Why are men more susceptible to severe COVID-19? It seems that globally, men are more susceptible to severe COVID-19 than women:

https://www.theguardian.com/world/2020/mar/26/men-are-much-more-likely-to-die-from-coronavirus-but-why

This is seen in other coronavirus diseases (SARS, MERS) but not respiratory diseases generally. Do we know the reasons for this?

Update -- In the time since this question was asked, two relevant articles have been published, one in Nature Reviews Immunology and one in medRxiv (note: medRxiv is a preprint server and is therefore not peer reiewed).
Scully, E.P., Haverfield, J., Ursin, R.L. et al. Considering how biological sex impacts immune responses and COVID-19 outcomes. Nat Rev Immunol (2020).
Takahashi, T., Wong, P., Ellingson, M., et al. Sex differences in immune responses to SARS-CoV-2 that underlie disease outcomes. medRxiv (2020).
Besides the genetic factors related to viral entry that I've explained below, these papers explain the immunological factors that may determine the higher susceptibility of males to severe SARS-CoV-2 infection, including sex-specific differences in early antiviral response, innate immune repsonse, and adaptive immune response.  Figure 2 of Scully et al. provides a graphic summary.

Genetic factors
SARS-CoV-2 entry into human cells is thought to depend on two human proteins:

ACE2 -- a transmembrane protein important for blood pressure control.1  The viral spike protein binds the enzymatic domain of ACE2, facilitating translocation of the virus into the cell.2
TMPRSS2 -- a serine protease with a transmembrane domain.  The proteolytic activity of this enzyme is thought to play a role in "priming" the viral spike protein.3

So, a place to start would be to ask if there are sex-specific differences in the expression or localization of these proteins.
ACE2
No significant differences in lung ACE2 activity have been found between male and female mice.4  In rats, however, lung ACE2 levels are reduced with aging in both males and females, with significantly higher ACE2 expression in old female rats compared to old males.5 Assuming that rats are a good model for sex-specific human lung protein expression, this observation counters the simple explanation that men are more likely to have severe COVID-19 due to higher ACE2 expression.
A recent preprint 6 presents an interesting hypothesis -- that ACE2 mosaicism due to X inactivation may be protective against SARS-CoV-2 in women.
From the abstract:

The fact that the human ACE2 protein is encoded on the X chromosome means that males who carry rare ACE2 coding variants will express those variants in all ACE2-expressing cells, whereas females will typically express those variants in a mosaic distribution determined by early X-inactivation events.

So, since males are hemizygous for the X-chromosome, males that have an ACE2 variant that binds strongly to the SARS-CoV-2 spike protein will only express that variant in their lungs.  Females have two X-chromosomes, though only one is expressed in any given cell due to X-inactivation.  If a female is heterozygous at the ACE2 locus, with one allele that encodes a protein that strongly binds SARS-CoV-2 spike protein and one allele that encodes a protein that weakly binds SARS-CoV-2 spike protein, mosaic expression of the maternal and paternal alleles may give partial protection from infection.
The authors found that ACE2 is generally intolerant of loss-of-function variants, though many missense variants occur at and near residues predicted to bind SARS-CoV-2.  Such variants were detected at a rate of 3.9 males per 1000 and 8.5 females per 1000.  However, the most popular missense variant, rs41303171, does not lie in a domain of ACE2 that is predicted to interact with SARS-CoV-2.  Additionally, this SNP is only observed in 1.7% of male and 3.1% of female samples, so it is not obvious that this explanation can account for the sex-specific discrepancy in severe COVID-19 at the population level.
TMPRSS2
Currently, evidence suggests that there are no sex-specific differences in TMPRSS2 expression in the lungs of humans or mice.7  Note, however, that only transcript levels have been evaluated in this context, and that TMPRSS2 activity would need to be evaluated to determine that proteolytic action is not different between sexes.

Non-genetic factors
Worldwide, men smoke five times as much as women.8
Smoking is co-morbid with severe COVID-19 9, likely due to decreased lung capacity, though possibly through a mechanism involving increased TMPRSS2 expression.7  From the same TMPRSS2 paper cited above:

regardless of sex, smoking significantly increases the expression of TMPRSS2, which reverts back to never-smoker levels in former smokers

Indeed, one recent study of more than 1,000 COVID-19 patients reported greater than two-fold increased risk for intensive care unit admission and death in smokers as compared with non-smokers.10
There may be cultural factors affecting disease progression, as well.  If men are less likely to wear masks or follow other guidelines to reduce the risk of infection, then infected men may be exposed to a higher infectious dose than women. Initial infectious dose may be positively correlated with viral load 11, and higher viral load is associated with a more severe prognosis for SARS infections.12
It could simply be the case that symptomatic men are less likely to be tested (a "tough it out" mentality), and therefore would be less likely to receive treatment that prevents a mild infection from becoming severe.

Citations

A Novel Angiotensin-Converting Enzyme–Related Carboxypeptidase (ACE2) Converts Angiotensin I to Angiotensin 1-9
SARS coronavirus entry into host cells through a novel clathrin- and caveolae-independent endocytic pathway
Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites
Sex differences in renal angiotensin converting enzyme 2 (ACE2) activity are 17β-oestradiol-dependent and sex chromosome-independent
Age- and gender-related difference of ACE2 expression in rat lung
ACE 2 Coding Variants: A Potential X-linked Risk Factor for COVID-19 Disease
No evidence that androgen regulation of pulmonary TMPRSS2 explains sex-discordant COVID-19 outcomes
Gender empowerment and female-to-male smoking prevalence ratios
COVID-19 and smoking: A systematic review of the evidence
Clinical Characteristics of Coronavirus Disease 2019 in China
SARS-CoV-2 viral load and the severity of COVID-19
Initial viral load and the outcomes of SARS


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

To answer your second question, one of the main reasons primers anneal before your target re-anneals to itself is not because it binds stronger, but because you add primers in large molar excess to their targets.  The primers will find your template faster than your template will find another matching template, and once the primer is annealed the template cant bind onto another template even if that reaction is more energetically favorable.  This molar excess is a requirement for the exponential amplification in PCR, and when you start to lose the excess primer concentration you lose exponential increase due to your targets re-annealing (and you get the production of unwanted PCR artifacts like chimeras).  As for the temperature, it depends on your template, but I guess it has to be somewhere between the primer annealing temp and the temp of your melting step.


All-or-nothing-law: law or general principle? The all-or-nothing principle indicates that a nerve cell fires at maximum potential or not at all, based on a threshold on the stimulus.

Is this a statement which is always true, or only mostly-always true?

In electrical engineering, a discipline I have studied, we have a similar rule, a logic signal is responded to as though it is either a high or a low.  However, in the middle are what are known as "metastable states," where the rules of thumb do not apply.  In fact, you can even theoretically lock up a logic circuit by presenting a steady stimulus in between two states.  Needless to say, designers of such circuits take great effort to ensure their logic is never exposed to such stimulus.

Do we have any evidence of neurons exhibiting behavior which defies the all-or-nothing law in some circumstances, or if not, what sorts of metastable behavior are seen when the stimulus is exceedingly close to that of the threshold?

I would argue the all-or-none principle is a rule of thumb. It is generally true if voltage hits a certain threshold then there will be a action potential with the same amplitude regardless the strength of the stimuli. But as you point out with the logic gate example, the threshold is notoriously hard to define mathematically. Furthermore Action Potentials don't always have the same amplitude, but as I will argue that doesn't matter all that much to the function of the neuron.

As most rules in biology we can find exceptions. I'll list some phenomena that confound the all or none principle.

Accommodation is the prime example that not all action potentials have the same voltage amplitude. Accommodation is the when the amplitude of the voltage of successive action potentials drops, and may even stop firing (Depolarization Block). This is usually the result of a too strong of a stimulating current, and occurs under pathological conditions.
Resonating Neurons These neurons fire when a certain frequency of input is achieved and can even fire when hyperpolarizing (negative) currents are injected. The reason I bring this particular neuron  type up is it shows that thresholds are not necessarily more depolarized (positive) than rest. They are complex manifolds (or shapes) relating to the gating variables of Ion channels in the membrane.

Another thing to note, is even though amplitudes of Action potential can change, the difference of a few millivolts in amplitude will not make a difference to the synapse and in that sense the all-or-none principle holds. Recall that voltage gated Calcium entry is required for a synapse to release it's neurotransmitter. Much like the logic gate, it will only enter at sufficiently depolarized (positive values) but the more positive the voltage, does not correspond to more Calcium entry. In other words it saturates at high voltages. In this way, to cause a stronger response at the synapse the neuron increases the firing frequency to stay "on average" depolarized longer. Thus more Calcium entry and thus more neurotransmitter release.


Earliest and latest onset of Huntington's Disease(Chorea)? Huntington's disease can hit at any age, although it tends to hit middleaged people most often. What is the youngest and oldest person that has exhibited Huntington's?

Clarification: By oldest I mean with no prior symptoms until the age.

Huntington's disease may become symptomatic starting from as low as 2 years old [1] and rarely after 55 years old [2] (yet there is evidence of onset at 65 years old [3] and even more according to newer studies).

Figure: Copyright © 2004, The American Society for Experimental NeuroTherapeutics, Inc.
Richard H. Myers. Huntington’s Disease Genetics. NeuroRx. Apr 2004; 1(2): 255–262. doi:  10.1602/neurorx.1.2.255. PMCID: PMC534940

Factors [4]:

CAG number (65%-71% of the variance in age of onset)
siblingship (11%-19%)

  [...] paternal age is negatively associated with age at onset of HD (Huntington's disease), particularly among subjects who inherit the mutant gene from grandfathers [5].

References:

Huntington's Disease Society Of America. What is Huntington's Disease (HD)? Available from http://www.hdsa.org/about/our-mission/what-is-hd.html (accessed 26.10.2014)
National Institute of Neurological Disorders and Stroke. Huntington's Disease: Hope Through Research Available from http://www.ninds.nih.gov/disorders/huntington/detail_huntington.htm (accessed 26.10.2014)
Myers RH, Madden JJ, Teague JL, Falek A. Factors related to onset age of Huntington disease. Am J Hum Genet. 1982 May;34(3):481-8. PMID: 6211092. Full text available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1685335/
Rosenblatt A, Brinkman RR, Liang KY, Almqvist EW, Margolis RL, Huang CY, Sherr M, Franz ML, Abbott MH, Hayden MR, Ross CA. Familial influence on age of onset among siblings with Huntington disease. Am J Med Genet. 2001 Jul 8;105(5):399-403. PMID: 11449389. Available from http://www.ncbi.nlm.nih.gov/pubmed/11449389
Farrer LA, Cupples LA, Kiely DK, Conneally PM, Myers RH. Inverse relationship between age at onset of Huntington disease and paternal age suggests involvement of genetic imprinting. Am J Hum Genet. 1992 Mar;50(3):528-35. PMID: 1531729. Full text available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1684271/


Entropy and Open Systems - AP Biology I had the following question on an exam of mine and I got the points for the question, but I am wondering if someone could please explain why it is correct, or rather, if it is correct at all:

  As living organisms grow, they increase in complexity and decrease in entropy. How does this relate to the second law of thermodynamics?

  (A) Living organisms, like everything else in the universe, spontaneously decrease in entropy over time.

  (B) The increase in entropy of the universe exactly balances out the decrease in entropy as the organism grows.

  (C) Energy cannot be created or destroyed, so the energy used for growth is later used to increase entropy.

  (D) The resulting increase in entropy of the universe is greater than the decrease in entropy associated with the growth.

I answered D, as it seemed like the most likely answer out of all of them, and I got the points.

According to the 2nd Law of Thermodynamics, the entropy of the universe will increase with time.

Please correct me if I am wrong, but from my understanding this only applies to closed systems--so how exactly would it apply to organisms (which are open systems)? Is it because organisms release heat through chemical reactions and thus add to the entropy of the universe while decreasing their own entropy?

Thank you!

-Aleksandr

You are correct. Anything within the universe is part of the closed system of the universe. Therefore, they must also increase the entropy of the universe. You are correct, they do release a lot of heat. Plus, while making ATP, the major source of cellular energy, they convert a complex molecule, glucose, to simpler molecules, H2O and CO2, increasing entropy as they release these chemicals.

Also, the key fact is that to lower entropy in their body, organisms must use up energy. Energy is required to avoid the entropy from increasing (which actually means they actually expend energy to prevent equilibrium; high entropy means reaching equilibrium). So they would follow the 2nd law of thermodynamics. Which reminds me of a joke!

Old chenists never die, they just reach equilibrium!


Praying mantis identification I found this praying mantis in Bangalore, India. It is around 6 cms in length and has a distinct marking on the forelimbs. Can I know the species ?

.. according to a taxonomical key that I found, I think it may belong to the genus 'Hestiasula'.

You're absolutely correct! This is of the species Hestiasula brunneriana, and is belongs to a group of praying mantis that are referred to as "Boxer mantises", due to their enlarged raptorial forelegs, of which are used for communication.

And though I can't quite tell, but at first glance this appears to be a female, due to what seems to be a longer than not abdomen; a female will only have 6 segments, whereas a male will have 8, however, the segments belonging to the female will be longer than that of the males. If you can somehow get an underbelly image, a much more definitive statement can be made.

The following image accurately matches your aerial image:

And then here's an image that demonstrates those distinct black markings on the raptorial forelegs:


How did Shulgin take cognizance of the dosage of a new substance? We know that Alexander Shulgin synthesized MDMA, 2C compounds and several other tryptamine derivatives and phenethylamines. But how did he find out that the average dosage of an unknown compound is X mg? For instance, if I synthesized a new psychoactive compound, how could I find out the dosage?

He didn't.
It was basically a matter of trial and error. Of course, having previous experience with other psychotropics of the same class helped him to have a rough estimate: in the case of MDMA, Shulgin was neither the first one to synthesize it nor the first one to use it, and he knew beforehand that the psychoactive dose was between 100 and 200 mg. Besides that, being a rational chemist, he started by what he supposed to be the smallest, safe dose.

Alexander Shulgin
For instance, regarding MDMA, Shulgin (2010) describes the following dosages (I'm copy/pasting only the start of each paragraph):

(with 100 mg) Beforehand, I was aware of a dull, uncaring tiredness that might have reflected too little sleep, and I took a modest level of MDMA to see if it might serve me as a stimulant...
(with 120 mg) I feel absolutely clean inside, and there is nothing but pure euphoria...
(with 100 mg of the "R" isomer) There were the slightest of effects noted at about an hour (a couple of paresthetic twinges) and then nothing at all...
(with 160 mg of the "R" isomer) A disturbance of baseline at about forty minutes and this lasts for about another hour...
(with 200 mg of the "R" isomer) A progression from an alert at thirty minutes to a soft and light intoxication that did not persist...
(with 60 mg of the "S" isomer) The effects began developing in a smooth, friendly way at about a half-hour....
(with 100 mg of the "S" isomer) I feel the onset is slower than with the racemate...
(with 120 mg of the "S" isomer) A rapid development, and both writing and typing are impossible before the end of the first hour...

Unfortunately, he doesn't explicitly say what was the sequence of the dosages he took... I can only assume it was the sequence of the paragraphs.
However, by far, the best example of how "blind" the chemist is regarding the adequate dosage of a unknown psychotropic is the famous case of Albert Hofmann, who invented LSD (not as a psychotropic) in 1938.

Albert Hofmann
When he decided to test LSD, in 1943, he ingested 250 micrograms... well, that's almost ten times a typical "street" dose of LSD nowadays, which is around 20 micrograms. Luckily for him, overdose of LSD (up to more than 100 times the amount he used) is not lethal.

Source: Shulgin, A. and Shulgin, A. (2010). Pihkal: A Chemical Love Story. Berkeley: Transform.


Why does the affinity of haemoglobin for oxygen decrease at high altitudes? My class 12 NCERT book says, Pg 226

  The body compensates low oxygen availability by increasing red blood cell production, decreasing the binding affinity of haemoglobin and by increasing breathing rate.

Why should the haemoglobin binding capacity decrease at high altitude?

I think it should increase for better oxygen transfer and uptake from air. The concentrtion of oxygen in the atmosphere decreases with height. Hence, if the haemoglobin binding increases, we will be able to draw more oxygen from the air and transport it to the cells.

The answer to this question is yes, a decrease in oxygen affinity will decrease the oxygen taken up by the haemoglobin (Hb), but it is an appropriate response because it will have a greater effect in increasing the release of oxygen to the tissues.

This is not intrinsically obvious. It happens because of the (sigmoid) shape of the oxygen binding curve, and can only really be appreciated if you examine the curves for the normal situation and that in which there is increased 2,3 Bisphosphoglycerate (2,3-BPG) producing the change in oxygen affinity. I have devised a figure to demonstrate this, although it is not based on actual data, so should only be regarded as illustratative.

At sea level the lungs pick up oxygen at 1 (say 100% saturation of
Hb) and when the oxygen pressure drops to 40 mm Hg in the tissues (2)
the Hb will be 55% saturated. Hence in this example they have
released 45% of a full complement of oxygen.
If we look at the same curve for high altitude, in this example the oxygen pressure at the lungs (1') will be such that the Hb is only 80% saturated. Thus at 40 mm Hg in the tissues (2) when Hb is only 55% saturated it will only have released and made available 25% of a full complement of oxygen.
Now consider the effect of high altitude acclimatization with increased 2,3-BPG production changing the equilibrium and the oxygen binding curve (red). At the lungs (3) the Hb will be less charged with oxygen — only 70% saturation — but at 40mm Hg in the tissues (4) it will be much less saturated than on the black curve — 30%. Thus it will have made available 40% of a full complement of oxygen.

This is not a perfect solution, which is why over a longer term there is increased production of red blood cells to provide more haemoglobin to compensate for the smaller amount of oxygen it can bind.


Do dingos show wolf 'characteristics'? I've read that Russians have been performing selective breeding on Red Foxes for about fifty years, aiming to make them tame. The wikipedia article says

  The experiment was initiated by scientists who were interested in the
  topic of domestication and the process by which wolves became tame
  domesticated dogs. They saw some retention of juvenile traits by adult
  dogs, both morphological ones, such as skulls that were unusually
  broad for their length, and behavioral ones, such as whining, barking,
  and submission.

I wonder, since dingoes are completely wild dogs that have only relatively recently split off from domesticated dogs, do they show more 'wolf-like' characteristics? That is, has their life in the wild selected against domestication genes?

I think any domestic animal that reverts to the wild is going to experience some genetic change given an evolutionary timescale. As you probably know, dingoes are descended from dogs introduced to Australia by early human migrants. Their ancestors were thus presumably domesticated or at least semi-domesticated.

Also, the Indian wolf is a subspecies of Canis lupus, which ranges across Eurasia and North America both.

I think this article may shed some light on your question:

It sounds like the dingo may have developed some traits that distinguish it from wolves and domestic dogs both.


Schizocoely and Enterocoely In terms of phyla, mollusca, annelida and arthropoda are schizocoelic, whereas echinodermata and chordata are enterocoelic.

I know that their difference lies in the formation of the coelom but how exactly is enterocoely more advanced than schizocoely?

Neither is "more advanced" than the other, they are separately evolved mechanisms to form a gut.

You may be misled by a human-centric view that treats humans and animals more humanlike as more advanced or "more evolved" than other animals but this is not true: all life has been evolving for the same length of time.


What indices can we use to describe fitness landscapes? We usually talk of smooth or rugged fitness landscape.

Are there any (standard) indices to measure the "structure" of fitness landscapes?

For example, one might consider the mean epistatic interactions (over all possible combination of loci)

This paper uses 4 metrics for discreet landscapes.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240586/

Deviation from additivity: How much your genes interact (normalized). Fitness in a purely additive landscape with three genes, for example, is F=f(x)+g(y)+h(z) where f,g, and h are each functions of one variable (the x,y, and z "genes"/coordinates). Deviation measures how far from additivity the fitness is. Higher is not always rougher but it is "trickier" since the effects of changing a gene depend on other genes.

Peak fraction: The % of points that are local peaks (discreet landscapes only), higher is rougher.

Tree component: The % of points that have at most one neighbor of higher fitness. Lower is rougher and indicates that there is a choice as to which direction to travel.

% monotonic paths: The fraction of paths (of all possible shortest paths from a given point to the peak) that don't go downhill. This calculation is averaged over all starting points in the landscape (excluding the peak). Lower is rougher.


Can 5 alpha reductase inhibitor drugs work for life or do they lose effectiveness? Do 5 alpha reductase inhibitor drugs like finasteride and dutasteride lose their effectiveness over time? Why do some drugs, like in an HIV regimen, work for a prolonged time without tolerance whereas other drugs, for example antidepressants, have tolerance issues after a short time?

As noted in a comment, a truly thorough answer to this question would require one or more books (1,2) or scientific journals (3), but a simpler, necessarily incomplete answer can be provided.

The short answer is: transmembrane drug transporters of the ABC family (4)

But what are those? Well, you should read the wikipedia article for a detailed description, but essentially they're proteins that burn energy in order to remove a broad range of drugs from the cytoplasm, making them less "bioavailable". The answer to why some drugs (or broad spectrum treatments with multiple drugs) are more or less susceptible to export by ABC family proteins is much more complicated (buy books from (1) and (2) or similar texts(5)), but the broad spectrum HIV regimen prevents resistance by a completely different mechanism (6).

Briefly, ABC transporter-mediated resistance involves no evolution, simply a "transcriptional response" to the presence of harmful drugs, while HIV actually evolves to become resistant or immune to antiretroviral drugs. However, it's difficult or impossible to be virulent (fast replication) and hardy (drug resistant and/or immune system resistant) at the same time, so mutations which increase resistance to one drug also decrease virulence - if you treat HIV with enough drugs then the mutations required to be resistant to all of them will result in a virus that has very poor virulence.

(1) http://www.wiley.com/WileyCDA/WileyTitle/productCd-0470927941.html

(2) https://www.amazon.com/gp/search?index=books&linkCode=qs&keywords=9781782620693

(3) https://scholar.google.com/scholar?q=human+drug+transporters&hl=en&as_sdt=0&as_vis=1&oi=scholart&sa=X&ved=0ahUKEwjVh6-a8aPPAhVK1B4KHfxABSsQgQMIGjAA

(4) https://en.wikipedia.org/wiki/ATP-binding_cassette_transporter

(5) https://www.google.com/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=human+drug+transporters&tbm=bks

(6) https://en.wikipedia.org/wiki/HIV_drug_resistance


Are there any arboreal mammals which eat leeches? Are there any tree-dwelling mammals which might be found taking a living leech and eating it?

(And do any hollow-dwelling birds of prey eat leeches?)

First I'd like to point out that there are over 500 species of leeches. Most of them live in fresh water (nearly 90%), and so most tree-living animals would not come into contact with these leeches. Because of this a leech's biggest predator would be fish.

According to The New World Encyclopaedia the predators of leeches are fish, crayfish, turtles, birds, frogs, dragonflies, and damselflies. It states that many of their predators have also been their prey. Ecospark also adds snails and other insects to the list. Biokids also points out that leeches will eat other leeches.

Britannica cautions humans about swimming and drinking water with leeches in it. They can attach to internal cavities - such as the nose and throat and then the leeches can drop into the lungs and cause suffocation. In Asia, it is common for a domesticated animal to die in this fashion.

According to Animals.mom.me monkeys and other omnivorous animals will eat leeches that live on land, but land leeches aren't very common. After over an hour of searching various websites and information about leeches, there is no other source stating that mammals eat leeches.

However, it is possible to eat leeches. They did it on a television show called Fear Factor (video of the leeches being eaten linked). Before you go eating leeches though, remember these people were monitored both during and after ingestion of the leeches.

Short answer: There are no recorded mammals as predators to leeches, but it is known that pets have eaten leeches (as well as breathed them in). And humans are also able to eat leeches. It's all about if the leech is within grabbing distance when the mammal is hungry.


Do I not have any alleles from my mom's mom & my dad's dad? So, I have an XX, & I got an X from my mom, & an X from my dad. My dad would have gotten his only X from his mother, & my mother could have gotten the X I got from her father or mother. That would mean I did not get either X gene from either my mom's mom or dad, or my dad's dad - does that mean that I have "less" of their genetics in me? Say I got my mom's dad's X, would that mean I have less of my mom's mom's genetic traits?

Speaking of your DNA in general, you have alleles from all four of your grandparents.  The 22 pairs of autosomes (non-sex chromosomes) can receive DNA from all four with random mixing.  On a few chromosome pairs you may be missing alleles from one of your grandparents due to the randomness, but on average you will have about a quarter of your autosomes from each of them.
The X (and Y, for males) chromosomes are special, though.  The X you inherit from your mother will have alleles from both your maternal grandparents.  The X that you, as a female, get from your father has no alleles from his father, so that grandfather's X alleles are always missing from your genome.
Because of the random mixing, you will have slightly varying amounts of DNA from each of your grandparents: it won't be exactly 25% for each of them.  Because of the special X inheritance, your paternal grandfather will on average contribute slightly less than the other three grandparents.  (Because of another quirk, mitochondrial inheritance, your maternal grandmother will contribute on average a very small amount more than the other three grandparents.)


Identification of a segmented black insect in France Found in the Lot department of southern France.

I think this is some sort of soldier fly larva (family Stratiomyidae). That would explain lack of legs. There are thousands of species world wide, with both aquatic and terrestrial larvae, so it might be possible to narrow it down a bit more.

Image from bugguide.net for comparison:

Thanks to @bli for reminding me of dipteran larvae!


Which concentration of BSA is recommended for dynamic light scattering experiments? What is the recommended concentration of BSA to be mixed with water so as to prepare a very dilute solution in order to clearly study the intensity-intensity correlation with single scattering ?

I want to plot the intensity vs time correlation curve/graph, and eventually calculate the hydrodynamic radius in each case. I've seen different journals and texts provide varied concentrations ranging from 0.001 g/L to 3 g/L.


What are the basic skills required to pursue future studies in theoretical ecology? I am a student and just about to choose a project for my Master's thesis in biology. I want to pursue studies in theoretical ecology in the future. Between field ecology and computational biology (as my two possible choices) what would be the best option to go for? Suggestions are needed as soon as possible .

Theoretical ecology
From wikipedia

Theoretical ecology is the scientific discipline devoted to the study of ecological systems using theoretical methods such as simple conceptual models, mathematical models, computational simulations, and advanced data analysis. Effective models improve understanding of the natural world by revealing how the dynamics of species populations are often based on fundamental biological conditions and processes. Further, the field aims to unify a diverse range of empirical observations by assuming that common, mechanistic processes generate observable phenomena across species and ecological environments. Based on biologically realistic assumptions, theoretical ecologists are able to uncover novel, non-intuitive insights about natural processes. Theoretical results are often verified by empirical and observational studies, revealing the power of theoretical methods in both predicting and understanding the noisy, diverse biological world.
The field is broad and includes foundations in applied mathematics, computer science, biology, statistical physics, genetics, chemistry, evolution, and conservation biology. Theoretical ecology aims to explain a diverse range of phenomena in the life sciences, such as population growth and dynamics, fisheries, competition, evolutionary theory, epidemiology, animal behavior and group dynamics, food webs, ecosystems, spatial ecology, and the effects of climate change.
Theoretical ecology has further benefited from the advent of fast computing power, allowing the analysis and visualization of large-scale computational simulations of ecological phenomena. Importantly, these modern tools provide quantitative predictions about the effects of human induced environmental change on a diverse variety of ecological phenomena, such as: species invasions, climate change, the effect of fishing and hunting on food network stability, and the global carbon cycle.

Computational Biology
from wikipedia

Computational biology involves the development and application of data-analytical and theoretical methods, mathematical modeling and computational simulation techniques to the study of biological, behavioral, and social systems.1 The field is broadly defined and includes foundations in computer science, applied mathematics, animation, statistics, biochemistry, chemistry, biophysics, molecular biology, genetics, genomics, ecology, evolution, anatomy, neuroscience, and visualization.2
Computational biology is different from biological computation, which is a subfield of computer science and computer engineering using bioengineering and biology to build computers, but is similar to bioinformatics, which is an interdisciplinary science using computers to store and process biological data.

Field Ecology
Ecology can be studied empirically through data analysis, through lab experiments or through field observations and experimentations. Field ecology refers to this last point that is, it refers to empirical ecology in the field.
Conclusion
Potential Misunderstanding
In your post, you seem to suggest that field ecology is a subfield of theoretical ecology. It is not! Either you work as a theoretician or as an empiricist (and then eventually as a field ecologist). Of course many people do both theory and empiric work.
Note that whether you are theoretical or an empiricist working in ecology, you will need to have a good understanding of the theory behind the science of ecology.
Computational biology vs theoretical ecology
In opposition to empirical ecology and field ecology, computational biology and theoretical ecology do not have a hierarchical relationship. If you work in theoretical ecology you can make analytical modelling or numerical (computer) modelling. If you work in computational biology you could analyze data in genetics, you could model cell processes, you could simulate interacting populations in ecology and many other things.
What should you chose?
What skills do you need?

Do you like data analysis (statistics and R and python coding)? You will have to analyze your data whatever you chose!

Do you like numerical simulations (lots of coding, incl. languages like C++)? If no, then maybe avoid computational ecology!

Do you like analytical modelling (lots of math)? If no, then maybe avoid making analytical models in ecology!

Do you like messy, complicated, tiring field work? if not, then maybe avoid working as a field ecologist.

What would you imagine to work on?

What question would you like an answer to? Think about it and try to understand how you would address the question you are trying to answer.

My advice

Do not be afraid of any field, any technics, any programming language, etc... You are good enough and have enough time to learn what you do not know.

Do whatever you like most!


difference between trisomy and partial trisomy Trisomy is having 3 chromosomes but then what is partial trisomy ?. I was reading about Patau syndrome and it is called trisomy 13 ( because instead of usual 2 chromosomes,it has 3 chromosomes). it was also wriiten that 20% cases are PARTIAL TRISOMIC...what is the meaning of partial trisomic?

Any organism with a partial polyploidy has got some tissues with a different number of chromosome set, unlike the rest of cell tissues.
These situations are often consequences of meiosis error and are more common in plants than in any other organism.


Why are fibroblast used so commonly in cell biology? Fibroblasts are some of the most commonly used cells in cell biology. What are the properties of those cells which makes them commonly used ?

From the comments by Shigeta and WYSIWYG :-

1.They are easy to get and they can be preserved and used over time.

2.They can be differentiated easily.

3.Due to historic reasons - someone getting lucky and finding a protocol for these cells.


What are the ESSs among hawks, doves, retaliators, bully and prober retaliators? In his book "The Selfish Gene", Richard Dawkins says that retaliator emerges as an evolutionary stable strategy. But I think dove is also a kind of retaliator and so if dove increases,  the hawks and others can exploit them.

Is retaliator an ESS? If not, which strategy is ESS?

Definitions:

hawk : They always fight hard and retreat only when injured.
doves : They merely threaten in a dignified way and never hurt anyone.

If a hawk fights a dove, dove runs away. If dove meets dove they go on posturing until one of them is tired and retreats. If a hawk meets hawk they fight until someone gets seriously injured or dies.

retaliators : A retaliator plays dove at the beginning of every fight. If opponent attacks, he attacks , if opponent behave like a dove he behaves like a dove. When 2 retaliators meet they behave like doves.
bully : A bully behave like a hawk until someone hits back. Then, he runs away.
prober retaliator : He is like a retaliator but he tries a brief escalation of the contest. He is hawk like if opponent doesn't strike back. If opponent strikes back he behave like a dove. If he is attacked he retaliates.

The pay offs: 50 for winning, 0 for losing, -100 for being seriously injured. and -10 for wasting time in a long contest.

Source: The Selfish Gene

I think Dawkins answers this in the book as well.

The point was that most strategies are not stable because the "random" introduction/mutation/evolution of some alternate strategies will disrupt a population of the first strategy.

The example was a group of doves being invaded by a single hawk (the conspiracy of doves). Because the hawk does relatively better (by winning every conflict against a dove), than even after generations of entirely doves, the random addition of a hawk (say by mutation) will take hold because the hawk always wins against a dove. Whatever feature/gene that created a hawk in the pool of doves will be passed to some offspring.

If I remember correctly, the only stable case was prober-retaliator, since all others get invaded by someone else.


What British bat is this? What kind of bat is this? I saw it flying quickly between trees in Buckinghamshire, UK, at about 4pm in September (so about three hours before sunset). I think it might be a common noctule but I was surprised to see that there are something like fourteen other British species to choose from.

Sorry the photo quality isn't amazing but it was hard to capture anything at all!

I would guess that it's a noctule (Nyctalus noctula) also.  The Bat Conservation Trust has a nice UK section with fact sheets for the 18 different species of bats found there.  It seems you can rule out the long eared bats by the photo and the pipistrelle because you didn't mention it flying eratically.  The fact that it was out so early seems to narrow it down to either the noctule, which is usually the first to appear, or the leislers (Nyctalus leisleri) which appears shortly after the noctule.  A distinguishing feature of the noctule is a mushroom shaped tragus, and for the leislers is long fur around the shoulder and back.  Although this is a great photo, it's going to be hard to make a definitive determination without knowing size and some of the other finer details.  Photos of the noctule and leislers can be found on the linked data sheets and the link to the UK section can help you determine if there are any other possible candidates I missed.


Effect of cold showers after intense training What is the effect of cold showers after very intense training (body fully covered in sweat, high pulse, increased body temperature)?

I'm especially interested in how it affects perspiration.

Taking cold showers(10-15 ℃) after training or workout have many benefits:

It helps in lowering the damaged tissues temperature by constricting blood vessels.
Cold helps numb nerve endings which provides instant localised pain relief.
Brings down heart rate and increases circulation.
It minimises inflammation and help you recover faster.
It is more effective in relieving delayed-onset muscle soreness,
which generally occurs one to four days after any physical activity.
It reduces uric acid levels, so it is beneficial for people suffering from gout.
It boosts glutathione levels in the body which is a very beneficial antioxidant.

Those who should avoid cold showers:

1] Those who suffer from heart diseases as constriction of blood vessels can lead to a heart attack.

2] People having high blood pressure, because blood vessels will constrict and can reduce the supply of blood to different organs, especially the brain.

Ice bath:

  In sports therapy, an ice bath, or sometimes cold-water immersion or cold therapy, is a training regimen usually following a period of intense exercise in which a substantial part of a human body is immersed in a bath of ice or ice-water for a limited duration. While it is becoming increasingly popular and accepted among athletes in a variety of sports, the method is controversial, with a risk of hypothermia, with the possibility of shock leading to sudden death. Many athletes have used cold water immersion after an intense exercise workout on the belief that it speeds up bodily recovery; however, the internal physical processes are not well understood and remain elusive. Generally research into the health effects of cold water immersion as part of an athletic training regimen is inconclusive, with some studies suggesting a mild benefit such as reducing muscle damage and discomfort and alleviating delayed onset muscle soreness, with other studies suggesting that cold water immersion may slow muscle growth and interfere with an overall training regimen.

[Source 1]

[Source 2]

You also maybe interested in:

[Question 1]

[Question 2]

References:

 - A cold shower maybe more beneficial to your fitness[Dr. Mercola].

 - Cold shower after exercise.

 - Effects of hydrotherapy on various systems of the body(NCBI)

 - The effects of cold water immersion and recovery of inflammation

 - Ice bath (Wikipedia)

 - 8 do's and don't's of Ice bath


Neuroscience and learning of a single neuron Can you teach an alphabet to a neuron?

If yes, how?

How does a neuron 'learn' new information, do all individuals learns similarly ?

No, you cannot teach a single neuron an alphabet.

In general, the way the brain learns and stores information is by adjusting the strength of connections between neurons. Therefore, there is not really any information in a given neuron, but in the pattern of how it's connected to other neurons.

For the example of the alphabet, there are a lot of different pieces of information to tie together: there will be different neurons that respond to the visual shape of a letter, the word that names the letter, the sounds that the letter represents in spoken language, the words that contain the letter, etc.

A general neuroscience textbook like Purves is a good place to start learning about how brains work. You might also learn about how artificial neural networks learn. They are definitely different from biological nervous systems, and the learning mechanisms vary, but they share some characteristics such as the information being represented in the strength of connections between units, usually called weights in an artificial network.


Why is pericardium muscle repolarizated earlier than endocardium? I was reading about heat muscle contraction and I read:

  The endocardium depolarization happens earlier than pericardium , but
  pericarduim repolarization happens earlier, therefore the T wave in
  healthy people is always positive.

I have two questions:

What's the reason?
Why doesn't it happen in atrium and atrial repolarization(T wave)?

I'm just going to link you to another post here, which I believe answers the same question. It's because the facilitation of the transient outward current if much more prominent in epicardial regions than in endocardial regions.

And the following citation, "Transient outward potassium current, ‘Ito’, phenotypes in the mammalian left ventricle: underlying molecular, cellular and biophysical mechanisms," provides some mechanistic insight.

To answer the rest of the question:

So in an ECG you have leads that record whether a charge is moving toward, or away from the lead. These net charges are reflected on the ECG as either positive or negative deflections. You have a signal from the sinoatrial node that causes a depolarization in the right atrium, then the left atrium (biphasic p wave). In each case, however, we see the positive p wave because in this depolarization the net charge is moving toward the electrodes. Studies on atrial repolarization note that yes, the atrial repolarization is generally obscured by the QRS complex but occurs with polarity opposite that of the p wave.

With the ventricles, and the T wave you end up with a special case. The endocardial regions and the interventricular septum are the first to depolarize, and you get the QRS complex. These regions have a longer period of contraction than the epicardial regions, however. The outside of the ventricles begin to repolarize quickly (transient outward current, surface becomes more positive), and this repolarization begins at the apex and propagates toward the base of the heart. Where you'd get a negative T wave with the change in charge, the direction that the repolarization travels causes you to get a positive reading.


High Blood Pressure - Na or NaCl? What is the cause of high blood pressure? or, Which foods can cause high blood pressure?
Is it just sodium, or sodium chloride? I'm confused because sodium chloride should ionise in the aqueous medium of the stomach.

It'd be great if someone could share the working details/mechanism of the same. Thanks in advance!

High blood pressure is caused by an excessive amount of fluid circulating in the blood vessels, or an excessively small mean blood vessel diameter. The later is more associated with stress situations and stressful lives, while the former is more related to the theme of your question: electrolyte balance.

An electrolyte is any molecule that produces an electrically conducting solution when dissolved in water (http://www.medicalnewstoday.com/articles/153188.php). In other words, they are or give rise to ions or charged molecules when dissolved in water. Examples are sodium, potassium, calcium, magnesium, chloride, phosphate, bicarbonate, ...

Water, even though on its own is a neutral molecule, it is still polar. This means that it has parts which are more negatively charged (in concrete, the oxygen atom) and parts that are more positively charged (the hydrogen atoms). These are called poles, and are due to different electronegativities.

The result of this is that water will form electrostatic bonds with charged molecules such as ions, or, in other words, which causes salts to be soluble in water. This also means that water is attracted to places with a lot of charged molecules - places with higher osmolarity. The travelling of water from places with lower to higher osmolarity is called osmosis.

That's what happens when the blood has an excess of ions (and thus higher osmolarity) when compared to the rest of the body and the normal, healthy values. Water starts travelling from the different parts of the body to the blood, being attracted by the extra concentration of salts, and pushing the blood volume over the healthy limits. This also makes it harder for the kidneys to excrete water from the blood, increasing further blood volume and giving rise to hypertension.

As you can see, any charged molecule in excess in the blood can increase blood volume (through higher plasma osmolarity) and create hypertension. In our bodies, the most common and impactful electrolytes are ions, being Sodium the most abundant.

Because sodium is the most abundant in the blood and the most ingested electrolyte, it is usually referred as its excess being the cause of hypertension. The common salt we use to cook comes in the form of NaCl, containing Sodium and Chloride, both electrolytes. They are very useful and fundamental to our organism, but in excess can cause diseases such as this.


Why aren't gene drives extremely common? The ability for gene drives to sidestep the Mendelian mechanism and rapidly spread through populations (even if the gene is slightly fitness reducing) is extremely powerful. Why aren't normal populations riddled with parasitic gene drives?  What mechanism keeps naturally occurring gene drives suppressed to (apparently) very low levels?

I have a feeling that the OP is confusing naturally occurring so-called selfish, or parasitic genetic elements and the CRISPR/Cas9-based gene drives that have been making news as potential tools to eradicate disease vectors like the aedes mosquito. My answer is working from that assumption.

The big difference between naturally occurring "parasitic" genetic elements (including bacterial CRISPR elements and things like transposons) and the gene drives that are being tested as vector control revolves around what we put inside the latter class of gene drive.

The OP hit on this difference in his question, when he mentioned the decrease in fitness caused by engineered drives. In the naturally occurring drive-like elements, there is rarely ever a decrease in fitness in the organism and when it does occur, it is unlikely to be passed on to future generations.

Transposons, for instance, are largely active in somatic cells, whose DNA is not passed on to descendants. Semi-randomly occurring genetic changes are sometimes passed on, but this is relatively rare and evolution favors those that are either neutral or that increase fitness. A brief search doesn't turn up, and I can't think of, any cases of naturally occurring deleterious genetic alterations caused by something like a transposon having been found to remain in a population long enough to be studied.

Engineered gene drives, on the other hand, particularly in the cases of those meant to combat mosquitos, are purposefully designed to reduce the fitness of their target host.

The last question, of what keeps naturally occurring drives at low levels, requires either a rather vague, or a very long answer. I'll go with vague and provide some links to longer ones. Briefly, our genomes have evolved a lot of ways to maintain genomic integrity, in the forms of proteins responsible for proof-reading DNA, repairing breaks, and destroying any "free" pieces of DNA found outside of a chromosome. We've also evolved a lot of mechanisms to maintain genomic integrity through small non-coding RNAs.

Here are some good papers (without paywall) on the subject:

How p53 restrains mobile genetic elements
Proteins that function to restrain mobile genetic elements in rice
Good review of transposons in general
Finally, how people are engineering gene drives to combat malaria

Hope that helps!


Why trust vaccine statistics from the mid-20th century, if ELISA tests were not available and disease diagnoses were completely subjective? Why trust vaccine statistics from the mid-20th century, if ELISA tests were not available and disease diagnoses were completely subjective? Any answer is helpful. Please let me know.

Diagnoses were not completely subjective; there are myriad assays besides ELISA.

Not back then.

https://emedicine.medscape.com/article/966220-workup

Although the diagnosis of measles is usually determined from the classic clinical picture (see Clinical), laboratory identification and confirmation of the diagnosis are necessary for the purposes of public health and outbreak control. Laboratory confirmation is achieved by means of serologic testing for immunoglobulin G (IgG) and M (IgM) antibodies, isolation of the virus, and reverse-transcriptase polymerase chain reaction (RT-PCR) evaluation.

None of this existed in 1970.


What is the name of this type of inflorescence? I was having a look at a rhizophora plant (from the mangrove family), and I got curious about its inflorescence. I can't make out what kind of inflorescence it is.

Here is a photo of the inflorescence.

Does anyone know which kind of inflorescence it is?

That is a woody compound umbel. A compound umbel is one with more than one set of pedicels between the peduncle and the flower. Hydrangeas also exhibit this type of inflorescence, although not necessarily woody.

In the picture below, I've marked all the levels where the pedicels branch.

End of peduncle, beginning of primary pedicels
Beginning of secondary pedicels
Beginning of tertiary pedicels
Beginning of quaternary pedicels, which bear flowers


Ferredoxin synthesis pathways I have been thinking about some alternative CO₂ fixation pathways. As almost all of them include ferredoxin reduction I started to wonder where does the ferredoxin comes from. I could not find any of the pathway in databases (ecocyc,kegg). Does any of you know if the biochemical pathway and the genes involved in synthesis are known?

Thanks,Martin

Ferredoxins and variants such as fladidoxins and rubredoxins are simply electron carrying protein that need to be regenerated, like the more energetic NADPH.
The key thing to remember is that redox balance is key. You cannot have electron pair accumulate so there has to be a terminal acceptor. In the case of aerobic resipration it is oxygen, in the case of iron or sulfur dissimilation it is iron(III) or sulfate, in the case of fermentation it is a small highly oxidised carbon (e.g. methanol, ethanol, butanediol, formate, acetate, propionate, lactate, succinate, fumarate). Carbon fixation requires electron pairs, which come from somewhere. The mechanism of how the carbon dioxide is assimilated can be via the Calvin cycle (plants and cyanobacteria), the Wood-Ljungdahl pathway or from the 3-hydroxypropionic cycle Prof. Fuchs described in Chloroflexi and Sulfolobus. In all three electrons come from somewhere (generally water, carbon monoxide and sulfur respectively).
The reason why there are both ferredoxins and NADPH is a tad harder to explain, but has to do with redox control and the fact that not always ferredoxin is regenerated by a NADPH reductase (also: NADH = catabolic, NADPH anabolic), but could be a fumarate reductase or similar.


Does mitosis include cytokinesis? I found that some books include cytokinesis within mitosis, but some other books I have referred to include only the dividing of the nucleus as mitosis and do not include cytokinesis.

Can anyone help me out? Please include a source in your answer.

Cytokinesis is separate from mitosis.

What edition are you looking at?  To quote from the Fourth Edition:

  The cell cycle culminates in the division of the cytoplasm by cytokinesis. In a typical cell, cytokinesis accompanies every mitosis, although some cells, such as Drosophila embryos (discussed later) and vertebrate osteoclasts (discussed in Chapter 22), undergo mitosis without cytokinesis and become multinucleate. Cytokinesis begins in anaphase and ends in telophase, reaching completion as the next interphase begins.

The mouse-over definition of cytokinesis there is:

  Division of the cytoplasm of a plant or animal cell into two, as distinct from the division of its nucleus (which is mitosis)


Why is uracil, rather than thymine, used in RNA? This question was posed on SE Biology some time ago, but all the answers, including the accepted one, answered a different question instead: “Why is thymine, rather than uracil, used in DNA?”. I therefore changed the title to match the answers, giving notice that, if the change were approved, I’d post the original separately question myself (and answer it, if necessary). Here it is:

  It is believed that thymine replaced uracil (the RNA base) in DNA because of the deleterious effects of slow spontaneous deamination of cytosine to uracil: by employing thymine instead of uracil, any uracil in DNA would clearly be aberrant, allowing a specific mechanism of repair (involving uracil DNA glycosylase) to evolve with impunity. As this was clearly advantageous, why didn’t RNA also evolve to use thymine instead of uracil?

N.B. By “why?” I mean “how can one rationalize the fact that?”. Obviously, the answer to this type of question is not, and probably cannot be, known with certainty.

Regardless of the question† of which came first*, RNA or DNA, it is possible to rationalize the absence of thymine in RNA by a cost–benefit analysis. There is a cost to using thymine, so there must be sufficient benefits to make this worth while.

Cost of using thymine rather than uracil

The most obvious cost of using thymine is the energy requirement for its synthesis (in terms of reducing power — NADPH).

An analogous conversion of rUMP to rTMP (if it existed) would incur similar costs. (There may be additional costs, but they may be contentious and this is indisputable, so it will suffice.)

Benefit of using thymine rather than uracil

For DNA the benefit is clear and stated in the question. By not using uracil as the complement to adenine, uracil produced by spontaneous deamination of cytosine can be recognized as abberant and removed by the DNA proof-reading repair systems. This presumably gives the organism an advantage (benefit) by reducing harmful mutations to DNA — the genetic material.

RNA is not the genetic material of contemporary autonomous organisms. Hence unrepaired C to U deaminations will not affect that aspect of the viability of an organism. How serious will they be for the cell, though? The largest and most long-lived RNAs are the structural ribosomal RNAs. Such mutations in the cells rRNA might have no effect on ribosome function as much of the RNA is thought to be structural. However, even if they did, the inactivation of a small percentage of the ribosomes of a cell would have little impact on protein synthesis. Likewise for the small tRNA molecules.

Messenger RNA poses a different problem as we can conclude that abberant proteins made from mutant mRNA are dangerous to the cell from the fact that a proof-reading mechanism exists to correct errors in the charging (aminoacylation) of tRNAs. I would argue that the relatively short half-life of mRNA compared with the frequency of deamination of cytosine means that the latter process is not responsible for a significant amount of mutant mRNA.

Conclusion

The benefits of using thymine — together with a repair system — in RNA would be marginal, and hence not worth the energetic cost this would entail.

†Footnote: We don’t need to argue about which nucleic acid came first

The current metabolic pathways for formation of dTTP from dUTP and the reduction of ribose to deoxyribose are strongly suggestive to me that RNA preceeded DNA in evolution. (They suggest nothing about whether RNA preceeded protein.) However, the rationalization presented here does not require this assumption. If DNA came first and RNA initially had T instead of U, the rationale could be used to argue why RNA changed bases from T to U. Indeed, the rationale can be employed by those who do not even believe in evolution — they could argue (and probably do) that some deity created things that way because it was more efficient in terms of cost–benefit.


Fermentation to acetic acid How much time is needed for the fermentation to acetic acid production cycle, and the conversion of apple vinegar in a sealed container incubated at 37 °C?
Should be in the fully closed?
What is right yeast?
I do it with powder, grated apple in a plastic soda bottle and I add a few peas and a slice of bread. I am waiting for make that.
If you have a better idea on what to do to get a good apple cider vinegar produce in my own house.

There are some recipes available on the web, my answer is based on this webpage and this information:
The process itself is rather easy and you can either use ready bought apple juice, homemade juice or apple cider (basically unfiltered apple juice). You will need some specially cultivated yeast, baker's yeast is generally not recommended since it might produce a lot of unwanted (and probably bad tasting) side products.
For the fermentation itself you need some (very) clean vessels in which the process can take place. These should be from a material which is not corrosive, as the vinegar would otherwise react with the vessel. Food-grade plastic, glass or stainless steel should be ok.
To have the reaction take place, the process need oxygen, otherwise the reaction will stop at the step of ethanol. This is also why acoholic fermentation is always sealed against the air, to avoid the oxidation of the alcohol the acetic acid. A cheese cloth will leave oxygen in, but keep insects and other contaminations out. If you need to filter the vinegar at the end of the process, a standard coffeefilter is good enough.
The following step by step directions come from this website:

Step 1 - Make or buy your apple cider or apple juice
Apple juice or apple cider is the starting point for making apple
cider vinegar. You can make your own, or buy it ready made, fresh,
bottled or frozen.  You can use a mechanical or steam juicer to
produce the juice / cider. To make your own juice (which is the same
as plain unfermented apple cider), see this page. Keep in mind that
you want to select sweet apples, like Fuji, Delicious, Mutsu, Gala,
etc. Green, unripe and unsweet apples (like Granny Smith) do not have
enough sugar to make good cider vinegar. Tips about selecting apples:
Apples used for cider don't have to be flawless. They do, however,
have to be free from spoilage. You can use blemished apples and small
sized apples. You can mix apple varieties together or use all one
variety. The only rule is to cut out any spoilage areas on otherwise
good apples. Spoiled areas will cause the juice to ferment too rapidly
and will ruin the cider. Don't use apples that appear brown, decayed
or moldy. Apples should be firm and ripe. Green, undermature apples
cause a flat flavor when juiced. The best cider comes from a blend of
sweet, tart and aromatic apple varieties. A bushel of apples yields
about 3 gallons of juice.
Step 2 - Make your starter yeast
Adding yeast to activate fermentation is not essential, but will speed
up the process and can produce a higher quality. Special cultivated
yeasts are available for this purpose at wine-making shops and
biological labs but bread yeasts are not recommended. To make a
starter, crumble one cake of yeast into one quart of cider and mix.
This makes enough starter for 5 gallons of cider; double the recipe
proportionately when making more.
Steps 3 - Making Alcohol and Acetic Acid
Pour all of the juice or cider into one or more containers to about
three-quarters capacity; do not close the lids on the containers.
Instead, cover the openings with cheesecloth secured with a rubber
band or string.
Step 4 - Store out of direct light, but some place with constant temperature
Stir the mixtures daily, making sure the cheesecloth is put back in
place. Keep the containers away from direct sunlight and maintain the
temperature at 60 to 80 degrees F.
Step 5 - Keep stirring daily, monitoring and tasting for the next 3 to 4 weeks
Full fermentation will take about 3 to 4 weeks. Near the end of this
period, you should notice a vinegar-like smell. Taste samples daily
until the desired strength is reached.
Step 4 - Filter Mother of vinegar
When the vinegar is fully fermented, filter the liquid through several
layers of fine cheesecloth or filter paper—a coffee filter works well
for this. This removes the mother of vinegar, shown at right,
preventing further fermentation or spoilage of the product. Mother of
vinegar is completely harmless and the surrounding vinegar does not
have to be discarded because of it. It can be filtered out using a
coffee filter, used to start a bottle of vinegar, or simply left in
and ignored.
Step 6 - Done! Storing Your Vinegar
The vinegar is now ready for storage in separate, capped containers.
Stored vinegar will stay in excellent condition almost indefinitely if
it is pasteurized. To pasteurize, heat the vinegar before pouring it
into sterilized bottles, or bottle, then place in a hot water bath. In
both cases, the temperature of the vinegar must reach at least 140
degrees F to pasteurize the product, and should not exceed 160 degrees
F. Use a cooking thermometer to ensure the correct temperature is met.
Cool the containers and store at room temperature out of direct
sunlight.


Influence of alcohol on brain cells As I am not related to biology, I would appreciate if you can keep your answers as simple as possible.

My question is about the influence of alcohol on the brain. As far as I know, drinking alcohol is killing cells in the brain. But is it linear? E.g. if I have 1.0 per mil and it kills 1000 cells will 2.0 per mil kill 2000 cells?

(An equation would be nice)

Thanks

The situation is definitely an extremely complex one, and you should probably forget about having an exact equation to define it.

When talking about the effects of a substance on the organism there are several factors to take into account. These are generally put together under the term pharmacodynamics.

Some of the factor to take into account are:

The dose of the substance
The route of administration
The metabolism of the substance
The target organ

The problem is, not all ethanol you drink will go to the brain, and it will not necessarily go there immediately, or all at the same time. All of this will change the effects on the brain. Also, there are several confounding factors, some of which I have tried to list.

I have summarized here a few information about ethanol metabolism, taken mostly from Principles of Forensic Toxicology - Chapter 10 by Barry Levine and Yale H. Caplan

Ethanol is normally taken through drinking, which means that it will have to pass through the gastrointestinal (GI) tract (i.e. stomach and intestine) before getting into the bloodstream. This route permits practically 100% of absorption of ethanol in the body, with the major site of absorption being the small intestine, absorbing ~75% of a dose of ethanol. The rest will be absorbed in the stomach and in the other parts of the intestine.

The absorption in the GI tract is dependent on the type of beverage: for instance carbonated alcoholic beverages are absorbed faster than "plain" ones.
The alcohol content also is important: a very diluted drink is absorbed slower than one with 10-30% of ethanol, as the latter will generate a bigger concentration gradient between the GI tract and the circulation, so it will diffuse faster. However, >30% ethanol will enhance mucus formation, which will slow down absorption. Furthermore, absorption depends on the status of the GI tract: preexisting conditions (e.g. inflammation) can modify the rate at which the alcohol enters the bloodstream.

But, we are still far away from the brain! After being absorbed, ethanol goes into the vena cava, and passes through the liver, where it can be metabolized (destroyed) by an enzyme called alcohol dehydrogenase (ADH), which converts ethanol into acetaldheyde, effectively reducing the ethanol concentration in the blood.
This is a well-known phenomenon for many drugs, and it is called first pass effect
Importantly, the human stomach also expresses ADH, so this first pass effect can start even before reaching the liver! The effects of ADH in the stomach obviously depends on how long the ethanol stays in there. So, it will be lower for an empty stomach then after a big meal.

Food, in fact, is also a well known factor that reduces the amount of ethanol in the blood.

For instance, these graphs show blood ethanol content in four healthy subjects after a 10 hour fast (filled circles) or after breakfast (empty circles), after drinking the same dose of 0.80 g ethanol/kg body weight, in 30 minutes.

From: Food-Induced Lowering of Blood-Ethanol Profiles and Increased Rate of Elimination Immediately After a Meal - Jones AW and Jönsson KA - J Forensic Sci., 1994.

As you can see, eating strongly decrease the ethanol blood content. Also see how there is quite a bit of variation between the different subjects (if you open the paper you will also see the graphs from other 6 subjects).

Also, you can look for instance at this paper (just got a random study, there seems to be a ton of them around):
First pass metabolism of ethanol. - Lieber CS et al. - Alcohol Alcohol Suppl., 1994

Coming out of the liver, ethanol goes into the right side of the hearth, and from there to the lungs. This poses no particular issue for most drugs, but ethanol is volatile! So, part of the ethanol is released through respiration (in fact the "classic" way of saying if someone has drunk alcohol is to smell his breath). However, this only accounts for a minor decrease in blood ethanol levels.

Finally, ethanol can start going around the body. Being a water-soluble molecule it will tend to diffuse into water-containing parts of our body (i.e. you will not find much ethanol in fat), which include the brain.

In the meantime, however, the process of elimination has started: ethanol can be excreted in urine, sweat and breath, although the major route of elimination is epathic metabolism by ADH, accounting for >90% of ethanol elimination.

There is a neat formula to express all of this, called the Widmark equation:

$A=\frac{Wr(C_t+\beta*t)}{0.8z}$

where

$A$ = number of drinks consumed
$W$ = body weight (important because of the content of water in the body)
$r$ = Widmark constant (depends on sex, age, etc.)
$C_t$ = blood ethanol concentration at time t
$\beta$ = acohol elimination rate
$t$ = time since the first drink
$z$ = volume of alcohol per drink

You can find examples of this formula in this PDF about Widmark equations

And now to the brain: ethanol does indeed have various effects on neurons. Short term effect essentially involve depression of neuronal activity, ethanol being able to modulate GABA signalling in the brain. Long term effect range from reduced neurogenesis (i.e. birth of new neurons) to reduced volume of certain brain areas, probably due to loss of neurons, to inflammation in the brain.

Again, the situation is very complex and it depends on the frequency of drinking, the amount of each drink and many other factors. A single dose of ethanol will probably have irrelevant effects on your neurons... as the amount needed (in one shot) for serious neurotoxicity will probably send you into ethilic coma. The exact mechanisms for these effects are only partially known and very likely to be derived by the interaction of numerous diverse effects.

This article explains some of the mechanisms for loss of neurons in the cerebellum.

Mechanisms of ethanol-induced degeneration in the developing, mature, and aging cerebellum. - Jaatinen and Rintala - Cerebellum, 2008

  These mechanisms include: (i) excitotoxicity; (ii) dietary factors, especially thiamine depletion; (iii) glial abnormalities; (iv) changes in growth factors; (v) apoptotic mechanisms; (vi) oxidative stress; and (vii) compromised energy production.

I will not go into the details of all of this, but it should be clear by now that all the things I mentioned so far (and many other factors I did not talk about) make it extremely difficult to give an exact quantification of the number of cells killed by ethanol. Surely the relationship is not linear, in fact, for instance, positive effects of small doses of alcohol have been reported numerous times.

A few more references on effects of alcohol on the brain:

Reduced neurogenesis

Long-lasting reduction in hippocampal neurogenesis by alcohol consumption in adolescent nonhuman primates. - Taffe et al. - PNAS, 2010

Adolescent binge alcohol exposure alters hippocampal progenitor cell proliferation in rats: effects on cell cycle kinetics. - McClain et al. - J Comp Neurol., 2011

Brain volume decrease

Decreased volume of the brain reward system in alcoholism. - Makris et al. - Biol Psychiatry, 2008

Amygdala volume associated with alcohol abuse relapse and craving. - Wrase et al. - Am J Psychiatry., 2008

Hyperhomocysteinemia as a new risk factor for brain shrinkage in patients with alcoholism. - Bleich et al. - Neurosci Lett., 2003


Relative Property of Alleles If there are three different alleles to a gene, is it possible that the first is dominant to the second, but recessive to the third?

Sure it is!

When we say that an allele is dominant on another what we really mean is that the phenotype obtained from that specific mutation of the gene somehow "masks" the phenotype of the other.

The easiest example would be that of pigment. A gene X could code for an enzyme which produces a red pigment. A mutation in X could result in a allelic variant x coding for a non-functional enzyme that does not produce pigment. In this case X will be dominant on x, as in the presence of both the pigment will still be produced (because you will have half functional and half non-functional enzyme molecules).

Things can, however be slightly complicated.

For instance, if the allele R codes gives a red pigment and r gives a white pigment Rr could give pink. This is called incomplete dominance.

On the other hand you could have co-dominance, where WW is white, ww is black and Ww is black and white.

The example you are asking for is called serial dominance and the "classical" example given is that of the rabbit coat color where you have for alleles with a dominance hierarchy like:

c+ > cch > ch > c

c+ gives a fully functional enzyme, called tyrosinase
c gives a non-functional enzyme, resulting in an albino phenotype
cch (chincilla phenotype) and ch (hymalayan phenotype) give partly functional enzyme (interestingly, the latter gives a temperature sensitive fur color).

In reality the rabbit coat genetics is even more complex, see this documents (PDF) for a more complete list of all the various loci and possible alleles involved.


What Websites Have Image Libraries for Bacteria and other Microorganisms What Websites Have Image Libraries for Bacteria and other Microorganisms?

With age of cell phone microscopes and hand held spectrometers it would be interesting and valuable to be able to compare in-home/at-work microbiology with data-banks. To be able to test for health or enjoy the visuals of tree of life seem relevant. What websites are out there?

While I doubt that this might be possible in all cases (and I would be careful about classifications), there are indeed some great ressources, which contain a lot of images. Since there is a vast number of bacteria present on this planet, there is of course a limitation to bacteria available in photos, representing only the most common or important.

These are:

Bacteria in Photos
American Society of Microbiologies Microbelibrary
Microbiology in Photos

Then there is an information page available from the CDC, which informs about parasitic diseases. These are non-bacterial, but probably also interesting. It can be found here:

Laboratory Identification of Parasitic Diseases of Public Health
Concern


Why are human titin and mice titin considered the same protein? I have a book that says:

  In humans titin is a chain of 34,350 amino acids, but in mice it is even longer with 35,213 amino acids.

If two polypeptides had different amino acid sequence lengths, how can they be considered the same protein? Or is it because they share in common one or more amino acid sequences - which, if a polypeptide contains, biologists consider it a particular type of protein - that they are both considered the same protein?

Human and mouse titin are orthologs, and can be confirmed through an NCBI query for TTN.

Orthologous proteins are not the same, per se. They retain the same function, and basically result from speciation: the common ancestral gene got divided between two species. However, the sequence may potentially differ because obviously the species have diverged.

Homology between the two can be confirmed computationally, through phylogenetic and alignment analyses, but I believe the naming convention Titin for both mouse and Human stems largely from the function of the protein in either organism.

Naming convention and explanations of homology are nicely outlined in this Bio.SE post.


Human brain is superior than till-date computers, yet why we perform poor than computer? Scientists found storage capacity of synapses by measuring their size.
They found, on average, a synapse can hold about 4.7 bits of information.
This means that the entire human brain has a capacity of one petabyte.
This is same as about 20 million four-drawer filing cabinets filled with text.

Striving around this stuff, I have a weird doubt crawling in my mind and it goes like this: Why is it like this that a human whose brain has got a capacity to store 1 petabyte, i.e. 1 million GB, cannot fully remember even the contents and information of a simple textbook which on the maximum would not be more than 1 GB, when he has to appear in exam? Why is storage capacity not directly linked with remembering capacity?

Three reasons:

Most of the storage capacity of the brain is used to store implicit knowledge. For example how to move your body, how to automatically recognise objects or how to hear and parse your language. These things may seem easy to you, but they require a lot of learning. Just look at how clumsy five year olds still are, they have been training how to use their body for five years straight and still skin their knees all the time.

Humans are actually able to retain huge amounts of information, both in their short term memory and in their long term memory. We know this because there are savants and hyperthymesia. It is likely that these abilities are actively suppressed in neurotypical people.

Because it is just not evolutionary adaptive to remember every detail. Intelligence depends on weeding out unnecessary information. If normal people learn huge amounts of information they often rely on memory abilities that are evolutionary adaptive, like the ability to remember a path from landmark to landmark.


Does this equation have a typo? (Systems Biology, singular value decomposition) I'm reading a systems biology paper, and I'm suspecting there's a typo in an equation, but I want to make sure.

The article is "Systemic metabolic reactions are obtained by singular value decomposition of genome-scale stoichiometric matrices." (Famili & Palsson 2003, http://www.ncbi.nlm.nih.gov/pubmed/12900206 / http://www.sciencedirect.com/science/article/pii/S0022519303001462). In equation 5, I wonder if the final subscript u_kr shouldn't be u_km, as the vector u_k^T is a column vector in the matrix U, which has dimensions m x m. Of course, some elements in u_k might be zero, in which case there would be less than m products in the sum, but I see no reason why there would be maximally r non-zero elements either (where r is the rank of the matrix S which has been decomposed). I worked out a simple example on paper where r < m and still got vectors with m non-zero elements. Can someone give me a second opinion on this?

Edit: Here are the main equations.
A model of a metabolic reaction network is described by a stoichiometric matrix S of dimensions m x n and rank r. For the metabolites in the model, changes in metabolite concentrations is equal to S multiplied with the vector of reaction rates, v:

${\frac{{dx}}{{dt}} = Sv}$

The singular value decomposition of S is given by

$S = U\sum {V^T}$

Multiplying on the left side with $U^T$ (The transpose of U) we get:

${U^T}\frac{{dx}}{{dt}} = \sum {V^T}v$

After matrix multiplication, we have for each row in $U^T$ and $V^T$, where $\sigma_k$ is the k'th singular value

$\frac{{d(u_k^Tx)}}{{dt}} = {\sigma _k}(v_k^Tv){\text{   k   =  1}},...,{\text{r}}$

And finally, equation 5:

${\text{u}}_k^T \cdot x{\text{  =  }}{{\text{u}}_{k1}}{x_1} + {u_{k2}}{x_2} + ... + {u_{kr}}{x_m}{\text{   (5)}}$

You are right this is a typo. Equation 5 is just a restatement of the definition of the dot product of two vectors:
$$\mathbf{u}_k^T\cdot \mathbf{x} = \sum_{i=1}^m u_{ki}^Tx_i$$
or written in another way
$$\mathbf{u}_k^T\cdot \mathbf{x} = u_{k1}x_1+u_{k2}x_2+\cdots+u_{km}x_m.$$

In the text Equation 5 is stating that one can find a linear combination of the metabolites described in $\mathbf{x}$ whose time evolution is described simply by a linear combination of the flux rates described in $\mathbf{v}$. The coefficients of the first linear combination are given by a row vector $\mathbf{u}_k^T$ in $U^T$. From this perspective, since there are $m$ possible metabolites ($\mathbf{x}$ is a $m\times 1$ vector), there have to be $m$ coefficients, so that the indices must range from 1 to $m$ in Equation 5. You are correct that $u_{ki}^T$ might be 0 for some $i$. But that doesn't change the fact that there should be $m$ (possibly vanishing) coefficients.


Any latest edition or successor of "Invertebrate zoology" by Ruppert & Barnes 2003? I have the 6th edition of the textbook "Invertebrate Zoology" by Ruppert and Barnes from 1993. I know there is a 7th edition from 2003, but is there and will there ever be a 8th edition? Assuming they should come every 10 years, shouldn't there have been one in 2013? So if Ruppert & Barnes retired, is there any more recent successor or alternative?

A worthy successor to this book series is "Invertebrates" by Richard C. Brusca et al. The latest edition being from 2016, so exactly what I was looking for.

https://www.amazon.com/gp/product/1605353752/ref=pe_353720_261047730_em_sp_C_1p_1_ti


Identify Bronze Coloured Beetle Spotted this beetle on Morfa Nefyn, a beach in North Wales, UK. The beach is a mixture of sand and stone, with large sandy cliff faces and rocky outcrops.

The beetle was about 3 to 5 mm or so long, running around on the rocks at the edge of a rock pool (not in the water though!), on a warm sunny day. It was moving are quickly, but not really fast, maybe around 1cm per second.

I've seen them on the beach before and sure I know what they were called but can't for the life of me remember.


Techniques to show a protein heterodimer-DNA interaction It is known that c-Jun and fos dimerize to form AP1 factor that binds to a sequence on DNA containing PyPuGACGTCNNNNGAGGTCPyPU.  In esophageal cancer cell lines there is no expression of the fos gene. However we still see expression of genes regulated by AP1 factor.  One of the possibility is another isoform of fos is expressed in these cells (e.g. fra1).

How will you check that fra1 is expressed or not in these cells.
How will you check that the heterodimer bound to the given DNA
contains fra-1 along with c-jun.

My thoughts on the above questions

For first question we can do immunofluorescence assay or we can do DNA affinity assay in which we chemically synthesize DNA sequence and bind it on agarose gel column pass through it protein extract of oesophageal cancer cells and our fra-1 protein if being expressed in cell line will bind to DNA. later we can elute protein DNA complex and by anti-fra1 antibody we can check if it is being expressed. But the drawback of both these technique is we should have knowledge of epitope of fra-1.

For second question - we can perform ChIP using antibody tagged Against c-jun and then eluting out DNA bound to c-jun. Then we can simultaneously label the complex with anti fra-1 in one sample and anti fos in another sample. We can check for results. If fluorescence is obtained in case of fra-1 sample that means both c-jun and fra are bound to probe and not fos.

How will you check that fra1 is expressed or not in these cells.

RT-PCR is a quick and an easy method to check for expression. However, it only tells you about the RNA level expression and you would have to work with the assumption that RNA concentration is directly proportional to protein concentration.

Considering that you do not have an antibody for fra1, you can go for mass-spectrometric protein quantification. It is good for a high throughput analysis and is generally wasteful when you just want to study one protein. However, people do carry out targeted proteomics to study a few proteins.

Alternatively, with some effort you can actually develop an antibody for fra1.

  How will you check that the heterodimer bound to the given DNA
  contains fra-1 along with c-jun.

Showing ternary complexes (fra-jun-DNA) are a bit difficult. It is relatively simple to show pairs. You can show that two proteins form a complex in vivo by doing a co-immunoprecipitation followed by detection by either western blot or mass-spectrometry.

You can also show interaction by biophysical techniques involving FRET and SPR but these cannot be performed in vivo (at least SPR. FRET can be done but there are limitations).

You can show the DNA-protein interaction by ChIP-seq as you mentioned in your question.

Showing all the three together is a bit tricky.

You can do it using in vitro assays that employ fluorescently labelled (one GFP and other RFP; or FRET pairs)/custom epitope tagged (for e.g. one FLAG and the other HA -tagged) proteins and a known DNA sequence generated by PCR/DNA synthesis. You can use EMSA along with antibody/fluorescence based detection to show the ternary complex.

You can indirectly infer the presence of the ternary complex when the ChIP-seq using antibodies for both the proteins shows up the same DNA sequence in the reads. You can also express a FLAG-tagged (or any other tag) protein, if in case you do not have an antibody for the proteins.


Why is water a polar molecule? Also, what is the definition of polar in this case? (9th Grade)

Does it have to do with the bonds it makes?

Polar means there's a higher density of electron on the oxygen and a lower density of electrons on the hydrogens. This has to do with the electronegativity of the elements in question. Hydrogen is in group 1 which likes to lose it's electron and oxygen in group 16 which likes to get two electrons (in this case one from each hydrogen) in order to complete the octet in it's valence shell.

Also it has to do with the shape, water molecules are not linear, but rather bent in a 'v' shape. the two sides are positively charged and the middle is negatively charged. if it were linear then the middle wouldn't matter, but because it is bent, on side has a negative charge and the other side has positive charge. It's not an negative/positive change the way it is in an ion, just a slight negative/positive charge.


What is the chemical composition of an egg shell? It ought to be some combination of C, O, and H, I presume. But really why should I care if eggshell gets in my eggs while I'm cooking?

It's the same stuff that makes up most sea shells, calcium carbonate, $CaCO_3$.

Incidentally, this explains why egg shells dissolve in vinegar (acetic acid which, since it is an acid, provides the Hydrogen ions in the reaction below):

$CaCO_3+ 2H^+ -> Ca^{2+} + H_2O +CO_2$

This simple reaction (which is what would happen in your stomach as well) produces water, calcium ions and carbon dioxide, none of which are particularly harmful.

The specific reaction with acetic acid is

$CaCO_3 + 2CH_3COOH → Ca(CH_3COO)_2 + H_2O + CO_2$

which also produces calcium acetate.

Anyway, there is nothing particularly toxic about $CaCO_3$, it's basically chalk. I wouldn't recommend eating a lot of it but you shouldn't freak out if some falls into your omelet either.

However, don't forget that an egg has exited a chicken's anus (well, cloaca) so their shells are likely to have come into contact with feces and they are porous so they are not necessarily the cleanest thing around. This is just not because of any chemical toxicity.


Aerobe or facultative anaerobe organism that metabolizes acetate? I'm assuming bacteria, but will take any suggestions.  Organism must survive primarily on the acetate (plus trace elements), but I can give/take electrons, if necessary.  Not interested in strict anaerobes.  I've tried Shewanella oneidensis, but have not succeeded in getting it to eat any acetate (just lactate).  Feel free to give journal refs.  Self-promotion won't be frowned upon if it's helpful.  :-)  Opportunity for joint pub, if successful.

You could try Paracoccus denitrificans.

Here is a study where acetate is used as the growth-limiting substrate: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.320.1692&rep=rep1&type=pdf

Here's the details of its version of acetate kinase: http://www.uniprot.org/uniprot/A1B9S8

I'd be happy to collaborate with you further on this.


Why do bees fly inside the gaps between the decoration on the exterior wall of a building and the wall? My house has decorations around the windows on the exterior wall:
There are gaps between those decorations and the bricks of the building:
During the summer, there are always bees looking for those gaps so they could fly into them while I rarely caught them flying out. I wonder why do they do that? What do they do inside? Is there anything I should do about this situation?
I guess that maybe they want to stay in a cooler place since it's quite hot outside? However, it's also worth noting that they seem to be interested in only one particular side of one particular window since I have never seen this happening to other windows of my house.

They just want to escape from.the heat. If there are no trees near your area, the bees can make a hive to live in. The bees don't constantly fly around; they only do so to gather food (or looking for a partner to mate).
Regarding the particular side of window, I'm not sure, may be that part is a little dry or (damp). What I mean is that the microenvironment of that crack may be more likeable to the bees, though that is just my wild guess.
Hope you found your answer. Thanks for reading.


Implanted neural recording system vs Electroencephalography Can someone help me to understand why in nowadays the scientists develop implanted neural recording system to measure and collect neural signals? Why the use of the electroencephalogram is not sufficient to record neurons? Which is the difference between these systems?

Thanks in advance

EEG records a rough average of activity from a large area of the brain, because it is located far away from the actual neurons. There is no way to separate out the activity of individual or even small groups of cells; instead, you record lower frequency synchronous activity among whole populations.

Implanted systems can record from small groups or sometimes even single neurons, which greatly increases the amount of information available.

Depending on the purposes of the recording or research, EEG might be sufficient; in other cases, implantable electrodes are required. EEG is sufficient to monitor sleep/wake cycles, for example; there is no need to record intracranially to monitor sleep (unless perhaps you are studying mechanisms of sleep itself). Implanted electrodes are often used before surgery to remove parts of the brain that are causing seizures. Using ECoG (basically an "EEG on the dura" rather than on the skull) or depth electrodes allows the surgeon to know more precisely which area is causing seizures, hopefully leading to a more successful surgery and needing to resect less tissue.

Implanted electrodes are also commonly used in animal experiments to learn about how single neurons and small populations encode or process information.


Was Earth's atmosphere more buoyant in the prehistoric era then today? The mass and size of the dinosaurs and prehistoric insects continues to amaze me. I read from an earlier post that oxygen was more abundant during the prehistoric era. However supporting the weight for me is still a mystery. Is it possible that the air was denser, allowing slight decrease in weight from greater buoyancy?

While it seems difficult to me to imagine any mechanisms that would allow significant changes to the total amount of atmosphere (and therefore density) in geologically recent times (< 100M year), it's quite difficult to find direct evidence about it.

In 2012 Nature published a paper that calculated the air pressure (and therefore the air density) by noting the distribution of sizes of puddles formed by raindrops in 2.7 billion year old ash. The conclusion was that the air was no more than twice as great as it is today.  This amount would be quite a bit for flying creatures, but would be almost completely insignificant for  supporting the weight of large creatures.

As an example, a large elephant has a volume of slightly more than $10m^3$, and a mass of over $5000kg$.  The buoyancy of the air only takes off the equivalent of about $12kg$ of that mass.  Even an atmosphere 10 times the modern density would be little help in supporting its weight.


Why didn't Escobar's hippos introduced in a single event die out due to inbreeding Today I read a BBC Report about how Pablo Escobar had once imported 4 hippos (1 male, 3 female) into his estate in Colombia for his private zoo. After his downfall, while other species were shipped out, hippos were considered too big to move and expected to not survive.
However, to the surprise of all the hippos are thriving and are so numerous that there have been calls to cull them. From the report:

Numbers are projected to only get bigger. [Colombian biologist Nataly] Castelblanco and her
peers say the population will reach over 1,400 specimens as early as
2034 without a cull - all of them descended from the original group of
a male and three females. In the study, they envisaged an ideal
scenario in which 30 animals need to be culled or castrated every year
to stop that happening.

My understanding is that since there was only 1 male, the gene pool would be limited and lead to lot of inbreeding in the descendants. This would cause population to not explode because some individuals would be unfit to survive.
Why has this not happened in case of hippos? Is it because there are 3 females (probably unrelated to each other) which keeps gene pool large enough? Or can mutations explain this phenomenon? Would results have been different if originally 2 females had been moved and only 1 retained?
EDIT - I have just found that current population is maybe less than 100 individuals which though big is not massive.
EDIT2 - I have edited the question title to keep focus on the hippos although a general answer would be welcome.

I think one of the important things to understand in thinking about this case is that it just hasn't been that long, generationally.
Escobar imported the hippos in the late 1980s. Hippos reach sexual maturity at an average of about 7.5 years old for males and 9.5 years for females, space births about 2 years apart, and live for 40-50 years.  Thirty years out, this means that only about 3 generations have passed for females. Moreover, the dominant males are highly territorial, which means that much of the breeding might even now be still coming from the initial male and not his descendants. Still, the initial male breeding with his own daughters would indeed produce a significant inbreeding coefficient.
The impact of inbreeding, however, is also affected by the density of deleterious alleles. In geographically restricted species, the higher natural level of inbreeding can result in purging selection that leads to a much lower frequency of accumulated deleterious alleles than in highly social and gregarious species like humans and dogs. Hippos appear likely to be such a species, as well as having overall lower genetic variation than other large African mammals, suggesting a fairly recent expansion.
In short: it hasn't been that many generations, and if the inbreeding sensitivity of hippos is indeed fairly low to begin with, it may indeed be that there simply isn't any significant impact from inbreeding at this point in time.


Best data repository to publish a large 'plotly' table containing all annotations on a transcriptome? I want to publish a transcriptome paper, along with interactive materials enabling readers to peruse the data behind the discussion. The R package 'plotly' enables rendering online-publishable tables that can be filtered & searched for specific entries.

I would like to publish such a table as supplementary to a paper (e.g. preprint version) however usually data repositories allow for uploading files and text. I intend to deposit the first version of my main manuscript to Bioarxiv, where they primarily publish .pdf files.

Would anyone here know an official data repository with a format such that would enable publishing online an interactive table?

A good example of such a table is given here.

Disclaimer: I have also asked this question at SE BioInformatics. Like me, they are unsure which would be the best fitting SE Community.

Journals and services where you can submit your script and manuscript and get DOI:

PLOS One
F1000
Zenodo
CodeOcean


Nervous system: Pain and Pleasure? If you have a constant pain in your body, why does a greater pain or pleasure make you not feel the original pain?

I'm not sure if why is referring to the biological basis or the reasoning for why it is beneficial but I've briefly summarised both. If you'd like more detail just accept and ask again clarifying your exact interest in this broad question.

Pain is taken up through the spinothalamic pathway but at may opportunities it may be blocked. It may be blocked by other ascending pathways or by descending pathways. There are a number of structures involved in this including endorphins and Interneurones which are part of the gate control theory of pain. Basically ascending sensory information is blocked when other sensory information is more acute or more pertinent. This is important for survival e.g. when feeling a lion it is important not to feel pain. That same endorphin pathway is highjacked by drugs such as morphine.