Why do we perceive colour? (i.e., distinct values?)

"But what reason is there to not perceive light as we perceive sound, in a spectrum?"

We do perceive light in a spectrum. Not just in a spectrum, but in a combination of spectral components (because we rarely in nature observe true single-wavelength light). If you are thinking about names of colors, those are just words we made up to describe colors to other people, and the range and spacing of those colors differs across language groups. We do the same for sound in the context of music: B-flat versus an E, for example.

  Or, to go one step further, why did we need an extra type of cone in the middle, the yellow-green wavelength?

Colors are perceived in vision by the ratio of activity of different cones, and intensity and spectrum can be confused. If you have no "green" cones, there are big stretches of wavelengths that only activate one of the other two cones. In that situation, there is no way to discriminate between intensity and color.

If, on the other hand, you are wondering about transduction, it's because sound and light have different physical properties. The cochlea effectively "maps" sounds onto a physical arrangements of hair cells. You could do something similar with a prism, but you would lose spatial acuity (effectively, you would need a whole spectrum analyzer for the receptive field of each photoreceptor: your retina would have to be absolutely massive). Instead, color vision works by differential chemical sensitivity to different light wavelengths.

Your question doesn't seem to be much about evolution, besides the title, so I left off that part.


There is no general therapy for cancer - as there is no general cancer. Cancer is the umbrella term for a disease where you have body cells growing without control, leading eventually to death. But since there is a wide variety of cells in the body, there is also a very wide variety of different cancers.

To treat these, surgery is often the first line of therapy. For some cancers this is already sufficient to cure the patient, examples are skin cancers (not only melanoma but the other forms as well) where you can cure a very high potion of the patients. This only works for early forms of the cancers when there are no metatases present.

Besides this, additional therapies are used - as you said yourself chemotherapy in the different forms as well as radiation therapy. Chemotherapy is given systemically and targets fast growing cells (cancer cells have these properties) and causes mutations or other problems which let the cancer cells eventually die. Radiation works with the same principle, but is more focussed.

Relatively new therapies are the targeted therapies where the treatment uses the occurance of certain common mutations. An example would be the mutated BRAF kinase in melanoma (and also in a number of other cancers) which can be specifically inhibited with an inhibitor. This avoids a lot of problems general adverse effects of the drugs. Additionally immune therapies are also new which use antibodies against surface receptors of T cells to prevent their inactivation. These T cells then attack the tumor.

These are all non-biological treatments. More biological ones are modified oncolytic viruses. In this therapy you inject genetically modified viruses which preferrably infect the tumor and then destroy it. These are relatively new, but an interesting option. See references 1 and 2.

An old method is the usage of bacteria to treat tumors - the first obervations on this where done in the late 19th century, see reference 3 for more information and a lot of further references.

A number of the chemotherapeutic drugs used today are originated from nature, but are today synthesized and used in a pure form and not isolated from their origin anymore. Examples would be vincristine, irinotecan, etoposide, and paclitaxel. See references 4 and 5 for details.

Besides this, there are no effective "natural" cancer cures, despite the claims of several "alternative medicine people". These are either based on wrong assumptions of biology or wrong ideas like Homeopathy.

References:

Advertisement Oncolytic Viruses and Their Application to Cancer
Immunotherapy
Oncolytic viruses: a new class of immunotherapy drugs
Strategies using bacteria to target tumors
Anti-inflammatory and anticancer drugs from nature.
Drugs From Nature, Then and Now


Why are there no large animals with chloroplasts?

I believe the gist of it is that chloroplasts simply cannot create enough sugar from photosynthesis to significantly power the energy-intense needs of any but the simplest of animals. Consider that plants maximize their surface area to the extent possible for a living organism, and still only have enough energy to grow and reproduce - movement is essentially impossible.

Here's a pretty good article I stumbled across a while back:
http://blogs.discovermagazine.com/notrocketscience/2012/09/18/will-we-ever-photosynthesise-like-plants/


Why was the Davson-Danielli model rejected?

The original figure that Danielli and Davson proposed looks like this (from the original publication):

It shows the phospholipid bilayer of the membrane (which is correct) embedded between two layers of globular proteins. The hydrophobic tails of the lipids are orientated towards each other, while the hydrophilic heads are oriented to the outside.

Although the membrane composition is correct (this was already published 1925 by Gorter and Grendel), there are some problems with the proposed model:

Membranes are not identical. The differ in thickness and the ratio of
proteins:lipids.
Membranes have distinct inside and outside layers (defined by the
membrane proteins which are present on the surface of the membrane)
Other than predicted by the model, the membrane proteins do not have
a very good solubility in water - in fact they are amphiphatic,
meaning they have hydrophilic and hydrophobic regions. The
hydrophobic side is anchored inside the membrane.
When the membrane proteins would cover the lipid bilayer, their
hydrophobic regions would be in contact with water, which
destabilizes this construct. Even if they would be oriented towards
the membrane, they would face towards the hydrophilic heads of the
phospholipids causing the same effect. Additionally the proteins
would also seperate the hydrophilic phospholipid heads from the
water. So there is no real stable solution in embedding the membrane
with proteins.


It seems like Euglena but I need more parameters than what you have provided.

(source: eastmarinedrive.com)

https://www.youtube.com/watch?v=ZHZZKwrYm4g

you can narrow it down by this:

http://goo.gl/XTEZ7S

Or

You can find them in commonly found microorganism in kitchen:

http://www.colorado.edu/eeb/EEBprojects/FiererLab/Flores_etal_2012_kitchens.pdf

Or

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0078866.t001/largerimage

Source: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078866


Is there any way to tell if a gene is functional for an individual with only a reference sequence and the individual's sequence of the gene?

In general, no.  There might be specific cases where you can, like if there is a stop codon, or a frameshift mutation early on, or someone else has seen your exact variant and experimentally proved that it has no function.

But in general, you cannot predict function from in silico data alone.


Why don't anti-viral drugs like "Acyclovir" work against coronaviruses?

Aciclovir specifically targets HSV-family viruses.

It is metabolized by a viral-specific enzyme into an inhibitor of the specific DNA polymerase expressed by the virus:

  in infected cells, HSV or VZV coded thymidine kinase facilitates
  the conversion of aciclovir to aciclovir monophosphate, which is then converted to aciclovir triphosphate by cellular enzymes. Aciclovir triphosphate acts as an inhibitor of and substrate for the herpes specified DNA polymerase, preventing further viral DNA synthesis.

https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2009-PI-00595-3

Other viruses don't express these specific enzymes, and even if they have similar enzymes they may not interact the same way with the drug. Even within the herpesvirus family, the drug is not equally effective against every virus.

Coronaviruses are RNA viruses, so even though the drug is not effective for DNA viruses outside the herpesvirus family, coronaviruses are definitely not going to be affected because they don't even have a DNA polymerase to inhibit.


Why these 2 dots frequently occur in dog's eyebrows? Do it serve/served any advantage?

I suspect but can't prove that these markings are not adaptive, but are accidents or epiphenomena of the general genetic system that determines coat colour.
On the one hand, an Australian Broadcasting Corporation documentary claims that canid eyebrows are adapted for social interaction: they have specialized muscles (which are not present in other carnivorous mammals such as cats), and ...

One study showed foxes who hunt alone had about half the facial expressions of wolves who work in packs. In fact, in wolves and dingoes, the eyebrows are often even a different colour, exaggerating the movement.

(they don't give any primary references).
On the other hand (supporting my guess) a lot of the evolution of these colour patterns seems to have occurred after domestication. These markings (not the eyebrow spots in particular) seem to be called tan points:

Red (tan) appears as pips above the eyes, on the sides of the muzzle extending to the cheeks, as pips on the cheeks, on the front of the neck just below the head, as two triangular patches on the front of the chest, on the lower legs and feet (and inside of the legs), and as a patch underneath the tail (and sometimes along the bottom edge of the tail too).

(I don't know whether eyebrow contrast in animals that aren't strictly brown/black is caused by the same genes ...)
A PhD thesis by Dayna Dreger (some material published in Journal of Heredity 2013:104(3):399–406 doi:10.1093/jhered/est012)

The black-and-tan phenotype, associated with the at allele, is a predominantly eumelanistic phenotype, with phaeomelanin restricted to distinct regions on the lower limbs, cheeks, eyebrows, chest, and around the anus. (p. 7)
Genome wide association study analysis, fine mapping, and sequence analysis identified a 16 bp tandem duplication in intron 5 of the hnRNP-Associated with Lethal Yellow (RALY) gene that segregates with the black-and-tan phenotype, versus saddle tan, in Basset Hounds and Pembroke Welsh Corgis. In breeds that never have the saddle tan phenotype, but frequently have the black-and-tan phenotype, the RALY duplication does not segregate with black-and-tan. This, together with further genotype analysis, suggests a gene interaction of ASIP, MC1R, DEFB103, RALY, and an additional modifier gene is required for expression of saddle tan or black-and-tan. (p. ii)
Neither the coyote nor 9 of the 10 wolves had the RALY duplication and the tenth atypical wolf was heterozygous (+/dup) (Table 5.1), suggesting that the lack of the duplication is the ancestral or wild-type allele (+). It follows then that the saddle tan phenotype is ancestral to the black-and-tan phenotype, despite the relatively limited number of breeds that currently express the saddle tan phenotype, making black-and-tan a modification of the saddle tan phenotype. The popularity of the black-and-tan phenotype across breeds and breed types is likely explained by artificial selection for the striking black-and-tan phenotype over that of saddle tan. Since the saddle tan pattern is found primarily in terriers, scent hounds, and a small number of herding breeds, this finding may also shed light on the development and relation of modern dog breeds, hinting at common ancestors between breed types.


What kind of worm is this in my food? (Tuna sandwich from canned tuna)

Looks like a maggot (fly larvae) of some sort — see for example the following image:

That particular image is of a common green bottle fly maggot, which has a distribution consistent with your posted location.


How many times can a human get chicken pox?

Usually you get chicken pox only once in your life, the recurring form are usually shingles.  But: It can happen (also in people which are not immunocompromized). I know two persons which got chicken pox twice and which are otherwise normal in regards of their immune system.

Persons with an HIV infection are more at risk here. They can develop both forms and depending on how much their immune system is already affected by the HIV infection can develop severe forms of the infection. It might be necessary to treat them with antiviral drugs. So it is clearly recommended to ask a MD about this. See here for more details.


Why is the gene regulation in eukaryotic cells needs multiple level of control than in prokaryotic cells?

I think you need to consider the overall amount of information that is needed to implement a proper control system in living organisms.

In prokaryotic cells, in most of the cases, you will find that one gene code for one enzyme, so if a simple organisms need 500 enzymes to stay alive you can expect 500 genes that code for that enzymes.
A more complex organism may need 100 times more enzymes to stay alive and so theoretically 100 times more genes. Now, evolution wise, to have a linear increase of DNA vs complexity is not a good option for very complex organisms. To keep everything compartmentalised in one single membrane is also not a good idea if you need to run millions of chemical reactions using thousands of enzymes that can cross react and need different optimal conditions to work properly, so multi-compartimentalization is a must.
Linked with it arises the problem of sending the right enzyme in the right place and this has been solved by adding tags, transporter enzymes, etc... in the pot... So, lots of more information is needed to make everything run smoothly.

It turned out that an efficient way to code for all that enzymes, tags, promoters and other regulators without increment the size of the DNA too much is by multi level control of the expression of a gene i.e. the same gene can be used to produce different enzymes (splicing etc...). The tradeoff to pay to have a more compact genome is to increase the complexity of its control system.

Lastly, consider that differently from normal electronic controllers, the biological one do affect each other. A biological controller system may produce an output molecule that interact with the system under control but also with other reactions going on all over... that is another burden that require an increase of complexity in the control system to make it work.


You would need to live a long, long, long, long time for this to become remotely problematic.

Your question seems to suppose that a memory is "stored" by a neuron, and since neurons have mass, then the more memories we have the more our brains will weigh. Actually, neurogenesis is pretty rare in the adult brain--most of the cortex is fixed, and new neurons do not grow. (The hippocampus is the best known counterexample, but it's important to note that contrary to lore, the hippocampus doesn't store memories per sé, though it is involved in the formation and retrieval of memories).

Memories are represented in the brain as patterns of firing neurons. Let's say, for simplicity, that each neuron can either be on or off. Since there are 86 billion neurons in the brain, we can experience 2^86bn possible brain states. That's a lot.

Of course there are a lot of simplifications here--most notably, there is a lot of structure to the brain, and so i'm not suggesting you can store 2^86bn memories--but the logic is the same. Even with only 1,000 neurons, we can store a ridiculous amount of information (2^1000).

I would like to comment on MCM's answer as well, because I don't think it's true that we "remove" old memories. Or rather, the topic is still being debated in cognitive science today. For an old take on it, see renowned memory researcher Endel Tulving's (1974) article, in which he says:

  When we forget something we once knew, it does not necessarily mean that the memory trace has been lost; it may only be inaccessible

The idea is that some memories are suppressed (no, not repressed), being rendered inaccessible. Robert Bjork and John Anderson have (separately) done some nice work in this area.

So before you worry about this becoming a problem, I suspect you need to work out the secret of immortality first.

  Tulving, E. (1974). Cue-Dependent Forgetting: When we forget something
  we once knew, it does not necessarily mean that the memory trace has
  been lost; it may only be inaccessible. American Scientist, 74-82.


By definition, will some children always be stunted?

You are correct, that under that definition; unless there were no variation (which would be impossible), there would always be individuals that fall below 2 standard deviations. However, "stunted" under this definition would not be a problem if variation was extremely low. So yes, it would be unfixable by definition, but if variation fell, then the "problem" would be fixed, because it would no longer be a problem.


White blood cells after dealing with an infection

White blood cells, especially neutrophils, rapidly leave the blood and migrate in tissues toward infections (or other forms of stimulations). Many of them do die at the location of an infection, but they can also migrate back. The simplest route for this is to follow lymph flow. Lymphatic fluid is picked up by lymphatic vessels, which work in parallel to blood vessels, and from there can move back into blood. Just as an example of migration through lymphatics

  Thus, we provide in vivo evidence that neutrophils, like DCs or inflammatory monocytes, migrate via afferent lymphatics to lymphoid tissue and can shuttle live microorganisms.

--Neutrophils rapidly migrate via lymphatics after Mycobacterium bovis BCG intradermal vaccination and shuttle live bacilli to the draining lymph nodes


Why doesn't the avocado turn brown when it is kept with its seed?

This is actually only partly true: When you cut the avocado in half, only the part where the seed really sits stays green, while the surrounding cut area gets brown over time.

Avocados turn brown because of an enzyme called polyphenol oxidase, which oxidizes the green contents of the avocado upon contact with oxygen. The seed blocks the access to oxygen, thats why it helps here (but only where it makes close contact). See this and this links.

There are two ways of preventing the browning of cut avocados (besides avoiding oxygen contact): Use either lemon juice, which inhibits the enzyme (by chelating the metal ion from its active center) or keep it cooled to slow down the procession rate of the enzyme (which will only work for some time).


Why do heterozygous individuals have increased resistance to malaria?

Very interesting explanation has been proposed by Ferreira A. et al. 2011. Briefly, red blood cells of individuals carrying homozygous point mutation in haemoglobin beta-chain tend to be more prone to disruption.

Red blood cells are full of haemoglobin, so once their membrane is damaged, they release free haemoglobin and heme to the plasma. This is called intravascular haemolysis. Too high level of free heme is toxic and you can read about its consequences, for example here.

In the plasma of individuals with heterozygous mutation also there is an increased concentration of free heme, but definitely below harmful level.

However, it is enough to trigger mechanism that protects us from toxic effects of free heme. Heme oxygenase-1 (HO-1)catalyses heme to biliverdin, iron and carbon monoxide (CO). CO makes the vascular environment very unfavourable for Plasmodium.sp and probably protects from infection.

The study was performed in the mouse model.


Why are insects unafraid when you tap at them from the other side of glass?

Since insect brains do not contain enough neurons for higher level emotions such as fear, much of their behavior is programmed and reflexive. When you approach them, they have evolved to fly away. Glass, on the other hand is not something they evolved to "understand". They likely are not programmed to see something approaching them from below their legs as they are sitting securely on a hard substrate as a threat. They can look down. They just don't "get" glass.


Is it possible for neurons themselves to manifest cancerous behavior?

Yes, but rarely.

Other types of brain cells are much more likely to form tumors. Oligodendrocytes, astrocytes, and more generally glial cells all form tumors with some regularity.

Nerve sheaths can also form benign growths.

Nerves themselves can even manifest cancerous behavior, even though they are nearly always benign and very slow growing. Unfortunately, they tend to cause seizures, increased intercranial pressure, and decreased neurological function in affected areas.


What is the anatomical term for a two jointed leg?

Welcome to Biology.SE!

I think you are talking about plantigrade, digitigrade and unguligrade.

Please note that the number of joints in mammals does NOT vary, but only the relative length (and shape) of the different parts of the leg.

A Plantigrade walks on the sole of the foot. 'Sole' translates to 'planta' in Latin hence the name.

Examples: Human, squirrel, raccoons, ...
Below is a chimpanzee skeleton

A Digitigrade walks on the digits (the toes).

Examples: dog, cat, hyena, ...
Below is a cat skeleton

An Unguligrade walks on the nails. 'nail' translates to 'ungula' in Latin hence the name.

Examples: cow, reindeer, goat, ...
Below is a cow skeleton


Preserved alpha complementation over evolutionary time?

Yes, there are cases where one gene has become two. Or, at least, where multiple  functions carried out by a single protein, the product of one gene, are carried out by distinct proteins, the products of different genes, in another species.

One case I have personally worked with is the bacterial SelB protein. It is essential for selenoprotein biosynthesis and has a dual function as an elongation factor and RNA binding protein. In eukaryotes, these functions are split between two proteins coded for by different genes. The Sec specific elongation factor EfSec and the RNA binding protein SBP2. See here [1] for more information.

Chimeric transcripts are also examples of this. One I happen to know of is the protein secp43 which in the mosquito A. gambiae is encoded by genomic sequences found on two different chromosomes [2]. Essentially, by two different genes.

The problem is that although we can easily find such cases of one protein's function being shared between multiple proteins in other species, or of one protein being coded for by multiple transcripts, it is hard to reconstruct the evolutionary history that gave rise to the current situation. So, whether the current situation has arisen because of alpha complementation or other causes is hard to know.

REFERENCES:

1) Lescure A, Fagegaltier D, Carbon P, Krol A., Protein factors mediating selenoprotein synthesis. Curr Protein Pept Sci. 2002 Feb;3(1):143-51.

2) Chapple CE, Guigó R., Relaxation of selective constraints causes independent selenoprotein extinction in insect genomes. PLoS One, 2008, 3(8):e2968.


The outermost layer of your skin consists mostly of dead cells, the Stratum corneum. Copper can't kill what's already dead.


Variation of fixation probability over time in Wright-Fisher model

The function probably look like $r(t) = A + B e^{-C t}$, where $r(t)$ is the rate of fixation at time $t$ (in generation). The reason for this exponential is that the probability that a mutation happens after $t$ generation is given by the exponential distribution.

As the rate of fixation at equilibrium must be at $2N\mu \frac{1}{2N} = \mu$, $A=\mu$, that is $r(t) = \mu + B e^{-C t}$

As at $t=0$, the rate must be 0. As $e^{0} = 1$, you should have $B=-\mu$. Hence,

$$r(t) = \mu - \mu e^{-C t}$$

$C$ here represents the steepness of the curve. I don't know how you could calculate it a priori but it must depends upon your population size $N$. As the expected time to fixation starting at frequency $p_0$ is (from Kimura and Ohta 1968)

$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0)$$

For $p_0 = \frac{1}{2N}$

$$\bar t\left(\frac{1}{2N}\right)=-4N\left(2N-1\right)\ln\left(1-\frac{1}{2N}\right)$$

or

$$\bar t\left(\frac{1}{2N}\right)=\left(4N-8N^2\right)\ln\left(\frac{2N-1}{2N}\right)$$

if you prefer. Maybe $C = \bar t\left(\frac{1}{2N}\right)$ leading to

$$r(t) = \mu \left(1 - e^{-\left( \left(4N-8N^2\right)\ln\left(\frac{2N-1}{2N}\right) \right) t}\right)$$

Let me know if it matches (I'd pretty amazed)!


This is an Atlantic wolffish (Anarhichas lupus). It's a very characteristic fish, with the teeth, the long dorsal fin and the small back fin.

https://en.m.wikipedia.org/wiki/Atlantic_wolffish


Explanatory answer

Rapidly-labelled RNA was the RNA labelled by radioactive precursor during a short period (the pulse), terminated by swamping the system with an excess of non-radioactive precursor (the chase). This is known as a pulse–chase, and is described in the methods section of the paper cited in the question and reiterated by @SeRe as an answer. Such a pulse–chase preferentially labels RNA species that have short turnover times (i.e. half-lives of the same order of the pulse), and was thus regarded as a way of studying messenger RNA.

This strategy and its interpretation was an extrapolation from what was known about mRNA in the regulation of bacterial gene expression, but the descriptive term ‘rapidly-labelled RNA’ was used rather than ‘mRNA’ because there was no direct evidence to support such an assignment in nucleated mammalian cells. Indeed, there were major problems because the rapidly-labelled RNA in the nucleus was of a different size to the RNA that subsequently appeared in the cytoplasm, and, indeed, there was no simple precursor–product relationship between the two. In retrospect this is not surprising given what we now know about the splicing of eukaryotic mRNAs and the fact that most of them have much longer half-lives than bacterial mRNAs. However, at the time there was a school of thought that interpreted these results as evidence against the idea of mRNA in eukaryotes, and one of the purposes of the paper cited was to demonstrate that some of the rapidly-labelled RNA that appeared in the cytoplasm had properties consistent with mRNA.

The historic context

It may be necessary to explain to younger scientists that this work was done before DNA cloning, before RNA sequencing (never mind DNA sequencing), before the discovery of polyadenylation of eukaryotic mRNAs (the ‘handle’ for purifying them), in short, at a time when no specific mRNA had yet been identified or isolated (see, e.g., the Wikipedia article on The History of RNA Biology). As documented in Mathew Cobb’s excellent article ‘Who discovered mRNA?’, mRNA wasn’t really discovered but was an idea to account for the rapid response of the lac system (observed in genetic experiments) in terms of a previous unexplained labelled RNA with a DNA-like base composition observed associated with more abundant stable RNA (ribosomes) when bacteriophage infected E. coli. Subsequent work, presented in papers by Brenner et al. and Gros et al. in the same issue of Nature in 1961, in effect documented this RNA more precisely in phage-infected cells and showed that it differed from ribosomal RNA. The importance of the work of Mathhaei and Nirenberg in establishing cell-free systems for translating polyU and subsequently other artificial polynucleotides cannot be underestimated. However, it is important to recognize that the genetic code was not deciphered using genuine mRNA.

It was natural to assume the mRNA model extended to eukaryotic cells, but at that time there was no convenient system with an abundant mRNA like that of bacteriophage and so the presumed differentiating characteristic of short half-life was used, as seen in a plethora of papers on ‘rapidly-labelled RNA’. Many of these were opportunistic, claiming to document anticipated hormonal or other effects on eukaryotic gene expression. Consequently the demonstration that much of the rapidly-labelled RNA in the nucleus never reached the cytoplasmic ribosomal location had the effect of discrediting not only these papers, but the very idea that mRNA existed in eukaryotes. This may seem rather absurd today, but the foremost ‘eukaryotic mRNA denier’ (as he might be termed in contemporary parlance) was the eminent Oxford Professor of Pathology, Henry Harris FRS, who developed man–mouse heterokaryons and set out his ideas in a published monograph entitled ‘Nucleus and Cytoplasm’ (a copy of which I once possessed). So it is relevant that Warner et al. (1966) refer specifically to Harris in the discussion section of their paper, which describes work that addresses the issues Harris had raised.

If there is a moral to this story (and it is always easier to draw morals after the event) it is perhaps that Harris was happy to confusticate lack of proof with disproof in an area that was peripheral to his main concerns, and that the groups in New York — and Jonathan Warner, especially, having previously described polysomes in Alexander Rich’s lab — were prepared to accept the fact that the situation was more complicated than originally thought, but were not prepared to throw out the baby with the bath water.


Did modern alligators and caimans come from prehistoric crocodiles?

This is the phylogeny of the Crocodilia, as best as we currently know it:

The order Crocodilia is a monophyletic group including all living crocodile and alligator species. That means that all of these species share a common ancestor and all descendants of that ancestor are part of Crocodilia.

Within the Brevirostres, three superfamilies exist - the now extinct Borealosuchus, the Gavialoidea, within only two species not already extinct, and the Brevirostres.

The Brevirostres are the monophyletic group containing the crocodiles and alligators (that includes the caimans).

  Did alligators come from crocodiles when the crocs swam into freshwater areas?

That very much depends on what you mean with "crocodile". If it's Crocodylidae, then no, these are sister groups. If it's only the true crocodiles (Crocodylids), no, those evolved after the split with alligators. If it's Crocodilia, then yes, alligators evolved from crocodiles.

  And since the alligators and caimans are 2 groups in alligatoridae did they have a common ancestor?

Yes. However, saying that is rather boring - all life has a common ancestor. If you mean whether they have a common ancestor and all descendants of that ancestor are either alligators or caiman, then yes.

Additional source: Crocodilian phylogeny inferred from twelve mitochondrial protein-coding genes, with new complete mitochondrial genomic sequences for Crocodylus acutus and Crocodylus novaeguineae


Ciliated Epithelium & Goblet Cells Lining The Trachea

There are two pipes from your throat, downwards. A foodpipe and a windpipe. One, called the trachea, feeds air into the lungs, i.e. connects your head with your lungs. Another pipe, called the esophagus, leads to the stomach.

Both pipes meet and share the same passageway in your throat and oral/nasal cavities. Let's call this the common pipe.

The lining of the trachea, made up of ciliated cells and mucus-producing cells, does indeed move debris UP and OUT of the trachea, away from the lungs. Once this debris is at the common pipe, it can go to the stomach or into the mouth or into your nose for clearance.


Are human fetuses more likely to be male?

The Fisher's principle is not applicable to the fetuses because it has been formulated for parental expenditure and basically states that the ratio of male to female parents (implying that both parties have reached the age of fertility) will tend to 1:1.

There are several mechanisms that we can use and that are mentioned in the canonical paper by James (2007):

  (a) there are equal numbers of X and Y chromosomes in mammalian sperms
  (b) X and Y stand equal chance of achieving conception
  (c)
  therefore equal number of male and female zygotes are formed, and that
  (d) therefore any variation of sex ratio at birth is due to sex
  selection between conception and birth.

James brings much evidence that none of these conventional beliefs is true. Rather, they are dependent upon many factors: exposure to stress during pregnancy, glucose level etc. He reports that there is an excess of males at birth in almost all human populations, and the natural sex ratio at birth is usually between 1.02 and 1.08. However, the ratio may deviate significantly from this range for natural reasons. (I really recommend reading the paper I linked, it is available for free).

Branum et al (2009) analyze birth statistics in the US taking into account many factors like ethnicity, gestational age and plurality and show that the ratio can increase even more with growing gestational age and has different values among different races.

So, taking everything together, I can say thay YES, the chances for human fetuses to be male are indeed higher.


Humans are diploid organism. So humans have two copies of every chromosome and gene.

When a person has B blood. We mean that the blood cells of that person expresses  the B antigen.

To produce the B antigen you will need at least one allele for the B antigen. Hence the B antigen phenotype can have a genotype of BB or BO.

Now if two people have the genotype of BO have children, a punnet square will show they they have a 25% of having a child with BB genotype, 50% of having a child with BO genotype and 25% of having a child with OO genotype.

Phenotypically, it means that there is 75% chance of having a child with B blood. And 25% chance of a child with O blood.

A similar system also occurs with rhesus +/- system. A person with +ve blood can have a genotype of ++ or +-. If two people with the genotype of +- have children together, there is a 25% chance that their child will have -- genotype and be rhesus -ve.

The two systems work together. So two people with genotype of BO blood type and +- rhesus antigen having children together, they can have a child with O blood and rhesus negative with a probability of 1/16 (6.25%)


Why do type 1 diabetics experience hypoglycemia?

Key to this question is that untreated, type 1 diabetics would never have hypoglycemia.  It is insulin treatment that causes the hypoglycemia.  Insulin brings sugar down and without insulin (as the case with type 1 diabetics) sugar just goes up.    Exogenous insulin will bring sugar down in anyone, diabetic or no.  Since Type 1 diabetics use insulin all the time, there is more chance for an accident (hypoglycemia).

Also, some Type 1 diabetics might not compensate against hypoglycemia or correctly perceive that they are hypoglycemic.  Reasons for this are laid out in the following article:

From Hypoglycemia in Type 1 Diabetes

  Three major defects in this homeostatic response contribute to the
  high frequency of hypoglycemia in type 1 diabetes.

The article summarizes what those are - basically a blunting of normal reactions to hypoglycemia stemming from the disease itself.  It then summarizes:

  Thus, the glucose counterregulatory defense against hypoglycemia in
  individuals with diabetes becomes impaired at almost every level and
  rendered even more defective through intensive insulin therapy


I think your reasoning is sound and your ordering very likely, but I wouldn't feel comfortable with deciding the side B is on. Actually, it's more than that: I think that by using basically the same number (~40) for everything that includes B, they want you to come to another conclusion.

Unlike eukaryotic cells undergoing meiosis, there is no crossing over in bacteria taking up DNA from the surroundings. Therefore, it shouldn't be possible for the cell to inherit A, B and C but not D, which is in the middle. Simply, from my understanding of the "experimental" setup, they added antibiotics A, B and C, so they have to assume the bacteria are wild type for D. However, it's basically for sure that those ABC-resistant colonies are also D-resistant.

Still, your reasoning is correct: comparing BC and AB should give you the side B is on, since the break could have been inside of the 3-gene cluster. However, the numbers are very close, and the "AB" and "BC" phenotypes are probably ABCD anyway, making the small difference even less meaningful (the true AB and BC are lost because they are mixed with the many ABCD).


How is cognitive ability linked to the presence of sex chromosomes?

If you are thinking that, say, a chromosome 1 triploidy will not result in cognitive impairment... that's not quite right.  Almost all triploidies result in death.   Same with chr2, chr3, chr4...just about every chromosome is lethal if there are extras.
It's not so much that having extra sex chromosomes is bad for cognitive function, it's that having extra chromosomes is usually lethal, only a few triploidies are even survivable, and they all cause lots and lots of problems, including cognitive impairment.  Having extra sex chromosomes is the mildest one, and it results in lots of comparatively mild problems.


Soon after asking this question I found a reliable source, the National Institutes of Health. It can survive for over 40 years.


Last-ditch efforts to maintain thermal homeostasis

Another factor at play here is the cardiovascular system.  Biro, Masudo, et al (2003) wrote an article about the benefits of the induction of systemic vasodilation for those with congestive heart failure.  This may be a short-term adaptation of the body stemming from the reduced ability to sweat in those conditions, or it may be a harbinger of the more serious circulation changes below.

Epstein and Roberts (2011) explain how the eventual results of heatstroke (which isn't the phenomenon that you are describing, but a sauna might induce some of the features of these same pathways) can cause a circulatory collapse due to an initial overtaxing of the circulatory system to compensate as well as the activation of certain heat shock proteins.

There are a lot of other references out there on sauna physiology, but many are not in evidence-based journals, so you can make your own decisions on those.

One factor that I didn't find mentioned explicitly was the basal metabolic rate.  It's probably safe to assume that the body will limit its own processes and reactions which produce heat.  I'm not clear on the extent to which factors such as the level of interleukins, etc. would play a role as they do in fever regulation.


Below the ladder means primer dimer.  You have no product.


bacterial cell wall degradation in humans

Humans have at least one enzyme which can break down D-amino acids, the D-amino acid oxidase (DAAO). They are able to break down these amoino acids, interestingly D-serine seems to play a role as a neurotransmitter. For more information have a look at these papers:

Physiological functions of D-amino acid oxidases: from yeast to
humans.
Human D-amino acid oxidase: an update and review.
d-Amino-Acid oxidase and its physiological function

We still need antibiotics, since only a small part of the bacterial cell wall is composed of D-amino acids. The cell wall is made of monomers from N-acetylglucosamine and N-acetylmuramic acid which are crosslinked by small peptides (these are short amino acids chains) to form the peptidoglycane polymer. A part of the amino acids in the crosslinking peptides are D-amino acids. I am not sure if the DAAO is able to attack these peptides in the polymer. Additionally most of the enzyme in the human body is present in liver and kidney, indicating that it breaks down D-amino acids that are transported there by the bloodstream.


Do model species evolve away from Batesian mimics?

I have found some papers that support the hypothesis that an overabundance of Batesian mimics creates a condition for model species to evolve differentiating characteristics -- in particular,  Franks, D. W., G. D. Ruxton, et al. (2009). "Warning signals evolve to disengage Batesian mimics." Evolution 63(1): 256-267.

The authors argue that new conspicuous traits in unpalatable species evolve in response to mimicry, since a mimic that evolves conspicuousness without being a good-enough match pays full cost of conspicuousness without the benefit of its predator learning advantage.


What happens to Km when enzyme concentration is *very* high?

Michaelis-Menten is often challenging for students because of the importance of the conditions that must exist in order for the model to hold. Walking through the derivation and the relevance of the assumptions can be helpful. Berg's Biochemistry is available via NCBI, and the section on Michaelis-Menten kinetics does a good job here, illustrating the following points:
Assumption 1:  The rates of all the relevant reactions are linear.
This assumption is what allows us to write down the equations the derivation starts with. We look at each separate reaction, and say that the rate of that reaction is equal to some rate constant times the concentration of each thing on the left side. From the equation $E + S \rightleftharpoons ES \rightarrow E + P$, we get the following

$E + S \rightarrow ES$

$Rate = k_1[E][S]$

$ES \rightarrow E + S$

$Rate = k_{-1}[ES]$

$ES \rightarrow E + P$

$Rate = k_2[ES]$

This assumption (the rate is linear) only matches the experimental evidence early on in the reaction, while most of the substrate is free $[S]$ (rather than bound up in $ES$).  Remember this. It will come into play when we evaluate assumption 3.
Assumption 2: The $ES \rightarrow E + P$ reaction is irreversible
In order for us to combine the above rate equations to derive the Michaelis-Menten equation, the only source of ES should be from $E + S \rightarrow ES$. We can't have any measurable $E + P \rightarrow ES$. Experimentally, for enzymes that follow Michaelis Menten kinetics, this is true when $[E]$ and $[P]$ are small relative to [ES]. So here we have our first requirement that $[E]$ be small. Biochemical reactions tend to not involve very high changes in free energy. The in situ free energy of ATP hydrolysis is the high end for a reaction in the cell, and that releases about $50kJ mol^{-1}$. We're not talking about combustion here. So in fact, these reactions are often reversible at appreciable levels of $[E]$ and $[P]$
Assumption 3: ES formation and breakdown is at steady state
This assumption is often described in a confusing way, i.e. the entire reaction ($E + S \rightarrow E + P$) is at steady state. Lets drill down to what we're actually talking about. In order to derive the MM equation. We need the rate of formation of $ES$ to equal the rate of breakdown of $ES$, that is, for $\frac{d[ES]}{dt} = 0$. That is steady state. Let's say that in words: the change in $[ES]$ needs to be zero. We only achieve steady state at an early point in the reaction (remember, we need most of the substrate to be free $[S]$ for assumption 1 to hold), if $[S]$ is substantially greater than $[E]$. $E$ needs to be saturated with $S$ while $S$ is still mostly in the free form. This is the key combination of assumptions that the situation you described violates.
Once we meet the three assumptions above, we can write down the following equality:
$k_1[E][S] = (k_{-1} + k_2)[ES]$
This equation says that the rate of formation of $ES$ (the rate from equation 1 at the top) is equal to the combined rate of the breakdown of $ES$, either into $E + S$ or $E + P$ (equations 2 and 3 at the top). Once we have this equality, we can derive the Michaelis-Menten equation: $V_o = V_{max} \frac{[S]}{[S] + K_m}$, where $K_m = \frac{k_{-1} + k_2}{k_1}$. Again, see Biochemistry to walk through this.


Identifying a beetle from northern California

This is a long-horned beetle, family Cerambycidae; the site http://www.sbcollections.org/cbp/DB_Query.aspx?Field=family&Value=Cerambycidae has a list of California species, with links to pages on each species (there are 387; not all species pages feature illustrations -- those that do figure museum specimens).  From that list the first that resembled your photograph is that covering Centrodera spurca (LeConte 1856), which has been found in Sonoma County; given that I haven't gone through the entire list there are likely other possibilities.

Centrodera spurca


How do high-throughput/NGS sequencers calculate quality scores?

I'm restricting this answer to Illumina. Even then, I don't know about the exact details of the raw data analysis (it is a proprietary software).

Basically Illumina records the sequence based on photographic images. Each nucleotide has a distinct fluorescent label. In a cycle, a nucleotide is pumped and unincorporated nucleotides are washed off (this is repeated for all nucleotides). A laser excites the fluorophore and the emitted light is recorded in the form of a photograph. The template DNA is present in the form of clusters of strands (at a given location), which enables easy visual identification of the fluorescence.

Base calling is done using image analysis. Each image is analysed for intensities of different colours and based on this the quality score is calculated. The quality score is basically the log likelihood of a occurrence nucleotide at a given position (based on its colour intensity) compared to other nucleotides.

This is the most simple explanation of how Illumina does base calling. There are different kinds of errors and biases and there are different statistical approaches to correct for them.

Have a look at following references for more details:

Ledergerber, Christian, and Christophe Dessimoz. "Base-calling for next-generation sequencing platforms." Briefings in bioinformatics (2011): bbq077.
Illumina MiSeq Imaging and Base Calling course
Genome Analysis Wiki


To be honest, you really shouldn't be buying such things if you're not prepared to handle them properly.  If you work with a proper lab, you will be inindated with vendors trying to sell you these and many others.

But to answer your question, if you are looking to purchase many such items ATCC is an excellent resource.  Not only will you have to meet regulatory requirements, but you will also have to deal with a great many MTA's depending on what you are trying to get.

In response to edit: Salmonella is actually not normally a serious pathogen to a healthy adult.  It is, however, still a human pathogen and should be handled under BSL2 conditions.  So if you have the funds and time to setup a BSL2 lab at your house, by all means go to town.  And I hope you don't live with any children, the elderly, or otherwise immunocompromised individuals.

In response to further edits:
If you just want to look at things under the scope, then I suggest you get started by making your own homemade culture plates.  If you can get your hands on some Lysogeny Broth (LB), agar, and petri dishes then you can make lb plates like a researcher in a real lab (minus an autoclave but you could use a pressure cooker).  These are items the public could get, but might be harder to come by.

I however will assume that you want to make your own plates from common household ingredients (I used to do this a lot as kid, whatever that says about me).

**

Making your own culture dishes:

**

1) The "plates" themselves.

I recommend getting the smallest Tupperware like
containers your can find that are microwave safe, dishwasher safe, and
really make a good seal (water tight at the least).  They really
don't have to be big, and you will make your life easier if you buy a
bunch to match.
They need to be super clean.  After running them through your
dishwasher at home, put them all in a boiling pot of water until you
are ready to pour in your "media." A mid-low simmer will work

Note that you won't probably be able to have perfect sterile technique at your house, but you should try to do what you can.

2) Your "Media" or Broth

I highly recommend using pectin as your gelling agent if you can't
get your hands on some agar.  After that comes plain unflavored
gelatin, but I recommend pectin.  You can get it at almost any
grocery store and my recipe is made assuming that.  You can determine
how much you want to make, just scale up the ratios.  I'm going to
list things as rough volume by volume so you won't need a scale.

i) Make the powder first:

45mL of pectin;
4 bouillon cubes ground as finely as you can (you can get different
types and results depending on if you start with vegetable, beef, or
chicken.  I recommend starting with vegetable.);
125mL of refined white sugar;
Additives (more on this later)

ii) Mix the powder into 500mL of water

Before you mix in the powder, hear the water to 50-75oC (mid low
heat), but not boiling.  Mix the powder in while stirring until
dissolved.

iii) Bring the mixture up to a boil.
Let it boil for about 2 min, stirring all the while.

iv) Cover the pot and let it cool for 4-5 min.

You by no means want it cool down to room temperature, you just want to get it a little below boiling.  If you are at 55oC or bellow it's definitely time move on.

v) Dip/fill your "plates" 1/3 full of media using clean/sterile utensils and seal while hot but not boiling.

You may have noticed this seems an awful lot like canning, and that's because it is.  Again you want to be as clean as possible in this step and of course try not to burn yourself on anything.

vi) Let your media plates set and chill over night in the refrigerator.

You really probably only have to wait a few hours if you are anxious to get going.  You are going to want to store the plates that you are not using in the refrigerator anyway.  Also if you made a bunch of plates, let the cool on a counter before you put them in the fridge so that you don't raise the temp of your fridge too much.

Remember the thing about additives?  You can play around with adding different amounts and different types of salts, vitamins, food, or other items to see how they effect the cultures you get to grow.  All kinds of fun there.  First go round, leave them all out.

Now you have your own home made culture plates!  The above recipe was empirically tested by my childhood, and repeated by my son's.  Not all pectin from the store may be equal, this is with Ball Classic (I have no relation to the company).  I'd love to know people's results in trying it, because I might need to re-think how/what I'm doing to get it to work.

Go around your house swabbing things with sterile swabs (you can get these at a drug store), and then streak them out on plate.  While it will be a little different with a swab and homemade plate, the idea is similar to what is done here.

Leave your plate in a warm wet place, but not in direct sunlight.  Ideal temp is going to be around 37, but you can leave them above and below that and still get things to grow.  On top of our dryer is where I leave.

After a day or so you should have colonies you can streak out on a slide and look under a scope.  You will find all kinds of things this way.  If you want a more formal way to put things on a slide, you can check out dry and wet mounting from a Google search.

You are actually quite likely to run into E.coli if you sample enough "areas" this way.  Obviously don't eat or huff the stuff that ends up growing.  Maybe you can post some fun pictures of this if you try it.


Do HIV particles die without host cells?

I've learnt that our circulatory system can clear foreign matters from blood stream. Phagocytes can engulf and breakdown virions. Our liver and spleen is the blood filter system, which sequesters foreign matters all the time. So free floating HIV virions can't stay indefinitely in our blood stream.

However, without an effective adaptive immune response, these mechanisms are still unable to suppress viral replication. That's why HIV patients still have high viral load if untreated.


Do we know the physical-nature of "senses" or qualia?

I'll try my best to give you my answer. But I maintain that this is still somewhat subjective.

Firstly, I think the short answer to your question as stated:

  Do we know the physical-nature of “consciousness”?

Is no.

I would personally say that our notion of 'sense' - that is, our ability to perceive stimuli, is not the same as consciousness (whatever "consciousness" means at this point). To me, and I think many others, the concept of 'consciousness' is simply being self-aware.

Science understands most if not all sensory pathways very well in terms of the electro-chemical and/or mechanical pathways involved.

To pick from your 4 options:

  Consciousness does not exist. It is just a myth.
  Consciousness    exists, but it is nothing more than information and computation.
  Consciousness exists, but we do not know its nature.
  Consciousness    exists, we know its nature, and that is more than information and    computation.

I think we can rule out 1 - we know we have something that we call consciousness - else we wouldn't be having this conversation!

We can certainly rule out 4 as well because we also wouldn't be having this discussion if it's nature was understood by now! :)

My own opinion steers me toward 3. Though I think understanding it might actually be impossible.

To run with your example of perceiving the colour red, I concur that we understand the physical processes that have occurred to enable us to see, and understand that we saw, red.

However...this puts me in mind of a kind of brain-teaser people sometimes mention: how do I know that what I consider to be red, is the same thing you consider to be red. Now, I don't personally think there's much to this, as colour is a physical property, but it does raise the possibility that the 'concept of red' is not immutable between individuals.

Some more food for thought is whether we actually possess a consciousness. By which I mean, it is an extant, natural phenomenon, like energy for instance, and you either have it or you don't. The alternative is similar to the debate about free will vs. the illusion of free will (I personally fall on the side of thinking the latter). That is to say, do we merely have the illusion of consciousness?

Taking the discussion from the comments about pain and expanding further; just because I feel pain, I do not believe equates to consciousness. How far down the evolutionary tree do you have to travel before you would decide a creature has no 'consciousness'. Sure, we probably agree dogs are conscious, but are they self-aware? Do they exist any further than to satisfy their biological needs? Even if we say yes... how much further do you need to go? Are sharks self-aware? Are hag-fish or nematodes self aware? And yet, we know that all these organisms are capable of sensing pain. So it's clear that simple sensing pain is not enough.

The last thing I recall reading about the basis of consciousness (and the closest thing I think we have to an answer as to what the physical basis of consciousness is) is that it is an emergent property of a complex system like our brain. The degree of 'inter-connectedness' in our brains is what makes us intelligent (not just size), and current thinking is that it's the density and number of networks inside the brain that is key.


Hybrid seed production requires a male sterile parent. Why?

To get a hybrid you need pollen from a different plant. Corn is likely to self-pollinate if some action is not taken to prevent it. I don't know of sterile males plants - in the US corn belt the self-pollination is prevented by detasseling. Many young people get summer jobs detasseling (cutting off the tassels) for seed corn.


Why do humans hear better between 2kHz and 5kHz?

Acoustically, we hear better in the 2-5 kHz range because our auditory canal resonates in that range (specifically, around 3 kHz). Our ear looks something like this (U Miami):

The auditory canal is part of the outer ear, which amplifies sound so that it can be converted into electrochemical signals by the middle and inner ear. We hear better in the 2-5 kHz range because the resonant frequency of the auditory canal is in that range.

The mechanical question of "how does this work" is usually easier to answer than the "why did this evolve?" question. Since reproductive fitness is the driving force of evolution, hearing babies crying (between 1-5 kHz) is the best guess I can come up with.


The blurry picture makes it hard to be sure, but I'm guessing it's some sort of louse fly (family Hippoboscidae). They are typically very flat, and can lack wings. They can bite humans, but the different species are dependent on their specific hosts to reproduce.

Image of a louse fly (found on someones neck) for comparison:

(image source)


What does this Barbary Macaque facial expression mean?

It looks like it is trying too threat.

Source:

Individual differences in scanpaths correspond with serotonin transporter genotype and behavioral phenotype in rhesus monkeys (Macaca mulatta)


Why are transcripts translated from 5' to 3' direction?

The tRNA is not acting alone, it has the help of the Ribosome.

The Ribosome assembles at the beginning of the transcript and starts the translation at the first AUG codon. It then binds the first tRNA which fits to the mRNA. The tRNA is then moved from the A-position to the P-position and the next tRNA is binding (the move around and bind by chance. A nice animation is found in the Wikipedia article on translation (which is also the source for the image above).

Translation can't go into the other direction, it is always in 5' -> 3'.

To recognize the right direction (and the right starting point) the Ribisome is not simply starting at the 5`end of the mRNA. Before the start codon AUG the mRNA contains a regulatory, untranslated region, the so-called 5'UTR. The end of the 5'UTR of eukaryotes contains the so called methylguanosine cap (and is only present in mature mRNA), in proaryotes this is done by the Shine-Delgano sequence. Both are recognized by the ribosome. After binding to the mRNA, the ribosome slides along the nucleotide chain until it reaches the first AUG to initiate translation. The image is from this description (which contains a lot more details, if you are interested in it).


Earliest and latest onset of Huntington's Disease(Chorea)?

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

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

Factors [4]:

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

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

References:

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


Why and how does falsifying sensory information work?

These are learning phenomena you describe. I'll try to explain a simple way to think about this.

By default, sweet foods are appetitive and, for instance, strongly bitter foods are aversive. However, it is possible to condition yourself to associate a stimulus, no matter how it presents originally, with a different valence (appetitive or aversive).

There are several well understood forms conditioning can take. I list a few here, and some subtypes. They are described well on Wikipedia:

Classical conditioning

-- Serial application of classical conditioning can be called second-order conditioning.

-- You can also condition yourself through self-evaluation, called evaluative conditioning
Covert conditioning is a technique more than a type of conditioning, it may directly apply to your question. It involves the use of imagery.
Operant conditioning

Operant and classical conditioning are the two major paradigms to know. Classical or Pavlovian conditioning involves pairing an "unconditioned" stimulus with a neutral "conditioned" stimulus. Operant conditioning involves providing a feedback, usually a reward or punishment, to reinforce learning.

You can self-learn or condition yourself. This does not mean necessarily it is intentional or conscious on your part, often things can be subconscious or unconscious. For instance, if you associate eating crisps with watching a movie, watching movies without crisps can become uneasy, in spite of the fact that watching a movie was originally a pleasurable activity. In a neuroscience seminar involving conditioning in fruit flies, I once recorded a saying which captured the spirit of the experiment quite well: An expected reward, not experienced, can feel like a punishment, and vice versa. Rewarding yourself after doing chores can also be a easy and practicable way to build good habits with doing chores.


Can one switch the DNA present in a sperm cell?

Not with present technology. There is next to no cytoplasm in a sperm cell. You cannot suck out its nucleus. If your remove its nucleus, the whole thing will just collapses on itself.

As for you question of replacing nucleus?. One current technique (Intra-cytoplasmic sperm injection - ICSI)  is to  inject a single sperm of a man with low sperm count with minimal mobility directly into an oocyte. (Ie sperm that is so bad that they effectively cannot swim on their own)

Unfortunately there is some indication, that this technology has made an entire generation of sons, who have also inherited their father's low sperm count and limited mobility. And now have a higher than average chance of needing IVF assistance.
https://www.newscientist.com/article/2108218-male-fertility-treatment-seems-to-pass-infertility-on-to-sons/


Almost definitely (I'm not a regular birder) European Green Woodpecker (latin name: Picus viridis) and it is native to your area according to its species distribution map.

  "Green woodpeckers are the largest and most colourful woodpeckers
  native to Britain. They are easily recognised by their laughing
  ‘yaffle’ call, which they use to demarcate their territory. They also
  drum on trees, though the sound is not as resonant as that made by the
  other two British species (the greater and lesser spotted
  woodpeckers). Green woodpeckers survive on a diet of insects and have
  a particular fondness for ants. They return day after day to their
  favourite ant hill to feed." - BBC nature


When is Pheophytin used in electron transfer to the q cycle in plants?

Not sure if there is a definite answer. However, from structural studies, its proposed that essentially the Chlorophyll a and pheophytin(Pheo) are positioned ~10A away, and the transfer of a radical electron from the P680 center to Pheophytin does occur. The exact mechanism is possibly mediated by a tyrosine

Durant J.R et al (1995). Proceedings of the National Academy of Sciences of the United States of America, 92, 4798–4802
Oleg Victorovich (2006). Retrived:5/25/16. Site: http://samlib.ru/o/oleg_w_m/cdocumentsandsettingsolegmoidokumentythefunctionandthestructureofporphyrinmoleculesrtf.shtml

3.Zouni A et al (2001). Nature, 409, 739-743


Do animals exist which have good vision, but see only grayscale?

Preamble & Overview.
This is a rather unsatisfying answer I'm afraid. I can't seem to find any animal that has exceptional eyesight and sees in monochrome.
Baring in mind the context of humans vs machines; machines cope better with shapes rather than colours however it generally appears that those animals which rely on exceptional eyesight to survive tend to see in colour and have other neurological systems to ease "data overload".
Animals that see in grey-scale.
Some pinnipeds (seals) see in grey-scale, but note that their survival doesn't seem to depend on visibility, and it is generally regarded as poor even in a typically healthy animal. According to SeaWorld, researchers have found blind seal mothers and pups that are otherwise perfectly healthy.
Dolphins are a similar story. It is so murky that they rely on bio-sonar. Fresh water dolphins are almost completely blind.
In fact, the more species that I have read about which have monochromatic vision, the more I see that these animals rely heavily on other senses.
Some land animals with "decent" monochromatic vision:

Lorisiformes
Bats
Raccoons
Nocturnal kinkajous

Note that these often have another much more acute sense like smell or hearing.
Surprisingly, there is also not necessarily a link between monochromatic vision and nocturnal state (there are some animals with dichromatic vision that are nocturnal, and some animals with monochromatic vision are crepuscular, or diurnal and visa versa).
From wiki:

Many species, such as all marine mammals, the owl monkey, and the Australian sea lion have monochromatic vision under normal conditions...

A trend I see is that animals that have exceptional eyesight tend to have also evolved some sort of colour differentiation.
Why not ditch the colour info to make it easier on the brain?
To bring this back to your context of machines I would say that identifying the difference between a ball, a chair, a human, and a car (the sort of things machines need to know about!) is much more dependent on shape than colour. A monochromatic person wouldn't struggle with that at all.
However in a "wild" environment telling the difference between grass and tiger stripes means that an animal with trichromatic vision may get to live another day whereas the animal with monochromatic vision might not see the tiger in time. Or spotting berries and fruit in some distant trees might mean food that would have otherwise gone unnoticed.
Those are obviously very narrow examples, but generally it seems animals always have one or more exceptional senses limited to smell, hearing, or colour vision (it would be great if someone could point out an exception to this in the comments, like touch or taste!).
You are right to hint that there is a lot of information in colour vision. Like your example with loss of colour in machines, data needs to be dumped very quickly in the human brain.
I'm not a neuroscientist, but I have read pop articles about how little we can remember with photo detail. Within seconds of looking at a scene all texture details are lost, most objects are forgotten about and all we can really recall are big shapes. But importantly, we would notice the tiger in the woods before forgetting and run for it! If we had no colour input, that wouldn't be the case.

Examples of more colour being used.
Hopefully the above demonstrates that colours are important to many animals. If anything it seems that more colours even than our perception of the EM spectrum are preferable, particularly into the UV range.
For prey identification reindeer rely on ultraviolet light to spot lichens that they eat. This same sight can spot the UV-absorbent urine of predators. This article has a few more examples.
Some birds of paradise like parrots have even more brilliant patters under UV light. Even starlings look to have an identifying pattern under UV light. Both those examples are thought to be involved in mate selection.

White light does not reveal the feathers' yellow fluorescence in images (left), but short wavelength illumination does (right). Photo: Science

This all hammers home that colour is more important to animals than machines and is involved in more than just camouflage.


If an insect becomes upside down, do they have mechanisms to turn themselves right side up?

Well, many insects have developed ways to right themselves when they get turned over.

One of the more interesting families are the Elateridae, or click beetles: so named because they press their prosternum and mesosternum against each other which causes pressure. That pressure is eventually released causing a "clicking" sound and springing the insect upward (or away from predators).

You can see an additional video of a click beetle doing so here.


A simple genome can be modeled, however imperfectly, on a computer, where some have taken experimental genomics data and built simulations from it.
For instance, from the paper A Whole-Cell Computational Model Predicts Phenotype from Genotype:

Understanding how complex phenotypes arise from individual molecules and their interactions is a primary challenge in biology that computational approaches are poised to tackle. We report a whole-cell computational model of the life cycle of the human pathogen Mycoplasma genitalium that includes all of its molecular components and their interactions. An integrative approach to modeling that combines diverse mathematics enabled the simultaneous inclusion of fundamentally different cellular processes and experimental measurements. Our whole-cell model accounts for all annotated gene functions and was validated against a broad range of data. The model provides insights into many previously unobserved cellular behaviors, including in vivo rates of protein-DNA association and an inverse relationship between the durations of DNA replication initiation and replication. In addition, experimental analysis directed by model predictions identified previously undetected kinetic parameters and biological functions. We conclude that comprehensive whole-cell models can be used to facilitate biological discovery...
We have developed a comprehensive whole-cell model that accounts for all of the annotated gene functions identified in M. genitalium and explains a variety of emergent behaviors in terms of molecular interactions. Our model accurately recapitulates a broad set of experimental data, provides insight into several biological processes for which experimental assessment is not readily feasible, and enables the rapid identification of gene functions as well as specific cellular parameters.

(cite)
Also:

Given the vast behavioral repertoire and biological complexity of even the simplest organisms, accurately predicting phenotypes in novel environments and unveiling their biological organization is a challenging endeavor. Here, we present an integrative modeling methodology that unifies under a common framework the various biological processes and their interactions across multiple layers. We trained this methodology on an extensive normalized compendium for the gram-negative bacterium Escherichia coli, which incorporates gene expression data for genetic and environmental perturbations, transcriptional regulation, signal transduction, and metabolic pathways, as well as growth measurements. Comparison with measured growth and high-throughput data demonstrates the enhanced ability of the integrative model to predict phenotypic outcomes in various environmental and genetic conditions, even in cases where their underlying functions are under-represented in the training set. This work paves the way toward integrative techniques that extract knowledge from a variety of biological data to achieve more than the sum of their parts in the context of prediction, analysis, and redesign of biological systems.

(cite)
Gentle advice: Avoid answers from cartoonists, whose domain of knowledge does not include biology.


What are the psychedelic effects of (star) anise and how many people are affected?

Interesting question! As this post has been sitting around for a while I am going for some speculations. First you talk chocolate, which essentially contains the alkaloid theobromine. Anise contains the propenylbenzene (E)-anethole (Idle, 2005). Theobromine is a caffeine-derivative and basically produces alertness, but also restlessness and perhaps anxiety when administered in large amounts (wiki). In extremely high doses there can be LSD-like effects (anecdotal report). Perhaps (speculative) your girlfriend is especially sensitive. Then (E)-anethole: the late Alexander Shulgin, Godfather of MDMA, has made the etheric oils (in)famous as precursors for amphetamine synthesis. In themselves the propenylbenzenes like (E)-anethole are quite harmless, as they do not contain an amine group (a prerequisite for being called an alkaloid). However, heating (E)-anethole in the presence of ammonia may lead to the production of PMA, a compound structurally and neuropsychopharmacologically related to MDMA (Idle, 2005). Although a bit of chocolate and a sip of Sambuca do not meet any of these conditions, both chocolate and Sambuca do contain certain psychoactive compounds, or their immediate precursors.


Googling your question showed that it is RNAse H that removes the RNA primer. DNA Pol I has both 3'-5' as well as 5'-3' exonuclease activity for proofreading and nick repair activities, respectively. See the wiki on Pol I


How can I measure bacterial alkaline phosphatase activity?

I found this kit that appears to be compatible with biological samples.  Rather than buying the kit you may also be able to imitate / modify their protocol to do the assay with your super natant.


Why are interspecies hybrids so often larger than either parent species

While they do not necessarily constitute the majority, it is true that there is a large number of interspecies hybrids whose members are larger in size than the parent species, and there exist explanations that account for this phenomenon.

What you are describing is an example of positive heterosis, or hybrid vigor.  While the rationale for plants is more complex, it commonly arises between related species in mammals as a sort of heterozygote advantage in which the contrast in genetic contribution during conception spawns some phenotypic benefit.  The exact implementation of this varies from species to species, but this link here is a nice, concise explanation for why ligers might be so large.


Significance of lipids in biological membranes...?

Membranes are built from a specific class of lipids, namely phospholipids, whose key property is that they are amphiphilic and so can self-organise to form bilayers. Not all amphiphiles do this, some prefer to adopt a micellar organisation. A bilayer composed of phospholipids produces the ideal combination of a hydrophobic barrier with a hydrophilic surface.

Although there are clearly amino acids with hydrophobic side chains, it is difficult to conceive of a proteinaceous barrier that would reproduce the properties of a phospholipid bilayer since it would not have a continuous hydrophobic phase.

Cellulose may be insoluble, but is full of polar groups so again would not create a hydrophobic barrier - I'm sure that ions can diffuse through a cellulose structure for example.

added later

@WYSIWYG raises an excellent point in the comments. Archeal membranes are composed of a different class of amphiphile in which the hydrocarbon tails (branched; derived from isoprenoids) are attached to glycerol by an ether linkage. It's instructive to note that the overall design principles are retained however, suggesting that the self-organising properties of these molecules was the key to the "invention" of biological membranes.


Why don't we see new diseases more often? Or, ever?

The first thing to note is that nothing is truly new, everything is a slightly different version of what existed previously, it's only on the very long term that you can see major change. Mutations occur continuously and new variants arise often. For example you need a new flu shot every year due to the high mutation rate of the influenza virus but we still call it flu because it's only a little different.

While disease causing organisms evolve at a relatively slow rate new diseases can appear suddenly when the effect on humans suddenly changes; the most obvious example of which is when a disease changes host species. For example the sudden appearance of HIV when Simian immunodeficiency virus (SIV) "jumped species" to infect human, most likely through the consumption and processing of Primate meat. While HIV appears new it is again ancient in the sense that it has caused a similar condition to HIV/AIDS in many African non-human primates for a significant period.


Cytosol is actually about as viscous as water
(i.e. ~1 cP or 1 mPa/s).

From the Introduction of Bicknese et al. 1993

  In fibroblasts and several types of epithelial cells, fluid-phase viscosity was 1.1-1.5 cP, not much higher than that of water (1 cP) (Periasamy et al., 1992). Recent measurements of cytoplasmic viscosity in CV1 and PtK1 cells by a novel ratiometric method supported the conclusion that fluid-phase viscosity in bulk cytoplasm is similar to that of water (Luby-Phelps et al., 1993).

And from the conclusion:

  Apparent fluid-phase viscosity near the cell plasma membrane was 1.1 ± 0.2
  cP (fibroblast) and 1.0 ± 0.2 cP (MDCK), not significantly different from the viscosity measured in bulk cytoplasm far from the
  plasma membrane.

Interestingly, the paper cites the following studies:

  In fibroblasts, fluid-phase viscosity was weakly temperature-dependent (Arrhenius activation energy 3-5 kcal/mol) and nearly independent of cell volume (Fushimi and Verkman, 1991).

Note:

cP = centipoise

A centipoise (cP) is a non-SI (non-System International) measurement unit of dynamic viscosity in the centimeter gram second (CGS) system of units. It is multiple of the CGS base viscosity unit named poise (P)
1 cP = 0.01 g/cm/s
1 cP = 1 mPa/s

Source:

Bicknese S., N. Periasamy, S. B. Shohet, and A. S. Verkman. 1993. Cytoplasmic Viscosity Near the Cell Plasma Membrane: Measurement by
Evanescent Field Frequency-Domain Microfluorimetry. Biophysical Journal 65: 1272:1282

Further Reading:

Beals et al 1999
Gyurov & Token 2011
Guthrie & Nettesheim 2012
Kalwarczyk 2011


How to bind antibodies to study their properties?

Like any other protein, antibodies will aspecifically bind nitrocellulose or PVDF membranes, but any other protein present in your antibody preparation will also do.

Depending on the antibody class, more specific binding can be obtained with protein A or protein G, that recognize the Fc domain. It's usual to have protein A/G immobilized on a stationary phase like agarose.

If you know the antigen used to develop the antibody, you can also use the immunizing peptide crosslinked to CnBr activated sepharose as a probe to bind your antibodies.

Knowing something more about your antibody preparation and what exactly is the 'behavior' your want to study could help obtain better answers.


Mucous-producing cells at the neck of the gastric pits create a layer of protective mucous covering the stomach lining. This mucous layer includes bicarbonate ions which act as a chemical barrier against the protons in gastric juice.  See here for some evidence.

The stomach lining stays protected because the mucous layer is continuously replenished.


What does z in lac z, y in lac y and a in lac a gene stand for?

The Jacob and Monod article on regulation is paywalled, but there do seem to be some PDFs floating around.
In this article, the terminology of z and y is introduced as designators for mutants (z+ and z-, y+ and y-).

The z appears to be linked to a term from a kinetic equation.
The y is not justified, implying that it is an arbitrarily chosen variable, and such choices are often by convention adjacent to the justified variable (e.g., the index variable i is often followed by additional indices j and then k).

The a component is not present in the original article, but its name seems likely to come as an abbreviation of its function as an acetyltransferase


Effect of 2,3-bisphophoglycerate (2,3-BPG) on haemoglobin

The oxygen dissociation curve for haemoglobin (Hb) in the absence and presence of 2,3-BPG is shown in (i) below:

It can seen that the curve has shifted to the right (MC-1 incorrect) and the oxygen affinity is obviously decreased, as it takes a higher concentration (pressure) of oxygen to achieve the same percentage saturation (MC-2 correct — and so is option MC-4 as far as I and @JM97 can see, agreeing with the poster. MCQs are an educational abomination!).

The physiological significance of this is  considered in detail in my answer to another question, but, in short, it ensures that an adequate proportion of the (smaller) amount oxygen taken up at the lower pressure in the lungs is released in the tissues (3 minus 4, cf. 1ʹ minus 2).

To address the interaction between the effect of 2,3-BPG and the Bohr Effect one needs to consider the corresponding curves for the effect of hydrogen ions (falling pH), shown in (ii), above (see also my detailed answer to this question).
It can be seen that the effect of hydrogen ions is similar to that of  2,3-BPG. Can these two have independent (additive) effects? It is known from molecular studies that they both interact with and stabilize deoxy-haemoglobin at different positions (see ii, below), and in one model of the allosteric mechanism they can be considered as shifting the equilibrium from the tense (deoxy-) to the relaxed (oxy-) state of haemoglobin:

(i) Generalized diagram of allosteric equilibrium of tetrameric protein between relaxed state (where it can bind substrate/ligand) and tense state. Negative effectors favour the tense state. (ii) Illustration of this for haemoglobin, where H+ ions protonate His-146 of the β-subunits and 2,3-BPG forms ionic bridges between the two β-subunits.

So it would appear that Bohr effect can still augment the 2,3-BPG effect, but I would imagine that the extent of this augmentation would depend on the initial position of equilibrium, and I would not expect it to be additive — I may be wrong. (Is MC-3 correct or not? A school student can hardly be expected to know unless he had been fed the ‘correct’ answer. Perhaps he is intended to interpret the option as meaning “does the 2,3-BPG effect work in the opposite direction to the Bohr effect”. You may now understand why I loath MCQs.)

Bibliography

The diagrams are my own, based on various sources I have used over the years. To check whether what I have written is correct, the reader may wish to check any of the many accounts online, including the following which have references to original material:

Wikipedia article on haemoglobin
Proteopedia article on
haemoglobin


Would that be a good thing?

Recent research from the Samson lab at MIT suggests that there are side effects from amplifying the DNA repair mechanism.

Hyperactivity of a base-excision repair (BER) protein called AAG in mice caused a positive feedback loop in DNA repair signaling that triggered macrophages to attack retinal cells, leading to a cycle of increased inflammation, photoreceptor (PR) necrosis, and ultimately blindness.

From the linked paper:

In this study, we demonstrated that programmed necrosis and subsequent inflammation are important mediators of AAG-dependent alkylation-induced PR cell loss in male mice... We showed that PR cells present necrotic morphology and oxidative DNA damage after the induction of PR cell death with alkylating agents; furthermore, we observed that PARylation in the PR nuclei is associated with the release of HMGB1, increased macrophage infiltration, and elicitation of an inflammatory response.

Another research project looked at a DNA repair protein called ATM in mice, where hyperactivity or overexpression may be implicated in Alzheimer's and Huntington's diseases. Knock-down mutants show reduced expression of this protein and reduced neural damage.

Ignoring the larger ethical questions of splicing genes into human beings, and the technical questions of how to get said genes inserted, transcribed, and translated in the right place at the right time in the right way, it would likely require considerable study to see what the systematic effects might be from expression of tardigrade or other organisms' DNA repair genes in humans.

At the very least, these papers suggest that the biology is complex enough that turning up the dial on repair machinery could cause serious health problems downstream, as much as it might confer greater protection from radiation or other environmental damage.


During DNA foot-printing, what is the purpose of radioactively labeling only one end of the DNA fragment?

Preamble

Although there is a Wikipedia page with a general account of DNA footprinting, this perhaps does not put sufficient emphasis on the general strategy, making reference to the Maxam & Gilbert DNA sequencing method, with which contemporary students are not likely to be familiar. Elsewhere on SE Biology I have summarized the strategy of different DNA sequencing methods, so I shall use that as a starting point for this answer.

The Strategy of DNA Footprinting

In DNA sequencing there are two conceptual pieces of information one is trying to discover: the identity of a base, and the position at which it lies. A third point of importance is the practical technique one uses to realize a strategy. The method of DNA sequencing developed by Maxam & Gilbert used specific chemicals to fragment pieces of DNA:

The particular chemical used identified the base as the last one on one of the fragments produced.
The length of the fragment indicated the position with respect to one of the ends, which was used as a reference point.
End-labelling of one end of the original DNA allowed fragments containing the reference point to be visualized, distinguishing them from others that were unlabelled and hence generated elsewhere.

In DNA-footprinting we are not concerned with identifying the bases: the DNA has probably already been sequenced or we can do that separately. We are in interested in positional information, and we shall see that this also involves fragments — generated by the non-specific DNase — and their visualization, as in the method of Maxam & Gilbert.

This is explained in the figure below, my own modification of Coutney2008.jpg, in the Wikipedia article mentioned.

The frame on the extreme left addresses the question of labelling and visualization by showing the fragmentation of uniformed-labelled DNA by DNase. In this example the DNase cleaves at three points (arrows), generating four fragments of different sizes, A, B, C and D. If these fragments are separated and visualized by their radioactivity (by autoradiography) there is no way of knowing their position in relation to the reference point. So whatever our strategy is in relation to protein-binding (explained below) the positional information is not revealed. We cannot tell that fragment A contains the reference point.

Now let us turn to Frame 1, which is in effect the Maxam & Gilbert strategy without the base-identification. The DNA is labelled at one end and treated with DNase at a concentration that will generate a range of fragment sizes. The ones we are interested in are those that include the reference point, which is the end we have labelled. These fragments have been coloured pink. Other fragments (light blue) that do not include the reference point will be generated — including some of the same size as those of interest — but these will not interfere with our analysis as they are not labelled and will not be visualized after the fragments have been separated according to size on denaturing gels and subjected to autoradiography (see gel lane 1). (The unlabelled ‘light blue’ portions may have been fragmented further, but this has not been shown for clarity.)

The footprinting strategy is shown in Frame 2. The experiment of Frame 1 is repeated with the DNA-binding protein (bright blue oval) added. Now the region of DNA to which the protein binds will be protected from DNase. Thus, fragments terminating within this region will be missing and be absent from lane 2 of the gel. Hence the position at which the protein binds is specified as the distance of the missing fragments from the labelled reference point. (There are likely to be fragments of the same size as the missing ones in the mixture, but, to repeat, because of the end-labelling they will not be visualized.)


Can oil be used instead of water in preparing wet mounts for microscopy?

Typically wet mounts are used to observe the mobility and behavior of microorganisms. A classical use for a wet mount would be to study something like pond water were you could see all the different organisms swimming around like they would in their natural environment. Oils are more viscus and would impede mobility and might impact behavior or even be toxic to the microorganisms.

If you were an olive oil manufacturer, and you thought you had some odd microbial contamination of your olive oil you might look at a drop of your olive oil between a slide and cover slip thus using an oil based wet mount like you are describing. You might also do this if you were studying the microbiology of an oil spill in water.

There is nothing saying you could not suspend a sample in oil. There may even be a unknown benefit of using this method in certain circumstances, that is waiting to be discovered.


Evolution - The ability to control ear muscles

Yes, humans have lost the ability to move their ears toward sounds like many other animals such as cats and rabbits.

It is thought that our ancestors lost the ability to move their ears around 30 million years ago when

  Ear size decreased and the associated musculature changed 1 (Steven Hackley).

A review from Steven Hackley outlines the evidence that the neural circuit remains in modern human brains. Apparently, the neural circuit still responds to directional sounds and may cause our ears to curl slightly (2 - 3 mm).


The known factors seem to be mainly oestrogen and genetic (although I haven't been able whatsoever to find detail on what genes):
Manning et al (1997): Breast asymmetry and phenotypic quality in women. Evolution and Human Behavior, 17 (2): 129–143.

Our data support the thesis that mammotropic hormones, particularly estrogen, are harmful because they suppress the immune system. Heavy women with high levels of body fat produce more estrogen and, therefore, bigger breasts. However, more estrogen leads to an increase in breast asymmetry. Women with “good genes” are able to produce symmetric breasts despite the presence of large quantities of estrogen. Large and symmetric breasts are therefore honest signals of high phenotypic quality in women.


Why Can't The Immune Systems of Uncontacted Tribes Handle Our Common Colds?

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

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

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

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

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

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

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

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

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

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

Guns, Germs, and Steel by Jared Diamond


Vigorous shaking for HFR interrupted mating

I remember doing this experiment many years ago in an undergraduate practical where we used vigorous vortexing of culture samples in glass tubes to achieve interruption and separation.

According to Griffiths AJF, Gelbart WM, Miller JH, et al. Modern Genetic Analysis. Bacterial Conjugation:

  ... sampling is accomplished by using a kitchen blender to separate
  the joined cells, resulting in interrupted conjugation.


What is the scientific name of such a fungus?

This looks pretty much like a Coprinus comatus (also known as: shaggy ink cap, lawyer's wig, or shaggy mane) to me. You can see the characteristic ring around the stipe of the fungus (see image below from Wikipedia). The fungus is edible and is also cultivated in China for this purpose. See here for more details.


How quickly do estrogens break down in the environment?

Months to years - although the actual duration in a specific environment depends on the nature of that environment and is tied to oxygen level. Higher oxygen, faster degradation. Less oxygen, the estrogen molecules interconvert among various closely related molecules which hampers both their detection and their degradation.

For more info, please see: Environmental science: The hidden costs of flexible fertility (Nature 485, 441 (24 May 2012))  and this Science Daily article.


How can carnitine enter the mitochondrial matrix without OCTN2?

Short answer -- looks like the image in my question might be flawed, and OCTN2 probably isn't even involved in inner mitochondrial transport. Lesson: don't believe everything you find on google image search!

Longer answer - So I went back to the page where I originally found the image and saw that Dr. Ikumi Tamai was featured as one of the researchers who originally described OCTN2 back in the late 90s.

So I contacted Dr. Tamai via email-- and he responded to me a few hours later!

In his response, Dr. Tamai stated that while OCTN2 is expressed in various places in the body -- it is mostly active in the kidney -- and works there to conserve blood carnitine by re-capturing it from urine and returning it to the blood.

He added that jvm mice (which have defects in OCTN2 that cause carnitine deficiency) respond favorably to carnitine supplementation because the defect mostly just lowers blood carnitine levels, and simply raising those levels improves the condition of the mice.

This seems to suggest that OCTN2 does NOT play any role in transporting carnitine within the mitochondria.

Dr. Tamai noted that the image, which seems to depict OCTN2 sitting on the inner mitochondrial membrane, might have been designed by someone who did not fully understand the science of OCTN2, and that different transporters are likely responsible for the transporting of carnitine into and out of cellular and mitochondrial membranes (not OCTN2!).

In short -- it seems like that little pink blob in the image above should NOT be OCTN2 (even though it is labeled as such) and should probably be another transporter altogether.


No, only virus or bacteria can cause you cold .Cold weather  causes increase in the spread of virus. Flu virus spread quickly in cold weather. Cold feet can slow down your immune system making you prone for virus attack.Means ,if you are wet you are susceptible to a viral  infection but the cause of cold then would be a virus not the cold weather itself.


You asked the single most difficult questions ever, so be proud of yourself! I've spent some time in the lab with a post doctorate trying to answer that particular question. It all is based on something called the hygiene hypothesis: the belief that as we are getting cleaner we are seeing less and less bacteria and so our immune system isn't working as it should so we get allergies. There's lot to this theory with regards to the different white blood cells in our body (specifically Th1, Th2 if you've ever heard of them). Of course there are reverse hypotheses, because we avoid eating stuff like peanuts, but minute amounts is found in dust, dust exposure (which also contains bacteria) makes us think peanuts are harmful so that's why we have allergies.

Realistically a bit of dust to the most of us isn't harmful but if it contains things like dust mite poop which many people are allergic to, cat skin (another seriously common allergy) or is leaking from a place with mould... you should be okay :)