What is a functional screen? I was going through this paper, but did not understand a term.
What is the meaning of functional screen?

(I am not a biology student, I don't understand much, and a small simple explanation would be enough)

From the abstract of the linked article (Guttman, 2002):

  We used an in vivo genetic screen to identify 13 effectors [...]. Although sharing little overall homology, the amino-terminal regions of these effectors had strikingly similar amino acid compositions.

And from the body:

  The screen relied on the type III secretion signal and the endogenous promoter of the hop gene and was thus highly specific.

Hence, the authors search and identify proteins with a secretory signal under the regulation of a hop promoter. A functional screen in this paper refers to the analysis of protein samples to detect the presence of proteins with a particular function.


Yeast Strain with squalene synthase / farnesyltransferase (ERG9) gene deleted I was interested in obtaining a yeast strain without the enzyme farnesyltransferase (Which catalyses conversion of FPP to Squalene). The Euroscraf database has thousands of yeast strains with individual genes deleted but when I search for "farnesyltransferase" I get a couple of hits that I am not being able to interpret.

Here's the link: http://www.euroscarf.de/search.php?search=farnesyltransferase&project=

What are all these different strains? In particular how does one interpret notation like which seems to be describing a particular strain:

BY4743; MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4

Yeast strains have two mating types MATa (since it secretes a pheromone named 'a factor'), MATα (secretes pheromone 'α factor'). Both MATa and MATα strains are haploid and when they fuse together they form diploid zygote. A haploid yeast has only one set of genes and utilize chemicals like histidine and tryptophan (amino acids) and adenine (part of DNA, ATP and other molecules) for growing. Yeast strains mutant with any of genes to
make these chemicals they will not grow unless they can get these chemicals from their food (yeast media) or allowed to mate with strain having normal genes.

Interpreting the strain notation:

BY4743; MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; Met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4

Strain name: BY4743
Genotype: MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; Met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4

To understand clearly, you can dissect the genotype in individual strains

BY4743;MATa;ura3Δ0;leu2Δ0;his3Δ1;met15Δ0;LYS2;YKL019w/YKL019w

BY4743;MATα;ura3Δ0;leu2Δ0;his3Δ1;MET15;lys2Δ0;kanMX4

Yeast genetics nomenclature:

Normal or wildtype genes are written in capitalized form - MET15 in MATα
Mutated genes are symbolized with small letter and Δ - ura3Δ0
ura3Δ0/ura3Δ0 - allelic mutation:  mutation in same genes of both strains (MATa/MATα) - They are two mutant alleles in the same gene locus. Both alleles of same gene are knocked out, so even both strains mate, they need external source of uracil in media to grow. Defect in one strain is NOT complemented by the other.
Met15Δ0/MET15 & LYS2/lys2Δ0 - Non-allelic mutation: Defect in one strain is complemented by the other. MATa has Met15Δ0 (mutation in methionine gene) and MATα has wildtype MET15 gene, capable of met synthesis. Complementation works here.
YKL019w/YKL019w::kanMX4 - Critical aspect of yeast strain in functional complementation assays. In all commercially available yeast strains, one gene will be double knocked out (both alleles of same gene) and replaced with an auxotrophic markers like antibiotics - tetracycline, kanamycin, ampicillin - for selecting the diploid cells after mating two strains. It is similar to plating Kanamycin mixed LB media to pick E.coli colonies harboring Kanamycin resistance vector in it.

The gene that is replaced is the gene of interest, i.e. if I am looking to study role of putative PGPS in Plasmodium falciparum, I get yeast strain knocked out with yeast PGPS (pgsΔ). When I do complementation test, I provide external DNA template cloned with Plasmodium falciparum's PGPS to check whether it complements in yeast genome and yeast grows - gene essentiality study.

I am not sure of the gene YKL019w/YKL019w, but it implies that wildtype of YKL019 is replaced with Kanamycin - kanMX4.


How does cancer of the larynx (laryngeal cancer) affect the respiratory system? The larynx is part of the respiratory system and is responsible for producing sound (our voices). My question is how cancer in the larynx (voice box) affect the respiratory system overall? I appreciate any answer, but if it's not too inconvenient, please don't use too complex terminology (I'm in grade 10 Canada).

Thanks

According to this website:

http://www.spirometry.guru/fvc.html

it causes difficulty with inhalation but exhalation is normal...

  "Typically the expiratory part of the F/V-loop is normal: the
  obstruction is pushed outwards by the force of the expiration."
  "During inspiration the obstruction is sucked into the trachea with
  partial obstruction and flattening of the inspiratory part of the
  flow-volume loop."

the exact symptoms of a laryngeal tumor depends on where it is located on the larynx... above the vocal cords, on the vocal cords, or below the vocal cords...

but more generally:

anatomy:
mouth/nose-->pharynx-->larynx-->trachea-->bronchi-->lungs

a tracheostomy may be necessary... basically the surgeon makes a connection between the skin outside the throat and the trachea... this bypasses the larynx (as well as pharynx and nose/mouth)...


What is this bizarre looking animal we found in the forest? Bug identification Please can someone identify this?

I can't find anything on the Internet like it. 2 cm long. North Bohemian mountains (Czech Republic).

That is the caterpillar of a lobster moth (Stauropus fagi), family Notodotidae. It is mimicking a scorpion to help protect it from predation. An amazing insect.


can magnesium bicarbonate be absorbed in the mouth? Can Magnesium Bicarbonate be absorbed in the mouth?"
  Magnesium Bicarbonate occurs naturally in some mineral waters.

Technically, the human mouth do not absorbed anything. The human mouth is just a first line of defense mechanism against external microbial (In terms of saliva). If in terms of physical aspect, it just helps you to reduce food size and shape it for consumption.

Real absorption do not happen in the stomach neither. Stomach is where acids are used to break down your food and subject to higher lethal effect to kill microbial. The absorption only begins in the small and large intestine. (This is why drug delivery is such a hot topic in research labs).

To answer your question, yes. We need magnesium to survive and so we do absorb magnesium. In fact we can't live without magnesium, we need it for certain vital functions for our body to be normal. (Only in small magnesium amount, we don't need a lot of it).

As for bicarbonate, our body do not need it. In small amount, it is not toxic to our human body but in high volume, this would be a serious issue. When we breath, on cellular level, gas exchange occurs. Oxygen is supplied into our healthy cells while carbon dioxide is removed from our cells into our blood.

This is where it gets tricky, we do not store carbon dioxide in the form of gas when removing it via breathing out. We actually store carbon dioxide in the form of Bicarbonate in the plasma of our blood (Do note that its plasma, not RBC). When it is transported to our lung, this bicarbonate will be converted to CO2 and removed as we breath out. Hence, we do not absorb bicarbonate unless it reacted with some other elements or salt to produce some byproduct that we could use.

I hope you find this useful.

Regards

Price


Are there animal species where some females have greater amounts of male-associated qualities than average males? In the human species, some women ( a meaningful, though not large percentage) are taller and stronger than the average man.

Is a similar thing true in the animal kingdom? Are there some meaningful percentage of hens that would make better fighters than the average (game) cock? Cows that would be better at pulling plows than the average bull? Lionesses that could beat the average lion in a stand-up fight?

The point of the question is are there overlapping "bell curves" of size, strength, etc. so that "strong" females, while a clear minority, are nothing freakish. Or is it true in most (mammal) species that male strength is "off the charts" compared to female strength, except for "freaks."

Spotted hyenas are a matriarchal society and female hyenas are larger than males. Also, female hyenas dominate males.


Does *E. coli Dh5 Alpha* strain has the ability to degrade polyethylene? Does E. coli Dh5 Alpha strain has the ability to degrade polyethylene? What are the bacteria that can be used as a control in the research of polyethylene degradation?

I am not aware of any wild E.coli strains that have been described to have the ability to degrade polyethylene. However, work to equip E.coli DH5α with the ability to degrade polyethylene, by means of transformation, has been done in the laboratory (Mahalakshmi 2012, Danso et al 2018)

Microorganisms that can be found in the wild/nature that do have the ability to break down polyethylene include (Source: article):

Pseudomonas spp
Bacillus spp
Staphylococcus spp
Aspergillus nidulans
Aspergillus flavus
Streptomyces spp


Genetics - Ancestry DNA relationships If my uncle and I both got our DNA tested and compared ancestry results, should we have 50% or 25% similarity? I get normally it would be 25% but since the mitochondrial DNA and Y chromosome are (mainly) used to figure this out using the test we did, shouldn't we share the same exact maternal DNA since it's my mom's brother and that doesn't recombine or anything and they got it from their mother? I just want to know if this is a different genetics problem than normal. Thanks!

The coefficient of relationship between you and your uncle is 25% (see wiki > coefficient of relationship for more info).

However, the percentage of similarity depends on the genetic diversity in the population of interest. If you were studying a population of fully homozygous clones (no genetic diversity), then no matter what the coefficient of relationship is between any two individuals, they would still be clones and therefore perfectly similar.


Why did they expect Astronaut Scott Kelley's telomere shortening to accelerate? (they got longer!) The NPR News article and podcast Scientists Share Results From NASA's Twins Study says:

SCOTT KELLY (NASA Astronaut): You know, the symptomatic stuff is fine. I don't have any long-term negative feelings, physically, from being in space. Now, there's the things you can't feel. And hopefully, I will never learn that those are a problem.
GREENE (Host): Those things you can't feel - well, it turns out they are as small as the protective structures at the ends of his chromosomes.
MARTIN (Host): Yeah. These are called telomeres, and normally, they get shorter with age. But what about in space?
SUSAN BAILEY (Principle Investigator): What we wanted to do was evaluate telomere length in both of the twins before and after so that we could see, you know, where they started and then where they ended.
MARTIN: Susan Bailey was one of the scientists who answered this question. She expected the stresses of space to shorten telomeres quicker.
BAILEY: And, in fact, we saw exactly the opposite thing - that during spaceflight, he had many more long telomeres than he did before he went up. So that really couldn't have been more of a surprise to us.

See also Radiation Biologist Dr. Susan Bailey Studies the Cellular Clocks of Astronaut Twins
Question: Why did investigators initially believe that Scott Kelley's year in space would accelerate the rate of telomere loss, relative to his baseline rate and the rate of his identical twin brother on the ground? What would be the postulated mechanisms?

Dr. Bailey wrote a short piece that hints at the reasons behind why she expected what she expected:

Telomeres are the ends of chromosomes that protect them from damage and from “fraying” – much like the end of a shoestring. Telomeres are critical for maintaining chromosome and genome stability. However, telomeres naturally shorten as our cells divide, and so also as we age. The rate at which telomeres shorten over time is influenced by many factors, including oxidative stress and inflammation, nutrition, physical activity, psychological stresses and environmental exposures like air pollution, UV rays and ionizing radiation. Thus, telomere length reflects an individual’s genetics, experiences and exposures, and so are informative indicators of general health and aging...
Our study proposed that the unique stresses and out-of-this-world exposures the astronauts experience during spaceflight – things like isolation, microgravity, high carbon dioxide levels and galactic cosmic rays – would accelerate telomere shortening and aging. To test this, we evaluated telomere length in blood samples received from both twins before, during and after the one year mission.


What is the rate of mRNA decay in saccharomyces cerevisiae? I am just looking for a number whether that is a mean or an estimate. I am having trouble finding this value on papers because the papers mention only the methods for calculating such a value. Is there a reason why a reasonable mean is hard to obtain?

Here is my best attempt at answering this question:

The median mRNA degradation lifetime is roughly 20 minutes in the case of yeast. Also, the total transcription for RNA pol II in a yeast cell growing in standard conditions is about 60200 mRNAs/h. I am going to go ahead and suppose that the transcription rate is constant throughout time. Thus we have that total transcription rate is equal to 1003 mRNAs/min. Furthermore, I am going to make the rough approximation that all mRNAs live exactly 20 minutes. Therefore, mRNAs will start degrading after 20 minutes. In one hour, 1003 mRNAs will degrade every minute for 40 minutes. It follows that the rate of mRNA decay in yeast is roughly 40120 mRNAs/h.


Why insects are so small compared to mammals? I was wondering what biological limitations make the dimension of the insects small compared to the dimension of the mammals. I know in other eras insect were bigger!

The standard answer to this question is - it's down to the delivery of oxygen to respiring tissues. Insects depend upon a process that is essentially diffusion-driven (via spiracles and the tracheal system) whereas vertebrates have a circulatory system that allows oxygen absorbed in the lungs to be carried via the blood to peripheral tissues. And of course the blood contains specialised carrier cells (red cells) which in turn are packed with haemoglobin which acts as a molecular carrier for oxygen.

The giant dragonflies of the Carboniferous (Meganeura) existed at a time when oxygen levels in the atmosphere were much higher than now (32.5% vs 20.9%), so the diffusion-driven gas exchange system could support a larger body size.


Are there examples of animals that live in groups, where all have the same role? For animals that live in groups, are there examples where all of them have the same role? For example, in animals we know there are bee queens or alpha, beta and omega mammals. But are there groups of animals where all the members have the same role? My question is aimed at 2 different groups actually, first animals in general (which includes reptiles, insects, etc.) and second to mammals only.

Yes, there are many examples. Those species are said to be gregarious. See below for examples.
Level of sociality
When it comes to social behaviour, it is common to categorize species into one of four categories: Solitary, gregarious, presocial, and eusocial.
Note that definitions may vary among authors and that there are limit cases that make the question of categorizing much richer than the simple definitions I am using below.
Solitary
Solitary species are species where individuals mainly live alone and are independent of each other (They may still meet to mate, though).
Examples: fox, polar bear
Gregarious
Gregarious species are species that gather into a group but do not share any labour. Each individual is selfish. Such gregarious behaviour can be driven by safety (typically during migration), to taxis toward a resource, or any other reason that may cause these individuals to gather!
Note, when you say "have the same role," it is clear that different individuals may use different life strategies (like typically territorial males vs. sneaker males in birds).
Examples: wildbeest (during migration), many insects attracted to a given lightsource.
Presocial
Presocial species are species that are gregarious and have a separation of labour but no separation of the the reproductive labour.
Examples: Humans, many hymenopterans, vampire bats
Eusocial
Eusocial species are species that have a separation of labour including separation of the reproductive labour.
Examples: Termites, ants, naked mole-rat


Is it a medical condition to not able to recall the word in a language while having a conversation While having a conversation it happens to some peopl that clearly they know there exists a perfect word to be used but can not recall it during the conversation in real time and hence forced to use some other word which may not be so perfect.

But after the conversation is done they will be able to recall it. This happens very frequently to some people. Is this some kind of medical condition. If yes what is the name of this condition called as. ?

The phenomenon you describe is known as tip-of-the-tongue phenomenon, where you know there is a word, and you feel it's "right on the tip of the tongue, but doesn't come out".

The phenomenon is normal and tends to worsen with age. Only in case it becomes so strong that it seriously interferes with daily life, it can be considered a medical condition (anomic aphasia) that may be indicative of damage to the brain, such as stroke, head trauma, dementia, or tumor.


Which Darwin book (and today edition) is illustrated by his own drawings? I am interested in buying Charles Darwin books and mostly drawings (nowadays editions, I am not a collector). Please, can you advise in which book and which edition I can find the most of his drawings? I found some books as On the Origin of Species ad the Geology of The Voyage of The Beagle but I am not sure if there are his drawings too. I am a student so I couldn't spend too much money on it, but I was interested in his texts and drawings, supporting each other in one book/journal/publication. Thank you !

I believe that there is only one drawing in the first edition of On the Origin of Species, and it is Darwin's.  Any good edition such as the fascimile edition with an introduction by Ernst Mayr, will include this drawing.  I'm not sure about other editions of the Origin or other books of Darwin's.  However, maybe you don't need to buy anything.  Darwin Online is a wonderful collection that includes many (all?) of Darwin's writings over the years, including images of many of them; the drawings are no doubt included.

It's possible that the History of Science and Mathematics StackExchange site would be a better place for this question.


Why is HIV so large compared to other viruses? The HIV-1 virus is about 120-150 nm in size and has a genome only about 10,000 base pairs long.

Other viruses are far more efficient, for example lambda phage has something like a tenth the volume and a genome five times longer. In other words, while half the volume of a lambda phage is taken up with DNA, in HIV it's more like 1%. Why is HIV so space inefficient?

There are many other things inside the HIV capsid besides RNA. The ssRNA is bound to the p7 nucleocapsid protein, the p6 late assembly protein, as well as integrase and reverse transcriptase, both of which are vital for infectivity. Also enclosed within the virion are Vif (Viral Infectivity Factor), protease, Nef (Negative Regulatory Factor), Tat (HIV Transactivator), and Vpr (Viral Protein R). Surrounding the capsid is a matrix formed by the p17 viral protein, and finally the lipid membrane envelope (taken from the host cell upon budding), which contains host cell proteins as well as the vital trimer of gp120/gp41 heterodimers, which bind to the target cell.

From Wikimedia

HIV (and many other viruses) depend on binding to certain cell surface receptors, and a larger total size increases the chances of binding to multiple receptors and potentially triggering receptor-mediated endocytosis, if that is part of the virus's entry strategy.

The naked λ phage binds to the lamB porin of single-celled prokaryotic E. coli by way of the phage's J protein and injects its DNA load into the bacterium, where host factors circularize and supercoil it, allowing for transcription to begin. While the phage's genomic material can be integrated into the host's chromosome, it is not required. Additionally, there is no nuclear barrier to cross.

From Wikimedia, numbers in parentheses are copies per virion.

On the other hand, HIV is a highly complex enveloped lentivirus that targets very specific cells in its multicellular eukaryotic host HIV requires reverse transcription and the assembly of a large pre-integration complex to transport the viral DNA into the nucleus and integrate it into the host's genome, all before it can even start producing new viral proteins.

Trying to compare the "packing efficiency" of HIV to the λ phage isn't just comparing apples to oranges, it's comparing apples to goats. The two viruses are completely different, with the only essential similarities being that they are viruses that infect cells.


Is this headlice or bed bug This is very small. About the size of a grain of rice. I Felt it crawling in my hair.  When I brushed my hair off this fell out in the sink. I was wondering if it's lice. I'm in Mojave county Az

That is a Thrips, order Thysanoptera. Not harmful. Not a bedbug or a louse. You can read about them here.
https://en.wikipedia.org/wiki/Thrips
(by the way the singular form of "Thrips" is "Thrips": there is no such thing as a "Thrip")


Why is Cysteine and Tyrosine used to calculate a sequence isoelectric point? Why are the amino acids - cysteine and tyrosine used in isoelectric point calculations for a protein sequence, yet neither of them are positively charged molecules? and are not used in net charge calculations.

Every amino acid has a different isoelectric point: a pH where they do not carry electric charge. This isoelectric point depends on the side chains:

By glycine the side chain $-H$ is neutral (while the amino and carbonic acid groups are not) so the IEP is 5.97.
By lysine the side chain $-(CH_2)_4\mbox{-}NH_2$ is alkaline $[R\mbox-NH_2 + H^+ \rightleftharpoons R\mbox-NH_3^+]$, so it will have a more alkaline IEP 9.74 than glycine.
By glutamic acid the side chain $-(CH_2)_2\mbox -COOH$ is acidic $[R\mbox -COOH \rightleftharpoons R\mbox -COO^- + H^+]$, so it will have a more acidic IEP 3.22 than glycine.

Every side chain has more or less contribution to the IEP of the amino acid. In your question

the side chain of cysteine $-CH_2\mbox-SH$ is a weak acid $[R\mbox-SH \rightleftharpoons R\mbox-S^- + H^+]$ so the IEP is 5.07
the side chain of tyrosine $-CH_2\mbox-Ph\mbox-{\scriptsize (p)}OH$ is an even weaker acid $[R\mbox-OH \rightleftharpoons R\mbox-O^- + H^+]$ so the IEP is 5.66

And every amino acid has more or less contribution to the IEP of a protein.

References:

Table of pKa and pI values
Amino Acids with Acidity Values
Introduction to Proteins; Amino Acids, the Building Blocks of Proteins
Electrospray Mass Spectrometry


Mutated and unmutated PCR product If I have a mutated colony containing the fusion protein, mCherry instead of the stop codon TAA, and an unmutated colony which does not contain the protein. Why will the PCR products of the two colonies have the same size?

I thought that since the mutated colony contains the protein instead of the stop codon, this would cause this product to be larger in size than the unmutated product. However, from experimental data it shows that both products are of same size. Could someone please explain why this is?

Thank you!

If mCherry was successfully cloned replacing the stop codon, you would indeed expect a fusion protein that is about 27 kDa larger than the original protein.
However, with a PCR you are not testing for the full length protein, but rather for a part of the target gene sequence.

The length of the PCR product very much depends on the position of your primers: If both primers are targeted at your unmutated sequence, the product size will not change by adding mCherry behind the targeted sequence. The product size of the PCR would only change, if one primer is located before or in your unmutated protein and the other one behind mCherry. This would probably result in a very large PCR product and hinder the PCR reaction from being effective.

To check for correct integration of mCherry, you would need to design a primer pair with the forward primer in your unmutated protein and the reverse primer in mCherry. This should result in a product in the fusion protein colonies, but not in the unmutated ones.

Alternatively, you could sequence your products.


Does the body have a mechanism for cleaning plaque buildup in arteries? Is there a self synthesized substance in the body, or a mechanism that can break down plaque in arteries ?

Atherosclerosis can be reversed to some extent by certain diets and change in life style that result in decrease of excessive weight, blood pressure and cholesterol levels.

Studies

1) Dietary Intervention to Reverse Carotid Atherosclerosis (Circulation, 2010)

In a study in Israel, in 140 participants, who were mostly age 40-65 and overweight, they observed an average of 5% reduction of the the volume of the carotid artery wall, which reflects the reduction of the plaque.

  Two-year weight loss diets can induce a significant regression of
  measurable carotid VWV [vessel wall volume]. The effect is similar
  in low-fat, Mediterranean, or low-carbohydrate strategies and appears
  to be mediated mainly by the weight loss–induced decline in blood
  pressure.

2) Intensive Lifestyle Changes for Reversal of Coronary Heart Disease (JAMA, 1998)

Forty-eight patients with moderate to severe coronary heart disease were randomized to an intensive lifestyle change group (10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support) or to a usual-care control group, and 35 completed the 5-year follow-up quantitative coronary arteriography.

  Experimental group patients (20 [71%] of 28 patients completed 5-year
  follow-up) made and maintained comprehensive lifestyle changes for 5
  years, whereas control group patients (15 [75%] of 20 patients
  completed 5-year follow-up) made more moderate changes. In the
  experimental group, the average percent diameter stenosis at
  baseline decreased 1.75 absolute percentage points after 1 year (a
  4.5% relative improvement) and by 3.1 absolute percentage points after 5 years (a 7.9% relative improvement). In contrast, the
  average percent diameter stenosis in the control group increased by
  2.3 percentage points after 1 year (a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% relative worsening) (P=.001 between groups. Twenty-five cardiac events occurred in 28
  experimental group patients vs 45 events in 20 control group patients
  during the 5-year follow-up (risk ratio for any event for the control
  group, 2.47 [95% confidence interval, 1.48-4.20]).

  The experimental group reduced LDL cholesterol levels by 40% at 1 year
  and by 20% after 5 years.

  When we began this study, we believed that the younger patients with
  milder disease would be more likely to show regression, but we did not
  find this to be true. Instead, we found that the primary determinant
  of change in percent diameter stenosis in the experimental group was
  neither age nor disease severity but adherence to the recommended
  changes in diet and lifestyle.

  those who gained weight were more likely to show progression of atherosclerosis.

  Experimental group patients had a 91% reduction in reported frequency
  of angina after 1 year and a 72% reduction after 5 years (Table 5). In
  contrast, control group patients had a 186% increase in reported
  frequency of angina after 1 year and a 36% decrease in frequency after
  5 years.

Mechanisms

Reversal of atherosclerotic plaques can be achieved by removing the causes. According to Atherosclerosis: Process, Indicators, Risk Factors and New Hopes, (Int J Prev Med, 2014), decreasing excessive body weight + exercise + cholesterol-lowering diet + cessation of smoking can result in:

Less damage to the arterial intima
Higher HDL/LDL ratio, meaning adequate removal of LDL (by HDL) from the blood into the liver and thus less deposition of cholesterol into the arteries
Less inflammation in the arterial intima


Two sets of chromosome and the sequencing output Humans have two sets of chromosomes that are not connected in each cell. Am I correct?

I assume while sequencing DNA both of these sets have to be sequenced and the output have to be provided in some order - i.e., paternal set followed by maternal or vice versa, though it may not be possible to know which is paternal and which is maternal.

(I know there are different types of sequencing techniques and output may differ depending on the technique. Here I am speaking of the general case). I tried clarify this question myself. But may be this is such a basic thing that no one seems to touch upon this aspect.

This is very similar to your previous questions, but apparently you are not understanding the explanations we are giving, so I'll try again, by giving a (hopefully not-too-technical) explanation of how next-generation genomic sequencing works. To avoid confusion, we'll assume we're working with human samples.

First, many individual cells are collected (the number depends on the application, it can range from 1 cell to millions or more), and their DNA is collected. This process destroys the cells, and all of the copies of all of the chromosomes are mixed together. As mentioned in your other question, there is no possible way to determine which chromosomal sequence is maternal, and which is paternal. Scientists typically don't even think about this.

Next, the collected DNA sample is purified and broken down into small pieces, then ligated to certain adapters to label them for the sequencing reaction. The sample is then amplified in a standard PCR to create starting material that is many times more plentiful than before. This is the DNA library.

Finally, the sample is ready for sequencing. What exactly happens next depends on which sequencer you're using - Illumina, Ion Torrent, 454, or SOLiD are the most frequently-used instrument brands. Within each brand, Illumina for example, there are multiple different kinds of sequencing.

However, we'll just gloss over all that and get right to the output - the instrument produces a file consisting of "reads" from the reaction. These reads are DNA sequences consisting of As, Ts, Gs, and Cs - the "letters" (also known as "bases") of DNA. The lengths of the reads vary by technology and instrument, generally in the range of 100 to 700 bases. One machine, though - the PacBio RS II, can produce high-quality reads up to 14,000 bases, although to my knowledge it is not in widespread use.

Here is where the computers come in. The individual reads overlap each other to varying degrees, depending on the quality of information you're seeking and whether or not you're looking for rare events, such as a small population of mutated cells taken from a heterogeneous tumor. For our purposes, we'll say our sequencing run resulted in a 25-fold overlap, meaning each base in the original DNA sequence of the sample donor was sequenced an average of 25 different times. The computers can then "align" the sequences, either just among themselves, without a template, or, more commonly, to a pre-existing sequence template, such as a reference genome. Eventually, the computer will spit out two sequences - the forward and the reverse strand (although typically you'd just pick one strand, and use the reverse strand for error-checking). This sequence is the average sequence of the chromosome, or other region of DNA being targeted.

From Wikimedia Commons: Mapping Reads.png

However, one can pretty easily detect mutations, such as single nucleotide polymorphisms (SNPs), deletions, insertions, etc. In the case of a SNP (pronounced "snip"), one allele of a gene has one sequence on one chromosome (lets say ATTCGTAAC) while another allele of a gene on the other chromosome has a single-base change (ATTCTTAAC, for example, where the G was changed to a T).

The point, directly relating to your question, is this: The final sequence that eventually comes out after all the computer wrangling is a single sequence with certain areas that may differ from chromosome to chromosome, or cell to cell in the original sample. There is no way to determine if the G in our example above was on the maternal or paternal chromosome. There is also no way to tell if, 20,000 bases down the line, another mutation is on the same chromosome as the G, because no single read can (currently) span that entire length. You might have a pretty good chance of determining that if the other mutation is, for example, 300 bases away, because many technologies can perform high-quality reads longer than that, so you'd just have to find the individual ones that contain both positions.

I know this was a little long-winded, but hopefully I was able to answer your question.


How can we know or measure pain in animals? Is there any standard way to know how much pain an animal feels when it gets hurt like when a bird loses it's wing or hen when killed etc. All pain sensation points?

Hey I'm new to biology. :)

Pain is subjective

Pain is a subjective experience; you cannot even tell with certainty how much pain your fellow human is experiencing, which is why we ask people; they then can tell us. Pain relief (both physical and emotional) is a significant part of medicine, yet we still have "pain scales" for self-reported pain, one of the more common ones being the Wong-Baker Faces Pain Rating Scale:

Now, note well that even this scale must be interpreted for the patients. For instance, a patient might look like a 6, but be reporting a 10, in which case, a nurse must try to ascertain their actual level of pain.

My point is evaluating pain is contentious even in humans who can express themselves.

Definition of pain

The International Association for the Study of Pain (IASP; www.iasp-pain.org) defines pain in humans as

  an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

Pain usually involves a noxious stimulus that activates nociceptors in the body that carry signals to the CNS where these signals are processed (and generate responses) including the “unpleasant sensory and emotional experience.”

The following are examples of common types of noxious stimuli for different tissues:

  Skin: thermal (hot or cold), mechanical (cutting, pinching, crushing), and chemical (inflammatory and other mediators released from or synthesized by damaged skin, and exogenous chemical stimuli such as formalin, carrageenan, bee venom, capsaicin)
  Joints: mechanical (rotation/torque beyond the joint’s normal range of motion) and chemical (inflammatory and other mediators released into or injected into the joint capsule)
  Muscle: mechanical (blunt force, stretching, crushing, overuse) and chemical (inflammatory and other mediators released from or injected into muscle)
  Viscera: mechanical (distension, traction on the mesentery) and chemical (inflammatory and other mediators released from inflamed or ischemic organs, inhaled irritants).

Animals need us to interpret their pain into language. For political and emotional reasons, humans are ill-disposed to do so (how could we then justify eating, exploiting, experimenting on animals, etc.). Even into the late '80's, veterinarians were taught that animals didn't perceive pain per se.

How we know animals understand pain

To determine whether animals can experience actual pain (not simply nociception), it is necessary to show that they

  can discriminate painful from nonpainful states; make decisions based on this discrimination in a way that cannot arise from evolved nonconscious nociceptive responses; demonstrate motivations to avoid pain; and display affective states of fear or anxiety if threatened with noxious stimuli. In addition, animals experiencing pain might be expected to exhibit spontaneous behavioral changes including sustained signals of distress and impairments in normal behaviors such as sleep.

Animals show all these behaviors. Additionally, there is ample evidence that emotional pain in animals is real. The mere threat of foot shock (electric) induces signs of stress in rats and mice that can be alleviated with anxiolytics (drugs that reduce anxiety).

Even fish show responses to a painful event: guarding behaviors, unresponsiveness to external stimuli and increased respiration, all of which improve with morphine. This is called analogous evidence: evidence that they are, mechanistically at least, directly analogous to pain responses in more complex animals.

Humans are animals

The nervous system of mammals is fairly identical to our own (we are animals). A chimpanzee who is afraid of a pin after being stuck with one 20 times in a row clearly feels physical pain and fear. That a chimp can mourn the death of a parent by not eating and not moving for days clearly indicates that they can experience emotional pain.

In summary:

Pain is subjective. I cannot really tell exactly what you feel if your arm is ripped off (your bird-wing example) or (don't read if queasy type)

   if you are given an electric shock, your throat is slit and, while still bleeding, you are dipped in boiling water to remove your body hair in a whole body hair plucker (which is how most poultry - usually males, not hens, btw - meet their makers).

By definition, only you can tell us.

But common sense and experience tells us it would be painful. And, yes, animals feel pain pretty much exactly like we do. Because we are exceedingly "more alike" than we are "slightly different".

Can animals feel pain?
Pain in Research Animals: General Principles and Considerations
Which Responses Indicate Pain and Which Nonhuman Vertebrates Display Them?<- read this if you really want to know
Evolution of pain


How can I change my buffer system for protein purification? I have a protein that I purified in PBS buffer, pH 7. I will do dialysis to remove salt and will then further purify the protein with ion exchange chromatography.

I will need to use another buffer (Tris-HCl) with pH 8 in the chromatography, and so my question is: Can I change the buffer system for my protein in the dialysis step? Or would you recommend me to use the Tris-HCl buffer from the very start and then just adjust the pH for the chromatography?

Thanks in advance!

Assuming that your protein can handle being in the new buffer, you have multiple options.

Dialysis will work although you might want to consider using a centrifuge spin filter with a suitable MW cutoff to gradually switch buffer and concentrate the sample. Be aware that some of your protein will stick to the filter, giving a loss of sample.

Alternatively you can perform size exclusion chromatography to switch into the new buffer, but you better be sure that the sample will remain stable or you may clog the column. If you can perform affinity chromatography, you can also opt to change buffer in this step.

You can of course try to start with a Tris based buffer and simply adjust pH by dialysis in a tris buffer with the desired pH. Just make sure that the dialysis volume is large enough to counteract the buffer in the sample.

Instead of using PBS you can also try with TBS (Tris-buffered saline), see wiki for details. https://en.wikipedia.org/wiki/Tris-buffered_saline


Human population growth - where can I find the data? Out of curiosity, I'd like play around with data of human global demography.

Where can I find data that describe the "per region (per continent for example) population size" versus time since the "Out-of-Africa Event" or earlier?

Here is for example the kind of graph I'd like to reproduce but if possible in a region per region basis.

National censuses are collected, published and disseminated primarily by each country's census or national statistical office (NSO) or its equivalent. Census data are published in each country's vernacular, and as appropriate, many offer English as well as other language versions.
Statistical offices of international agencies (e.g. United Nations, statistical organizations for member states like the ASEAN, Eurostat, and OECD), also publish statistical data including population figures. The most consistent data in terms of format and frequency, whether online or in print are usually generated from them.

The US Library of congress provides some interesting links here:
http://www.loc.gov/rr/business/census/intlcensus.html
Also Cornell provides a few resources also:
https://www.ciser.cornell.edu/ASPs/datasource.asp
If you still need some information, your best bet is to then contact social scientists and ask for their opinion.


What is the armpit hair for? Modern human beings, especially women, cut their armpit hair. It seems to me the armpit hair is trivial/useless. Shortly speaking, what is the armpit hair for?

I have been trying to read up a bit on this. I started out looking on wikipedia and it seems there are three hypotheses which are not necessarily mutually exclusive.

1.Aid the wicking of sweat away from the skin

2.Reduce friction between the thorax and upper arm

3.Facilitate the release of sex pheromones

The first would seem possible because it would help to prevent over-heating of the lymph nodes under the armpits and that also fits with the fact there are a lot of sweat glands there.

The second, I can't find any citations which support this but I understand that people who shave their armpits tend to suffer from dry underarms. This could be a result of increased friction.

The third is apparently controversial although it seems perfectly reasonable and highly likely to me. There is a famous experiment by Claus Wedekind who got men to wear a t-shirt for a few days. He then got women to choose a most preferred male purely by the scent of the t-shirt and found interesting results relating to the MHC profiles. The armpit hair could help to trap the odour produced by the sweat and help with mate attraction, like some kind of scent sponge. I don't understand why this is so controversial, loads of animals influence mate choice with scent - perhaps people don't like to think we are genetically attracted to each other by sweat because it seems animalistic and less romantic.

In summary, there is no sure answer and it could well be all of the above, or something entirely different.


What is this fleshy-stemmed plant? This plant came (seemingly by accident) with another pot plant a few years ago in a plant sale.  Unfortunately, we do not remember what the original plant was that it came with.

It was initially one of the small 'fleshy stems' you can see in the photos, about 2cm in length.
If you do not water it, the leaves fall off and leave the fleshy stems
If it is watered, a new section of stem is grown with leaves.
Its existing stems do not seem to regrow their leaves if they drop off.
It was acquired in the South-West of England.
It does not appear to be affected by the time of year.

Photos (click to enlarge):

Reminds me of Senecio articulatus (Candle Plant; hot dog cactus), a succulent plant in the broad (aka polyphyletic) Senecio genus (Asteraceae).

 Source: U. Wisconsin-Eau Calire

Based on my limited knowledge of the plant and the variable leaf shape, I am not sure if this is your species or not. However, I'm sure some additional searching using this species as a guide will get you to the correct species/cultivar.

World of Succulents provides some additional information on Senecio articulatus.

You can see a video of a Senecio succulent identified as S. articulatus for better comparison to your plant:


What is the cause that angina pectoris is felt in your left arm? When someone has heart problems sometimes they feel pain in their left arm. But why is the left arm painful?

It has mainly to do with the embryonic origin of organs, with the heart being a typically left sided organ, it develops sharing some nerves with the left thorax and left arm.

There is however high variability, typically among patients but also among coronary vessels. For instance, right coronary stenosis may lead to abdominal pain, whereas left circumflex artery stenosis may lead to no pain at all.

References:

Essentials of Medical Physiology

Cardiac Pain. Anatomic Pathways and Physiologic Mechanisms

Changing Features of Anginal Pain After PTCA Suggest a Stenosis on a Different Artery Rather Than Restenosis


What species is this bushy thorny yellow-flowered angiosperm from Morocco? What species is this bushy thorny yellow-flowered angiosperm from Morocco? Photographed in spring in a dried up river bed. The bush is about 1 metre high.

I happened to come across a photo of a similar leafless shrub (without flowers) that also had 120 degree branches and looked thorny, or Spiny is probably a better description. It helped me to identify the plant in your photo as a Launaea arborescens. It is an unusual species of Chicory in the dandelion family, Asteraceae. Being tolerant of arid locations, it native to northwest Africa and southern Spain.

http://encyclopaedia.alpinegardensociety.net/plants/Launaea/arborescens

https://en.wikipedia.org/wiki/Launaea

https://en.wikipedia.org/wiki/Launaea_arborescens


How would one go about identifying unknown cell cycle checkpoint proteins (i.e., cyclins)? No this is not 'homework'. I'm a PhD student, and this was something brought up at the end of a journal club recently, and one of the PIs posed this question and told us to think about it. It sounds simple, but it sort of has me baffled.

Western blot: No. Need a known antigen and so, since we don't know what we're after, this won't work.
Total protein gel: Collect cell lysates from different cell populations that are in different parts of the cell cycle, run it on a gel and observe any cyclic expression. This seems sort of ok but I feel like there are a few problems with it: 1) identifying the cell populations that are in the different cycle stages; 2) other proteins of same/similar size that cannot be differentiated.
Some sort of RNAi, knockdown, etc.: Like the western blot, we don't know what we're dealing with and so can't target anything.
Pulldown assay with mass spec: I don't know a lot about it aside from that it looks at protein-protein interactions. Unsure if it would be appropriate here.

As far as a model, I was thinking either yeast or some immortalized mammalian cell line.

I've actually been involved in a hunt for checkpoint proteins in diatoms (a type of eukaryotic algae), the cyclin family has been greatly expanded in these organisms and we were trying to figure what these extra cyclins were sensing/signalling[1].

In a nutshell, the first author looked at different conditions which were likely to affect cyclin expression. Most of these conditions prevented cell division (e.g. lack of nutrients, G2/M chemical inhibitors or light) and samples were taken before and after the blocking conditions were removed. Afterwards mRNA's were quantified of suspected cell cycle genes. As the checkpoint genes' mRNA and protein cycles extremely transiently this took some doing. Cyclins that reacted to the conditions were characterised using complementation assays and other techniques.

Afterwards yeast two hybrid assays were used to identify interacting proteins to build up the network[2]. In general, these experiments were not that straightforward and messing with essential genes causes a lot of trouble but it still nothing compared to the original yeast cyclin work where they were slogging through mountains of temperature sensitive mutants defective in their cell cycle (see the work of Lee Hartwell and Paul Nurse who got the Nobel prize for this in 2001 with Tim Hunt).


Why are red blood cells preferred to study the structure of plasma membrane? If we wanted to study the structure of a plasma membrane, why are red blood cells a more attractive cell type to work with than other cell types such as liver cells or kidney cells?

Human RBCs are relatively simple in structure compared to the other cells in question; they contain no cell organelles (so far I knew; please correct me if there is any new theory) and therefore contain only one membrane.

RBCs do not have significant amount of extracellular matrix making them very easy to work only with the cell membrane. RBCs float in a fluidy medium (blood-plasma), so easy to collect, distribute in containers, keep into various solution. no need of maceration. Human RBCs are very uniform in shape and size, and do not divide. That makes it useful for various experiments like demonstrating plasmolysis and deplasmolysis as well as quantitative experiments on membrane biomolecules.

One classic example is Edwin Gorter and F. Grendel that first showed that cell membrane is bilayer; that is upon observation on RBC. They took known number of RBC, denatured the membrane, extracted the lipids and spread that as a lipid monolayer on water-air interface. They found that the monolayer is twice bigger than total surface area of taken RBC ! *

  Source:  * The Cell/ Cooper/ 4th Edition/ASM-Press and Sinauer publication.

However this is not a reference-based answer, but these are the features more than enough to make me so lazy that I would choose only RBC and flyaway from any-other option.


Meaning of "primers IL-2" in a scientific article From an article ("Amelioration of Experimental Autoimmune Encephalomyelitis in Lewis Rats by FTY720 Treatment", 2003):

  We performed PCR amplification in a 100-μl reaction mixture containing 200 μM of each of the regular dNTPs, 10 pmol of each primer, and 2.5 U of TaqDNA polymerase (TaKaRa) using primers IL-2 (300 base pairs; bp), 5′-CAGCTGTTGCT GGACTTACAGG-3′ and 5′-CACAGTTGATGGCTCATCATCG-3′; IL-6 (294 bp), 5′-GACTTCACAGAGGATACCC-3′ and 5′-TAAGTTGTTCTTCACAAACTCC-3′; INF-γ (310 bp), 5′-GGATATCTGGAGGAACTGGCAAAAG-3′ and 5′-GCTAGATT CTGGTGACAGCTGGTG-3′; β-actin (461 bp) 5′-CATCGTGGGCCGCTCTAGGCA-3′ and 5′-CCGGCCAGCCAAGTCCAGACGC-3′.

I'm not completely sure: do they mean that the primers are "specific to the IL-2 gene"?

Do they mean "5′-CAGCTGTTGCT GGACTTACAGG-3′ and 5′-CACAGTTGATGGCTCATCATCG-3′ are primers that are specific to the IL-2 gene"?

From the description, yes, those primers are supposed to be specific for the IL-2 gene. The way they would be used would be on mRNA, not DNA, so you could use them to quantify the level of IL-2 transcription. However, there seems to be some glitch in there, because while the first sequence (5′-CAGCTGTTGCT GGACTTACAGG-3′) matches rat IL-2 mRNA starting at 120 in the sequence,  the second one (CACAGTTGATGGCTCATCATCG) does not match any IL-2; a BLAST search only turns up random and irrelevant matches.

This may be an error in the paper (copying and pasting the wrong primer, which is extremely common, unfortunately); it may have been an error in design (someone used the wrong primer and got lucky results that seemed to match what they expect); or I may be doing something wrong, which I'm not going to try to troubleshoot any more than this.

(Edit, as @VonBeche points out in comments the reverse primer is almost a match at 398, with a one-nucleotide mismatch that screwed up my search -- possibly allelic variant, but equally possibly a mistake)


Are the fossil sites in Hadar geographically separated? The Hadar fossil record is made up of, from oldest to youngest, the Basal Member, Sidi Hakoma Member, Denen Dora Member, and Kada Hadar Member.

Are these regions geographically distinct, or, are they layers on top of another on the same geographical region?

Here is a map of the region where they found the Lucy skeleton.

The researchers speak of the Hadar formation at Dikika, so they are giving it an expanse of 10-15 kilometers at least.

it's quite flat as well.

Why do you want to know?


Which bird species/families worm-dance and is this learned behaviour? Today I saw a Herring Gull and a Common Gull (UK common names) "worm-dancing" on an area of wet grass. Worm-dancing is when the bird taps its feet on the ground rapidly in order to drum worms to the surface (that its a worm hunting behaviour might be conjecture, I'm not sure it's been proven).

Shortly after, a pair of Jackdaws landed and also began hunting, but without dancing. They walked over the area poking about in the grass, whereas the gulls stayed in the same place.

So my question is firstly, which species/families has worm-dancing been observed in, and secondly is this thought to be learned behaviour (this might be determined by it being a local phenomenon in certain populations)?

EDIT: Originally misidentified a common gull as a black headed gull (corrected above). Today I saw a black headed gull alongside the two larger gulls, and it was hunting like the jackdaws, not worm-dancing. There might possibly be a size/weight requirement to be able to worm-dance effectively, if we accept the hypothesis that it's a method of bringing worms to the surface.

Short answer
Sea gulls indeed tap the ground to surface earth worms, which is known as worm charming. Traditional human societies have practiced a similar technique known as worm grunting, involving vibrating the ground. Worm grunting is obviously a learned behavior passed down for generations in Florida. In other animals, such as gulls, I wasn't able to find evidence whether it is learned or innate behavior.

Background
From wikipedia:

  Worm charming is especially [observed] among birds. The methods used vary; however, tapping earth
  with feet to generate vibrations is widespread. One common example is
  the "Seagull dance". The wood turtle also seems to be adapted for worm
  charming, as it is known to stamp its feet – a behavior that attracts
  worms to the surface and allows the turtle to prey on them.

It is popular belief says that the charming mimics the drumming vibrations made by rain and that worms are attracted by it. However, studies have indicated that the charm vibrations sound similar to those made by burrowing moles, a voracious worm predator and that the charming behavior of worms surfacing reflects an escape behavior of worms, namely the abandoning of their safe burrows to expose themselves to the real danger once surfaced (Catania, 2008).

The authors investigated the charming reaction of the worms by studying human-indiced charming, a technique used by fishermen. For generations, many families in and around Florida's Apalachicola National Forest have supported themselves by collecting the large endemic earthworms (Diplocardia mississippiensis). This is accomplished by vibrating a wooden stake driven into the soil, a practice called “worm grunting”. This worm grunting is obviously learned behavior.

However, I couldn't find evidence whether the worm charming in birds and turtles is learned yes or no.

Reference
- Catania, PLoS ONE 3(10): e3472


Hydrophilicity and polarity If any given molecule is polar, and is capable of hydrogen bonding, I can be sure that it's hydrophilic.

However, are those two the only conditions that make a molecule hydrophilic?

I think the answer is no.

The definition of polarity is basically that a molecule has a dipole, and as water has a very large dipole, if a molecule will mix with water readily, its usually pretty polar.

Water also can share its hydrogens in hydrogen bonding, which is an actual shared covalent bond where a hydrogen atom is shared between two acceptors.  The hydrogen bond is fairly weak (~ 0.5 kcal/mol) but water does a lot of hydrogen bonding.

So hydrogen bonding and polarity are often a shared characteristic of an molecule, but are not the same thing.

Ions are quite hydrophilic but do not need to be hydrogen bond donors or acceptors.   Chloride  (Cl - ) is not a hydrogen bonding atom - its so acidic that it exists nearly entirely in the Cl- form in water solution. But its definitely electro negative and really soluable in water. Are Ions polar though?  Chloride is symmetrical and so its not really polar.

Still is there a polar molecule which is neither a hydrogen bond donor or acceptor?  Acetone and the cyanide ion (CN-) are a polar molecules which have no hydrogen bond donor, but can accept them.

I think sulfate is an example of a polar molecule which does not form hydrogen bonds.
Sulfate (SO4 -- )  has four S-O bonds arranged in a tetrahedron but each of them is highly polar - with 90% of the negative charge on the oxygen.  But like the Chloride ion its so acidic that it much prefers its free ionic state.  It would have very little hydrogen bonding character even when its in water.  Sulfate can form hydrogen bonds, but I think they will only be stable when there are several of them at once.  Sulfate binding protein has seven hydrogen bonds when it binds sulfate, using the chelation effect to make the binding strong enough to be stable.


Why does migration distance depend on log of molecular weight in SDS-PAGE? I really want to know why in the result of SDS PAGE, log of molecular weight(MW) and migration distance (distance from the loading well) have a linear relationship. Why is it log(MW) instead of MW? Thank you!

An SDS-PAGE standard curve of Rf vs LogMW is linear because the standard you're given is engineered to behave that way. An expanded SDS-PAGE curve would show that the actual graph is sigmoidal: Structues that are too large can't enter the matrix, and too small they pass right through. Your standard has taken into account the % composing the gel, and the size of the proteins which the standard consists of that ensure you get the linear data points on the semilog graph.

If we look at the raw data though plotted linearly, the graph isn't entirely linear. The data is much prettier, and trivial to convert back to MW if we log transform the MW. It's the same data, just mathematically transformed. Some more reading on it here.


Why isn’t Haemoglobin a plasma protein, rather than being encompassed by the erythrocyte? Erythrocytes (red blood cells) are a common feature of almost all vertebrates. What evolutionary advantage do they provide in containing haemoglobin, rather than it being just a plasma protein? In fact, haemoglobin is dissolved in plasma in a few annelids and haemocyanin in cephalopods.

The only reason I can think of is that haemoglobin is small enough to get filtered into the tubules of the kidney and is renotoxic. Maybe that's why it had to be packaged into erythrocytes. But isn't this a greater cost than reducing the pore size to prevent it being filtered out? Also, doesn't haemoglobin or haemocyanin get filtered into the primitive kidneys of annelids and cephalopods?

To the man with a hammer, everything looks like a nail.

The poster’s hammer seems to be kidney function. Mine is the biochemistry of the erythrocyte (red blood cell). Others, no doubt will be able to provide yet different perspectives.

From a biochemical point of view the erythrocyte has a limited repertoire of metabolic pathways compared with other tissues. However it does have an extremely active pentose phosphate pathway (not universally found in tissues) and the function of this is to provide the reducing cofactor NADPH, which is needed to maintain glutathione in a reduced state. The importance of reduced glutathione in these oxygen-carrying cells is that it provides protection against reactive oxygen species — something that could not be done — or at least not controlled so well — in the blood plasma.

Another feature of haemoglobin is that the equilibrium between the oxy- and deoxy- forms involves the small triose molecule, 2,3-bisphophoglycerate. This is described in the answer to another question. The ability of the erythrocyte to synthesize this molecule allows the sophistication of this control.

I imagine there are many more examples. (Any added in comments will be added.)

One could argue that these metabolites are not indispensable for organisms (glucose phosphate dehydrogenase deficiency does cause haemolytic anaemia in man), and this presumably explains why the simpler organisms you mention (and about which I know little) can dispense with red cells.

But a question certainly worth asking.


Is there any record of an Albino (Not leucistic) peacock Wikipedia says there are, however gives no source to one. Does anyone know if an albino peacock was ever recorded?

There is a breed of White Peacock. I could not find any record of 'Albino' Peafowls (the gender neutral term for peacock is peafowl (females are peahens). This white variety of peafowl is similar to how there are white chicken which have been bred over many years.
Albino animals do not produce the pigment 'melanin'. Albinism can be a dangerous trait in some organisms such as birds. The lack of melanin makes albino animals very sensitive to the sun's UV rays which can cause their vision to become impaired. Therefore most birds that are adult and white are usually either a variety of bird that is naturally white or is suffering leucism which is similar to albinism but does not remove melanin from organs such as the eyes.
But not all white birds are albino and not all albino birds are white. Just because the melanin pigment is non-existent in albino birds, doesn't mean other pigments couldn't still exist. Some animals don't even need pigments to achieve a certain color and do so instead by reflecting light in interesting ways.
It must also be noted that sometimes, white varieties of birds (or birds with leucism) are interpreted as albino and mistakenly presented that way online. This goes for other animals as well.


What does vaccine efficacy mean? In the last few weeks, Pfizer/BionTech, Moderna and AstraZeneca have each released preliminary estimates of the efficacy of their SARS-COV-2 vaccines.
But what do their respective efficacy percentages actually mean? Is the Pfizer/BioNTech vaccine 95% effective in any person? Or is the success of provoking the desired immune response limited to 95% of the population?
Put very simply: is it 100% effective in 95% of the population, or 95% effective in 100% of the population?

Vaccine efficacy
Pfizer's target measures for efficacy (see the study on clinicaltrials.gov) seem to be:

Confirmed COVID-19 in Phase 2/3 participants without evidence of infection before vaccination

Confirmed COVID-19 in Phase 2/3 participants with and without evidence of infection before vaccination

From Pfizer's study plan (VE = vaccine efficacy):

VE will be estimated by 100 × (1 – IRR), where IRR is the calculated
ratio of confirmed COVID-19 illness per 1000 person-years follow-up
in the active vaccine group to the corresponding illness rate in the
placebo group from 7 days after the second dose. VE will be analyzed
using a beta-binomial model.

(note: they also have other time windows and checkpoints in their analysis plan; which one is reported will shift from press release to press release as they get more data. If you are interested in the details the study plan also describes the planned interim analyses, and some of the press releases discuss deviations they've made from their original interim plans in consultation with regulatory agencies)
This measure is called relative risk, and can be written like this:
%InfectedPerTimeplacebo = NInfectedplacebo / (NStudiedplacebo * AverageFollowUpTime)
%InfectedPerTimevaccine = NInfectedvaccine / (NStudiedvaccine * AverageFollowUpTime)
Efficacy aka VE = %Infectedvaccine / %Infectedplacebo
If you assume risks are the same in the placebo and vaccine groups (they "should" be, but might vary if, for example, people who experience vaccine side effects change their behavior) and the average follow-up time is the same (they should be approximately the same, because they are giving the vaccine and placebo to patients enrolled at the same time), this ratio would tell you that a vaccine efficacy of 95% means that if you took 20 people who would have had a positive test after the placebo, you would only expect 1 of them to test positive if they instead got the vaccine.
Population vs. individual statistics

Put very simply: is it 100% effective in 95% of the population, or 95% effective in 100% of the population?

These are population-based measures. They can't say anything about efficacy in particular individuals by these outcome measures. For example, there is no way to know from a study like this whether the vaccine is 100% effective in 95% of the population, or if it raises the infective dose in everyone by some amount which causes the number of people exposed to this critical viral dose in their environment to decrease by 95% (or some other effect with the same end result).
Other approaches like challenge studies, where vaccinated individuals (or animal models) are intentionally exposed to a certain dose of the virus, can help understand the individual effects of vaccination, as can indirect measures of immune response like antibody titers. These approaches have other drawbacks, however (safety, translating animal results to humans, translating a given immune response to an infection chance, etc).
Beyond just 'vaccine efficacy': disease severity, real-world efficacy
These particular outcomes also say nothing about disease severity. It could be that the people who do test positive despite getting the vaccine get just as sick as the sickest people who don't (interpretation would be that the vaccine protects mostly against mild illness). It could also be the reverse, and that people who get the vaccine and still test positive have a milder illness than they would have otherwise. Efficacy defined by this relative risk ratio does not say anything about this, it only compares positive vs negative rates.
An additional note: these numbers report efficacy in the trial environment. "Real-world" effectiveness (the same measure of effect, but in real world use rather than under trial conditions) might depend on other factors such as differences in the people enrolling in trials vs the general population (both in terms of things like age and preexisting conditions as well as behavior and exposure risks), failure to administer the vaccine properly (including improper storage), failure to complete both doses in timely fashion, etc. This measure of effectiveness also refers only to "primary" effectiveness. One would expect that if enough people were vaccinated, the effect on the population could far exceed the primary effectiveness, because not only do vaccinated individuals have a lower chance of infection, but everyone else in the population also has a lower risk if there are fewer people available to transmit the infection.


Are prions a recent biological phenomenon? Is there evidence to suggest whether prions have existed for a large portion of evolutionary history, played a role in evolutionary history, or could they actually be a recent biological technology invented by mother nature? Is there evidence or biochemical data that prions may predate cells?

Knock-out experiments on non-pathological prion proteins ("PrP") show damage to neurons. So there is evolutionary pressure to conserve their sequence and expression. Mutations to PrP and related regulatory regions appear to be deleterious and the organism will not likely get to reproduce.

A paper here explores this question and demonstrates empirically that pathology-causing prions — normal PrP that refolds into a form that causes disease — themselves undergo selection pressure:

  In summary, prions show the hallmarks of Darwinian evolution: They are subject to mutation, as evidenced by heritable changes of their phenotypic properties, and to selective amplification, as documented by the emergence of distinct populations in different environments.

To the extent that organs susceptible to aberrant prions have undergone evolution, one could infer from this that prions themselves would be under selection pressure to adapt, as their host environment changes.

Further, there is another paper that discusses sequence-level similarity of PrP between clades:

  The presence of the human and mouse PrP genes within conserved syntenic groups (Sparkes et al. 1986) and the presence of aPrP gene in chicken (Gabriel et al. 1992) argue that the PrP gene existed before the speciation of mammals. In mammals, DNA sequences of the ORFs encoding PrP generally exhibit ∼90% similarity. As expected, the degree of similarity at the amino acid level increases to >95% when PrPs of different primates are compared (Schätzl et al. 1995) but is much lower when human PrP is compared with that of a marsupial (∼70%) (Windl et al. 1995). An even lower degree of homology is found when human PrP is compared with that of the chicken (∼30%) (Harris et al. 1989; Gabriel et al. 1992). Attempts to find PrP-related genes in lower eukaryotes have, to date, been unsuccessful (Oesch et al. 1991).

There is an estimation of 600M years of evolutionary distance between humans and chickens, back to their common ancestor:

  The last common ancestor of birds and mammals (the clade Amniotes) lived about 310 – 330 million years ago, so 600 million years of evolutionary time in all separates humans from Aves, 300 million years from this common ancestor to humans, plus 300 million years from this ancestor to birds.

This would suggest to me that PrP has been around for a while, at least 330M years and probably longer, and that aberrant and pathological folds of PrP would have been evolving since (along with PrP, itself).


What phase of Action Potential (AP) exactly defines the Relative Refractory Period? I am posting below, word for word, two statements made on Relative Refractory period - the first from the text: Human Physiology for Medical Students by Magdi Sabry, and the second from a web page with the URL:
https://content.byui.edu/file/a236934c-3c60-4fe9-90aa-d343b3e3a640/1/module5/readings/refractory_periods.html.
In addition, I've attached a photo from Google which appears to be in support of the second statement.
But which of these is correct?

"Relative refractory period (RRP)...corresponds to the remaining part of the descending limb of the AP till the start of after-depolarization (i.e. during the later 2/3 of RP)"

2."...there are two types of refractory periods; the absolute refractory period, which corresponds to depolarization and repolarization, and the relative refractory period, which corresponds to hyperpolarization. "

Neither is an accurate definition; both are correct and not conflicting if you interpret "corresponding" to mean "typically/approximately corresponding".
The absolute refractory period is any time in which you cannot evoke another action potential no matter the strength of stimulus, due to an action potential in progress/that has just occurred.
The relative refractory period is any time in which you can trigger an action potential but need a stronger stimulus than normal.
Neither of these definitions refers to specific phases of the action potential in terms of voltage or change in voltage. Yes, typically the absolute period includes the ascending and descending phases of the AP, but there's no reason it can't last longer depending on the gating properties of the sodium channels. Similarly, the relative refractory period starts with the end of the absolute refractory period and continues through the hyperpolarization phase, but there is no reason it cannot end sooner or later, again depending on gating properties.


What insect is this? (India) Can anyone tell me what kind of insect (if it is one) is this...!! Or is it the pupa of some insect?

Well I don't think that the whole big thing is the insect itself, it appears to be just a kind of protection or shelter which moves along with the tiny little thing that keeps on popping out and going it so as to move.
Location:  India

This is mostly a guess and loose suggestion, since the picture is not very clear (would need to see the larvae in more detail). However, Bagworm moths (Psychidae), Case moths (Coleophoridae) and Caddisfly larvae (Trichoptera, almost exclusively aquatic) all build similar cases. They construct their cases out if silk and often include debris, pebbles and other materials. I wouldn't be surprised if the larvae in your picture belongs to one of the first two taxa. Bagworm moths and Caddisflies generally include lots of external materials in their larval cases, which could point to Case moths for your specimen (which seems to have a weaker case mostly made of silk).

Here are two pictures of first a UK Case moth larvae (Coleophora deauratella) followed by a Bagworm moth (Dahlica triquetrella), just as comparisons. If you do google image searches of "group name + larvae" you will see many examples of what they can look like.

And just as a cool example - the larvae often use random material lying around to build their cases, which can give the following result, if caddisfly larvae are bred in a tank containing pieces if gold and pearls. For further information see this link.


If animals aren't getting tooth decay because they don't eat processed foods, could similar work for humans? In previous question here on stackexchange biology I read that animals don't get dental caries because they aren't exposed to refined carbohydrates like sugars. My question is: in theory, could a human be completely dental caries-free if he followed the diet of not eating any processed food? :))

And also, are fruits like apple or orange 'safe' against dental caries? (since they're not 'processed' sugars?) Thank you kindly for answers.

I think your assumption is wrong : Our small mixed breed had to have all her teeth pulled in 2 operations a year apart. The caries were so bad it damaged her kidneys.  i have had other dogs with caries but not so severe .


Does biofuel production by microalgae need an extra source of CO₂? It is necessary to have extra source of CO2 i.e. from a nuclear reactor or factory chimney to produce bio-fuel by microalgae or is it able to do it with the normal CO2 density in the atmosphere?

Maybe this is easiest understood comparing to our current rate of CO2 consumption to the possible industrial CO2 absorption rate.

Human non biological CO2 production is 29 Gtons.  A little more than four tons of carbon per human being each year.  The natural carbon cycle on the planet through CO2 is otherwise about 788 Gtons.

Is it possible to grow enough algae to balance our current rate of industrial production? I think so - it would be an additional 2% of the current carbon cycle.  In a first pass, that implies turning 2% of the non-productive earth surface into an average patch of ocean or forest/jungle.

This is possible, but it would be expensive.  we're talking about flooding a desert basin for algae production. (numbers are from google).

2% * (area of earth surface = 197million miles^2) = 3.9 M miles^2.

Sounds doable, but remember that 70% of the earth's surface is already water and producing algae at a pretty good clip.  We'd be using ~6% of all the land for the algae farm:

For comparison,  3.9M miles^2 is larger than the continent of Australia.  (2.97 Million miles ^2), and bigger than the Sahara desert (3.6 M miles^2).

just to get into the questions raised in the comments.... To DEPLETE the CO2 level in the atmosphere, we'd have to produce more fuel from the algae than we use - which seems to be impractical from a market standpoint - the fuel would be sitting around in warehouses while the plants die.  I can't imagine anyone making any money from this, and it would be expensive... so it'd be a strange set of circumstances that would deplete the atmosphere from carbon dioxide.  Also more oxygen probably would encourage more combustion and more animals too... so hard to see this happening.


ATP cost for gene expression How would you estimate the number of ATPs required to transcribe, export and translate a single eukariotic protein?

The cost of transcribing and translating a hypothetical average gene in yeast has been calculated as 551 activated phosphate bonds ~P per second (Wagner, 2005).

  The median length of a yeast RNA molecule is 1,474 nucleotides, and
  the median cost of precursor synthesis per nucleotide (derived from
  the base composition of yeast-coding regions) is 49.3 ∼P. With a
  median mRNA abundance of R = 1.2 mRNA molecules per cell and a median
  mRNA decay constant of dR = 5.6 × 10−4 s−1, the mRNA synthesis costs
  calculates as 49.3 × 1,474 × 1.2 × (5.6 × 10−4) = 48.8 ∼P per second
  and cell. This is a fraction 48.8/1.34 × 107 = 3.6 × 10−6 of the total
  RNA synthesis cost per second. The median length of a yeast protein is
  385 amino acids, with a combined biosynthesis and polymerization cost
  of 30.3 ∼P per amino acid. The median abundance is 2,460 protein
  molecules per cell. No currently available data allows a meaningful
  estimate of the median protein half-life, but a protein of an
  intermediate half-life (see below) of 10 h (decay constant dP = 1.92 ×
  10−5 s−1) yields an overall synthesis cost of 30.3 × 385 × 2,460 ×
  (1.92 × 10−5) = 551 ∼P s−1.

For your question about a single gene, the cost would be 49.3 * 1474 ~P for the mRNA and 30.3 * 385 ~P for the translation, which would result in around 84 thousand ~P. This is probably a very misleading statistic as you can transcribe multiple proteins from a single mRNA.

How the cost of mRNA synthesis and translation are calculated is described in detail in the paper. A large part of the cost comes from the synthesis of the basic building blocks, the nucleotides and the amino acids.

Wagner, A. Energy Constraints on the Evolution of Gene Expression. Mol Biol Evol 22, 1365-1374 (2005).


What kind of insect is this found in North America in April? I noticed this small insect that probably measured 5 mm in length on my coat lapel. Not sure whether or not it had been inside or landed outside on my coat. Photos were taken in Nashville, Tennessee, USA in April. It was alone and I have never seen an insect like this one before. Just trying to figure out whether this bug is harmless or something that could be a problem. . Here is another photo taken of the same insect.

It is a ladybug larva.  They eat aphids.  I have handled many and never been bitten.

https://test.whatsthatbug.com/2010/10/25/ladybird-beetle-larva-ladybug/


Where can I download a list of all plant species of the world? Where can I download a complete list or dataset of every plant species in the world?

This website claims to contain all the plant species we know of (and also contains some statistics on the state of their collection). Keep in mind that there are many species that have yet to be found or assessed correctly. The world is a big place.
http://www.theplantlist.org


What is the meaning of Sequestered germline? What is the meaning of Sequestered germline. I understand the meaning of Sequestered in English but what is its meaning in context of germline.

For eg-"  female germ cells are Sequestered early in development ".

"The germ line cells are sequestered" means "the germ line cells are separated from the non-germ line (somatic) cells."


How do place cells switch their response patterns when the subject moves to a different environment? So I understand that place cells form a map of each environment the subject has been in and responds accordingly in each environment. Question is how do they switch to represent a different environment when the subject moves to a new environment? It seems unlikely that a different set of place cells represent each environment the subject has ever encountered because it seems that would require too many place cells (and since the cell counts in the hippocampus is I presume relatively fixed, "free" place cells run out at some point), so it must be the same place cells "remembering" different response patterns to different environment and responding accordingly in different environments.

From the wikipedia page on place cells: "In a different environment, typically about half the place cells will still have place fields, but these will be in new places unrelated to their former locations."

Muller, R. U.; Kubie, J. L. (1987). "The effects of changes in the environment on the spatial firing of hippocampal complex-spike cells". The Journal of neuroscience : the official journal of the Society for Neuroscience.

Imagine a 2x2 grid. Starting on the bottom left, how many different ways can you move to each box of the grid?

Two times: 1) up, right, down; 2) right, up, left

Now, say each of those combinations are used to store the memory of a different location. In order to activate either sequence, a different input signal would be required to tell the axon to send it's initial signal right, or up.

Your eyes will receive a signal in the form up light, and a specific electrical impulse will be sent down the optic nerve that allows your brain to perceive an image.

There are millions of nerves in your brain, and each combination of impulses serves to store a different memory.

Now, imagine a grid that has a million by a million boxes. How many combinations can you use to fill each box?

And, actually if I recall correctly, the hippocampus is one of the few areas in the brain that is consistently undergoes neurogenesis.


Antibacterial hand soaps (and related products); what are they good for? From Wikipedia:

  Household use of antibacterials in soaps and other products, although not clearly contributing to resistance, is also discouraged (as not being effective at infection control).

Following the links led me to this paper:  Larson EL, Lin SX, Gomez-Pichardo C, Della-Latta P.,  Effect of antibacterial home cleaning and handwashing products on infectious disease symptoms: a randomized, double-blind trial.  Ann Intern Med. 2004 Mar 2;140(5):321-9.

They conclude:

  The tested antibacterial products did not reduce the risk for symptoms of viral infectious diseases in households that included essentially healthy persons. This does not preclude the potential contribution of these products to reducing symptoms of bacterial diseases in the home.

Upon reading this, my thoughts were:  Why would one test whether antibacterial products have an effect on viral infections diseases?  Since the authors used a control group (those whose soaps didn't have an antibacterial agent), they are only testing for the effect of the antibiotic.

This leads me to the main question:

  Question:  Which common diseases would likely be more affected by antibacterial hand soaps (and other antibacterial products) than their non-antibacterial counterpart?

This may be related to this question on Skeptics SE:  Does regular handwashing with antibacterial soap prevent disease?  Since it is closely related, I will copy my answer from there to here:
See this related answer.
To answer your specific questions:

Has something changed?

Well, we have access to these products now, whereas we didn't before.

Does this sanitizing really make people healthier?

That is a subject of debate.  While it can prevent rapid spread of some things, keep in mind that anti-bacterial soaps should only have specific uses.
The CDC has concerns about the prevalent use of these products.

Scientists are concerned that the antibacterial agents will select bacteria resistant to them and cross-resistant to antibiotics. Moreover, if they alter a person's microflora, they may negatively affect the normal maturation of the T helper cell response of the immune system to commensal flora antigens; this change could lead to a greater chance of allergies in children. As with antibiotics, prudent use of these products is urged. Their designated purpose is to protect vulnerable patients.

Also, there is some concern as outlined by the hygiene hypothesis (WP).  However, that is mostly associated with childhood immunities and allergies as opposed to the effects on adults.

“The natural immune system does not have as much to do as it did 50 years ago because we’ve increased our efforts to protect our children from dirt and germs,” says McMorris.
“Allergies are on the rise because our society has changed the way we live. As a result, people with allergies are having children with others who have allergies, which in turn creates a natural increase in the prevalence of allergies in our society.

The bottom line on this hypothesis is that more research is required.

He (Richard G. Barbers, M.D., USC professor of medicine at the Keck School) also gives credence to the hygiene hypothesis in that "we may be over-protecting kids, and their immune systems, consequently, do not become well-developed."
Barbers notes that only time and a lot more research will tell whether the hygiene hypothesis is valid, and whether, once again, parents should let their kids play in the dirt.

It is generally understood that interaction with beneficial germs is good for you.  However, normal cleaning will not destroy these germs since they reside within you (unless his germaphobia induces him to take antibiotics).  The human immune response doesn't particularly work that way.

The investigators show that "good" bacteria in the gut keep the immune system primed to more effectively fight infection from invading pathogenic bacteria. Altering the intricate dynamic between resident and foreign bacteria - via antibiotics, for example -- compromises an animal's immune response, specifically, the function of white blood cells called neutrophils.

Using too many anti-bacterial soaps has raised quite a few concerns even still.

Soaps and lotions that include antibacterial agents have no benefit over ordinary soap and water, but more research is needed to allay or substantiate concern that these substances may be leading to increased rates of antibiotic resistance. This is the conclusion of the Food and Drug Administration's Nonprescription Drugs Advisory Committee, which met last month to consider the use of these products outside of the health care setting.
"In the absence of proven benefit, there's no real reason to encourage the use of these products," said Alastair J.J. Wood, MD, committee chair and associate dean at Tennessee's Vanderbilt Medical School.

That is not to say that their use should be discontinued entirely.  Two MDs weigh in and conclude:

Opt for regular soap and water, unless you’re at a hospital or doctor’s office, where it’s best to use antibacterial soap. But if you’re out and about and antibacterial soap is the only kind around, it’s fine to wash with it—and it’s worth keeping in the kitchen to use after handling raw meat.

Hope that helps.


Is a bone marrow transplant limited by sex? Can a female patient get transplanted with bone marrow of a male donor and vice versa?

Short answer: Yes. Because in almost all cases of organ transplant, the organ recipient will be administered immunosuppressive drugs.

There is some literature on the effect of sex on the outcomes. I have included two hints here.

from: http://www.nature.com/bmt/journal/v35/n6/full/1704861a.html

The impact of the donor gender on outcome in HLA-identical sibling donor hematopoietic stem cell transplantation for multiple myeloma was studied in a retrospective registry study of 1312 patients (476 male to male (M → M); 334 female to male (F → M); 258 male to female (M → F); 244 female to female (F → F) reported to the European Group for Blood and Marrow Transplantation (EBMT). The best overall survival (OS) from the time of transplantation was found in F → F (median 41 months) with no significant difference between other groups (median 25 months in M → M, 18 months in F → M, 19 months in M → F) despite a significantly higher nonrelapse mortality in F → M. This was due to a significantly lower relapse rate (REL) in F → M compared to all other groups. Before 1994, OS was poorer in F → M than in M → M, which improved to similarity from 1994 onwards (median 29 months in M → M and 25 months in F → M). The reduced REL contributed to this improvement in F → M indicting a sex-specific graft vs myeloma effect. Therefore, a female donor is as good as a male one for male patients, while for female patients gender disparity is a negative factor for outcome.

from: https://www.broadinstitute.org/news/1386

"It's been clear for some time that bone marrow transplants involving a female donor and a male patient pose a higher risk of GVHD," said Bradner. "This ‘sex mismatch' arises from genes that are carried on the male-specific Y chromosome and are therefore present in males but not in females..."


Do trees grow from the bottom or the top, or is that oversimplifying? I was wondering how trees grow. I wonder if it was similar to hair growth which occurs from the follicle. but clearly branches grow from the trunk so there is definitely a difference with hair growth.

I looked here and couldn't find a verifiable source, there are contradicting answers.

Here it says trees grow from places in places called meristenes, and it denies trees grow from the bottom, but more like from the branch tips and root tips.

If I carve and inscription in a young tree, will it get up with time?

It appears you are mostly interested in the vertical growth of trees. As @Joe Healy points out, this is done only by cells in the apical meristem. This region always remains at the top tip of the tree, that is where the upward growth occurs. The apical meristem, as it continues upward with growth, will leave portions of itself behind that may result in branches (axillary merristems). So yes, unless you carve at the very tip of the tree, your initials will remain at the same height you carved them.

A very simple experiment that I've done many times with students demonstrates this. Germinate some corn seeds until the shoot and the root are about 2 cm long. With a fine Sharpie, mark each with lines every 4 mm or so. Continue the germination. After a few more days you'll note that the line spacings nearest the kernal are the same as when you drew them. But on the very outboard end, near the tips of shoot and root, the spacing will appear stretched out.

Another type of meristem, the vascular cambium, is responsible for the increase in diameter of a tree. It is a sheath that lies between the bark and wood producing new wood to the inside and new bark to the outside.


Red flower with yellow star in center with fig-like leaves This plant has red flowers with a yellow star in the center and has fig-like leaves.

Location: Toronto
Size: 4ft tall by 3ft wide
Date: July 25th, 2020

What is it?

They are common hollyhocks, they come in many colors. As a little kid from Chicago , I was impressed by flowers taller than me when visiting rural Wisconsin . Then the standard for hiding/decoration outhouses.


How to calculate or know by experiment the entropy of enzymes or protein? How do you calculate or experimentally determine the entropy of enzymes or protein?  In particular, I am interested in Boltzmann and conformational entropy, and Gibbs free energy.  Any references are welcome.

In practice, like Energy calculations, Entropy is a relative numbers and difficult to get.  Computational chem and bio have been working on this problem with mixed success.  The summary of what I'm going to say here is that when you try to calculate the differences in entropy (or energy for that matter), the Gibbs Free Energy differences in most biological processes such as enzyme/substrate binding, protein/protein or protein/DNA interactions or protein folding etc is so small compared to the errors in these calculations that the computations are hard to believe.

Entropy is ultimately a term one would use in calculating the Gibb's free energy which will tell whether a given chemical or molecular process will occur.  So it's a valuable number to have.  Gibbs Free Energy (G) equals Enthalpy (heat) minus the temperature (T) times the change in entropy.

G = H - T$\Delta$S

The Entropic term, $\Delta$S is described in chemical systems often as a change in the combinatorial change of the system and the change in the heat capacity of the system. The first of these could broadly described as a 'mixing' term.  When more than one solvents or a solvent and a solute diffuse into each other mix completely, the number of possible states is maximized.

The heat capacity of the system is a more often the focus of entropy calculations for proteins and biological molecules.  This is because the conformations of the biological molecules, especially how free they are to move around are thought to contribute to the entropic part of G.

So attempts have been made to estimate from NMR and crystallography as well as molecular dynamics how much domains and side chains are free to move.  Unfortunately this is only an insufficient proxy for biological entropy.  A substantial if not dominant contribution to the T$\Delta$S term comes from solvent.

How is this so?  Water molecules form structures around proteins which are not static, but do involve many water molecules residing there on the average to see them in crystal structures and NMR experiments.  While the individual waters are exchanging rapidly, they are not in the same entropic state in water solution as they are when they form a hydration shell around an aromatic or charged side chain.

Attempts have been made to parametrize the solvent entropy by looking at the buried nonpolar surface in a folded protein, looking at the mobility of sidechains before and after folding/binding, but these metrics appear to be configuration dependent to the point that they can't calculate the protein entropy via these efforts, at least heretofore.

Conventionally, molecular dynamics tries to calculate this by surrounding the proteins or other molecules with water molecules and some approximation of the overall entropy is calculated on the entire system.  It turns out that small differences between the water molecular models and the simplifications in ball and stick/Hooke potential water models we make are also problematic approximations when there are hundreds or thousands of water molecules in the simulation.


Do people even notice when insects other than butterflies and beetles go extinct? Lists of endangered animals only include beetles and butterflies if they bother to mention insects at all. Here is an example from where I live:

http://www.dec.ny.gov/animals/7494.html

All of the insects are beetles, dragonflies, moths, butterflies and there is a mayfly, but that is kind of similar to a butterfly when it comes to their "fanbases." Where are the ants, lice, silverfish and aphids? Is there a better list?

I am not aware of a better list, but you are right that (1) many insects have gone extinct recently, and (2) documentation of insect extinction is poor.  An article in Conservation Biology (2005) says

  The biodiversity crisis is undeniably an insect biodiversity crisis. Yet insect conservation remains the awkward “kid sister” to vertebrate conservation. Nowhere is this clearer than in what we know, or rather do not know, about insect extinction, particularly for those extinctions that may have already occurred. ... What accounts for the tens of thousands of expected but undocumented insect extinctions? What does this discrepancy mean? How important is it to our understanding of extinction and the future of ecosystems? These should be questions at the heart of species conservation, yet they have hardly been addressed. No peer-reviewed articles have been published reviewing modern insect extinctions, and no estimates of global extinction rates have explicitly focused on insects.

--Modern Insect Extinctions, the Neglected Majority (my emphases)

The book Insect Conservation Biology (2012) may have more info, though it still seems to focus heavily on the more charismatic species like butterflies.


Why do mutations in Drosophila dsx (double sex) affect both males and females? Reason: Loss-of-function mutation of dsx gene in female embryo leads to production of a nonfunctional protein that fails to repress male specific gene expression. So somatic characters of both the sexs persist forming an intersex.
...This is all that I have figured out.

But what is the reason of appearance of intersex characters in male drosophila? Is it due to gain-of-funnction mutation.

Expression of the double-sex gene is rather unusual, so it is not surprising that you are having difficulty understand mutations in it. The simplified diagram below (adapted from Gilbert’s Developmental Biolgy — available on-line) should help clarify the matter.

The key concept is that although the double-sex gene (dsx) is expressed in both male and female flies, the gene products (DsxF add DsxM) are different in the two cases. This is achieved by alternative splicing of the RNA transcript, controlled ultimately by X and Y chromosome dosage. (If you are unfamiliar with alternative splicing, see e.g. this section of [Molecular Biology of the Cell (http://www.ncbi.nlm.nih.gov/books/NBK21558/).)

The second important concept (the details of which, I admit, I am less familiar with) is that sex is determined by both activating genes specific for the particular sex and inactivating genes for the opposite sex. Thus, the diagram shows that DsxF both activates expression of genes for female sex differentiation and represses expresses of genes for male sex differentiation. Likewise DsxM activates expression of genes for male sex differentiation and represses expresses of genes for female sex differentiation.

Thus, according to this schema, if dsx is completely knocked out there will be consequences in both male and female. In the female, in the absence of DsxF, the genes for female sex differentiation will not be activated, but those for male sex differentiation will not be repressed. This presumably results in the intersex phenotype. Likewise, in the male, the absence of DsxM prevents the expression of the genes for male sex differentiation, but does not repress those for female sex differentiation. Again, I presume this results in the intersex phenotype.