enter into the bacteria. Naturally, this process is very traumatizing to the E. coli, especially since chemical transformation has the added insult of temperature shock (0°C to 42°C then back down to 0°C).

Substituting LB for any rich broth, such as SOC, will greatly improve transformation yield. If a protocol calls for SOC media, and you don't have any, you may substitute for another rich media. I have used 2xYT for SOC many times quite successfully, and as I stated earlier, only the valence number for the various ions seems to matter, so just make sure they are present.

It was my understanding that sucrose/glucose was added as an additional nutrient source for E. coli to expedite their recovery from the transformation protocol. I speculate that this is the case. Hanahan refers to sucrose as a stabilizer but does not define what it is stabilizing. I speculate that it acts as a cryopreservation aid and prevents ice crystal formation when undergoing cooling on ice in the heat shock method. Given the earlier bio.SE question about shifting E. coli feedstocks, it seems unlikely that sucrose will be used as a nutrient source in the one hour growth period immediately after transformation because that article quotes 4-12 hours as the common time range to shift metabolism from amino acids to carbohydrates.

Sources:

Hanahan D. Studies on transformation of Escherichia coli with plasmids. J Mol Biol 1983 166(4):557-80.


How do painkillers prevent shock? I was reading about the Placebo effect and came across this little story:

  The roots of the placebo problem can be traced to a lie told by an
  Army nurse during World War II as Allied forces stormed the beaches of
  southern Italy. The nurse was assisting an anesthetist named Henry
  Beecher, who was tending to US troops under heavy German bombardment.
  When the morphine supply ran low, the nurse assured a wounded soldier
  that he was getting a shot of potent painkiller, though her syringe
  contained only salt water. Amazingly, the bogus injection relieved the
  soldier's agony and prevented the onset of shock.

https://www.wired.com/2009/08/ff-placebo-effect/

I also read that Morphine specifically lessened the effects of shock:

  Only when it is severe, or when a severely wounded or injured person must be moved quickly (as from a wrecked vehicle or aircraft) it is wise to give Morphine at once. It may not always relieve the pain entirely, but will certainly lessen shock.

https://web.archive.org/web/20140420133119/http://www.med-dept.com/morphine.php

So, how do painkillers prevent wounded soldiers from going into shock and dying? What physiological mechanisms are responsible? Is it something to do with blood pressure? Heart rate? Pain itself?

1) Pain can aggravate hypotension, so painkillers may help to prevent shock.

A severely wounded person with significant blood loss can develop hemorrhagic shock due to drop in blood volume and consequently drop of blood pressure and insufficient perfusion of vital organs.

It is known that pain can trigger vasovagal syncope, also known as neurocardiogenic syncope in which a person faints due to sudden drop of heart rate and arterial vasodilation resulting in drop of blood pressure and reduced brain blood perfusion.

Here is an example how carbamazepine, which prevented pain, also prevented the episodes of neurocardiogenic syncope (The Korean Journal of Pain):

  A 65 year-old male patient diagnosed with glossopharyngeal neuralgia
  complained of severe paroxysmal pain in his right chin and ear
  followed by bradycardia, aystole and syncope. We report a case
  successfully treated with a permanent pacemaker and carbamazepine in a
  patient with GPN who had syncopal attacks preceded by paroxysms of
  pain.

In an injured person who is at risk to develop hemorrhagic shock, severe pain could cause neurocardiogenic syncope that could proceed into shock, so, it sounds logical that painkillers could help to prevent shock.

From the first quote in the question (the patient was convinced he was receiving a strong painkiller), we cannot conclude that the painkiller prevented shock, because this has not even started to develop.

2) Analgesics for a person in severe pain who has lost blood and is in danger of developing shock.

According to Pain Control in Trauma Patients (Trauma Reports, 2011, fentanyl can be appropriate painkiller in shock since it does not aggravate hypotension:

  Fentanyl is the best known synthetic agent and is widely used in pain
  control. It is 50 to 100 times more potent than morphine and has the
  added benefit of not causing histamine release and peripheral
  vasodilation, as found with morphine administration. Based on this
  physiology, fentanyl should not impact blood pressure as much as other
  narcotics and, therefore, is preferential in the critically ill trauma
  population who may have tenuous cardiovascular status from hypovolemic
  shock.

Morphine can cause hypotension, so it may aggravate shock. According to prescribing information for morphine sulfate oral solution by FDA.gov, 2018:

  In patients with circulatory shock, Morphine Sulfate Oral Solution may
  cause vasodilation that can further reduce cardiac output and blood
  pressure. Avoid the use of Morphine Sulfate Oral Solution in patients
  with circulatory shock.

In conclusion, painkillers may help to prevent shock by reducing pain.


Is water movement across cell membrane purely diffusive or it always requires channels? If we see nephrons, in the descending part of Loop of Henle (LoH), water movement is allowed but solute movement is not. On the contrary, in ascending LoH, solute movement is allowed but not water. What exactly restricts this movement?
I am particularly interested in understanding the movement of water across cell membranes and then answering the above query.

Water across cell membranes occurs due to osmosis( which is based on a concentration gradient). so water diffuses through the cell membrane. sometimes water channels called aquaporins can be found.
https://www.anaesthesiamcq.com/FluidBook/fl1_2.php
https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/aquaporin
In the loop of Henle, the water, and Na+ & Cl- exchange occurs due to the counter-current principle takes place. the interstitial fluid has a certain sodium chloride concentration. the filtrate that is entering the descending limb of the loop of Henle, has a particularly low NaCl concentration.so because of that water moves from the loop of Henle to the interstitial fluid.simultaneously, at the ascending limb of the loop of Henle just adjacent to that particular point, water concentration is high in the interstitial fluid. so because of that NaCl moves to the interstitial fluid (Na+ actively, and for ion balance, Cl- passively.) this happens along the length of the loop of Henle. what restricts water movement from the ascending limb of the loop of Henle is that that limb has no aquaporins and the descending limb has numerous (with relative to other places in the nephron). anyway, here's a link for you.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468499/


probability of hairpin vs self-dimer formation? I have a linear ssDNA oligo that is designed such that the ends are complementary, and conducive to hairpin formation (see attached figure). My question is, which has a higher likelihood of formation, a hairpin, or a self-dimer? Would the likelihood of hairpin formation increase if I decrease the concentration of the ssDNA oligo during the annealing process? If I enter the sequence in IDT oligo analyzer, the gibbs free energy for formation of self-dimer is significantly lower compared to hairpin.
The melting temperature of the complementary part of my oligo is 50 deg. The annealing will be done in nuclease free water, without any Mg+.

I have tested a similar design to this. With a duplex protocol the chance of forming a hairpin is much higher than that of forming self-dimer, even at concentration of 25 μM. You can run a 3-5% agarose gel to test the outcome.


What is this insect in India? I found this insect today in front of my room.

I am just curious to know what kind of insect it is? And, is it poisonous?

Location: India

Its a black Cricket .

Crickets, (family Gryllidae) are related to the Grasshoppers Family.

It should have grasshopper like hind legs .
Crickets usually emit  noise from its body.


Why does my anti-ubiquitin antibody visualization not work on my PAGE gel? I am using 2D gel electrophoresis to visualize polyubiquitinated proteins. However, while I can see actin and heat shock protein using when appropriate antibodies, I cannot visualize them using anti-ubiquitin antibody. Could it be degradation problem?

I run isoelectric focusing at 200 V overnight (at least 18 hours) and 700 V the last 30 minutes. I am worried that I am applying more volts than needed, because the standard protocol is 200 V for 20 minutes, 450 V for 15 minutes, 750 V for 15 minutes, 2000 V for 30 minutes, but due to problems with the power unit I cannot do this.

I am sure I have polyubiquitination because I use a drug that triggers polyubiquitinated protein accumulation inside the cells.

I would like to add also that cells are collected by scraping in cold PBS and then they are placed in ice and the pellet is also collected at 4 degrees to prevent protein degradation.

There are stable ubiquitinated proteins in mammalian cell lysates even if active proteosomes exist in cells.

First, you might want to make sure that the antibody is applicable to WB.

Then, you would ask if your WB system using the antibody works. You could optimize the condition using just 1D SDS-PAGE followed by WB.

For the condition for isoelectric focusing, when focusing is completed, you get very high electric resistance, so you might want to monitor current after you change the voltage to 700 V. Current decreases gradually, and get stable at some level. But I do not know you can see stabilization by 700 V.

You also might want to check if major proteins such as actin form spots nicely at the expected pI. That could tell if forcusing is completed roughly.


How to find a PDB structure of a protease with a peptide like inhibitor I wonder how, for purposes of just illustrating some concepts like substrate alignment in the catalytic triad active site, I can quickly and efficiently find a protease structure (irrelevant of what organism exactly) that has a peptide like inhibitor on the PDB database.

Hints appreciated.

Here's one: http://www.rcsb.org/pdb/explore/explore.do?structureId=2IPH. It was crystallized with the inhibitor bound to the protein.


How do wild animals get rabies? I can see the chain of spreading disease: Humans usually get rabies from domestic animals, those usually get it from wild animals, wild animals in their turn get from the other wild animals and here I'm stuck. Well, so where do wild animals get it from initially?

I know that rabies is a virus and it needs warm-blooded animals to live out. Also according to Wikipedia once an animal is effected it lasts, let's say, no longer than for 2 weeks.

In other words, does it mean that there is a constant population of rabid animals that exists in order to pass this virus from one animal to another every 2 week on the average?

Such viruses have a natural host, which might get sick, but is usually not killed by the virus. From there, the virus can get zoonotic (jump over species barriers) and infect other animals when it comes to contact. For Rabies the reservoir hosts are different, for the US these are bats, skunks and racoons. For more details, have a look on this PDF.

Another example for this is the SARS virus (a corona virus) which most likely lives in bats naturally and has jumped from there onto birds and from there infected humans.


Nomenclature for mutations at specific nucleotide positions I'm sure this is a basic question, but I couldn't find an answer anywhere. Let's say I'm provided with the location of a nucleotide as location as  FGFR3:c.1843-35A>T. What does "1843-35" mean?

As 'c.' stands for 'coding' sequence (instead of 'g.' for 'genomic'), according the HGVS guidelines it denotes the A to T substitution at nucleotide -35 of an intron (in the coding DNA positioned between nucleotides 1842 and 1843).


How does the enzyme ATP Synthase use a proton concentration gradient to make ATP? I understand what the enzyme ATP synthase does, but I'm not exactly sure how it does it. I've heard that it uses rotary catalysis, but how exactly does this work? How is the energy from the H+ ion harnessed, turned into mechanical energy, and then finally into the chemical energy stored in ATP? Why does the spinning of parts of the enzyme need to occur for this to happen?

Image from wikipedia page on ATP synthase

In brief, the addition and release of protons to the structure cause a conformational change that leads to another conformational change.  This series of conformational changes occurs in such a way that it induces a rotational motion.

The rotation of the central axel that extends through both hemispheres of this large complex is driven by the proton gradient.  Specific residues in the c12 ring are protonated in order to drive this rotation.  A high concentration of protons (in this picture the high concentration is found above the complex) allows each of the subunits in the membrane to be constantly loaded with H+ ammunition, ready to fire when it comes to be their turn.

The function of this axel is to slightly but significantly change the shape of one subunit at at a time in the red part.

Changing the conformation of subunits in the red part is what allows for the three steps in ATP synthesis to occur: binding of ADP and Pi, catalysis of the formation of ATP, and release of ATP.

All of these changes occur at the molecular level.  The proton forms a bond with a single amino acid of the entire protein complex, but this is sufficient to cause a difference in the most stable 3-dimensional structure of the whole.  This could cause either a cascade of changes that result in a net rotation or it could cause a re-stabilization of the structure due to electrostatic forces.

According to Vinit K. Rastogi & Mark E. Girvin in their 1999 Nature paper on the subject, it's more like the former:

  Earlier models proposed simple rotational diffusion of a rigid c12 ring, possibly driven by electrostatic forces. The structural data on protonation-linked conformational changes in subunit c indicate that the process may be more mechanical, with local rotations within subunit c driving larger-scale rotations of the c12 oligomer as a whole, in a `wheels within wheels' type of mechanism.

The whole paper's a good read.  But this is as current as I am on the topic, and it's likely that a more detailed mechanism has been determined for the action of ATP synthase since 1999.


Do male animals visually perceive females as more/less attractive? If we somehow remove pheromones, do animals experience a phenomenon similar to human "visual beauty" when looking at members of the opposite sex? For example, given a set of 20 female ducks observed through a glass panel, would male ducks attempt to court/mate with a small subset of female ducks first(more attractive ones), or is it based on some other criteria (most receptive, random, closest, fittest, pheromones, etc?)

If there is some "visual attractiveness selection criteria", is there a requirement of certain complexity of the brain and/or visual system for an animal before this phenomenon starts to occur?

I'm aware of the existence of this question: Why does sexual selection evolve beautiful features?, and my question deals with the members of the same generation, not long-term evolution.

There are numerous examples of visual attraction in animals. An absolute classic of an experiment, taught to most/all evolutionary biology students, is the widowbird tail length experiment by Andersson. He experimentally manipulated the tail lengths of male widowbirds at random. Some tails were made longer and some shorter. From this experiment Andersson showed that females choose males with longer tails more preferentially. Another classic example is the lek mating system where there is a bias in reproductive success towards attractive males, in some cases 10-20% of the males get 70-80% of the matings.

  A lek is an aggregation of males that gather to engage in competitive
  displays that may entice visiting females who are surveying
  prospective partners for copulation. Leks are commonly formed
  before or during the breeding season. A lekking species is defined by
  the following characteristics: male displays, strong female mate
  choice, and the conferring of male indirect benefits. Although
  lekking is most prevalent among avian species, lekking behavior is
  found in a variety of animals such as insects, amphibians, and
  mammals

Beauty could be a an example of a an indicator trait:

  Indicator traits are those that signal good overall quality of the
  individual. Traits that are perceived as attractive must reliably
  indicate broad genetic quality in order for selection to favor them
  and for preference to evolve.

I'm sure there are some studies in fish, likely guppies or zebra fish, which gave individual fish the opportunity to visually assess potential mates (placing tanks next to each other and observing courtship) which would be very similar to your hypothetical duck example. Despite often being a paradox, female mate choice is well documented. Further, male mate choice is now coming to light, even in species where female mate choice and male-male competition exists.

I don't think selection on "beauty" would require some kind of particularly special neural system, obviously some visual capacity is necessary for visual attraction and some basic neural pathways linked to that. I have done experiments myself in Drosophila simulans which looked at good gene benefits of mating with attractive males (indirect genetic benefits of female mate choice) and another which assessed precopulatory selection (female mate choice) for a secondary sexual character in the same species. Even in such a small-brained species there appears to be some degree of (partially visual) mate choice going on.


What is the reason behind choosing the reporter gene when experimenting on your gene of interest? I noticed within example experiments in class that different reporter genes are chosen to be inserted near your gene of interest to prove whether or not the gene is being expressed. For example, you may insert the gene for fluorescence next to your gene of interest so you know if it is transcribed or not by whether the organism's cells are fluorescent and to what degree they are fluorescing at.

I have noticed in some experiments that have multiple versions that in one case they use the fluorescent gene and in the next a different gene (for example lactose). Both portions of the experiment use almost the exact same steps so why would they not choose the same reporter gene?

Different genes will serve different purposes. For example, if you want to perform colocalization studies, then fluorescent genes like eGFP and DS-Red (or any variation of those, namely Emerald, mCherry, etc) will be quite useful, since you can use different filters on your microscope for the various fluorophores. For morphological assessments, perhaps a LacZ gene or alkaline phosphatase may be better suited, since the detection of these enzymes is compatible with standard histological techniques and you get usually much better contrast than with fluorescence. For quantification purposes, you would use probably firefly luciferase or CAT, since there are very good quantitative assays for these enzymes.

The decision will also depend on the degree of experience of the lab with each detection technique and even in the availability of the constructs. If a reporter is already made by the lab next door and if it fits your needs, you'll just use it, instead of creating your own, even if the reporter gene would not have been your first choice.


Are the genes for transcriptional factors close to their targets in the genome? Transcriptional factors (activators and repressors) are proteins which regulate transcription. Being proteins, they themselves are also made from expression of certain DNA sequences/genes.

For example, the lac operon repressor is coded for by the lacI gene. Now, in the case of the lac operon, the gene for the transcriptional factor is next to the promoter sequence. It is, in fact, a part of the lac operon. Similarly, the trpR gene is a part of the trp operon.

Is this always the case? Is the gene coding for the transcriptional factor always present next to (or close to) the transcription unit?

The two mentioned operons are only in prokaryotes. Could it be that this fact is valid for prokaryotes only, and not eukaryotes' DNA?

Is the gene coding for the transcriptional factor always present next
  to (or close to) the transcription unit?

Not necessarily. You can find several counter-examples. Even for prokaryotes this is not necessarily true. The genes regulated by a common factor are called regulons and though the target genes need not be proximal to the regulator, it has been observed for E. coli and B. subtilis that operons within a regulon are clustered in the genome (Zhang et al, 2012). In the same study, the authors note that small regulons have the regulator proximal to them (See the figure below).


(Why) are polar bears more common in Labrador than in southern Greenland? The Labrador Sea is between Greenland, Labrador, and Qikiqtaaluk:

Map source.
A Greenlandic source on polar bears states:

In Greenland the polar bear lives and breeds in the northernmost parts of West Greenland and in Northeast Greenland, but is also occasionally seen elsewhere in Greenland, as it moves with the drifting ice.
However, it is extremely rare for either local inhabitants or tourists to see a living polar bear. The chances of seeing a polar bear are greatest when sailing by ship along the coast.

On the other hand, Parks Canada for Torngat Mountains National Park (northern Labrador) states:

Polar bears are true carnivores and can be a significant risk to human beings. Visitors travelling and camping in the park are in polar bear country and are at high risk of encounters. Polar bears are almost always present along the north Labrador coast.

The observation that polar bears are more common in Labrador than in southern Greenland is supported by Derocher (2010), Nature:

Derocher (2010), Nature
Polar bears like the sea ice edge, but this is very far from either Labrador or Greenland when at its fall minimum.  When sea ice is at its spring maximum, both Labrador and almost all of Greenland are packed deeply in ice (see maps below).
Then why are polar bears so much more common in Labrador than they are in southern Greenland?  Arey they really?  And how do they survive all summer long, when the sea ice is very, very far away?  The occasional tourist might not be enough, I guess.

Arctic minimum sea ice from NSIDC

Arctic maximum sea ice from NSIDC

I think the lack of sea ice coverage would point you somewhere- even with the maximum sea ice coverage picture, the SW corner of Greenland has next to none, which may impact the carrying capacity for both bears and prey animals on that narrow strip of land between the ice cap and the sea- less space and less things to hunt, less ways to get around, etc. And then there's not much continental shelf over there, either.

Labrador is surrounded by more continental shelf, which might contribute to higher levels of sea ice at high levels and greater seasonality. Might lead to more prey?

This article might get you somewhere:Polar Bears in a Warming Climate


Stability of DNA double helix conferred by base stacking Our school textbook states that base pairs confer stability to the B-DNA double helix in two ways:

1) Hydrogen bonding between purines and pyrimidines of opposite strands.

2) "Stacking of one base-pair plane over the other"

It's the second point that I'm not able to understand. I did try looking it up on the internet, but I'm not able to find anything relevant in that regard.

So could someone please try explaining that second point to me?

When you carefully look at the structure of DNA helix, you will notice that consecutive bases are partially layered i.e. one base is "on-top" of the other base. Stacking is a chemical phenomenon in which the cloud of the pi-electrons in an aromatic molecule interact with that of the other. This interaction is non-covalent. Since the DNA nucleobases are aromatic molecules, they also exhibit stacking which stabilizes the structure of the DNA. A study by Yakovchuk et al. (2006) suggests that base stacking has higher contribution to DNA stability than base pairing. Sponer at al. (1997) found that there is no great difference between the stacking energies of B- and Z- forms of DNA helix.


Why we shiver/tremble/shake while performing some work which requires high accuracy? Shivering when nervous or anxious is a common thing.

But, shivering or trembling sometimes also occurs when we are performing a work which requires high accuracy. In such case, our whole body doesn't shivers but a part (usually hand) which is involved with that work shivers. The most common example is threading a needle. It requires great accuracy and you might have noticed that when you are doing so, your hands are continuously shaking which prevents you from accomplishing that task flawlessly. Even when we aren't in a state of nervousness, our hands tremble. It's un-resistable.

Yet another quick example - Try to stretch your one arm and try to keep it straight (have it loose, don't try to force it straight), you might notice that your arm is actually shaking a little bit. You can't hold it exactly straight without moving even a little bit.

It's also noticeable when we try to pin-point a small spot with our hand(finger) without actually touching it. (that finger and the hand as a whole starts trembling)

So, what's the reason? It isn't anxiousness as we shiver even when we are calm.
Perhaps, it's gravity which is pulling our hand down and we are trying to lift it continuously which creates a imbalance? But, then we should shiver always?

If you thread needles often - like a dozen times a day for many days - you will eventually be steady as a rock, because practice improves the process (you will also unconsciously maneuver to steady both hands.) It's not inevitable that all people have involuntary muscle movements with very fine motor skills; it's a matter of ability/practice for most.

The steadying of larger muscle groups like the upper arms - especially against gravity - is less controllable (e.g. threading a needle with arms fully extended), but not even closely outside the realm of possibility. Think of what great athletes, dancers, craftsmen are able to do that is "impossible" for mere mortals.


Why Can't The Immune Systems of Uncontacted Tribes Handle Our Common Colds? I'm sorry if this is a stupid question, I'm just starting my first year of a biomedicine degree and I'm curious - googling didn't find me any answers.

I know that the Aboriginal Australians and many other native peoples have been wiped out by diseases such as smallpox, influenza, the common cold, and malaria. A lack of immunity to our diseases is currently an ethical concern of contacting previously uncontacted tribes.

Seeing as we can't properly develop full immunity to the common cold - as it's always changing - but we manage to always fight it off, and (I think) our immune systems are all fundamentally the same, why can't their immune systems just quickly learn to handle something like the common cold? Can't they simply develop antibodies? Why does it become fatal when introduced to a new group?

Thanks!

I think your question stems from your assumption that different human populations share an immune system that is fundamentally the same. This is not the case. In fact, some of the greatest genetic variability in human populations can be found in the human leukocyte antigen (HLA) gene complex. The HLA genes codes for the major histocompatibility complex (MHC) proteins in humans. These cell-surface proteins are involved in regulating the immune system.

Different human populations have different levels of innate immunity to certain pathogens based on their historical exposure to different pathogens at different frequencies over evolutionary time.

I'm going to use the generic terms 'indigenous person/people' to refer to non-European indigenous people who encountered Europeans for the first time between the 15th-late 18th centuries. They can be Aboriginal Australians, Native Americans/First Nations, Amerindians, etc.

The primary reason that indigenous people were historically so vulnerable to European diseases is that the Europeans had been exposed to these pathogens for a long time, which led to them developing resistance to the pathogens. This is natural selection at work. The individuals most likely to survive were those with an immune system able to fight off those particular diseases.

Prior to European contact, indigenous people would never have encountered the pathogens that the Europeans brought with them, they lacked any immunity to them as a result. This allowed contagious disease like smallpox to spread quickly and kill a lot of people these groups.

You might ask why didn't Native Americans' diseases wipe out the Europeans when they came into contact with them?

One of the main reasons for that was domesticated animals. Europeans, by mainly the luck of the draw, had lived in close contact for centuries with a large variety of domestic animals, and thus, got exposed to a large number of species-hopping diseases, thus developing immunity. Native Americans had very few domestic animals, and got far less exposure.

References:
Riley E, Olerup O. HLA polymorphisms and evolution. Immunol Today. 1992
Sep;13(9):333-5. Review. PubMed PMID: 1361325.

Patterson KB, Runge T. Smallpox and the Native American. Am J Med Sci. 2002
Apr;323(4):216-22. Review. PubMed PMID: 12003378.

Markov PV, Pybus OG. Evolution and Diversity of the Human Leukocyte Antigen(HLA). Evolution, Medicine, and Public Health. 2015;2015(1):1. doi:10.1093/emph/eou033.

Guns, Germs, and Steel by Jared Diamond


Why is glycerol kinase absent from adipocytes but present in the liver? Why don't adipocytes have the enzyme, glycerol kinase? Wouldn’t it be more efficient for them to utilise glycerol present to synthesize triglycerides than to get it from the liver? So what is the advantage of its absence?

The short answer to this question is given in the Wikipedia article on glycerol kinase:

  Adipocytes lack glycerol kinase so they cannot metabolize the glycerol produced during triacyl glycerol degradation. This glycerol is instead shuttled to the liver via the blood where it is: phosphorylated by glycerol kinase to glycerol phosphate and/or converted to dihydroxyacetone phosphate which can participate in [glycolysis or] gluconeogenesis.

[My de-emphasis of glycolysis]

To understand this requires one to consider the different functions of liver and adipose tissue and how they should respond to the fed and fasted state. Then one can appreciate that the differences in enzyme complement are one of the ways by which this is achieved. (The other is their differential responses to hormones.)

The role of the adipose tissue is to store fat (triglycerides) in the fed state and make it available for the other tissues in the body in the fasted state.

The role of the liver is to divert metabolism to the synthesis of fat in the fed state (at the appropriate stage) and to ensure that there is a supply of glucose in the fasted state for those tissues that depend on it (brain, erythrocytes) or a supply of ketone bodies for the brain.

The substrates for triglyceride synthesis are L-glycerol phosphate and fatty acids. There are two enzymes that can catalyse its production, glycerokinase (glycerol kinase) in the liver and glycerol 3-phosphate dehydrogenase in both liver and adipose tissue, as shown in my diagram below:

Fed State

The liver has surplus glucose so it can switch to fatty acid production from acetyl CoA (from pyruvate) and generate L-glycerol phosphate from the dihydroxyacetone phosphate intermediate of glycolysis, catalysed by glycerol 3-P dehydrogenase. This allows the synthesis of triglyceride, which is exported as lipoprotein.

When the triglyceride reaches the adipose tissue it is broken down to fatty acids and glycerol by the hormone-sensitive lipase. The glycerol cannot be used by the adipose tissue, but adipose tissue can synthesize L-glycerol phosphate itself in the same way as liver as there is glucose available for glycolysis in the adipose tissue. Hence the triglyceride can be resynthesized and stored.

Fasted State

The hormone of starvation, glucagon, initiates the breakdown of triglyceride in the adipose tissue. As already stated, the glycerol produced cannot be used to synthesize L-glycerol phosphate as the tissue lacks phosphoglycerate kinase. In starvation uptake of glucose is prevented hormonally, so that there is no glucose for glycolysis and hence no hydroxyacetone phosphate as a source of L-glycerol phosphate. Hence the fatty acids cannot be re-esterified and are released into the blood for other tissues, i.e. the response of the adipose tissue to starvation is that required.

The glycerol diffuses to the liver where it can be converted to L-glycerol phosphate because of the presence of glycerol kinase. What is the fate of this? It is not converted into triglyceride, it is converted to dihydroxyacetone phosphate by the reverse of the reaction shown. This is not glycolysed, but converted to glucose by gluconeogenesis, the enzymes for which are present in the liver. The glucose is released into the blood where it can be utilized by the brain, i.e. the response of the liver to starvation is that required.

References

This answer is based on lectures I delivered to undergraduates some years ago, which were drawn from various sources. The problem is that most biochemical texts tend to be organism-agnostic, and any discussion of mammalian tissues tends to be limited. Thus, I can’t find much useful to refer to in Berg et al. on line, except for support in section 16.3 for my assertion that glycerol returned to the liver in starvation is used for gluconeogenesis. I’ll update this later if I find anything more useful.


Why did some animals evolve inward-slanted legs? Something I noticed looking at reference images is some animals have legs that are slanted inward relative to the length of their body, like in the two images below. Why have animals evolved this instead of having their legs pointing more straight down like lions or elephants?

Sorry no references other than illustrations for the moment.
If a running biped has it's feet further away from the line of gravity, then it's got less efficiency in forwards motion and more instability of the line of gravity falling left and right.
When you consider the kinetic downwards weight in kilos that goes into every step, a runner/sprinter who doesn't have aligned steps wastes a lot of energy.
here's are dinosaur footprints:
https://australianmuseum.net.au/Uploads/Images/7919/footprint%20comparisons_big.jpg
The hips joints tend to point sideways to give a strong musculature, lots of running muscle, and a wide base of more than 90 degrees, for a wide birth canal and other reasons.
So the tendency for efficiency of running bipeds is to have aligned footsteps and their hips tend to be a strong and wide base.
That's only the resting position, the walking angles actually vary a bit outwards and straight too, the knee goes outwards when it's rising.
https://cdn.pixabay.com/photo/2016/01/18/02/04/footprints-1145883_960_720.jpg
here is a comparison of ostrich and human bone angles: http://rsif.royalsocietypublishing.org/content/13/122/20160529


How does the Golgi Apparatus perform its function? The Golgi Apparatus is an organelle with a great number of functions, I am particularly intrigued in the role it plays in packaging macromolecules and sending them to their target organelle or to leave the cell in exocytosis.  I would love to know more about how this process works.  How does the Golgi Apparatus recognise which molecules are which and how does the vesicle it places the molecule into navigate to where it is needed?

This is actually is an awesome story: both how it happens and how it was discovered. This is one of those stories people get Nobel Prize, and this was Günter Blobel who was awarded this highest possible prize for his discovery, which is according to his Nobel prize certificate:

  "for the discovery that proteins have intrinsic signals that govern
  their transport and localization in the cell"

If you watch or read his Nobel prize lecture you will find answers to your question formulated much better than I can do it here. His Nobel lecture was opened with the following words which might already answer you question:

  Imagine a large factory that manufactures thousands of different items
  in millions of copies every hour, that promptly packages and ships
  each of them to waiting customers. Naturally, to avoid chaos, each
  product requires a clearly labeled address tag. Günter Blobel is being
  awarded this year's Nobel Prize in Physiology or Medicine for having
  shown that newly synthesized proteins, analogous to the products
  manufactured in the factory, contain built-in signals, or address
  tags, that direct them to their proper cellular destination.

Still, I recommend you to read (or watch) to the end, there are some interesting points on how it was discovered and what experiments were done to do it.


What arthropod is in the picture? I am from Philippines and I found this in my room.
This arthropod has 6 legs and have a bit long Chelicerae like spiders that can fold to hold its food. It's about half an inch long. It also looks like a
scorpion but I could not find anything like it on the internet. Thank you!
I've also noticed that it can jump and it also produced spider silk.

It is not a pseudoscorpion as those would have 8 legs and then the two front large pincers. This is most likely a kind a jumping spider where the two large front legs count as two of the 8 legs.
Depending on your geography (not given in the question), this looks to resemble a jumping spider in the genus Chalcolecta (or some regional variant of that based on where you are). Hard to see any detail (like eyes and body segments) from your photos. But have a look at some of these and see if any of them match your specimen. Here are some pics of C.prensitans and C.simon.


Why mosquito bite is confined to a certain shape? I think this problem should be asked in a physiology forum rather than biology@ stackex but I'll give it a try.
So my question is simple - why a mosquito bite is usually confined to a certain shape (shape = red area) and not just disappearing continuously? Can our body cells tolerate some level of antigens without changing color from that?

What you're referring to as a mosquito bite is actually the "wheal" (red swollen bump in the skin) that forms from an immune system reaction to antigens (foreign molecules) in the saliva of the mosquito that it leaves behind inside the bite.  It's not technically a toxin, just something that causes an immune reaction.

It's also not an infection, it's inflammation.  Infection might set in if the skin is scratched open and bacteria move in.

The reason it's red is that immune cells release cytokines (like histamine and that cause cause edema that leads to swelling, heat, itching, etc - and recruit other cells to do the same.

The cytokines that act locally have a range of effect, especially histamine.  The degree of immune reaction determines the size of the wheal and how long it lasts.  Scratching it contributes to irritation and can prolong resolution.  Scratching it open can lead to infection.


iPSC in drug discovery Pluripotent stem cells are very popular and lots of research has been conducted to use these cells as a tool for drug discovery. My question is how many years would it theoretically safe is we could use iPS cells during the process of drug discovery?

People are doing small molecule screens with stem cells right now (albeit embryonic stem cells). Probably a lot more screens of that kind are in progress behind closed doors in the pharmaceutical industry, and we can expect iPSC culturing to get better and cheaper, so sometime in the next decade we'll see them become a common model.

iPSCs will probably be an improvement on existing cell culture models, and will also allow things like the creation of cell lines for specific genetic diseases, but they wont' be a quantum leap forward for drug discovery in general.


Do animals only breathe through one nostril at a time like humans? Humans breathe through one nostril at a time.

Do non-human animals also do so, or do they breathe through both nostrils at once? Has any actual study been conducted on this topic?

The post linked by @Remi.b says

  The nasal cycle is a natural ultradian cycle (see here and here. Not only is it present in humans, the nasal cycle has been observed in rats, rabbits, domestic pigs, cats and dogs (see references in Eccles 1996).

Proceeding to Eccles 1996 (p. 372):

  The nasal cycle is not only limited to the human nose, as it has been found in the rat and rabbit [31], the domestic pig [32, 33], the cat
  [34] and the dog [35], and appears to be a universal phenomenon at least in all mammals and possibly other animals.
  ...

  Bojsen-Moller F, Fahrenkrug J. Nasal swell bodies and
  cyclic changes in the air passages of the rat and rabbit
  nose. Anat 1971; 110: 25–37.
  Eccles R. The domestic pig as an experimental animal
  for studies on the nasal cycle. Acta Otolaryngol (Stockh)
  1978; 85: 431–436.
  Campbell WM, Kern EB. The nasal cycle in swine.
  Rhinology 1981; 19: 127–148.
  Bamford OS, Eccles R. The central reciprocal control
  of nasal vasomotor oscillations. Pflügers Arch 1982;
  394: 139–143.
  Webber RL, Jeffcoat MK, Harman JT, Ruttimann UE.
  Demonstration of the nasal cycle in the beagle dog. J
  Comput Assist Tomogr 1987; 11: 869–871.

A Pubmed search for '"nasal cycle" animal' gets a total of 18 hits, including refs 32 and 35 above, as well as

  Spontaneous nasal oscillations in dog. A mucosal expression of the respiration-related activities of cervical sympathetic nerve. Asakura K, Hoki K, Kataura A, Kasaba T, Aoki M. Acta Otolaryngol. 1987 Nov-Dec;104(5-6):533-8.
  Proceedings: Studies on the nasal cycle in the immobilized pig. Eccles R, Maynard RL. J Physiol. 1975 May;247(1):1P.

A bit more digging forward & backward through citations finds the article on cats (also by Eccles):

  R. Eccles & R. L. Lee (1981) Nasal Vasomotor Oscillations in the Cat
  Associated with the Respiratory Rhythm, Acta Oto-Laryngologica, 92:1-6, 357-361, DOI: 10.3109/00016488109133272

You might find more if you poke around (Google scholar/Pubmed, look at citations backward & forward, try search terms like "'nasal cycle' bird" or "'nasal cycle' reptile"), but at this point I doubt that anyone's bothered to check this in non-mammalian animals ...


What are the short/long term effects of chloroquine on fundamental cell processes? Does chloroquine, which affects the endosomal membrane traffic pathway (by affecting the acid environment used for fundamental endosomal reactions), have short/long-term effects on cell growth/proliferation/signaling?

This paper provides many experiments about changes to the endosomal system and autophagy and should be a good starting point.
Most of the treatments are done in the 5h to 24h range typical for cell culture studies. In theis relatively short time frame Chloroquine is well tolerated by cells. However, long term treatment will very likely be different.


Correlation between threat and odour, taste Is there any sort of correlation between threat and taste/smell?
Are we evolved such that things which are harmful to life taste and /or smell bad and things(food) which are useful to us taste, smell good?
How far this conjecture correct?

The compounds that smell bad to us are often the same ones produced by the anaerobic metabolism of bacteria, such as hydrogen sulfides or butyric acid. These types of compounds are the ones that make excrement and rotting food smell bad, and if something is giving is giving off a lot of them it's a pretty good signal to not put it in your mouth. Vomit also has quite a lot of butyric acid in it, so we may be particularly sensitive to it.

Plants produce toxic compounds to stop herbivory, many of them taste bitter. Alkaloids are often toxic and uniformly bitter, terpenoids are another example.

There's nothing obviously different from a chemical perspective in chemicals that smell bad. Butyric acid is just a 4 carbon chain with a couple of oxygens on the end and reeks, while the compound propanediol (which is 4 carbons with an oxygen on each end) is used in deodorants. If a compound has a strong smell or taste to us, it is because that compound has been important to us during our evolution. That doesn't mean it's a perfect indicator; cheeses can stink and be totally edible, but that's because the compounds in that cheese usually are a sign of something dangerous.


where to find the relative frequency distribution of synonymous codons Most amino acids can be encoded by more than one codon. For example, Serine can be encoded by any one of {UCU, UCC, UCA, UCG, AGU, AGC}.

My question is in two parts:

1) what are the relative frequencies of those codons? This question can be equivalently phrased in probabilistic terms: What is the probability that a given amino acid was encoded by particular codon?

2) Is this probability dependent on the context (the neighboring codons/amino acids)?

The phenomenon of using different codons with different probabilities is called codon usage bias. How the different codons are used is sometimes pretty different between species and requires some care. This is especially true when you want to overexpress sequences in bacteria to produce protein, which may need codon optimization to ensure an optimal codon usage (otherwise rare tRNAs can slow down the translation process). There is a database (based on the NCBI Genbank) which gives you the codon probabilities for different species:

Codon Usage Database

Additionally, these papers might be interesting:

Synonymous codon usage in bacteria.
An evaluation of measures of synonymous codon usage bias.

Regarding your second question, I don't think (and I haven't found any evidence either) that the codon usage is dependent on the neighbours.


Which of the response is faster? voice or hand action? After taking certain stimuli and making the the decision to do certain action, which one response (output) (out of 2 possible output-ways, voice and hand-movement) would act faster?

For example lets say I'm playing a car video game that can be controlled by voice.

If i say "left" it will turn left and so on.

If I'm controlling that car by hand then I could just steer to the left.

So, if i'm not considering energy required for hand to move and all.

Which will get the signal to my brain faster, my mouth or my hand?

Assuming that we are talking about a situation at the physical limit of the brain:

Speaking a word will always be slower than pushing a button.
A whole word requires a contraction of the diaphragm to push out air so this air can be modulated by another sequence of contractions and relaxations of the vocal chords.

So contracting finger muscles is very similar to speech initiation however for a computer to respond (in the example you were playing a video game) the computer needs to recognize the full word and then map it to an output before actually implementing the left turn.

So adding the extra processing time of the computer and the actual extra production time of the vocalization you're better off pushing buttons.

As a matter of curiosity if the physical limit situation is relaxed; whenever there is a mismatch in both sensory receptors as well as outputs, the brain does its best to compensate. Think of something dropping on your foot, the visual information is actually delayed so that the sensory stream (that has to go up all of your leg and spine) catches up.


What is the formula to calculate $R_0$ (basic reproduction number)? What is the mathematical formula for $R_0$ and what does each variable represent?

I have tried searching this to no avail.

$$R_0 ∝ \left(\frac{\text{infection}}{\text{contact}}\right) · \left(\frac{\text{contact}}{\text{time}}\right) · \left(\frac{\text{time}}{\text{infection}}\right)$$

  More specifically:

  $$R_0 = τ · \bar{c} · d \quad \quad (1)$$

  where $τ$ is the transmissibility (i.e., probability of infection given contact between a susceptible and infected individual), $\bar{c}$ is the average rate of contact between susceptible and infected individuals, and $d$ is the duration of infectiousness.

Notes On $R_0$ (2007)

Further reading:

https://en.wikipedia.org/wiki/Basic_reproduction_number
Complexity of the Basic Reproduction Number (R0), emerging Infectious Diseases (2019)
Theory versus Data: How to Calculate R0?, PLoS One (2007)
The R0 package: a toolbox to estimate reproduction numbers for epidemic outbreaks, BMC Medical Informatics and Decision Making (2012)


Why does chewing enrage me? Whether it's snacking on chips, munching on salad, or simply chewing gum, when I hear someone do it within an earshot, it drives me completely bonkers!

It doesn't matter if it's my girlfriend, my mom, someone sitting next to me at the office, or random stranger on the train, it bothers me just as much. The "mouth open" chewing type makes me want to get violent, and I often find myself in a blind rage. I also notice the slower, and more "deliberate" the chewing/munching is, the more I get tense and more it bothers me.

Sometimes I feel like they are doing it on purpose, and completely fake, sort of like a commercial where they exaggerate the act of eating.

I want to know more about Misophonia or "Hatred of Sound"?

Misophonia

  Misophonia is a relatively unexplored chronic condition in which a
  person experiences autonomic arousal (analogous to an involuntary
  “fight-or-flight” response) to certain innocuous or repetitive sounds
  such as chewing, pen clicking, and lip smacking. Misophonics report
  anxiety, panic, and rage when exposed to trigger sounds, compromising
  their ability to complete everyday tasks and engage in healthy and
  normal social interactions.1

Physiology

The auditory pathways may be functioning normally, but there is an abnormally strong reaction of the limbic (emotional system) and autonomic nervous system (body control system) to which the auditory system is intimately connected.

Several definitions are listed for the disorder, including:

“Abnormally strong negative reactions of the autonomic and limbic systems to specific sounds resulting from enhanced functional connections between the auditory and limbic systems for these sounds.  The auditory system works in a normal manner, without abnormally high activation.  At the behavioral level, sounds specific for a given patient evoke strong negative reactions.  This situation may cause general negative attitude to sound as well.  When fear is dominant emotion (patient is afraid of sound) phonophobia occurs (phobia – fear).  Phonophobia is a specific case of misophonia.”
“Selective sound sensitivity should be considered a type of misophonia, where soft sounds (typically eating and breathing sounds made by emotional attachment figures) are the focus, and the quality of those sounds causes annoyance and rage in the listener.”

“Pre-puberty seems to be a very common age of onset for the majority of those with misophonia, with lifetime persistence for most cases, and there appears to be a genetic component.”
“Misophonia can be considered abnormally strong connections between the autonomic and limbic resulting from enhanced connections between the auditory and limbic systems.  These connections encompass both a high level of cortical level loop with involvement with cognition as well as subconscious connections, most probably involving the link between the medial geniculate body and the amygdale. The functions of these connections are governed by the principles of conditioned reflexes.”

source:

1 Misophonia: physiological investigations and case descriptions
[2] MISOPHONIA 4S Provider Network USA

Great Site: http://lifewithmisophonia.wordpress.com/


About the quality of microsatellites I built a script to detect microsatellites in a FASTA file. However, there are thousands of possibilities.
So, my question is:

what are the markers of a "good" or "useful" microsatellite?
- How many base pairs, how many repetitions?

And, are there any other heuristics that can be run to further detect usefulness of the microsatellite?

thanks.

Try running software like Censor. If checks in the reference repeat databases and detects microsatellites. So, you can most probably be sure of the microsatellites generated. Moreover, the microsatellites have their information present in the GIRI database. So, you can get more information, if you find the microsatellite in your sequences. Hope this helps.

~Rama.


In humans, are diseases inevitable during old age? Considering that dying "from old age" actually means that one dies from an illness related with aging, is it inevitable to eventually acquire diseases in old age?

There is a thought that aging itself should be considered a disease. In which case, death by disease is inevitable with our current level of medical technology.

  During the last 25 years, by targeting the underlying processes of aging biomedical scientists have been able to improve the health and lifespan of model organisms, from worms and flies, to rodents and fish. We can now consistently improve the lifespan of C. elegans by more than ten-fold (Ayyadevara et al., 2008), more than double the lifespan of flies and mice (Bartke et al., 2001; Sun et al., 2002), and improve the lifespan of rats and killifish by 30 and 59%, respectively (Valenzano et al., 2006; Zha et al., 2008) (see Figure Figure11 and Supplementary Table 1). Currently, our treatment options for the underlying processes of aging in humans are limited. However, with current progress in the development of geroprotective drugs, regenerative medicine, and precision medicine interventions, we will soon have the potential to slow down aging (Bulterijs, 2011, 2012).


How does a new species survive without suffering inbreeding? Just what the title states. The thought came from reading When has an organism evolved enough to be called a new species?

I'm probably wrong but I understand new species happen sporadically rather than in whole-sale lot during breeding season. Is the new species capable of breeding with members of its parent species? How does a new species survive inbreeding initially?

Well, speciation is a process, not a single event thing.

Usually what happens initially is geographic isolation of some members of a species, so in that sense the inbreeding is something that is influencing and you can also think of it as causing the speciation process. The presence of special harmless or semi-harmless disadvantagious mutations - which increases in frequency from this isolation - influences how the species is going to evolve, but eventually shapes this species to better cope adapt to some environment, or evolves the new species out of existence.


flavivirus virus genome, methylated guanine I'm looking at the sequence of a flavivirus virus genome (mRNA). Kindly see the link MH900227.1. How can I identify the Guanine nucleotide that is methylated in the capping process?

Thanks,

Why do you think the methylated G is present in these sequences?

I have two reasons for thinking your question isn't answerable.

As I said in my comment, based on BLAST results I don't think your sequence is complete — it appears to be missing the 5' end.
If the 5' end is missing then the end that gets capped is missing.

The 5' cap gets added post-transcriptionally and has a linkage (5′–5′ triphosphate) that prevents it from being sequenced.
That means that sequencing reaction don't see the G that gets methylated in the 5' cap.
This is why I suggest that you make sure you understand the capping process.


Can I make an population genetic analysis from incomplete protein? I have an dataset of fasta sequences. This proteins are not complete (My sequences have 700 nucleotides,while complete sequences have 1725 nucleotides)I would like to know if i can make an population genetic analysis from it(like TAJIMA-D test) and similars.

It very much depends upon what type of analysis you want to perform. For a Tajima's D, all you would need is a single nucleotide sequences in a sample of individuals, so yes you can. Whether or not the sequence came from a gene or any other sequence is not relevant to whether you can compute Tajima's D (although the type of sequence will likely affect the resulting D).


How to download different kinds of data from NCBI eutils? I have been researching NCBI eutils and wish to get some 'big data' from it. I know that I can construct queries to query one of (I think) 8 databases, like this:

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/einfo.fcgi?db=nucleotide&id=2765657

which queries the nucleotide database for an id 2765657.

I am looking for a query that will return:

genetics sequences.
functional annotations of the sequences (e.g. exons, introns)
metadata (e.g. chromosome)

Would anyone be able to show an example of how to search the eutils to get samples of records as described above?

I would need to know:

Which database to search?
how to list available records?
how to query for a sample of the records?

Any help would be greatly appreciated.

Many thanks.

Downloading all this using an E-utils search would be cumbersome as you would have to search against multiple databases. For your specific needs, a GTF/GFF3 file would be good. Basically, a GTF/GFF file has genome annotations (positions of features) and includes features like exons, CDS and in some cases even special codons (such as that for selenocysteine). This file would not have the sequences but you can retrieve the sequences from the corresponding genome sequence fasta file using the co-ordinates described in the GTF file. There are several software tools that can do this; for example gffread and bedtools-getfasta (you can even write your own script which would not be very difficult).

You can download the GTF and the corresponding genome fasta files from these sources:

ENSEMBL (many organisms)
NCBI-RefSeq (many organisms)
UCSC genome browser (many organisms)
GENCODE (for human and mouse) and modENCODE (for Caenorhabditis worms and Drosophila)

You should look at the details of the genome assembly. Different releases/sources may have different extents of curation.


Are there dichotomous keys for identifying medical conditions? I know dichotomous keys are often used to identify flora and fauna.

I was wondering if they are also used in medicine for identifying diseases -- are they? If not, why not?

For histopathology they use them all the time to describe cells and tissues, very much as they are used to describe biological entities.  Characteristics like size, cytoplasm to nucleus ratio, grouping, staining characteristics, immunohistochemistry and now molecular attributes are all used to categorize a cell of interest.  For cancer, the identity of the malignant cell is crucial to diagnosis and subsequent effective treatment - based on successful treatments used in the past for people with that type of cancer.

Here is a histopathology dichotomous key I found at Noelways.com


Name (and meaning of the absence) of the white semicircle at the base of the fingernail? At the base of fingernail, there is a white semicircle (see on the first picture). But sometimes there isn't one.

My questions are: what is this white semicircle on the fingernail, and what causes it? What is the explanation when there it isn't on all of the fingernails (see on the second picture)?

The lighter crescent-shaped part at the base of the nail is called the lunula. It is a normal part of the nail matrix, and indicates nail growth. The faster your fingernails grow, the more obvious the lunula.

Absence of the lunula without any other abnormalities of the nail is not uncommon, and while it can indicate anemia or malnutrition, it is often found normally, and with aging. In this case, careful inspection of all the nails will usually reveal a lunula on the thumbs and the fingers closest to the thumb, but a very small or absent lunula on the other fingers.

In your picture, there is clearly a lunula on the middle finger, and, I suspect, a larger one on the index finger, and a relatively normal one on the thumb. This is not a finding of great concern in the absence of other pathology.

  The lunula: The small, whitish, half-moon shape that you sometime see at the bottom of your nails is called the lunula(pronounced loon-yoo-la). It's actually part of the matrix. You might be able to see it only on your thumbs, or maybe not at all. Don't worry if you can't see a lunula on any of your fingers. It's no big deal. It's there, just under your skin.

Examining the Fingernails When Evaluating Presenting Symptoms in Elderly Patients
Examining the Fingernails
Nails


How is the size of a gene defined? Is there an agreed definition as to how many nucleic acid bases constitute a gene?

If not, why not? I'm not sure I understand how the exact sizes of genes are defined.

Is there an agreed-upon definition as to how many nucleobases constitute a gene?
If not, why not?

There is no such definition. A gene is a region of the DNA that is transcribed. Typically a gene should have a transcription start site dictated by a promoter and a transcription stop site marked by termination signals (like terminators and poly-A signal etc.)
There are some little RNAs (~18nt) that are produced from TSS of usual genes but are probably products of failed elongation. These are not really considered genes as they are heterogeneous in size and are not marked by any boundary.
There may technically be a minimum cutoff on gene length which could be the length of DNA necessary for the RNA-polymerase to sit and also include the termination signals. As indicated in the comments, the smallest gene may be the tRNA. However, the smallest annotated gene from the GENCODE annotations is TRDD1 (just 7nt long!!!). This is not based on gene prediction; it is manually annotated by the HAVANA team.

What is the average length of a gene?

I just did a rough calculation from the GENCODE human genome annotation file (version 23).
The average transcript length seems to be around: 1.5kb
The average gene length seems to be around: 29kbp
The genes would be longer than (or equal to) their corresponding transcripts because the latter gets shortened due to splicing.
I made a histogram plot of these lengths for convenience:

Transcript length distribution

Gene length distribution

Note the sharp peaks at 100bp. Quite interesting!

Remi has user19099 have mentioned that the longest gene in humans is titin. It seems that it is the longest gene in many other diverse animals. See What's the longest transcript known? for more details.

Methodology (so that limitations can be identified)
To calculate gene length distribution: I parsed the GTF file for "genes" (third field i.e. feature) and subtracted the fifth field (stop) from fourth (start).
To calculate transcript length distribution: Got the transcript fasta file from the annotated locations. Calculated their lengths. Plotted the distribution.


Standardized Selection Ratio (SSR) In this article the athors used the Standardized Selection Ratio (SSR) in order to infer what is the preferred host (anemone) of anemonefish.

Here is a quotation coming from their methods:

  The “preferred host” of anemonefish was assessed calculating the “Standardized
Selection Ratio (SSR)” (values between 0 and 1) (Manly et al. 1993). Manly’s standardized
selection ratio represents the probability that an individual will use a particular habitat
type, taking into account the different resource availability. For each anemonefish species (i) inhabiting an anemone species (j), SSR was calculated as:

$$SSR = \frac{wi}{\sum{}{wj}} $$

where $wi = \frac{oi}{pj}$

    `Oi` is the relative frequency of the anemonefish species i and `pj` the relative frequency
of the anemone species j. Higher values of SSR indicate a strong preference for the
selected resource. The Log- Likelihood statistic (χ2L) (Manly et al. 1993) was used to
check the significance of the observed distribution under a null hypothesis of a random
host choice.

Here is the book they cite (Manly et al. 1993).

Can you help me understanding basically what they did and how they calculated their SSR and p.values. If $wi = \frac{oi}{pj}$ what does wj equals to?

I can see why you might be confused! The authors chose bad notation, since the way they wrote it $w_i$ clearly depends not just on the choice of anenomefish species $i$ but also on the choice of anenome species $j$. And it is not clear how exactly they are performing their sum in the definition of SSR: sum over all possible anenome-anenomefish species pairs or only over all anenomefish species? The former makes sense but is extremely unclear, and the latter doesn't make sense because there's no way to interpret that as a probability that an anenomefish will choose a particular anenome because the sum of the SSR for all the different anenome species would not necessarily be 1, so the probability of an anenomefish species choosing some species of anenome would not be 1!

NOTE: The reference to Manly 1993 was incorrect (you cited a 1995 paper); they actually cite a book: Manly B, McDonald L, Thomas D (1993) Resource selection by animals. Statistical design and analysis for field studies. Chapman and Hall, London. This would probably be the best place to look to get an exact answer to your question. I think that would be the best place to look first.


Wild bee hive indoors - can I move it? Wild bees decided to build their hive in my shed, right above the table where I work on occasion.

The image is rotated 90 degrees left.

It started out as a single bee from what I could see two weeks ago. I thought fine, we won't bother each other and I like the company. But now two weeks later the bees are busily constructing and it is quickly growing larger. It started with a smallish dome, and new layers are being added from the outside. Every now and then a drop of some fluid falls out of the hive, and also small black grains, perhaps bee poop? Any ideas what these are?

Anyway, I have no idea how big this hive will become, so it is is probably a good idea to move it (it is around 15 inches from my head ;-)). Any suggestions?

Those aren't bees, they're a kind of paper wasp. As you observed, they start small and seem innocuous at first, but be warned, as the nests grow in size, the inhabitants become more protective of their nest and are more likely to see you as a threat to attack than as a peaceful cohabitant (at least this has been my experience.)

  Nest construction starts in late spring and continues throughout the summer. The last brood raised includes males and next year’s queens. Due to the importance of these reproductives, the worker wasps become very protective and aggressive toward those who venture too close to the nest this time of year.

Somehow we seemed to have a number of attractive habitats for paper wasps (and mud wasps) and had to deal with them when too large or in a dangerous place (e.g. in a door frame.). A honeybee relocation service will do you no good in this situation.

You have a few options to consider, I recommend sooner than later. First, at night and while wearing protective clothing and gloves, you can simply whack the nest off at the base and run away as quickly as possible); Plan/clear your escape route in advance! Stay away for a couple of days as it often takes this long for them to completely abandon the young inside. If these are bald-faced hornets, their sting is quite painful, much more so than a bee or a yellow-jacket.

Or, if this doesn't bother you (it does bother me), you can light the nest with a burning roll of paper (it is, after all, paper, and will burn quite rapidly. The 'good' part of this is that the flame usually destroys the wasps' wings as well, and they're less likely to be able to attack you. This is best done on a cool night after all or most activity around the nest has ceased. The fire flares brightly and burns the nest very quickly without setting fire to adjacent structures, but a fire extinguisher should be kept nearby just in case.

Third, you can buy a spray, but I found them to be ineffective against the kind of paper nest shown in your picture, because the envelope protects the wasps inside. I used up two large cans of foaming spray (in spite of hating insecticides, as it wasn't a spot I could safely whack) without any obvious result. I ended up doing multiple whack-and-runs.

Finally, you can hire a professional, something I never did in my 28-odd years of dealing with them, but which is often recommended.

Yes, it's probably poop.


What are the advantages of blood's redness? Although this page (http://evolution.berkeley.edu/evosite/evo101/IIIE5aNotadaptation.shtml) denounces the idea that blood's redness is not an adaptation, I remain inquisitive on the matter since no scientific research has been performed in studying its possible advantages.

Does anyone have any ideas on the advantages of having red blood?

Thank you for your time and effort

The reason why blood is red is rather simple: It is the iron atom in the middle of the heme, which plays the central part in binding oxygen. Depending on the oxidation state the blood looks either dark or light red. The structure is the following (taken from here):

That the color only depends on the coordinated metal atom is shown by another related molecule, the hemocyanin, which is the oxygen carrying molecule in the hemolymph of insects. It contains copper which is colorless in one oxidation state and blue-green in the other. The function is the same, the color is different.


How is gene expression estimated? I'm reading this fantastic article on estimating body time: Molecular-timetable methods for detection of body
time and rhythm disorders from single-time-point
genome-wide expression profiles and one of the things that is not very clear to me is how the researchers estimated which genes are expressed and which ones are not:

  Total RNA was prepared by using Trizol reagent (GIBCOBRL). cDNA
  synthesis and cRNA labeling reactions were performed as described (5).
  Affymetrix high- density oligonucleotide arrays (Murine Genome Array
  U74A, Version 1.0, measuring 9,977 independent transcripts) were
  hybridized, stained, and washed according to the Technical Manual
  (Affymetrix). Affymetrix software was used to deter- mine the average
  difference (AD) between perfectly matched probes and
  single-base-pair-mismatched probes. The AD of each probe was then
  scaled globally so that the total AD of each microarray was equal. The
  resulting AD values reflect the abundance of a given mRNA relative to
  the total RNA popu- lation and were used in all subsequent analyses

I'm not sure if I'm reading this correctly - did the researchers look at all RNA available in the cells and calculated the levels of messenger RNA produced by expressed genes? if not, how can the level of expression of a gene be estimated?

The technique described here is called microarray. Your question has given me an opportunity to put forth one of my opinions about certain problems of gene expression studies.

Gene expression is a measure of the activity of any gene. If the gene performs its activity in the form of a protein, then its expression should be a measure of the protein. If a gene makes a non-coding RNA then its expression is a measure of the RNA concentration.

[You can omit the cases of post-translational modification because of signal transduction. They are highly expressed and transiently but frequently used. ]

Like your example there are many studies which use mRNA concentration as a proxy for protein activity. This proxy works in many cases because transcriptional gene regulation is more frequently used mechanism for imparting stable changes. But the best strategy would always be to measure the proteins also.

Apart from microarray there are several techniques to measure RNA concentration:

RNA sequencing (high throughput)
Real-Time PCR (medium throughput)
Northern Blotting (Low throughput, semi-quantitative)

Many techniques exist for measuring proteins also:

Mass spectrometry (high throughput)
ELISA (Low throughput, quantitative)
Western blotting (Low throughput, semi-quantitative)

Usually the "proxy method" is used because protein quantification is comparatively more difficult. Antibody based techniques like ELISA and Western blotting have problems of cross comparison of proteins because of the variability of the antibody binding efficiency.


Is fucus filamentous or colonial algea? Am a bit new to biology SE. My question is wether fucus is filamentous or collonial form of algea?Does a form of algea have to be collonial or fillamentous or it can be something else?
https://en.m.wikipedia.org/wiki/Fucus_vesiculosus

I would suggest looking up some basic sources on types of algae. For example, that source that I link to says this:

Algae vary considerably in size, shape, and growth form.
They can be:

Single celled
Many celled - either colonially or as filaments of cells; or
Elaborate plant bodies with differentiated cell types

In this case, I believe that Fucus would be in the third category ("elaborate plant bodies").
But note that these are informal categories, they don't really correspond to taxonomy or evolution or anything.


Doubt in a multiple choice question involving cell organelles Find the odd one out and state the category of the rest.

  Chloroplast
  Mitochondria
  Nucleus
  Grana

Now my answers are :

1st possibility : grana

Category : presence of DNA in others

2nd possibility : grana

Category : all others are cell organelles

Are their any more possibilities and are my answers reasonably correct?

I would say Nucleus is the odd one out. Chloroplast (which have Grana in them) and Mitochondria are involved in the process of creating/breaking down energy, whereas the Nucleus is, so to speak, the blue-prints of the cell.

To summarize:

Chloroplast is involved in Photosynthesis to create energy

Grana are in the Chloroplast, which is involved in Photosynthesis

Mitochondria are "the powerhouse of the cell" and help break down energy (ATP > ADP)

Nucleus is the cell's blue-prints

Therefore, it seems that the Nucleus is the least like the others.


How do you define a gene list? So I wrote in a chapter that I will be checking for publications with gene lists in them. I got a comment asking "How would you define a gene list and what criteria did I use". I know that gene lists are usually generated by microarray studies, NGS analysis etc but what is the best way to define a gene list?

I am running blank except maybe say that its a list of genes.

EDIT: "I defined a gene list as a list of genes generated as a result of a microarray analysis or a next generation sequencing study." Sounds good?

The comment seems useful as your current definition of a gene list lacks context.

  How would you define a gene list?

There are many different kinds of gene list. Specifying gene lists from microarray and next-generation sequencing provides some context but both technologies are used to analyse many different kinds of DNA and RNA samples. Define the molecules that are being referenced by the gene lists.

Defining DNA or RNA isn't sufficient as each gene list is compiled to perform a research task. Genomic projects may provide lists of genes that were sequenced or mutated or contained single nucleotide polymorphisms. An RNA transcript project may create lists of genes where transcription was occurring in a tissue or whose RNA transcripts were influenced by experimental factors or whose splicing was altered. Most publications also include multiple gene lists and some of those will include rows that were removed following data evaluation. Define the kind of lists that you are collecting.

There's value in defining your search criteria well. It allows you to communicate your work to others and it can provide focus to your search efforts.

  What criteria did I use?

This was mostly answered above. I would also consider including some rules for the publications that you will search for gene lists.