Where can I find historical data on world-wide ecology parameters?

Adding some additional database sources:

-- Climate --

Prism

The PRISM Climate Group gathers climate observations from a wide range of monitoring networks, applies sophisticated quality control measures, and develops spatial climate datasets to reveal short- and long-term climate patterns.

WorldClim

WorldClim is a set of global climate layers (climate grids) with a spatial resolution of about 1 square kilometer. The data can be used for mapping and spatial modeling in a GIS or with other computer programs.

NOAA's NCEI

NOAA's National Centers for Environmental Information (NCEI) are responsible for hosting and providing public access to one of the most significant archives for environmental data on Earth with over 20 petabytes of comprehensive atmospheric, coastal, oceanic, and geophysical data. See NCDC (climate), NODC (Oceans), NGDC (Geophysics), and NCDDC (Coasts).

NCEI has a HUGE repository of datasets. Sometimes you have to dig (e.g., here).

TROPICAL STORM TRACKS DATABASE

The storm tracks database is derived from the storm data published by the National Hurricane Center (NHC). This web page provides a convenient user interface for casually browsing storm information, including location, category, and wind speed.

-- Traits --

TRY

TRY is a Plant Trait Database. More formally, it's a network of vegetation scientists headed by DIVERSITAS/IGBP, and the Max Planck Institute for Biogeochemistry, providing a global archive of curated plant traits.

BioTraits

This is an online resource for empirical data on how biological traits respond to environmental drivers such as temperature, light, and salinity.

-- Species --

GPDD

The CPB / NCEAS Global Population Dynamics Database largest collection of animal and plant population data in the world, and brings together nearly five thousand time series in one databa

Global Invasive Species Database

The GISD is a free, online searchable source of information about species that negatively impact biodiversity. It focuses on invasive alien species that threaten native biodiversity and covers all taxonomic groups from micro-organisms to animals and plants.

Movebank

Movebank is a free, online database of animal tracking data hosted by the Max Planck Institute for Ornithology. They help animal tracking researchers to manage, share, protect, analyze, and archive their data.

Global Plants

Global Plants is the world’s largest database of digitized plant specimens and a locus for international scientific research and collaboration.

COPEPOD

The Coastal & Oceanic Plankton Ecology, Production & Observation Database (COPEPOD) is an online database of plankton abundance, biomass, and composition data. COPEPOD's online zooplankton and phytoplankton data content ranges from long term ecosystem monitoring surveys to detailed process studies

COMPADRE & COMADRE

COMPADRE Plant Matrix Database and COMADRE Animal Matrix Database site. Contain matrix population models of hundreds of plant and animal species

Catalogue of Life

One of the most comprehensive and authoritative global index of species currently available. It consists of a single integrated species checklist and taxonomic hierarchy. The Catalogue holds essential information on the names, relationships and distributions of over 1.6 million species.

-- Forests --

FAO Forestry Database

The FAO Forestry Department maintains an array of online databases where information covering various aspects of forestry is stored for analysis and further dissemination.

FIA

U.S. forest Service's Forest Inventory and Analysis database contains continuous forest census data for the United States.

European Forest Institute Database

EFI is running a number of online databases with data and information on different aspects of European forests, forestry and forest research.

CTFS-ForestGEO

The Center for Tropical Forest Science - Forest Global Earth Observatory (CTFS-ForestGEO) is a global network of forest research plots and scientists dedicated to the study of tropical and temperate forest function and diversity

-- Other --

NutNet

The Nutrient Network (NutNet) is a grassroots research effort to address pervasive human impacts on ecosystems (via alteration of global nutrient budgets and changes in the abundance and identity of consumers) within a coordinated research network comprised of more than 40 grassland sites worldwide.

...Also see the Ecological Databases page on INNGE Wiki for more resources!!

Ex: Ecological Data Wiki:
The site is a source for finding ecological datasets and quickly figuring out the best ways to use them. Just think of it as the Wikipedia of ecology data.


Is one single antibody binding its antigen enough to elicit an immune response?

This is a wonderful question, because it addresses a common misunderstanding.
Short Answer: We have no clear data about the effectiveness of a one single antibody molecule in the immune response of an entire organism, but since many different antibodies can recognize the same pathogen, and . Just as antibodies in a healthy individual are able to find, bind to antigens, and produce an immune response, antibodies from transfusions of IVIG can do the same. They can block, opsonize, activate complement, and regulate B-cells and T-cells.
Long Answer: Surprisingly, brilliantly, our innate immune system is able to generate transmembrane and secreted proteins that bind every possible antigen (or almost every possible antigen, depending on who you ask). See my answer to this earlier question, and the associated general references. We get very excited when we teach this. With our focus on teaching the diversity of antigens and binding regions, it is easy to get the idea that there is a single unique antibody for every possible microbial invader. For students that really take in the problem of antigen diversity and the solution of antibody diversity, this question, or some variation, often follows: how can a single antibody ever do any good? Usually, with some wonder about how to quantitatively match up this diversity with any specific pathogen. This is an example of that question. Here is the answer:
Many different antibodies can recognize a pathogen
A single pathogen has many many antigens, or molecules that, e.g., an antibody could bind to. A single antigen has many epitopes, or specific binding sites for an antibody paratope (the part of the Fab region of an antibody that is specific to the binding site). A single paratope can bind more than one epitope. This is called cross-reactivity. Additionally, a single epitope can be bound by more than one paratope. A good discussion of this principle can be found in Chapter 4 of Frank's Immunology and Evolution of Infectious Disease.
Antibodies are produced in massive quantities
Lauren Somparyic, in How the Immune System Works, estimates that, in the pre-immune state, of the roughly 3 billion B-cells, a single clone is comprised of about 30 cells. Each clone contains many copies of the transmembrane version of its single antibody, and many different clones (as discussed in the paragraph above) will recognize a single pathogen. Once exposed to a pathogen, B-cells that recognize it divide many times over, undergoing a series of changes beyond the scope of this question. At the end of this process, plasma cells, the B-cell progeny that produce secreted antibody, then each secrete hundreds to thousands of antibodies a second. Without ongoing antigen stimulation, many of the plasma cells die, but long lived plasma cells migrate to the bone marrow and continue to secrete enough antibody to allow for the rapid response seen in a subsequent exposure to the same pathogen. The majority of antibodies in the blood of a healthy adult come from these long lived plasma cells in the bone marrow. You can read about this process in chapter 3 and 10 of How the Immune System Works and chapter 7 of Abbas Basic Immunology. Essentially, the circulating antibodies in the $\gamma$-globulin fraction of plasma contain large numbers of each antibody produced in response to exposure to a pathogen. Because of this, we don't have to wonder how one lone antibody in the vast expanse of an organism can be effective in response to many pathogens. We have many, many antibodies that can do this.
IVIG
IVIG is from, as the OP states, pooled samples of antibodies from many thousands of blood and plasma donors. 75% of these are IgG antibodies, meaning they've already undergone class switching and are a result of exposure to antigen. I'm not aware of a good study that clearly catalogues the populations of different clones in IVIG samples, but we can say the set of antibodies in IVIG represent the collective immune memory of the population from which it was pooled, but behave in a similar way to the circulating antibodies in a healthy adult.  You can read more about this here and here. Because of this, the same principles discussed in the above paragraph apply here. We don't have to worry about the lone antibody lost in the massive sea of the human body. Even pooled from thousands of donors, each dose of IVIG contains many, many antibodies that can recognize each important human pathogen.
Transfused antibodies retain their effectiveness
There are a variety of clinical uses for IVIG, but there is clear evidence that the antibodies in these samples retain their effectiveness in their roles as effectors of the immune system. Not only are the antibodies in IVIG effective at blocking and neutralizing pathogen receptors and toxins, but they activate and clear complement, opsonize pathogens and damaged cells for clearance by neutrophils and other phagocytes, control and regulate the B cell population, and interact with the T-cell population, much as they do in the healthy individuals who haven't been given IVIG. The NEJM article I linked above discusses much of this (though it focuses on modulation), this review, which you can access without a paywall, also discusses this.


Can you please help me identify this insect?

That is a bean weevil, family Chrysomelidae, subfamily Bruchinae. If you have dried beans at home, check for an infestation. Throw out the contaminated beans, and put your others in sealed plastic containers, or in the fridge. https://bugguide.net/node/view/13857


Can the body always find the right antibodies?

Yes and no. Yes, it's possible that some individuals won't be able to (or happen to) make antibodies to a specific part of a pathogen. But most pathogens are large and complex enough that they have many different targets for antibodies, and it becomes increasingly unlikely that someone won't be able to target any part of the pathogen.

An example is given in Influence of Immune Priming and Egg Adaptation in the Vaccine on Antibody Responses to Circulating A(H1N1)pdm09 Viruses After Influenza Vaccination in Adults. A subset of adults (who were exposed to a particular influenza virus as children) have poor antibody responses to a vaccine to a different strain of influenza virus:

  Significantly reduced antibody reactivity to circulating viruses bearing K163Q was observed only in the USSR/77-primed cohort, whereas significantly lower reactivity caused by egg-adapted Q223R change was detected across all 3 cohorts.

(This is not an argument against vaccination, I feel obliged to point out, because the vaccinated people were still better off than unvaccinated, just not as well protected as they could be.)


What are the variables that control/influence the color of oranges(Citrus sinensis)?

Naturally, ripe orange skins are usually green-yellow. In colder climates, they will turn orange over winter, since in the cold the chlorophyll will start degrading and stop masking out yellow/orange carotenoids in the skin. If the fruit is picked in fall (and not let ripen or degreened) they will have green color.

Ehtylene gas, which is a natural plant hormone, is sometimes used to give them more uniform, orange color (degreening). Also, some oranges cultivated in the US are dyed with Citrus Red 2 to make their peels orange.


Tryptophan side-chain structure, how should it be orientated?

Good question, this regards rotamers!
Basically, the side chain of amino acids can rotate as shown in the figure below for glutamate (Glu; E). The various option for side-chain rotation is called rotamers! Some amino-acids side chains have the potential of many rotamers (such as glutamate) while some can only adopt a few (such as tryptophan) due to steric restraints. You can read about it here on FolditWiki or in the article 'Rotamers: To be or not to be?: An Analysis of Amino Acid Side-chain Conformations in Globular Proteins'.

The set of amino acid side-chain conformations in globular proteins
cannot be considered as normally distributed around some rotamer
points. Outliers occur systematically. The rotamericity of an amino
acid depends essentially on the different environments the amino acid
meets in real protein structures. Factors such as the backbone torsion
angles of the residue itself, the secondary structure and tertiary
contacts influence the rotamericity. (...)

When solving a protein structure, scientists spend a lot of time on placing the amino-acid side chains into their correct rotamer position. Which rotamer a particular side chain should adapt, depend on the surrounding environments. Some amino acids side-chain are also very flexible and will move around the various rotamer position that they can adopt. In the example of glutamate (figure above), it would most likely adapt a rotamer position pointing either out towards solvents (if the the side chain is on the surface of the protein), or perhaps towards a positively charged amino acids side chain such as Arginine (R) or Lysine (K) to form salt-bridges or H-bonds.
In the case of Tryptophan (W), it is often involved in pi-stacking and would therefore be found in a rotamer position that stacks with other aromatic amino acids side chains. It is also a very bulky amino acid, and might therefore only have space in one particular conformation. Note that tryptophan (W) only has two rotamers, which are similar to the two that you drew in the updated figure, and again shown below. Note that both of these are correct, and that my hand-drawn bond angles are a bit off. These two rotamer options for tryptophan are even found in enzymes catalytic site, where the 'flipping' from one confirmation to the other is the key-mechanisms the allows substrates into or out of the active site!

These structural arrangements are a lot easier to understand in three-dimensions, if you are still struggling then it could be a good idea to use a visualisation program (e.g. PyMol or Coot) and take a look at tryptophane's and other amino acids side chains by downloading some protein structure from the PDB database.
Here are also some related questions

Protein Structure Parameters
How to convert PDB file of Amino Acids to rotamer tuples list of all AAs instances


How does life change when you dig deeper?

Extremophile bacteria and archea are living very deep beyond our imaginations. This is what you need for general composition at different depths. And this and this is for the deepest living organism known ! Following is image from (Manson et al 2010) which shows at what depth you will get bacteria

Even more deeper, Wold's single species ecosystem, Desulforudis audaxviator which can be found 3 km below sea level.


Are sizes of potatoes normally distributed?

According to Evaluation of the Effect of Density on Potato Yield and Tuber Size Distribution potato tuber size was estimated using a normal distribution but they are not normally distributed
They found that a Weibull distribution with specific parameters estimated better than a normal distribution.
In fact you should not expect a normal distribution because there are no potatoes of negative size  As such you expect a gamma distribution.  The Weibull distribution is in the same family of distributions.
But in many cases the normal distribution is used since the probability of a negative number is negligigble.
Does this mean that potato sizes are still the result of many factors? It would seem so


How is information sent from the skin to the brain?

The accuracy of sensation is actually quite variable depending on the region of our body. Highly innervated areas such as our fingers have a higher degree of accuracy than sparsely innervated areas such as our legs.

There is a simple experiment you can do to illustrate this. Close your eyes and then get a friend to lightly and slowly run their finger from your wrist, up towards the bend in your elbow on the inside of your arm. Try to guess at what point the reach the joint of your elbow.

In terms of how the brain knows where it came from,  there is part of your brain called the sensory cortex. This sensory cortex has a pattern that corresponds to areas of the body. This pattern is known as a the sensory homunculus (google images will find this). As signals pass up the various different spinal pathways and into the brain they are sent up to this sensory area and the appropriate region of the homunculus is stimulated thereby giving the sensation in the appropriate body area.

Interestingly in some brain surgery a patient may be kept conscious so that these areas can be directly stimulated by electric current and the patient will experience sensations.

There is also a matching area, called the motor cortex, which corresponds to movement rather than sensation.

The above is a simplified version of what goes on and there is lots more detail which would be covered in neuroanatomy books


How does inbreeding depression cause infertility?

One of the main contributors to inbreeding depression are recessive lethal alleles. Suppose you have an individual who has the genotype Aa, where A is the dominant, non-lethal allele and a is the recessive lethal allele. This recessive lethal allele is likely very rare in the population (selection would decrease the frequency of a recessive lethal allele), so our Aa individual can breed with almost any individual without consequence because most other individuals are AA, so the offspring of this individual will be either Aa or AA.

However, if the Aa individual breeds with itself or with a close relative who has the Aa genotype, its offspring will have a chance of inheriting the two aa alleles, which is lethal, decreasing the fitness of the Aa individual that bred with itself (or a close relative). This decrease of fitness resulting from self-breeding will cause selective pressure to outcross instead of self.

It is important to note that the recessive allele doesn't need to be strictly lethal for this effect to happen - if the recessive allele causes infertility (for isntance, failure to produce gametes or something similar) the same effect will happen.

In short, inbreeding can cause detrimental recessive alleles to become paired, causing lethality or infertility.


Could a mammal convert ingested dissolved CO2 to usable energy?

There isn't any biologically useful energy in CO2. In fact, humans and all other animals produce CO2 as a waste product at the end of metabolism specifically because it is low-energy. You don't need to ingest it or breath it in as a gas, and if you didn't breathe it out you would die.


Proteins with alpha helices alone and beta sheets alone?

You may consider taking a look at the SCOP structural classification of proteins to check all beta proteins and all alpha proteins. As per specific examples and though not belonging to the SCOP classes mentioned above, Porin for a beta protein (PDB:1A0S), and Rhodopsin for an alpha protein (PDB:1F88) are two nice structures to look at.


Female preference for males who are already in a relationship

This is a widely researched topic in the overlap between social sciences and evolutionary biology.  Evolution has become very influential in understanding human interaction and preferences.

This chapter from "The Adapted Mind : Evolutionary Psychology and the Generation of Culture" will give you an idea of how all this plays out in the big picture - its a fairly comprehensive review of many factors considered in human mate choice.  The study may be psychological, but the logic is derived from biology these days.  (stackexchange won't let me link to google books - you can search for the title and look at chapter 6).

Evolutionary tendencies will favor more successful offspring.  But for people it includes not only the genetic qualities of the mate (appearance, height, disease resistance, health) but also social qualities (how reliable or willing a mate is to support offspring).

First off you can see that there are many many factors which women take into consideration in their preferences.  Its commonly said they are more complex than men, but that's another question.  You have to take a range of factors holistically including the social environment.

I can't find this particular issue addressed in the literature, but I think that it might be attractive to women in some social settings.  If there is a lot competition for 'quality' mates or resources for instance - if you have very few secure males or pessimistic females might create pressure which would cause females to prefer males which were successful.

Its pretty easy to feel good about hypotheses like this.  I couldn't find a specific study, but perhaps someone else will.  There's a lot of such papers out there.

I should say that men are as easily led to do things by 'mate choice' psychology that aren't totally healthy or socially acceptable.  That's biology.


Does the yolk sac for Danio rerio form at the vegetal pole?

Generally, yes, yolk is at the vegetal pole. There may be exceptions but I am not aware of them.

You can read about zebrafish (Danio rerio) embryology in great detail in this paper. Figure 3 from this paper (see image) shows the immediate post-fertilization zygote, in which the animal-vegetal axis is first set up by the migration of non-yolk to the animal pole.

UPDATE: very explicitly labeled yolk figures.


What is a Mitochondrial Eve and Y-chromosomal Adam

When talking about a maternal unbroken linage and a paternal unbroken linage, is the meaning that Mitochondrial Eve had a linage of only women reaching every person today, and the same with Y-chromosomal Adam and men?

Kind of, yes. The concept behind Mitochondrial Eve and Y-Chromosomal Adam has to due with cell replication and basic genetics.

The Mitochondria ("Power Generators" of the cell) are directly inherited from mother to daughter cell. That is, new cells do not start with 0 and are forced to make them de novo. Some Mitochondria are replicated before division and some are 'given' to the daughter cell to start with.

Because of the unique way that Mitochondria are inherited, when it comes to creating new humans it means that only the Mother's Mitochondria are given to any children she gives birth to regardless of the sex of the child. So I, being male, have my Mother's Mitochondria - which the same as my Grandmother's - and the same as my Great-Grandmother's - etc. etc. etc. until you can trace that line back to "Mitochondrial Evel" whose Mitochondria are the origin for all humans on the planet and are inherited Maternally.

In that sense it is an unbroken lineage of genetic information as inherited from mothers, though not exclusive to women.

"Y-Chromosomal Adam" is a similar concept - Women do not have a "Y"-Chromosome, so every Y-Chromosome men have today had to originate from somewhere. It's trickier to do than tracing Mitochondrial DNA because while Mitochondria are inherited exclusively from mother to child, there could have been multiple Fathers to Mitochondrial Eve's children and other similar complications that muck things up.

  How is the specific "identity" or time period of those persons is known, assuming that researchers didn't check the Mitochondrial DNA or Y-chromosome of every single living human being today?

For "Y-Chromosome Adam" it's still more or less in the data-gathering phase as far as I was last aware. It's not as concrete as "Mitochondrial Eve", which has a very solid body of work supporting her.

The "identity" is known because the more in common a person's genes have with the genes of another, the more closely they are related. The researchers took a lot of genes from very divergent populations, and compared them. The researchers were then able to tell which portions were common among all of the Mitochondrial DNA, which had changed the most, and which had changed the least from each other. Using that data, you can construct a rough image of what the originator (or LCA - Last Common Ancestor) had for their own genetic makeup.

You can construe a time period because portions of your DNA (either Mitochondrial or Nuclear) acquire/tolerate mutations at an expected rate - say 1 mutation every 1.5 Million Years. So as long as you have a rough idea of what your LCA's genes looked like (see above), then a modern day sample with 5 mutations is 7.5 M.Y. away from the LCA.

  how can they know for sure that there aren't some tribes in the Amazons, which have a direct female linage to Mitochondrial Eve's sister?

They didn't when they started testing. That's part of the fun of the project.

The "Out of Africa Hypothesis" rose in prominence partially due to the findings of the research. It basically posits that the ancestors of humans evolved once in Africa, and then spread from Africa to the rest of the world. Because the Mitochondrial Eve research concludes that "Eve" was around before we spread throughout the rest of the world, it implies that every ancestor already had Eve's legacy when they started migrating into Europe, Asia, the Philippines, etc. Thus every human on Earth, no matter where they are today, shares traits with Mitochondrial Eve.

For the Amazonian tribes, they would have inherited it from their ancestors in North America, which were ancestors of tribes in Asia who crossed an ice bridge into North America, and the tribes in Asia came out of Africa.


How did this spider evolve to mimic exactly a human face and arms?

I think this really is just a case of what you refer to in your question as anthropomorphism. We are very, very good at seeing faces. Here are some more examples.

Addendum

This site has pictures of quite a few peacock spiders, and as far as I can tell these are all the same species (The only peacock spider mentioned on Wikipedia is Maratus volans).

The remarkable thing about these images is that individual spiders seem to have very different patterns on thorax and abdomen, and many of these are much less like human faces. This seems to me to weaken the case for some sort of mimicry.

Interesting fact: seeing faces and other forms where they do not exist is a psychological phenomenon called pareidolia.


No, it won't happen

Even geographical isolation failed to allow speciation in humans (see Does it make sense to classify all humans in a single species?). So if there is some small reproductive isolation between working groups, it is definitely not going to be strong enough to cause speciation.

In an imaginary world

If there was strong reproductive isolation

In an imaginary world where there is a more important reproductive isolation that lasts for long enough between blue and white collar workers, sympatric speciation might be possible. Such reproductive isolation could be caused by very important social stigmas.

Wallace effect

Wallace effect is a type of speciation that is mediated by a reproductive isolation that has been selected for as fitness of offspring is higher when mating is assortative.

There is probably relatively little genetic predisposition to being blue collar or white collar worker. But in an imaginary world where there is very strong genetic predisposition to being a good blue collar or white collar worker, and where worker quality will affect income which will affect fitness, then yes, wallace effect could be a thing.

But really, we do not live in one of this imaginary world. In our world, speciation won't occur between blue collar and white collar workers.


The other answer is most certainly incorrect. Silverfish are silver/grey and (like all members of the Zygentoma order) have three distinct, tail-like caudal appendages from their posterior end -- really, two large cerci with a central long filament.
 [Sources: 1, 2, 3].

The OP's specimen resembles the larva of a dermestid carpet beetle of some type; specifically, the location and appearance make me think it might be a black carpet beetle (Attagenus spp) -- for example A. unicolor.

 Source: Univ of California Master Gardener Program of Contra Costa County Blog

Description:

Tell-tale characteristic: the tuft of numerous "hairs" on the posterior end:

  The larvae of the black carpet beetle, which may reach 12.7 mm in length, are very different from other carpet beetles’ larvae. They are elongate, carrot-shaped, golden to chocolate brown, and have a tuft of very long, curled, golden-brown hair at the tail end of their body.  [Source: Penn state Dept. of Entomology]

A description from IFAS suggests that larvae develop stiff, bristlelike tails when older.

See bugguide.net for more pictures, such as this one

Pest:

According to many of the sources I've linked to already, the larva is the damaging life stage of this beetle.


Is it possible for a human to live forever if he/she didn't catch any diseases?

No that is not possible ever. There is something called telomere which is present in the chromosomes of cell .These Telomere triggers the action of ageging and leads body towards death. When we are in growing age the amount of telemere is very less but as we get older and older the amount of telemere get increases .
The rate of increase of telemere increases with each succesive cell disivision. Hence death is sure no matter what ever you do.


Is there any measure by which the Germans today could be called a genetically superior race?

I am leaving the word 'superior' aside (it's ill-defined and strongly valuing).
In any way - unlikely. If any ethnic group is 'superior' (at least, intellectually) - then, ironically, Nazi main victims - Ashkenazi Jews. But while there is some genetic component, it is impossible to disentangle it from societal and historical factors. Here are some links, is you are interested.
When it comes to Germans, as far as I remember, they are not a group genetically distinct from, say Poles. Yet Slavs were considered by Nazi also an inferior race, to be enslaved or eradicated.
In any case, culture and socioeconomic factors seem to be much stronger than (relatively small). In particular, for Germany itself, there was a huge difference between West and East Germany, prior to the fall of Berlin Wall. It can be hardly explained by 'genetical superiority' of West Germans. An excerpt from Race, IQ, and Wealth by Ron Unz:

Consider, for example, the results from Germany obtained prior to its 1991 reunification. Lynn and Vanhanen present four separate IQ studies from the former West Germany, all quite sizable, which indicate mean IQs in the range 99–107, with the oldest 1970 sample providing the low end of that range. Meanwhile, a 1967 sample of East German children produced a score of just 90, while two later East German studies in 1978 and 1984 came in at 97–99, much closer to the West German numbers.
These results seem anomalous from the perspective of strong genetic determinism for IQ. To a very good approximation, East Germans and West Germans are genetically indistinguishable, and an IQ gap as wide as 17 points between the two groups seems inexplicable, while the recorded rise in East German scores of 7–9 points in just half a generation seems even more difficult to explain.

See also The East Asian Exception to Socio-Economic IQ Influences and The Myth of American Meritocracy (on how ethnicity can affect admission) by the same author.


What percentage of a cell's volume is occupied by protein?

The tricky part is to define what is the volume of a biomolecule as it is a folded chain full of bumps and holes. Water is all around and in the folded structure and is actually important to keep the conformation of at least some of the proteins/RNA/DNA.

At the same time we know that 60% of your body in mass is water. Let's visualize that. Bio molecules have roughly the same weight per volume than water. Now add into the equation that a good third of the filled actually is water due to the structure holes, adsorption etc. You now have roughly:

  % empty space = 60%-(40%/3)= 47%

To help think about it imagine a grid with roughly one cell out of two being filled. That looks pretty crowded to me. Then you of course have variations with blood and secretions on one side and bones on the other but you have the big picture.

For an example look at an electron microscopy picture of a striated muscle cell: http://histology.med.umich.edu/sites/default/files/muscleQ4.jpg. It looks pretty much like the half filled grid isn't it? Of course seeing individual molecules is hard but the white space correspond to mostly empty space with a couple of actine fibers. The dark corresponds to actine+myosine fibers: an extremely tight space. And we have roughly half of each :-)


Trouble understanding overlapping genes.

A gene has got nothing to do with a stop codon. As you might know there are non-coding RNAs as well and the genomic regions responsible for transcription of these RNAs are also called genes.

Genes that have an overlap in their genomic locations (without considering the strand orientation) are called overlapping genes.

In case of same strand overlaps, the genes should have a different transcription start/stop site. Alternatively spliced RNAs are not considered overlapping transcripts. In certain cases, transcripts with an alternative transcription start/stop site are not considered separate genes but rather, isoforms, especially if the gene produces an mRNA and the alternate transcription start/stop sites just affect the untranslated regions (UTRs) and not the coding region (have a look at this article).

Your confusion is quite valid and gene nomenclatures need some redefinition/clarification.


In DNA repair, how is it determined which strand contains the error?

There are many types of DNA repair. Let us limit to the following three different types to answer this condition.

1. UV damage

Exposure of a cell to UV light can result in the covalent joining of two adjacent pyrimidines (usually thymines), producing a dimer. These thymine dimers prevent DNA polymerase from replicating the DNA strand beyond the site of dimer formation.

In such cases, UV-damage specific endonucleases cleave both the 5' and the 3' end of the lesion. Along, with the lesion some normal DNA is also lost as an oligonucleotide. Here modifications are being made only on one strand, the other is taken as a template (correct) and the DNA in the lost part is replaced.

The UV-damage may occur on both the strands but locally, one is affected and the other is the template (since you can't have thymine both sides)

2. Base Excision

Normal DNA bases can get deaminated spontaneously or on insult to an abnormal base (not on DNA).The abnormal base is excised by glycosylases and gap is later filled by considering the other strand the template.

3. Mismatch repair

What you are talking of in your example is not a case of deamination or UV damage but a mismatch repair. There can be errors in replication too where such a case could set in. There are specific enzymes for this repair, but discrimination is based on the degree of methylation. GATC sequences, which are found approximately once every thousand nucleotides, are methylated on the adenine residue. This methylation is not done immediately after synthesis, so the newly synthesized DNA is hemimethylated (that is, the parental strand is methylated but the daughter strand is not). The methylated parental strand is assumed to be correct, and it is the daughter strand that gets repaired.

The above said mechanism of discrimination is only in the gram negative bacteria. To quote Wikipedia,

  However, in other prokaryotes and eukaryotes, the exact mechanism is not clear. It is suspected that, in eukaryotes, newly synthesized lagging-strand DNA transiently contains nicks (before being sealed by DNA ligase) and provides a signal that directs mismatch proofreading systems to the appropriate strand. This implies that these nicks must be present in the leading strand, and evidence for this has recently been found.

There are other cases where there is damage occuring to both strands that I'd suggest for further reading.

References

Lehninger's Principles of Biochemistry, Ed. 6
Lippincott's Illustrated Reviews, Biochemistry, Ed. 5
Wikipedia. DNA mismatchrepair


What factors cause males to be more common than females in humans, from an evolutionary perspective?

Nice question! The answer is in your linked article. I quote:

  When you put this all together, it turns out more males are born because more female fetuses are lost during pregnancy.


This paper describes some PCR strategies with LINE and SINE PCR identification (Shedlock and Okada. SINE Insertions: powerful tools for molecular systematics. BioEssays (2000) 22:148-160.).

I have no experience with PCR amplification of SINEs or LINEs, however I can think of two strategies right now.

1) You may be able to find a unique 18-20 nt region flanking those regions. If you can, great. If not, perhaps there is a unique site somewhere in the middle of these regions, then you can amplify from the middle outward to both upstream and downstream regions.

2) If there are no unique sites that you can exploit, that would imply a highly regular (ie, repetitive) pattern, but you can take advantage of this too. You can pick primers such that they are on the extremes of the repetitive subunit within these structures. For example, if your sequence looks like this:

A------>BA------>BA------>BA------>BA------>B

Then you can pick primers A and B for PCR use. You will have non-specific primers, and therefore when you amplify the DNA, you will get all possible permutations of DNA that these primers will produce. Specifically, you will get:

A------>B

A------>BA------>B

A------>BA------>BA------>B

A------>BA------>BA------>BA------>B

A------>BA------>BA------>BA------>BA------>B

         A------>BA------>BA------>BA------>B

                  A------>BA------>BA------>B

         A------>BA------>BA------>B

and so forth.

This last approach is obviously inefficient, because your possible products scale exponentially, and will be produced with equal likelihood, minimizing the DNA yield of any particular segment.


Can motor neurons in the brain stem start movements?

Yes, movements (including fairly complex ones) can start in or be driven by the brainstem (and spinal cord).

Central pattern generators are key to producing coordinated rhythmic movements, including those for locomotion, chewing, and breathing: these are also located in the brainstem and spinal cord.

There have been many experiments done to study brainstem control of locomotion (see Shik and Orlovsky, 1976), particularly in decerebrate cats. You can induce a walking motion independent of cerebral control in these animals just by moving the floor (e.g., using a treadmill).

More generally, voluntary motor commands from cortex are mostly just a "suggested plan" - the specific patterns of muscle activation are determined in the brainstem and spinal cord, with input from proprioception and modulation by the cerebellum and brainstem nuclei such as the red nucleus.

In humans, spontaneous movements are also common in ~50% of brain-dead patients (Saposnik et al. 2005), although definitions of brain death typically include the brainstem, so these should be thought of as spinal rather than brainstem movements.

Saposnik, G., Maurino, J., Saizar, R., & Bueri, J. A. (2005). Spontaneous and reflex movements in 107 patients with brain death. The American journal of medicine, 118(3), 311-314.

Shik, M. L., & Orlovsky, G. N. (1976). Neurophysiology of locomotor automatism. Physiological reviews, 56(3), 465-501.


Are there multicellular isogamous species?

Our knowledge about the sexual transmission of mitochondria and
  plastids (hereafter organelles) in isogamous eukaryotes comes mostly
  from studies of the yeast Saccharomyces cerevisiae and the green alga
  Chlamydomonas reinhardtii which are both unicellular species. To
  investigate organelle inheritance in a multicellular organism with
  morphological isogamy, we studied the filamentous brown alga
  Ectocarpus siliculosus, in which each gamete contributes one plastid
  and at least one mitochondrion to the zygote. ...

2004 - Inheritance of organelles in artificial hybrids of the isogamous multicellular chromist alga Ectocarpus siliculosus (Phaeophyceae)

So it is possible, but it seems like very rare.


Amino acid characteristics that determine their chemical properties?

Sounds seriously like your homework, so it'd be better if you researched. However as a starting point amino acids can be polar and non-polar. These properties cause varying forces of attraction between amino acids and their surrounding environment. The location changes the way they can interact. Ask if you are unsure about something :)


What is the difference between hilum of the lung and root of the lung?

Short answer: Hilum is an area(has only 2 dimensions) where as root is a body( has 3 dimensions).

  The root of lung is a short broad pedicle connecting the medial surface of the lung with the mediastinum. It consists of structures entering and leaving the lung at hilum. The root of lung is surrounded by a tubular sheath derived from the mediastinal pleura.

and

  The hilum is the area on the mediastinal surface of the lung through which structures enter or leave the lung.

Source: pg no 239

Consider the following image( edited by myself):

If the cylinder is root of lung then lateral opening(blue) is hilum.

The region bounded( within the limits of pleural membrane) by those two planes is root of lung and the area bounded by the lateral plane is hilum.


If you think about the boiling of water, I'm sure you can understand that heat breaks hydrogen bonds. Next consider that the hydrophobic effect is driven entropically and so, by the equation $\Delta G=\Delta H-T\Delta S$, its strength increases with temperature (to a point). See here and here for further explanation. Also, this paper for a more empirical view.


Can two arms-racing species be stabilized?

To rephrase Cort Ammon. It depends on how you setup the system.

Imagine each combat strategy as a point on a landscape. Good strategies are on higher ground, poorer strategies are on lower ground.

A and B each have their own combat strategy and thus start at different points on this landscape. Mutations allow a species (say A) to explore the strategies around its starting point. Selection will cause the curtail that exploration.

If A find itself on a slop of a hill, selection (ie your combat and mating system) will cause the A population to drift upwards on this slop. However if A find itself on the peak of a small hill, it has no where else to go.

So how the scenario will play out will depend on the initial start conditions of population A and B. The mutation rate/genetic variability of the population (ie how many strategies population can explore around its initial strategy).

Additional factors is the genetic system that you have. If individuals of your species can only have one strategy (haploid), the species will be bound to its local hill. However if an individual can have more than one combat strategy at a time, (ie a diploid or gene duplication in RL), then the individual can have a combat strategy that work (local peak) and have a second strategy that is free to evolve... free to explore the landscape... going down valleys of bad strategies... and may eventually find the foot of a mountain... which a peak fitness higher than even the local peak it started.


How does Vibrio cholerae benefit from infecting its host?

After V.cholerae gets into the human intestine it starts to multiply its numbers, and then becomes virulent after sufficiently expanding its numbers. This virulence drives the diarrhea which in part causes the bacteria to slough off into the intestinal lumen, and then into the external environment again.

So in short it uses the human intestine to increase cell numbers.

See work by Bonnie Bassler for a really fascinating understanding of the complexity of this infection.


What protocol does the nervous system use?

An analogy to a computer bus can easily mislead you. Neurons do not communicated via a multiplexed "bus" with different targets; rather the complex connectivity of the neurons itself works as a computing device as a whole. The area study for understanding the communication among neurons is called "neural coding".

If you are talking about just the motor and sensory peripheral nerves, they innervate specific targets.


Protein - one polypeptide molecule or a collection of molecules?

This sort of question is easily answered by consulting and carefully reading an introductory biochemistry text, like this section of Berg et al. on line. However, as the diagrams of β-sheets can be confusing, I will summarize.

The amino acids linked by covalent peptide bonds produce a protein molecule in the form of a single polypeptide chain.
This polypeptide chain folds into a specific shape in three-dimensional space, its conformation being maintained by weak non-covalent interactions — ionic bonds, hydrogen bonds and Van der Walls interactions. (Often referred to as protein tertiary structure.) Proteins that have a roughly spheroidal shape (rather than being long and extended) are referred to as globular proteins.
Often the three-dimensional structure has large regular components (often referred to as secondary structure) because of the potential for repeated hydrogen bonding between the CO and NH of the repeating peptide bonds.

Molecular diagrams to illustrate the type of secondary structure known as the β-sheet generally show just a section of the polypeptide chain for clarity, as in the left-hand illustration from Berg et al., below:

This may give the impression that two separate chains are involved†, but cartoon representations such as the one on the right (also from the same section of Berg et al.) show that for globular proteins this is not so.

In the diagram the flat blue arrows represent β-strands that are hydrogen-bonded to one another to form a twisted barrel-shaped β-sheet. The yellow ‘rope’ between the arrows represents the continuation of the chain in the non-sheet areas of the structure.

So the possibility for confusion arises primarily from the difficulty of showing the detailed pattern of hydrogen bonding in the whole of a large protein. (Although it may also arise from the fact that it is easiest to illustrate β-sheets using the diagrams of silk fibroin — historically the first to be described — in which the sheets are very regular and flat. To an extent this is misleading as the right-hand side of my diagram indicates.)

†Footnote

Fibrous proteins, such as silk, exist in which β-sheets are formed between many different chains. The identification of the individual chains can be made unequivocally, e.g. on the basis of the gene sequence, and it is clear that the higher-order structure is composed of many individual molecules. In smaller higher-order structures, e.g. tetramers of globular proteins held together by weak non-covalent interactions, the semantic question of whether a molecule can be made up of several individual chains arises. In my opinion, this question is best ignored, unless one is studying the biophysical chemistry of proteins.


What is this thing that is growing in my yard? And should I get rid ot if?

Myriostoma is a fungal genus in the family Geastraceae. The genus is monotypic, containing the single species Myriostoma coliforme. It is an earthstar, so named because the spore-bearing sac's outer wall splits open into the shape of a star. Source: Wikipedia.

But this recent article shows otherwise https://pdfs.semanticscholar.org/08ea/2ee6be93787f2e0034b85222b751a5281167.pdf


On the effect of polluted air on health. Is it more gradual, or more immediate?

The main factors of urban air pollution are nitric oxides, carbon monoxide, and what is called in german "Feinstaub" (very small carbon-rich particles from diesel exhaust). However, do not forget heavy metals: street dust is especially metal-rich and is swept into the soil near the streets where children and farmed plants can take it up. Lead is a heavy metal that can be breathed in with the air. Last not least noise over a certain threshold is proven to be a cause of illness, even loss of life time (10 years near an airport, if I recall correctly, but airport noise is getting better while machines become more fuel-efficient).

To answer your question one would have to look at every single factor. Lead accumulates in bones and destroys your brain. I just see Brazil banned it too in the 80's so this one killer is no more.

http://en.wikipedia.org/wiki/Tetraethyllead

I have found a meta-study that reviews about 80 papers on the subject, especially the Sao Paulo studies, so this should fit exactly your questions:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093800/


Cell proliferation limit and senescence of embryonic stem cells and fibroblasts

Telomeres (caps on the ends of chromosomes that are gradually shortened during each cell division) determine the maximum number of times a cell can divide, known as the 'Hayflick limit'. Cells that are able to express telomerase, an enzyme capable of extending the telomeres, can divide indefinitely.

There are various types of stem cell in a body which replenish the 'pool' of cells in the tissue once they reach the end of their useful lifespan. Each stem cell expresses telomerase to lengthen the telomeres after a round of cell division. The inhibition of telomerase in somatic (normal) cells is a major 'challenge' for cancerous cells - in order to achieve uninhibited proliferation, they must express telomerase. Thus, there are many molecular similarities between stem cells and cancerous cells (well, with regards to telomerase, anyway!) [ref].

Fibroblasts are somatic cells - they are the 'normal' cells that make up the vast majority of organsisms. The only cells not known as somatic are gametes/germ cells and stem cells. They thus do not express telomerase, and have a replicative lifespan, also known as a Hayflick limit.

With regard to your question about engineering organs, there are many resident stem cells in tissues (and thus organs) that 'top-up' the somatic cells when required. As organisms age, this pool of stem cells becomes depleted [ref]. Artificially engineering an organ such as the heart (I assume this is what you mean) would be inherently difficult, as many vascular cells are not replaced, but can last a whole lifetime - this is also true for many neuronal cells. So replicative lifespan is not necessarily related to lifespan!


Are hybrid-species individuals considered to be of the same species as their parents?

TL/DR We usually don't give specific names to those hybrids.

This is a fairly complicated question, actually, without an easy answer. Hybridization can have different outcomes, depending on how different the hybridizing species are. The cases you mention (liger, mules) actually do not deserve a specific names, because, first, they don't occur in nature, and, second, they are sterile, so there's no reproduction, hence no progeny. This lack of descendants goes against any defenition of species that we have in biology. There are cases where hybrids might become their own species, for example the butterfly Heliconius heurippa appears to be a species that evolved through hybridization between two closely related Heliconius species. There are also many examples in plants and more are being discovered in animals. These cases do receive a species name, because they occur in nature and populations can be predictably found.

Another case, similar to the cases you mention, involve hybridizations that occur in nature, but are rare and the individual rarely has any significance effect on the population. Sometimes those individuals are fertile, but look so different that might not be able to reproduce. Other times they can only reproduce with one of the parental species and if this happens successfully, new alleles can be introgressed into the parental genome. But for what we know, reproductive barriers between species tend to be successful in nature, tend to be broken down with human intervention (captivity, movement of species, among others) and, in most cases, don't have a significant evolutionary impact, except the cases when they do.


Determine which seed will germinate first

You'd have to know the individual germination times for each family.  I'm linking a table for vegetables, but it doesn't include the three plants you're looking at.  A google search for each one individually shows that yes Mung does have the shortest germination time.  It's a memorization question.

To add to that here is a paper where they review variation times between over 600 seeds and find that the variation in time is mainly constrained within families.


Is there a definition of species where Lions and Tigers are the same species?

The concept this would fit under would be the "Biological Species Concept."

Concerning this concept, the Evolution site for Berkeley says "members of populations that actually or potentially interbreed in nature..." constitute a species. By this definition, since lions and tigers can (and do) interbreed, they would be considered the same species under this concept.

EDIT: As Bryan pointed out, though, lions and tigers do not breed outside of captivity. NatGeo and Britannica both second this. With this, then, the Biological Species Concept would not be viable.

EDIT2: With the above in mind, there don’t seem to be many options.

Mate-Recognition: This idea posits that organisms who “recognize one another as potential mates” (Wikipedia, “Species”) make up a species. By this, it could be argued lions and tigers are the same species, but I would be hesitant for this to be the concept, for the same reasons against the Biological Species Concept (not occurring in nature).

Ecological: Using this definition, a species is made up “of organisms adapted to a particular... niche, in the environment” (Wikipedia). Again, this is very fuzzy, as I wouldn’t define them in the same niche (though this might depend on how specific you get).

Conclusion: These seem to be the most likely, though that’s a very loose term. I couldn’t find any others that would fit nearly as well. I would say the answer is “no”, but I don’t think I found all of the concepts.


How can parentage test be accurately done even though crossing over occurs?

Crossing over is an event that occurs during meiosis, which produces the gametes. This crossing over occurs between 2 homologous chromosomes, which are both from the parent. Hence, even though crossing over occurs, the recombinant chromosome that is passed down to the child will contain an allele that matches with the allele on one of the parent's chromosomes. Within the allele, the base pair sequence would not change.


A reflex arc is sometimes called the reflex pathway. While there is no involvement of the brain in the output/response to stimulus, it does receive signals via the spinal cord informing it of the action. In other words, the reflex action is registered in the brain as soon as it occurs.


Cultures of growth-arrested feeder cells have been used for years to promote cell proliferation, particularly with low-density inocula. Basically, feeder cells consist in a layer of cells unable to divide, which provides extracellular secretions to help another cell to proliferate.

From this paper's abstract:
Feeder Layer Cell Actions and Applications


To understand clearly extraintestinal diseases

Certain intestinal diseases have symptoms that appear concurrently in other systems of the body, but the bowel diseases themselves are not extraintestinal.

  Extraintestinal manifestations of inflammatory bowel disease are prevalent in both ulcerative colitis and Crohn's disease. The most common manifestations involve the musculoskeletal and dermatologic systems. Other manifestations involve the hepatopan-creatobiliary system (eg, primary sclerosing cholangitis) as well as the ocular, renal, and pulmonary systems1.

One of the key differences between extraintestinal manifestations and comorbid conditions (though seemingly not a necessity, the article cites primary sclerosing cholangitis as an counterexample) is that the extraintestinal effects will subside once the disease of the bowel is treated.

1 Levine, J.S., Burakoff, R. (2011). Extraintestinal Manifestations of Inflammatory Bowel Disease. Gastroenterol Hepatol (NY), 7(4), 235–241.


Long-term efficacy and absence of side effects of anti-covid vaccines

You are correct that we have been creating and approving vaccines for a very long time, so the procedures for looking at efficacy and side effects of vaccines in general long-term are quite well developed. They occur via so-called "Phase IV" trials, also known as post-marketing surveillance.
However, one complicating factor with at least the Pfizer/BioNTech and Moderna vaccines is that they're the first mRNA vaccines ever approved. While I hope the companies have been following some of the volunteers from previous clinical studies of other mRNA vaccines, we're in somewhat uncharted territory right now. The vaccines appear to be safe and effective, at least on the scale of tens of thousands of Phase III test subjects, but we just don't know exactly how they'll behave long-term. They were approved in the US as "Emergency Use" products, meaning the upside of having them available outweighs any known or potential downsides at this point.
So, the technical answer to your question "how does one prove the long-term efficacy and absence of side effects in such a short time?" is that they can't prove it. Based on the available data to date, there's no reason to suspect that some previously-unobserved deleterious effect will become common, but we can't be 100% certain until the products have been in widespread use for years and possibly decades. However, given the seriousness of COVID-19 and its currently unchecked spread across much of the world, the benefits of having "highly, strongly, very most likely safe" vaccines (that are also very effective) are huge.


How does a drastic change to the genome persist and spread?

It isn't necessarily true that individuals with different numbers of chromosomes are infertile. Even though common wisdom has it that horse (64 chromosomes)/donkey (62 chromosomes) hybrids are invariably infertile mules, that's not true; a significant number of fertile horse/donkey offspring have been documented.  Here is an example where the chromosomes were checked and confirmed to be 63 in the fertile mule parent.

Even more dramatically, the common shrew (a single species) has many different chromosome numbers as natural variability (at least 50 different chromosomal variants were identified in one paper) and this doesn't affect their interfertility.

So there are three general answers to the question here, though I don't know which is the most likely.

The extra chromosome arose and the original variant was very fortunate to have offspring; similar to the rare horse/donkey fertile hybrids.
The extra chromosome arose but had little effect on interfertility; similar to the common shrew. (The quote from the article in the question argues against this, but I don't know if it's a presumption made by the researchers, a presumption made by the writer, or a demonstrated fact.)
The extra chromosome arose in a single litter, so that several siblings shared it, and then interbred. Although incest avoidance is generally quite strong, animals that colonize islands or distance geographic areas (invasive species, often) commonly do interbreed this way.


Role of drift in evolution of sexually dimorphic traits

[C]an drift overcome sexual selection in the evolution of sexually dimorphic traits?

Short answer

Yes

Long answer

There are many ways to consider the effect of genetic drift. Here is one: One can approximate the probability of fixation of new mutations (using diffusion equations) with

$$P_{fix}≈\frac{1-e^{-4Ns} }{1-e^{-4s}}$$

, where $s$ is the selection coefficient and $N$ is the populations size. As you can see, a larger population size (the lowest is the genetic drift) corresponds to a higher probability of fixation of a beneficial mutation (to reach frequency of 1 in the population). If you don't have a good intuition of why genetic drift is inversely proportional to the population size, please have a look at this post. The most important point to keep in mind about the effect of drift is that when drift is high, every mutation pretty much behaves like neutral mutations.

This approximation is accurate under some assumption, for instance that the population is panmictic (=random mating). This equation holds true regardless of the reasons why a mutation affects fitness. The mutation may affect the activity level of an enzyme or it may influence how attractive an individual is to the other sex. So yes, in any case, a beneficial mutation may fix although it is deleterious (because of drift), or it may not fix although it is beneficial (because of drift).

A mutation might be beneficial in both sexes, detrimental in both sexes or beneficial in one sex and not in the other. In such cases, I suppose it is possible that the above equation must take a slightly different form. In any case where the mutation has a different impact on the fitness in each gender, I don't know how the above formulation would solve to but I'd think that you could simply replace $s$, by $\frac{s_m+s_f}{2}$, that is the average of the effect in both sexes (where $s_m$ and $s_f$ are the selection coefficients in males and females respectively). Intuitively, I think this should hold true as long as the sex-ratio is 1:1. The exact calculation of the probability of fixation doesn't matter to your question though. Note that mutations having the opposite effect on fitness in each gender often end up being on sexual chromosomes (if any) or at least being expressed in one sex but not in the other. In such case, a fixed mutation often end up being beneficial in one sex while neutral in the other. In any case, genetic drift will obviously affect the evolution of sexually dimorphic traits.

EDIT

  could you clarify "As you can see the highest is the population size (the lowest is the genetic drift),"?

The impact of genetic drift can be measured in terms of how it affects probability of fixation or how it affects the rate at which heterozygosity at a neutral site is lost. An intuitive explanation for why $N$ and genetic drift are inversely proportional can be found here.

  Are you referring to the positive correlation with P fixation and Ne?

Yes. I could have referred to that as to something else though. Note that the correlation between $P$ ans $N_e$ is perfect ($r^2=1$) because $N_e$ is defined on the concept of genetic drift.

Definition of $N_e$

Let's WR (stands for Wright-Fisher) be a population of size $N_{WR}$ where mating is random and there is no variance in fitness.

Consider now the population A. Let's its size be $N$. A experiences a given level of genetic drift based on its mating system, population structure, variance in fitness, etc.. the effective population size $N_e$ of A is (by definition) the size of the WR population ($N_{WR}$) that experiences the exact same level of drift, that is the same probability of fixation for a new mutation and the same rate of heterozygosity lose at a neutral site.


Could inhibition of progerin formation slow the rate at which a body ages?

Progeria (and related) syndromes are essentially a collection of 'accelerated aging' phenotypes caused by single mutations; Progerin is a shortened version of the protein Lamin A, and is therefore not found in individuals without a loss-of-function mutation in the LMNA gene (the wiki page you reference). As far as we are aware these genes do not 'cause' aging in individuals without the mutations.

LMNA is a normal component of the nuclear lamina (a structure inherent to the nucleus). This review discusses the various diseases associated with mutations in this gene, some of which present 'accelerated aging' phenotypes. However, as far as I know, there is limited evidence to suggest that LMNA, or indeed any Lamina associated protein, is involved in 'normal aging'. A recent GWAS meta-analysis found a variant in LMNA that is associated with longevity in humans, however the association is relatively weak (OR=1.18, P=7(x10)-4), so even if this is a true association, it seems that (as usual in aging research) there are many other factors to consider, and it is not a single gene that is doing the aging.

So to stress the point: progerin has no function in 'normal' human aging - it is a defective protein caused by a germline (or novel) mutation in the LMNA gene.  Accelerated aging is the symptom of this genetic disorder, and is not completely analogous to normal aging (as you point out, there is no cognitive decline that is associated with normal human aging).


Are there land animals that use gill-like organs instead of lungs?

Terrestrial crustaceans are land animals that use gills (or gill-like structures) for gas exchange, though these gills must be kept moist for efficient respiration.

Specifically, animals like hermit crabs have a branchiostegal lung that looks like gill tissue but is better adapted for absorption of oxygen from air instead of water.


No. Cell-plasmolysis is not necessarily fatal for the cell. Plant cells normally recover from this condition when water is available. (But cell death can take place in excessive or prolonged lack of water).

It is an incomplete truth that during plasmolysis, plant cells get detached from the cell wall. Actually the plasmodesmatal connections remain there and a portion of the cortical (outermost)-layer of cytoplasm, mainly containing "cortical endoplasmic reticulum", a group of endoplasmic reticulum spanning close to the cell wall; remains there.

Now, when plasmolysis take place, the cell-membrane shifts apart from the cell wall; but at the place in-between, there forms fine cytoplasmic threads called Hechtian strands. So the connection is retained. (As well at some portion of cell-wall, the bulk protoplast remain touched there)

Here are photos showing hechtian strand; taken from the book Plant Cell Biology- structure and function, by Gunning and Steer, Jones and Bartlett publishers, Copyright 1996;

  Image-1 (Book image 16-C)

  Hechtian strands of stretched plasma membrane extended from the plasmolysed protoplast to the cell wall (K. Hecht , 1912, was the first to  study them in detail). This confocal micrograph shows strands in a 16 μm- deep zone. Some strands extend from plasmodesmata (arrows), where the membrane passes through the cell wall, butmany attached to other sites. in 1931 another early investigator J. Plowe, pushed plasmolysed protoplast along inside their cell walls, observing that existing strands stretched and broke, and that new strands could form. In today's terminology we would say that new strands arise when freebinding sites on the plasma membrane contact and bind their ligands in the cell wall.

Reference:

  Plant Cell Biology- structure and function, by Gunning and Steer, Jones and Bartlett publishers, Copyright 1996

Update: An interesting information; there is one method of plant protoplast isolation without enzymic digestion of wall; which uses plasmolysis. Since the protoplast(and cell membrane) get shifted from part of cell wall; it becomes easy to rupture the wall without rupturing the cell-membrane. (Discussed in this website). The protoplast remains alive after plasmolysis otherwise we won't be able to use this method for protoplast culture, cell fusion etc.


Natural enemies boost deep evolutionary fitness?

The question is interesting.

I am afraid about the use of the word "fitness" in you question. The fitness is usually defined as the number of offsprings an individual can sire in its lifetime. Most often we talk about relative fitness which is the relative number of offspring in an individual can sire in its lifetime compare to the individual in the population that sire the greatest number of offsprings.

How would you compare fitness of individuals between different species? Just by counting the number of offspring they left behind? Or did you mean that most fit species are actually those species that can outcompete others? If yes, then I would say that saying

  Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) fitness

can be restated

  Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) species competition ability

and it is actually just a special case of

  One species that evolve under many strong selection pressure ends up being a very competing species.

The explanation is the following:

One species that undergoes one selective pressure, will see its genetic variance decreases. The weak individuals will disappear letting places to the strong individuals. Then newly arisen variance (mutation) will come up only in the strong individuals (as the other ones disapeared). This is what J.Gould meant by saying "Natural selection creates the fit". As a consequence a species that undergo many successive selection pressure will end up with purified and very strong genotypes while, in a species that were free to evolve without selection they would have evolved many different genomes with some good mutations nested in very poor genetic background.

You could as well use the concept of lineage selection and states that lineage that succeeds to outcompete others will thrive while species that suffer from competition with other species will get extinct. As a result, if you compare all species that were in competition with another species in the past with all species that were not in competition, you will find out that those that were in competition are more resistant to competition. But I guess this is not exactly what you meant when saying: "Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) fitness"

Finally you might think of the ability of species to evolve better. This ability is called "evolvability" (see this book for example). You might say that species that undergo many selection pressures were selected to resist to newly arisen selection pressure. As a result, species that are under competition might end up with a greater evolvability than those that were not under selection. Resulting that species that were under competition will tend to increase to always increase their fitness in the long term.


This looks like an Aplysia, or "sea hare", a marine gastropod. Some of them sometimes get stranded and look like fat violet/green/brown blobs, around 10cm diameter. In the water, they swim slowly. I've seen some in Brittany (France) and in Algarve (Portugal).


Could someone explain the join in the SARS-cov-2 genome at location 13468?

In the reference genome browser, it seems you are looking at the first Coding Sequence (CDS) line, YP_009724389.1, which shows the translation to LNRV...:

If you look lower down, you'll see a line for CDS YP_009725295.1, which shows translation to LNGF... as you expected.

So, these are two different interpretations of possible translations for this area of the genome.  Why does the first have the weird peptide sequence?  If you hover over the CDS line, the browser will pop up more information about it.  For the top CDS, that includes this comment: "pp1ab; translated by -1 ribosomal frameshift".  This suggests that someone believes that sometimes the ribosome translating the RNA glitches at that point and advances only 2 nucleotides instead of 3 after the "N" codon.  This shifts the interpretation frame as if there were another C present.

If you search for "pp1ab", you'll see it's mentioned in the Feb. Nature article on the sequence.


Training Data for Secondary Protein Structure prediction using neural network

The standard benchmark dataset is the one from Lindahl, which consists of 976 × 975 target-template protein pairs.

  Lindahl, E. & Elofsson, A. Identification of related proteins on family, superfamily and fold level. Journal of molecular biology 295, 613–625 (2000).

It is for example used in the following articles:

Improving Protein Fold Recognition by Deep Learning Networks
Improving protein fold recognition by random forest

Another resource is SCOP: Structural Classification of Proteins.

  Nearly all proteins have structural similarities with other proteins and, in some of these cases, share a common evolutionary origin. The SCOP database, created by manual inspection and abetted by a battery of automated methods, aims to provide a detailed and comprehensive description of the structural and evolutionary relationships between all proteins whose structure is known. As such, it provides a broad survey of all known protein folds, detailed information about the close relatives of any particular protein, and a framework for future research and classification.


Are there organisms which have compartments of different body temperature?

For most of the multicellular organism; different part of body would exist in  different temperature; however there are more extreme/ drastic examples too.

Bombardier beetles; a group of beetles; that have a specialized reaction chamber in the body; where they can produce a hot and noxious reaction-mixture. They project it towards the enemy; and can throw by bending their pygidial region to wide range of directions. They do it as a defense mechanism.

Wikipedia image of bombardier beetle. They are some members from the tribes  Brachinini, Paussini, Ozaenini, Metriini of family Carabidae.

The reaction mixture can attain a temperature up to 100°C , more than enough to cause thermal death of normal protoplasm. But the reaction take place in a specialized compartment inside their body... and nothing else happen to the life of the beetle.

Here are some image of the anatomy of bombardier beetles (from here)

pygidial glands within a Bombardier Beetle; highly diagrammatic.

 more detailed diagram of the gland, however, diagrammatic.

 this is a more realistic diagram of the gland in bombardier-type carabid beetles; whole diagram showing forms of this glands in other-type carabid beetles  is available in the main website.

This paper includes a simplified diagram of chemical reaction in the chamber. reaction summary.

Here is an image from BBC showing bombardier beetle in action.

  Reference: Wikipedia


What is the biological mechanism underlying caffeine intolerance? (CYP1A2 or other?)

I have found that caffeine is mostly metabolized over CYP1A2 (as we know), but also over CYP1A1, CYP2E1 and CYP3A4. The question is how much the individual can cope with this alternate pathways if he is a CYP1A2 poor metabolizer. [1]

Secondly I found in my pharmaceutics textbook that CYP2A1 activity determination is indicated due to undesirable side effects to caffeine and theophyllin.[2]

UPDATE: 19.03.2013 12:30 GMT+1

@dd3: To clarify the second statement: I used the approach that theophyllin and caffeine are similar xanthin derivates. Since theophyllin is used as therapeutic drug in respiratory diseases (COPD etc.), I thought that scientific interest would be greater. And yes CYP1A2 plays an important role in both theophyllin tolerance and intollerance.

I found some new sources:

At first a study with CYP1A2 knock-out mice, which shows that the elimination of theophyllin takes 4-times longer in CYP1A2(-/-)mice. And they also assume that the same behaviour is also applicable to caffeine. [3]

Also there are two clinical studies by Japanese and Turkish scientists. The Japanese conclude, that theophyllin should be used with care in CYP1A2 poor metabolizer (even in haplotype poor metabolizer), since theophyllin has a narrow therapeutic range.[4] But the Turkish scientist assume that according to their findings, theophyllin is also metabolized over alternative pathways such as CYP2A13, CYP1A1, CYP2E1, CYP2D6 and CYP3A4. And according to this the genetic status of CYP1A2 is not as important as expected. [5]

Conclusion:
Assuming that theophyllin and caffeine are metabolized similarly, you can conclude that a mutation in CYP1A2 would lead to caffeine intolerance. In my experience people with caffeine intolerance describe severe nervousness after drinking a cup of coffee. Fatal cases I know were due to high consumption of energy drinks in children without or at least not known caffeine intolerance.

Sources

[1] http://informahealthcare.com/doi/abs/10.1081/DMR-120001392
[2] german source: http://www.medizinische-genetik.de/index.php?id=2642
[3] Derkenne S, Theophylline pharmacokinetics in mice: http://www.ncbi.nlm.nih.gov/pubmed/15970798
[4] Obase Y, Polymorphisms in the CYP1A2 gene and theophylline metabolism in patients with asthma. http://www.ncbi.nlm.nih.gov/pubmed/12732846
[5] Ahmet U, The effect of CYP1A2 gene polymorphisms on Theophylline metabolism and chronic obstructive pulmonary disease in Turkish patients http://www.jbmb.or.kr

Further Reading:

Xanthines as therapeutic drugs: http://web.carteret.edu/keoughp/LFreshwater/PHARM/NOTES/Xanthines.htm


I'm not completely sure as it's very difficult to determine frog species with just one picture taken from the side.
Morphology-wise it looks like this is a Afrixalis dorsalis, although it's colour doesn't comply with the most comomon pattern. You can find pictures of this species with specimen looking exactly the same or very similar.
Colour deviations occur in several frog species...

interesting article about frog species in Gabon
AmphibiaWeb Afrixalis dorsalis (this also mentions differences in patterns and light coloured populations)

Source: Wikimedia Commons

Source: http://calphotos.berkeley.edu

Common colours and pattern
Source: http://calphotos.berkeley.edu


The term "irreversible" means that the reverse reaction occurs so rarely that it is considered negligible. This means that you do not have to consider equilibrium, as you have to for reversible reactions. Instead, you can assume that all of the reactants will eventually become product.

As you stated, this is true for reactions that have a very negative Gibbs free energy.  Remember the formulation of the Gibbs free energy in terms of the equilibrium constant:
$$
\Delta G^o =  -RTln(K)
$$

This can be rewritten as follows:
$$
K = e^{-\Delta G^o/RT}
$$

As $\Delta G^o$ gets very negative, you can see that $K$ gets very positive.

The equlibrium constant has two definitions that are both useful. First, it is the ratio of the products to the reactants. Therefore as $K$ gets very positive, the equilibrium ratio of products to reactants approaches infinity, implying that all of the reactants will be consumed.

More useful is the definition of the equilibrium constant as the ratio of the rates of the forward and reverse reaction. From this definition we can see that as $K$ gets very large, the ratio of the rates of the forward and reverse reaction approaches infinity. This means that the rate of the reverse reaction becomes negligible compared to the rate of the forward reaction. This is exactly what it means to be irreversible.

Note that it is possible to make (what I think is) a more convincing argument using the concept of activation energy, using Hammond's Postulate to describe the character of the transition state. If you'd like, I can write this out. However, I think the argument given above is more easily understood with a basic chemistry background.


Boys born in excess - how can the nature draw from non-natural distributions?

Welcome to Biology.SE.

"Natural" vs "non-natural" Distribution

There is no such thing as a "natural probability distribution". Actually, biological system often produce distributions that does not match with commonly used distributions just because the assumptions yielding to these distribution are sometimes poorly met in nature. In other words, many biological variables meet more complicated distribution than the standard uniform, binomial, geometric, beta, exponential, and other distribution you know of.

Of course the gaussian distribution is kind of a special one that is often approximatively reproduced by biological system as a consequence of the central limit theorem.

Some distributions are more used than others but there exist an infinite number of definitions and anyone can construct one. Here is my distribution of the day. $P(x | y,z) =  C \frac{y^x - exp(-yz)}{x+z+y}$, where $C$ is a constant of integration to ensure $\int_{-\infty}^{\infty} C \frac{y^x - exp(-yz)}{x+z+y} = 1$. I will call this distribution the "remi.b distribution". I have no idea what kind or process it can model and nobody will probably ever use it but it is a legit distribution.

Developmental mechanism

You can read this post and that post about the developmental mechanism that yield to such bias sex-ratio at birth.

Evolutionary processes

  how can the nature know beforehand that boys should be made in excess?

Organisms producing a bias sex-ratio are selected for as they increase the average fitness among their offspring. As such the population is selected toward creating such bias sex-ratio. Organism don't know, they just do.

In order to understand the evolution of sex-ratio a bit better, you should have a look at this post.


Is returning cholesterol to the liver really performed by HDL?

According to Reverse Cholesterol Transport: Molecular Mechanisms and the Non-medical Approach to Enhance HDL Cholesterol (Frontiers in Physiology, 2018), both HDL and LDL are involved in reverse cholesterol transport.

In short: HDL takes cholesterol from the blood (from lipid-laden macrophages) and delivers it to the liver 1) via scavenger receptors (SR-B1) or 2) via LDL and LDL receptors (LDL-R). (For a detailed explanation of the diagram, see the Figure 1. in the linked article. There's a similar diagram (Fig.1) in Journal of Cardiology.)

Petter Atti says in his blog (emphasis mine):

  Historically this process of returning cholesterol to the liver was
  thought to be performed only by HDL’s and has been termed reverse
  cholesterol transport, or RCT [...]

  This RCT concept is outdated as we now know LDL’s actually perform
  the majority of RCT. While the HDL particle is a crucial part of
  the immensely complex RCT pathway, a not-so-well-known fact is that
  apoB lipoproteins (i.e., LDL’s and their brethren) carry most of the
  cholesterol back to the liver. In other words, the “bad” lipoprotein,
  LDL, does more of the cleaning up (i.e., taking cholesterol back to
  the liver) than the “good” lipoprotein, HDL!

He says that LDL does "more of the cleaning" than HDL, which may be technically correct in the sense that more LDL than HDL particles may be involved, but this alone does not change the concept of good or bad cholesterol. In the image, you can see that the initial cleaning (step 2 and 3) is done only by HDL, so without HDL no cleaning might occur at all.

Low HDL and high LDL levels in the blood are known risk factors for atherosclerosis (NCBI Books, 2019). Not all LDL particles are bad, though, the most harmful are oxidized small dense LDL particles (Hindawi, 2017).


How to measure growth of algae with colorimeter

Let's be clear, you are using a colorimeter, not a spectrophotometer?

Can you provide the brand name and model number of this colorimeter?

Have you learned about the Beer-Lambert Law? It states that A = Ecl where

A is the Absorbance

E is the molar extinction coefficient

c is the concentration of the unknown

l is the length of the light path through the sample (the standard path length is 1 cm in spectrophotometers).

The first thing you need to do is measure lambda Max, the wavelength of light that is absorbed the most (or transmitted the least) by your sample. The Beer-Lambert law is linear when A is between approx. 0.1 and 1.0.

So take a dilute solution of the algae and starting at the smallest wave length of light that the device can emit (you can vary the wavelength?). Take readings of the Absorbance and then increase the wavelength by 10 nm. Starting at deep purple, and ending at far red, write down the A values. Plot this data with A on the Y-Axis and wavelength in nm on the X-axis. There should be a distinct maxima in the curve, that is the most sensitive wavelength, and is the one you should use for all your experiments. If the algae is green, then the maxima should be over in the red end of the spectrum (like chlorophyll).

Next you need to make a standard curve that correlates the Absorbance at lambda max with the number of algal cells in the cuvette (the test tube you put in the colorimeter). That means you need an independent method of counting the number of algal cells. If they were bacteria or yeast then you could plate them on agar-filled Petri dishes and count the number of cells per mL (for example). For some cells if you have a high powered microscope and a hemocytometer then you could visually count the number of cells per mL. If neither of these methods are available then you could measure the mass of algal cells by weighing them on a balance.

So by some method you will be able to plot the number of cells in the broth vs. the Absorbance (plot A on the Y-axis).

From this you can empirically determine the molar extinction coefficient of these algal cells.  Then you just need to measure the Absorbance at lambda max on  dilute aliquot of the cell culture and you will have an accurate measurement of the number of cells per mL.

With this assay working then you can inoculate a bunch of identical cultures, that vary by the pH of the growth medium. By removing small aliquots of the cultures at the same time points you will be able to plot the number of cells (on the Y-axis) versus the time they have been growing, and you will see if varying the pH alters the shape or magnitude of these growth curves.


“Swine flu” is an obsolete name.  The official name for the virus that was briefly called “swine flu” is “H1N1pdm09”.

H1N1pdm09 has a mortality rate of around 0.01-0.1%. That’s roughly 10- to 20-fold lower than COVID-19. Its R0 was estimated at between 1 and 2, which is roughly half the estimates for SARS-CoV-2 (the virus responsible for COVID-19].

A vaccine for H1N1pdm09 was available in the fall of 2010.  It was possible to make it that quickly because it’s just another influenza strain, and the normal techniques for for vaccines against influenza strains worked fine.

Most importantly, H1N1pdm09 never went away.  It is still one of the main influenza strains circulating today, and if you were vaccinated for influenza since 2010 you received a vaccine against it.

CDC info here: 2009 H1N1 Pandemic (H1N1pdm09 virus)
WHO info here: Evolution of a pandemic:
A(H1N1) 2009, April 2009 – August 2010, 2nd edition


Why does HPV Infect Squamous Epithelial Cells and Not Others?

The answer usually lies in whether the cell of interest expresses the correct receptor.

Check this:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820467/

This excerpt from that review explains why:

"Although both the α6β4 and α6β1 heterodimer were capable of binding VLPs in vitro, only the former was supposed to function as a HPV receptor, which was concluded from the results that the α6 subunit associated preferentially with the β4 in epithelial cells [12], and the α6β4 complex was expressed exclusively in the basal cellular layer of the stratified squamous epithelium [13], which was presumably the only site of productive PV infection"


Detailed mechanism of the cause of diabetes mellitus type 1?

Diabetes mellitus is divided into four  type 1, type 2, gestational diabetes, and specific type of diabetes. Type 1 diabetes is commonly called as Juvenile diabetes or Brittle diabetes.
It is also called as "Insulin-dependent diabetes mellitus (IDDM)". For our bad-luck the causes of Type 1 diabetes remains obscure, and scientists believes its mostly related to genetics and other environmental factors like mutations or virus attacks. I found some articles that may help.

  But it
  is believed that genetic and environmental factors (possibly viruses)
  may be involved. The aetiology ('cause') of type 1 diabetes is
  unknown, but a good deal is known about its pathogenesis (the way in
  which it develops). As with other complex diseases, the outcome is
  determined by the interplay of multiple genes and (most likely)
  multiple environmental determinants, together with an element of
  happenstance. The risk of developing diabetes is strongly influenced
  by genes affecting immune function, particularly the HLA system,
  but other factors are involved. The best evidence for this comes from
  the study of identical twins: if one twin develops diabetes in
  childhood, the other (who has identical genes) has no more than a one
  in three chance of developing the disease. Prospective studies in
  human populations reveal that circulating auto antibodies directed
  against the islets typically appear in the first 5 years of life, and
  may be present for many years (sometimes 20 years or more) before the
  disease develops. A similar latent period is seen with coeliac
  disease, and implies that some sort of regulatory balance has been
  achieved within the immune system, and subsequently lost. This opens
  the door to the possibility of 're-education' of the immune system by
  various forms of immune intervention.
  Reference

  The pathogenesis of Diabetes mellitus type 1 shows a strong tendency towards genetic related factors,

  Reference


How many agarose gel bands are typical for circularised DNA

I don't have hands on it, but I will not be surprised if supercoiled DNA migrates at different distances according to some inner topological conformation (i.e., more or less coiled AND/OR more or less nicked). Similarly, this picture highlights >8 conformations. What is run in the gel is circularized phage DNA with some degree of knotting due to the circularization (phage DNA is otherwise linear).

Figure from: Arsuaga et al. 2005, PNAS 102 (26) 9165-9169 (free on PubMed Central)

Another theoretical possibility is that two or more plasmids of different sizes were grown in the same maxiprep because of some contamination. But in this case, you will spot the problem also in the digestion, so it does not seem to be your case.


Decreasing signals in assay measurements

Freeze-thaw cycles are often suspected of causing degradation in organic molecules 1,2. My first guess would be that your fluorophore is breaking down due to those repeated cycles. Alternatively, you might be getting precipitation of a calcium compound from the buffer you are freezing that your colleague is not.
Standard laboratory practice is to make aliquots of frozen solutions. Before thawing the solution for the first time, set up pre-labeled smaller containers (e.g. Eppendorf tubes) and then aliquot the amount you expect to use for each experiment. That way potentially sensitive compounds are only thawed twice.
References:
1: Kozikowski, B. A., Burt, T. M., Tirey, D. A., Williams, L. E., Kuzmak, B. R., Stanton, D. T., ... & Nelson, S. L. (2003). The effect of freeze/thaw cycles on the stability of compounds in DMSO. Journal of biomolecular screening, 8(2), 210-215.
2: US Food and Drug Administration. (2008). Guidance for Industry. Drug Stability Guidelines.


About the plight of Elephants and efforts to conserve them?

Dehorning of rhinos has been tried with limited success. Poachers have killed dehorned rhinos anyway, either out of spite or to avoid tracking worthless prey in the future. There is the problem of anesthesia (always a risk) and the fact that rhino horns are usually not destroyed but saved in the event of decriminalization. But at least horn grows back.

Considering the strength of horn and ivory, and the force applied in their use, plastic would not be of much use to them (especially elephants with long tusks).

  They are used for digging for water, salt, and roots; debarking or marking trees; and for moving trees and branches when clearing a path. When fighting, they are used to attack and defend, and to protect the trunk. - Wikipedia

To detusk elephants would be akin to declawing a lion, though much more dangerous and painful. Though this might help prevent poaching, the future of these animals lies in prevention.


Here is a report addressing this, I haven't read it in detail, but I've skimmed it and it looks like they've done a pretty good job, and address a number of key points, talk about the emission spectra of certain organisms, etc.
Bioluminescence – a source of marine energy?

From the conclusion: "The low light output of bioluminescent species relative to solar light may render the conversion of bioluminescent light into electrical energy uneconomic as a stand-alone option."

I agree with them that it would be possible to extract energy that way.  I also agree that its not even close to economical.  You lose energy at so many steps, you have chemical energy in whatever the cells eat to grow, then some small fraction of that chemical energy will be turned into light energy, most of that light will shoot out in the wrong direction and just get absorbed by other stuff in the culture.  If you want to use bugs, a better option would probably be a microbial fuel cell, where microbes sit on an electrode, oxidize some chemical, and take that electron and dump it straight onto the electrode.  This is still a pretty inefficient process as far as energy production technologies are concerned, but at least it skips the waste associated with conversion of the chemical energy into light energy and then back into electricity.


Why rectus abdominis is not proximal muscle?

It's not clear what "proximal" means in this context. It's not a standard use of that anatomical term in English. I'd also say that the figure on the left actually does show the pectoralis major.

The author of this figure might be trying to show the muscles that cross the proximal joints in the upper and lower limbs. For example:

Upper limb

Pectoralis major
Biceps brachii
Triceps brachii
Latissimus dorsi

Lower limb

Adductors (brevis, longus, magnus)
Rectus femoris
Semimembranosus, semitendinosus, biceps femoris (long head)
Gluteals (maximus, medius, minimus)

Muscles that do not cross the shoulder or hip are not included. This explains the lack of rectus abdominis or subclavius. Though it is not clear to me which the paired muscles in the posterior view are running craniocaudally from the thorax to the gluteal region.


I think it is part of a Australian trigger fish skull. check the pictures below, unfortunately someone sawed off most of the spine on the skull photo, but you can see the base of it, it is probably not the exact same species, but it is certainly part of a triggerfish skull. There are a half dozen species in Australia.

Cool find.


The answers are:

Yes, they know when to stop eating. See this paper.
Yes, they store extra energy as fat in the intestine.
This one is a little more complicated. They can use extra energy, but not to move faster. Movement doesn't take much energy, and until they're close to death from starvation, they continue to move quite well. As for eggs, they do indeed slow down the rate of embryo production when nutrition is inadequate. But the total number of eggs is limited by the supply of sperm, so there is an upper limit on how many they can produce, even in unlimited food. Probably the main benefit of stored nutrients is to allow them to survive longer if the food runs out. They are very, very good at dealing with a variable food supply -- much better than you, for instance -- and they do it partly by storing up extra energy. This paper and references therein describe some starvation responses. You can also look up L1 diapause, the dauer larva, and adult reproductive diapause.


Does any animal species have two sexes and more genders?

Many organisms have multiple sexes. For instance, here is one which apparently has 7 (and each sex, or "mating type" can only mate with the others). The "gotcha" is that, mostly, they're unicellular organisms where mating in itself is weird to begin with. I haven't ever heard of a metazoan which truly has more than one sex (there may be variation within the males or females, but I think the sperms or eggs are always interchangeable).

Gender, I think, is more of a social term relevant to human behavior. Especially nowadays, so much of the literature and understanding of what is referred to as "gender" is closely linked to things such as gender identity, sexuality, gender roles and personality that is difficult to see how you could meaningfully speak about the "gender" of (non-human) animals.

It's analogous to the idea of "animal language" - certainly some animals may be said to behave in stereotypical ways which influence their mating behavior. Does that mean that what is written about human gender applies? I suspect precious little of it would. I would be quite skeptical of someone discussing gender (in the modern sense) for even uncivilized humans, let alone non-human animals.


Plant identification: San Francisco, USA

I'm going to refrain from giving you the answers because the point of the assignment is to  learn how to do it yourself.

You should likely start  by using a dichotomous key (likely provided by  your instructor).

You could also try  searching the Jepson California eflora or CNPS Identifying Native Plants for online keys.

Check out  the California Native Plant Exchange website if you don't know the name of the plant but know the general area where you saw it.

If you don't know what general type of plant  you have,   you should try keying  the plants to family  first  to get better search terms.  Try here.

If you don't know plant terminology  used  in  these keys,  try  "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001)


What is the name of this plant with leaves having two different shades of green?

So after searching a bit, I think this plant is of the genus Ficus:

I am still unaware of the species but the nearest I could find was Ficus retusa. I hope I have been of help.