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Was the recent "conservation hunt" of a black rhino supported by science?
CNN recently covered a sanctioned black rhino hunt in Namibia by Texan Corey Knowlton, who bid US$350,000 for the license. In the story, he claims that the hunt was actually supporting conservation of the critically endangered species, as they were looking to kill an older, non-reproducing male that was consuming resources and potentially threatening younger, breeding males. The Namibian government has a list of 18 rhinos in the country (out of a total population of about 2,000) that meet the criteria.

Knowlton is targeting one of four black rhinos at the top of the government list, the ones considered "high priority threats to the herd."

Knowlton eventually caught up to and killed the animal he was targeting, and donated the meat to a local village.
CNN.com later published two opinion pieces, one in support of the hunt by Dr. Mike Knight, the Chairman of the International Union for Conservation of Nature (IUCN) Species Survival Commission's African Rhino Specialist Group (AfRSG) and the South African Development Community Rhino Management Group (SADC RMG), and one opposed to it by Jeffrey Flocken, the North America Regional Director of the International Fund for Animal Welfare (IFAW). Knight cites black rhino-specific data in his piece, arguing that in the case of this particular species, limited hunting is actually beneficial. Flocken instead uses a wider argument, citing hunting of polar bears, elephants, and lions, among other species, and claiming that the idea of "conservation hunting" as a whole is flawed. He does not, however, directly address the situation of black rhinos.
I have evaluated each side's argument, but have not yet formed a solid opinion, which is why I'm asking here. In the specific case of the black rhino, does the science support the notion of limited elimination of older males? Are there studies that show this has led to an increase in other types of conservation efforts? Does the money spent for licenses actually go towards conservation and assistance for locals?
As a second, optional question: Are the arguments posed by Flocken against "conservation hunting" in general supported by independent research? Just thinking logically I can imagine they are, as a lot of what he says makes sense in a broader context, if not necessarily in the case of the black rhino. Is there a scientific case for limited, situation-specific hunting, or should all forms of it be discouraged?
Note: I'm asking this here instead of Skeptics because I'm looking for a scientifically-supported answer. If you think it's better suited there, let me know and I'll move it.

"Support" how? For instance, I think that there are different answers to different questions depending on whether you're looking at it from the perspectives of population biology ('can we remove some individuals without affecting the long-term population growth rate?'), conservation biology as a coupled human-natural system ('where does the money go?', 'what effect does this example have on poaching?'), ethics ('does this harm animal welfare?'), or aesthetics ('is this distasteful?'). Part of the issue with those two editorials seems to be that they addressing different questions.

I see no reason why you can't post it on both sites, I have crossposted to Skeptics on occasion.

There are a bunch of meta posts about cross posting and it seems that the community still disagree on the question. I think however that most people think that cross posting is bad (see this meta post)

This question is still unanswered, partly because as @Oreotrephes points out, the question isn't actually clear on what its asking. Otherwise this is a nice question on a stimulating and interesting topic.

Looking at the question again, I think that someone could very easily put together a well-cited answer to the final sentence: "Is there a scientific case for limited, situation-specific hunting, or should all forms of it be discouraged?"

Not supported by "science," but supported by logic.  The bottom line is this:  the rangers were GOING TO KILLER THE RHINO ANYWAY.  The older male rhino was aggressive and actually killing other rhinos.  So, we have three scenarios:

Leave the rhino, letting it kill several more rhinos.
Have a park ranger kill the aggressive rhino (so that one rhino dies instead of many), which costs money.
Kill the aggressive rhino (so that one rhino dies instead of many), but auction away the rights to someone willing to spend big money, which will go toward paying the park staff to protect the young rhinos that remain.

There are economic arguments in favor of this practice [1].  The idea of culling individuals to either maintain or increase a population is also derived from the idea of "Compensatory Mortality" and has been demonstrated for a variety of ungulates [2][3][4][5][6].
I think the major flaw of any argument against this practice is the assumption that the rhino would not have been killed if there hadn't been an auction... The rhino was already on death row.  They marked it for culling because they wanted to preserve the maximum number of living, breedable rhinos...  It was only a matter of how to go about doing it, and I think they made the right choice by raising funds.
P.S.  I don't hunt, and I love animals.  In fact, I was a little bummed about this story when I heard about it, but once I learned that the rhino was going to be killed anyway, I realized it's the best, most logical answer available.
P.P.S.  Check out the Radio-Lab about this story [7].  They site that rhino populations rebounded following the creation of hunting ranches, because it gave a monetary value to the animals on ranchers' land, and they wanted to maintain that resource (by creating a breeding population).

[1] Lindsey, P.A., Rouletb,P.A.,  Romañach,S.S. 2007. Economic and conservation significance of the trophy hunting industry in sub-Saharan Africa.  Biological Conservation.  Volume 134, Issue 4.  Pages 455–469
[2] Staines, B. W. 1978. The dynamics and performance of a
declining population of red deer (Cervus elaphus). Journal of
Zoology 184:403–419.
[3] Burnham, K. P., and D. R. Anderson. 1984. Tests of
compensatory vs. additive hypothesis of mortality in
mallards. Ecology 65:105–112.
[4] Peek, J. M. 1986. A review of wildlife management. PrenticeHall,
Englewood Cliffs, New Jersey, USA.
[5] Bartmann, R. M., G. C. White, and L. H. Carpenter. 1992.
Compensatory mortality in a Colorado mule deer population.
Wildlife Monographs 121:1–39.
[6] White, G. C., and R. M. Bartmann. 1998. Effect of density
reduction on overwinter survival of free-ranging mule deer
fawns. Journal of Wildlife Management 62:214–225.
[7] Radiolab. (2015, September  07). The Rhino Hunter [Sound recording]. Retrieved from WNYC Radio website: https://www.wnyc.org/widgets/ondemand_player/radiolab/#file=%2Faudio%2Fxspf%2F529748%2F

Yes it is.  Besides Dr. Knights article which is very focused on the issue and describes numerous benefits, there are other sources of research that show this can be good not only for the animals but also the community.  And specifically that this has worked in Namibia (where the black rhino was hunted) extremely well.
Namibia has encouraged communities to see their local animals as resources to be protected and that they can profit from.  In cases of endangered species, the federal goverment abides by CITES and only allows so many to be killed. Other than that limitation communities are allowed to profit from their local animals both from trophy hunts but also tourism.  This has led to a reintroduction of many of these animals (endangered and not) onto private lands.  The survival and thrival of these animals is now an economic concern to the communities and land holders, and are protected as such.  This has worked for the recovery of many animals in Namibia.  In summary, the selling of a license to hunt one black rhino brings big profits to the community and therefore encourage the people to protect these resources.
The CITES articles are also a good resource when looking at this.  It's very clear in the resolutions to allow quotas for endangered animals that it is not harming the population.
And one other paper, though it's behind a paywall, describes how South Africa's white rhino population went from fewer than 100 to over 11,000 as privatization and legal hunting were legalized.
As a side note, the wildlife conservation department where I live receives almost half its funding from hunting licenses.  Since it has been in operation the deer population has gone from nearly wiped out in the state to over half a million animals.
Flocken's arguments are based on fact but are really targeted at examples of bad wildlife management rather than against the practice of conservation hunting.  There is some concern that allowing the legal killing of any endangered animals will lead to more poaching, but I haven't seen any evidence in the literature of that.


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Primers for human tissue?
If I wanted to examine human tissue samples, such as hair, blood, fingernails, etc, for their DNA, what primers would I use for the amplification of the DNA when extracted(PCR)?
edit: To look at the STR in the human genome based off of the FBI's CODIS system http://en.wikipedia.org/wiki/Combined_DNA_Index_System
from wikipedia:
"CODIS identifies genetic markers at 13 STR loci, plus Amelogenin (AMEL) to determine sex.
CSF1PO
D3S1358
D5S818
D7S820
D8S1179
D13S317
D16S539
D18S51
D21S11
FGA
THO1
TPOX
vWA

"
I read something about CODIS, but I don't know too much about it, if any one could give me some specifics that would be helpful.

The human genome is 3 billion letters long.  You aren't going to look at all of that, are you?  You have to know what you want to look at.  Are you just trying to examine the microsatillites that are used in DNA fingerprinting?

@swbarnes2      Sorry I was not thinking, I want to look at a microsatillite area, a subset i believe is called STR(single tandem repeats), since they have been used before in identification historically?

Saying that you want to look at the STR is still pretty broad.

@Chris          I guess I want to do the same type of identification that the FBI does with its CODIS system

The References and External Links sections of the Wikipedia article in your question contain a great deal of relevant information to get you started. There is a link to the FBI's CODIS and NDIS (National DNA Index System) Fact Sheet, which contains a lot of relevant information, including part numbers for validated kits from several manufacturers. DOI numbers for some journal articles are given in the Wikipedia article as well, wherein you may be able to find specific primer sequences or references for them. Finally, there is a link to the main CODIS page on FBI.gov, which contains an abundance of useful information, including the NDIS operational procedures manual.
You just need to look to find what you seek.

Extracting genomic DNA and PCR are different processes. Extracting genomic DNA means that you get all the DNA sequences from human genome. Using extracted DNA, you can amplify a specific region from the whole genomic sequence.
A primer set is usually set at the both ends of a sequence you want to amplify the sequence. In your case, you the region highlighted in yellow in the figure "CODIS markers" of the wiki would be amplified.
Different people may set primers differently even if they want to amplify the same region; however, in this case, primer sequences are already determined to get consistent results. If you would like to know the actual sequences that FBI is using, you (or someone or I) have to search to find them.

By the way, some protocols may skip the extraction process--taking several micro litters of buffer-suspension of samples or something like this. It may depend on whether  the PCR enzyme can overcome inhibitory effects of crude DNA solutions to amplify fragments.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Can nociceptors die because of too much mechanical stress?
In martial art people hit their body (e.g., with small bean bags) to become more insensitive to pain. Can the sensory neurons die during this procedure? I think this is just an urban legend. Instead, I think the skin receptors desensitize, but they don't degenerate by the constant mechanical stress. However, I cannot find any research in the topic.

As far as I know, adaptation of peripheral receptors, including pain receptors, is transient (Giniatullin & Nistri, 2013)
Instead, my educated guess is that the increase in subjective pain threshold plays an important role. Pain thresholds differ between the sexes (Chesterton et al., 2003), and depend on disease and physical status (Kosak et al., 1996). Repeated exposure to painful stimuli hardens one mentally (I have practiced martial arts for two decades ).
Morever, there is an interesting answer on Martial Arts SE on the question How should I expect my fist to change over time from punching? Here it is shown that extensive training stimulates the growth of additional skin and bone. Extra skin (calluses) may dampen the impact of painful pressure stimuli.
References
- Chesterton et al., pain (2003); 101(3): 259–66
- Giniatullin & Nistri, Front Cell Neurosci (2013); 7(245): 1-9
- Kosak et al., pain (1996); 64(3): 415–23

Ok. I can accept this. Btw. the technique I referred is called as "bone hardening". I have found a lot of interesting articles about bone remodeling. It appears to depend on mechanoreceptors. http://www.researchgate.net/publication/239942205_Osteocytes_are_not_only_mechanoreceptive_cells http://www.bme.sunysb.edu/people/faculty/documents/2012-gene-mechanotransduction.pdf http://www.sciencedirect.com/science/article/pii/S1063458412000192 http://link.springer.com/article/10.1007/s00018-005-5175-3

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Tree identification from dried branch
I found a very interesting branch last week, and have been trying to identify it but cannot seem to find the answer. If anyone has any suggestion, I would be grateful.
I found it near the forest, around WA area.
Here's some picture:

I just reviewed an edit which seemed to be updating the original answer, but was not by the original poster. If it is actually the same person, I would recommend you recover your password

This looks like dried cholla cactus, although it will be hard to determine the species. It is sold commonly for fishtanks, so might even be found in places where it does not grow naturally if someone cleaned out their fish tank.

EDIT by Ilan: on this image you can clearly see that the tree identified right:


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Is there a protocol for freezing and thawing Bacillus subtilis cells?
There is a book that says to store Bacillus spores in 50% glycerol at -70 degrees Celsius (doesn't mention if the 50% is final concentration or not). But from what I know, the cells themselves can be stored in any % glycerol as long as the final glycerol concentration is 15% (v/v) at -80 degrees Celsius.
Is there a difference between preserving spores and cells? Because the book said to preserve the cells at a certain glycerol concentration and the spores at a different glycerol concentration.
Also, say I scrape some B. subtilis out from the cryovial for reuse, and they are frozen. Do I wait for the scraped cells to thaw and then plate them, or plate them while they are still frozen?
And if I want to sporulate these cells, should I recover these frozen cells by plating and incubating overnight, or can I just drop them directly into the sporulation medium? I want to get the details down properly.

Welcome to Biology! You wish to store B stubtilis and be able to grow them again later, or to what purpose are you asking this question? Also, why do you think a standard glycerol stocking procedure for E. coli will not work for you? Background info helps folks to answer your question.

I advise you to edit your original question and add these details

Thanks for the edits. I just added a few spaces here and there

This is just anecdotal and I don't know the best method, but I used to store B. subtilis cells in 50% glycerol at -80C. For protein production, I'd thaw the stock completely, plate them to obtain log phase cells and then inoculate the growth medium. Worked every time.

While I have never done bacterial stock cultures from spores, I don't think it is necessary, as the standard procedure for making bacterial stocks should work without problems.
For that you grow your bacteria in liquid culture until you reach the late log phase (so you have a lot of bacteria in your media), take 1 ml of the culture, mix it with 100% glycerol to reach a final glycerol concentration of 50% and then freeze it a -80°C. At this you can store it for long times (probably not indefinitely but for years is possible).
When you want bring your cultures back to life, take the tube and either use an inocculation loop or a pipette tip to scrape a bit of the frozen culture and plate it on an appropriate agar plate. If you want to scale up, pick one colony from the plate into liquid media.
Since glycerol is a pain to pipette (and can also have sterility problems), I have switched over to DMSO as a cryo-protective agent for bacterial cultures as well. Simply add 15% (end concentration) DMSO into the cryo vials (so 150ul DMSO to 850 of culture), mix and then freeze the cells. In my experience this works as good as glycerol.

+1 - just out of philosophical curiosity, you say When you want bring your cultures back to life; do you regard your cells as dead at -80°C?

At least they are not growing and doing metabolism. I would say dead, resting fits probably better.


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How pronounced is the difference if we would change the running direction for runners?
I was jogging when I asked myself this question:
In running contests the standard running direction is counterclockwise; I also believe to remember that the regulation is very old (right back to the Greeks and Romans). I suppose the reason is that most people have a stronger dominant right leg and running counterclockwise feels more natural.
Now there are people who are "left-legged": They have a stronger and dominant left leg. What I ask is: How would the times change overall if we revert the direction and let the runners run clockwise ? Has someone experimented with it ? Is the effect discernible or even decisive ? Would left-legged people get an advantage ?

I'm not a track runner, but surely even on track there must be more to it than a dominant leg vs a non-dominant leg! I would imagine the difference is minuscule when compared to training regime and the on-the-day morale of the racer. Even small things like pre-race diet and windspeed will affect the racers much more I would have thought. I'm interested to see if a sports-scientist can provide an answer that says otherwise!

I know that if you take a former racehorse and try to make them go the other way around the ring, they are confused. But it is necessary to exercise them in a balanced way. (And to have a useful riding horse.) I imagine human runners having nightmares of having to go the wrong way around the track!

Been a sprinter for 12 years, so from that perspective, I don't think it would matter. The angle that you take when turning is not drastic enough to have a musculoskeletal difference; step height differs only a few inches. Additionally, turns never account for more than 50% of a race (barring a couple distance events, where turns act much more like straightaways anyway due to the lessened speed), so a bigger imbalance would be disadvantageous for straight sprinting. In practice, I think it would take a little bit to get used to, but not more than a year.

Could you actually test it ? Run 800m (to see if it makes actually a difference) two times continously over two weeks (if you have holiday), switching the directions (1. day counterclock clock 2.day clock counterclock 3. counterclock clock) every day to level out any order influence and look if the times are equal. In the first days a difference is to be expected because you are unused to it, but if your assumption is correct after two weeks the difference should be neglible.

I could do this, but as I am a sprinter, generally the longest that I run is around 150m. If I run 800m, it would increase the amount of turns taken, but it would be very slow. As your original question pertains to competition, I'm not sure that that speed would be relevant to your line of questioning. Additionally, I have no turn bias, since my event, 100m hurdles, doesn't include turns, so I think that the times would be pretty similar even without taking an average over a longer period of time.


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Why is it difficult to bend the waist while keeping the knees straight?
It's easy to keep your legs straight when you're standing up or laying flat on your back, but as soon as you try to sit up or bend down, you need to bend your knees as well as your waist.  (Try it.  Lay down flat on the floor, then try to sit up straight while keeping the backs of your knees pressed against the ground.  You'll have trouble long before you reach 90 degrees.)
Why is this?

First off, I would be careful generalizing people's experiences with this exercise (..."Try it...You'll have trouble long before you reach 90 degrees"...):

Source: Yoga Tune Up
The muscles you are feeling at 90o, and the lady pictured above perhaps not even at 180o are the hamstrings. They run along the back of your thigh, attaching at both the hip and the knee. They flex the knee and extend (straighten) the hips.

Source: Precision Nutrition
When you do the exercise you are describing, the pelvis starts pulling on the hamstrings from the top because your knees are staying in place. Bending the knees releases the stretch.


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Are there any papers arguing against vaccination in French?
Disclaimer: This question is NOT about challenging the safety or efficacy of vaccines. It is only asking for tips on providing credible references that may show harmful effects of vaccination, if any.
In my French class, we were asked to debate an issue in current events. My topic is vaccines in children or adults.
The challenging part is that I was assigned to argue against vaccination, and I have to back up my arguments with credible sources (not blogs) that are in French. Hopefully some of you could point me towards some links to articles or research papers in French.
Please avoid discussion on safety and efficacy of vaccines, including local and global policies on their use. I just need help with this topic for my French class

What about looking into positive studies and say that all distributions have negative-side tails that cause death etc. In real science there are studies like "X is good for you", only "in p% cases X helps to increase Z by q%". Take (1-p)% cases and use that as an argument

*there are no studies like X is good for you

Out of curiosity, did you pick this topic or did your teacher?

Strangely, it seems that all of the debates about science aren't actually based in science at all. Vaccines, evolution, global warming, etc…

Maybe instead of a direct approach you can find arguments on why death by disease isn't so bad after all?  But seriously, you're not going to find much in biology; you might be better off looking for non-scientific arguments.  For example, some religions view disease as an expression of divine will and discourage medical treatment.

I guess you can find interesting material following the links in this article: http://rougeole-epidemiologie.overblog.com/2015/05/vaccin-dt-polio-faut-il-signer-la-petition-joyeux-ipsn.html

I'm voting to close this question as off-topic because it asks evidence for a wrong claim. There are no evidences yet for vaccines having bad effects. This question is also likely to attract anti-vaccination supporters who may claim this post as a support for their cause.

@WYSIWYG so when people get disease after&due to vaccination it is OK? science is about measuring real effects, not saying that something is bad or good.

@WYSIWYG - asking for references for any claim should be on-topic. Whether it has proven correct or incorrect. Stuff being considered correct now is proven incorrect tomorrow. Isn't that science? Moreover, the Wakefield study  is an important study, as it stands example for total non-sense making it into one of the most respected journals worldwide.

@aandreev and AliceD I am not questioning the scientific process. I am just saying that the way the question is worded, it is likely to get into controversies. We can always say no it doesn't happen like that as per the research till now and many of you have said that. Questions about specific formulations of drugs/vaccines are fine. This post needs to be protected if not closed and even then there may be people with enough rep who will come up with theories. We can't keep moderating it forever.

You could find credible sources arguing against specific vaccines but not against vaccination in general. That's like looking for credible sources arguing that the earth is flat.

@terdon: That would actually be my strategy: find many credible sources arguing against several specific vaccinations, and paint the pro-vaccination crowd as zealots trying to stuff vaccines down everybody's veins.

Not an answer, but just a hint -- I know that there's an angle that condemns vaccines because they (some of them) contain aluminium compounds, which in turn is claimed to cause Alzheimer's disease. Highly controversial and certainly not my POV, but perhaps this provides you with a couple more keywords.

can we probably add a disclaimer that question is not for discussing vaccines, but for providing credible references that show harmful effects of vaccination?

There is no scientific dispute that modern vaccines are brilliant. The anti-vaxxers rely only on pseudo scientific fear mongering and ludicrous, offensive campaigns to further their profiteering. The only (off topic) debate to be had is whether or not one has the right to refuse vaccination for non-medical reasons and (rather selfishly in my opinion) rely on herd immunity, which is very risky for the individual.

I wish you good luck, as 99.99% of the anecdotal claims out there that conclude vaccination is bad are based on unfounded rumors.
Note that much of the negative public opinion is based on a fraudulent (and retracted) paper by Wakefield in The Lancet (1998). Unfortunately for you, however, it is in English.
My French is a bit rusty, but if you go to Google Scholar and type in a search term like vaccination results in autism (les résultats de la vaccination dans l'autisme) or Wakefield vaccination autisme something might pop up in French that advocates against vaccination.

I do wonder if Wakefield regrets the damage he has done. 5% of children under 7 in California are not vaccinated. Measles is a preventable condition! One I've never had to endure!

The Wakefield study has collapsed as fraud, and there are no credible sources that make persuasive scientific arguments against being vaccinated in today's world -- not even in French.

did you mean "in English"?

@MarchHo I meant "in French". Apparently certain types of humor fail to translate well to the written word.

You will not find good, credible sources arguing against vaccination. However, spewing nonsense is not necessary for winning your debate. You can collect good, credible sources arguing against specific vaccinations and use them to paint the opposing side as pro-vaccination zealots who unquestioningly want to stuff vaccines down everybody's veins.
Vaccines, like other treatments, have to be approved by health authorities, and therefore, the possible side effects are being studied in clinical trials. All you have to do is find a few cases where there side effects were a bit more severe than anticipated.
A good start for your research could therefore be publications about the risks of vaccination. On Google Scholar, "risques vaccination" brings up hits like Risk-Benefit assessment of hepatitis B vaccination in France (in French) that can give you a good basis for gathering material against vaccination.

@AliceD: I reverted some of your changes to keep the original meaning of my post. If you feel the first paragraph remains problematic, I'd rather take it out completely.

If you don't mind - I've taken it out. As it was previously, it could have lead to anti-vaccination people (ab)using your answer in favor of their stand point. OPs question is kind of problematic in that it may lead to endless debate

@AliceD: I tried another version that states why am trying to give the OP what he needs rather than what he seems to be asking for.

The only angle I can think of that isn't "Haha, I can't believe these people are allowed to vote" is that the enemy we know is better than the enemy we do not know.
I see no reason why the classic argument of selection pressure doesn't apply. (See Warfrin(spelling?) resistance in rats, the resistant rats required more vitamin-k, thus more time out in the sun, so in a warfrin free environment are at a disadvantage, but thrive in an environment with warfrin)
Unfortunately (fortunately) evidence doesn't really support that, in fact we have eradicated several diseases already entirely and nothing replaced them.
(Long comment sorry)
By the way! Do tell us some of the arguments that come up!

I don't think the resistance angle helps much here, but if one wanted to pursue it, this question is relevant: http://biology.stackexchange.com/questions/30166/why-vaccines-do-not-cause-bacterial-resistance/

@Corvus indeed, no doctor is going to say "Let them die!" (side note: "overprescription of antibiotics" is a hot topic in the UK because bacterial resistance is actually becoming a problem! However that's not vaccination)

Also @Corvus thanks for that link, I was wondering while I was writing!


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A question on glycolysis

In the first step of glycolysis, the glucose ring is phosphorylated.
  Phosphorylation is the process of adding a phosphate group to a molecule derived from ATP. As a result, at this point in glycolysis,
  1 molecule of ATP has been consumed.

Is it the phosphate group, or the molecule, that is derived from ATP ?
http://www.sparknotes.com/biology/cellrespiration/glycolysis/section1.rhtml

Welcome to Biology! What is the molecule in your concluding question Is it the phosphate group, or the molecule, that is derived from ATP ??

This is an issue of grammar; clauses should be used properly :P The sentence should be  "Phosphorylation is the process of adding a phosphate group derived from ATP, to a molecule."

@WYSIWYG - absolutely positively agreed - it wasn't critique, just a request to clarify the question. The answer below is great and I retracted my close vote.

See this post too an addition to Koustav's answer, which pretty much summarizes the phenomenon.

The question is a bit unclear, it should be reframed as suggested by AliceD. To simply answer the question,
Glucose is the substrate, and in the first step it is converted to Glucose-6-phosphate.
Only the Phosphate group is added which originates from ATP, your notes also are a bit misleading because it tends to suggest that Hydrogen is released, which is not the case, the phostphate group in ATP loses an OH and Glucose loses an H in an SN2 reaction giving rise to Water in the process.
Always remember that ATP is categorized as an energy donor which drives chemical reactions in your body by breaking chemical bonds. ATP or Adenosine Triphosphate has three phosphate groups. The last Phosphate in ATP produces the highest amount of energy in any given chemical reaction where ATP is involved.
This is an ATP molecule.

The first P that you see is the Phosphate which gets released, and the ring that you see is a five member ring called a ribose sugar, while glucose is a six member ring.

"Is it the phosphate group, or the molecule, that is derived from ATP ?"
The Phosphate group is derived from the ATP molecule (thus why Adenosine triphosphate) NOT from the molecule it would be attaching the phosphate group to.
Phosphorylation - The process of taking this phosphate group and adding it to another molecule in the energy chain.
I hope this clears things up.


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Comparison of gene expression time series in vitro and in vivo
I have to analyse two datasets consisting of time-series measurements of gene expression. One set are in vivo data from the expression profiles obtained between a few days before birth to several days post-partum. The second data set was obtained in a C2C12 cell line, where t = 0 was defined as the day in which 100% confluence was reached.
Is there an optimal way to align the two time series? Simply aligning the two series using the two t= 0 samples as starting point seems arbitrary.

Welcome to Biology! I attempted to clarify the question. Feel free to roll back if it doesn't reflect your question anymore.

I would start asking myself: does it make sense for the two series to be aligned? In other words, do you have any evidence that the events in the in vitro experiment may correspond to events in vivo? It would help if you describe you experiment in a bit more detail, (if possible, this may be sensitive information). Which species, what tissue, what experimental conditions, what is your scientific question.

Hi, yes, it is sensitive information... however thank you for the answer, I will try to find out if there is a best shift that globally maximises the correlation between pairs. If not everything will be traced back to up/down regulation...

This is a mesenchymal cell line that differentiates in vitro after reaching confluence (and serum deprivation). There are likely similar cells in the animals, but they might be a small percentage of the total number of cells. During differentiation in vitro you'd expect to see some genes going down and others going up over time. In the animals that signal would likely be swamped by tissue-specific genes from the dozens of tissues and hundreds of cell types.

Direct comparison of the course would be difficult between tissues and cultured cells. In stead of time scale, you might want to use markers.
For example, Kislinger et al. show the expression peak of SIX1 is 2 days after differentiation; SMAD3, 4 days. I am not a right person who can tell which markers are good, but I believe you could find more information by literature search.
http://www.mcponline.org/content/4/7/887.full


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How do I know which alleles the parents have?
I have the following assignment where I am to look at the "tree" (not sure the english word) and assign whether or not they can be autosomal dominant or recessive as well whether they can be X-linked recessive.

My way to try and complete this assignment is by drawing a punnet's square but I quickly run into some confusion. When I draw my square, I know that is I'm checking for autosomal dominant, then I would draw the mother as A'a, the A' denoting the sick dominant allele. What I'm not sure is this: Can't I also draw her as A'A'? That would also mean she would be autosomal dominant but with 2 sick alleles. What about the father? Do I draw him as Aa, aa or AA? I'm a bit confused here!

Let's go step my step here.
Going by your notation I'll call the square as Male and Circle as female.
So from this information I can confidently say that you disease is not X linked dominant.
Why?
Because Females carry XX, that would mean to be X linked dominant she had to be X'X' for the disease allele to manifest it's phenotype. But if it were X'X, it would lead to a loss in fitness. And since the Male is normal and XY he does not carry the disease which tells us that the disease is definitely not X linked dominant.
Therefore in a cross of X'X' and XY you get individuals X'X and X'Y in the ratio 1:1
Coming to AD Autosomal Dominant may mean A'A' as the disease allele is present in homozygous condition. A heterozygous condition would lead to loss in fitness, not necessarily a disease.
A Father may be AA or AA'
so this cross would give you individuals

AA' for A'A' x AA
A'A A'A' for AA' x A'A'

so in this case you always get the disease in autosomal dominant, what remains is recessive.
AA or AA' Father x A'A' Mother
Products AA' for AA x A'A'
or AA' and A'A' for AA' x A'A'
which tells us that the disease is actually Autosomal recessive on the mother.
The father's genotype for the allele is AA or homozygous dominant
and the disease is autosomal recessive for the disease in the mother.

Why can the father not be Aa or aa?

the Aa that you are talking about is the AA' condition and the aa or A'A' cannot exist because in the diagram the father is a normal individual. So he can be either homozygous dominant for the wild type fit allele and heterozygous leading to a loss in fitness.

I don't think loss of fitness is relevant in this situation. In any case, there is nothing in the question to suggest that the disease is incompletely dominant and would result in a loss of fitness in a heterozygote


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In protein-protein interactions what is the difference between a binding site and an interface?
I see binding site and interface used almost interchangeably in the literature, but I'm not sure if it is exactly the same thing or not - what is the difference?

By PPI do you mean protein-protein interactions? I see binding site more in the context of transcription factor binding sites (i.e. protein-DNA interactions; I may be biased here by my own experience though). It would help if you quote examples from the literature.

We can't give you an answer without more context. Neither of those terms is really standard, so what they mean will depend on context. Could you give some examples?

A protein-protein interaction (PPI) binding site is a type of interface. If it has been established that the interface is a PPI binding site, then the terms can from that point forward be used interchangeably. But the word "interface" is very generic and does not have any specific scientific meaning so the nature of the interface must be defined or else the term is fairly meaningless.

Just thought I'd add a dictionary entry. As you said, the term interface doesn't have a special meaning. http://dictionary.reference.com/browse/interface


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Insect Identification - Black Cicada

I came across a black cicada in northwest Missouri last week (May 2015). I am only familiar with brown cicadas. What makes this black one different? Is it a different species, or do the brown cicadas change color at some point in adulthood?

A little digging on wikipedia seems to have answered my question. This picture of a 17 year cicada, Magicicada septendecim is pretty close to what I saw.

Furthermore, this seems to match the time and place, as the Kansas Brood of 17 year cicadas is scheduled to emerge this year and should appear in the Missouri-Kansas area. It also explains why I'm not familiar with these cicadas, 17 years ago I wasn't paying attention to them.

It is a 17-year periodical cicada, but you got the species wrong. See my answer for evidence for another of the three 17-year species!

 Short answer
This is Magicicada septendecula, one of the three species of 17-year cicada (colloquially, "17 year locust") native to the Eastern United states.

 Credit: C. Simon, Fontaine et al (2007)1
 Long answer
Periodical cicadas are the only group of dark-bodied cicadas with bright red eyes and orange/red-tinted wings (at least I don't know of any others). These cicadas, all of which are in the genus Magicicada, can be divided into 13-year and 17-year cicadas, each with multiple potential species:

17-year species: M. septendecim, M. cassinii, M. septendecula

13-year species: M. tredecim, M. neotredecim, M. tredecassini, M. tredecula

These species tend to form mixed-species cohorts called broods in which all members of a brood synchronously emerge at the same time (every 13 or 17 years). There are 23 broods found in the US that emerge in different years, and the broods are identified by Roman numerals (I-XXIII). [Source: Scientific American]

You can read more about periodical cicada broods on Wikipedia, and you can see range maps of both 13- and 17-year species here (from here) and all together in one map here: Liebhold et al (2013)2.

Importantly, only 3 broods are found anywhere in Missouri: one 17-year brood (Brood IV, the Kansan Brood) and two 13-year broods (Brood XIX, the Great southern Brood, and Brood XXIII, the Mississippi Valley Brood).

 Modified from: Liebhold et al (2013)

Brood XIX is by far the biggest brood in terms of coverage in Missouri, but these 13-year cicadas last emerged in 2011 (not 2015).

The other two broods both emerged in 2015, when the OP photographed the specimen in question, but only Brood IV is found in Northwest Missouri. So we can safely narrow the potential species down to just one of the three 17-year cicadas.

However, Brood IV does contain all 3 species of 17-year cicadas, so we'll have to keep digging...

CicadaMania.com provides the following tips for IDing these fairly similar looking species:

M. cassinii: Smaller (2.4-2.7 cm long) with black ventral abdomen

M. septendecula: smaller (similar to M. cassinii) with orange/yellow stripes on ventral abdomen

M. septendecim: larger (2.7-3.0 cm long3) with orange/yellow stripes on ventral abdomen.

We don't have the greatest view of the abdomen and we have no definitive reference for size (at least to differentiate a couple of mm), so this makes ID a bit more difficult.
However, it does appear that there are bands of orange striping seen on the lateral sides of the abdomen in the OP's image, suggesting we can rule out M. cassinii.

Lucky for us, there is one additional way to identify between the other two species. Again from CicadaMania.com:

The pronotal extension is an extension of the pronotum that lies between the Magicicada’s eye and its wing (outlined in green in the photo below). M. septendecim have orange coloring in that area, which gives us a key way to visually distinguish them from M. septendecula.

 Orange pronatal extension of M. septendecim ; Source: Cicada Mania
Sure enough, the OP's specimen does not have an orange pronatal extension...

...suggesting that the OP's species is M. septendecula!
Also, FYI: cicada adults do not change colors. The 5th molt prior to the adult stage,  which leaves behind the familiar exuviae clinging to a tree trunk, is the final anatomical change cicadas undergo in their life cycle. [See here for more]

Citations:
 1. Fontaine, K.M., Cooley, J.R. and Simon, C., 2007. Evidence for paternal leakage in hybrid periodical cicadas (Hemiptera: Magicicada spp.). PloS one, 2(9), p.e892.
 2. Lloyd, M. and Dybas, H.S., 1966. The periodical cicada problem. I. Population ecology. Evolution, 20(2), pp.133-149.
 3. Evans, A.V., 2007. National Wildlife Federation field guide to insects and spiders & related species of North America. Sterling Publishing Company.

It's difficult to be sure without seeing the specimen more from the side (or ventrally), but the lack of visible orange color between the eye and the wing articulation suggests that it could be one of two other 17-year cicada species, Magicicada cassinii or M. septedecula (all three species emerge synchronously; their different songs isolate them reproductively).  M. septendecim has the lateral orange color.  M. cassinii is the most common of the three species in the 17-year brood that came out in 2015.
Cicadas do not change much in appearance during their short adult lives.

Welcome and thanks for your answer.By convention we ask for sources, a verifying image of your ID and additional background info such as the distribution and habitat of your species ID. As of now, it's more of a question comment.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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How does a virus reach its host, it is always passive?
We know that viruses are non motile and cannot metabolise, and that it enters the host cells via binding to the receptors. But how exactly it reaches the host
(that is, how it go from the transmission medium (e.g. the aerosols) to actually make contact with the cells in the host)
If it rely on simply diffusion to bump into the host cells' receptors, what makes the odds high enough so that such proliferation strategy is efficient enough to ensure the virus to multiply and proliferate?
In addition, once it has released its DNA into the cell, what helps the DNA to reach the nucleus and not drifting randomly within the cell for a long time, that is, is there exist mechanisms or transportation pathways that actually guide the DNA from the perimeter of the cell through the cytoplasm in the middle and towards the area where the nucleus lie?

Different viruses have different modes of spreading- some are water borne, some are transported via aerosols, some are sexually transmitted etc. Your question is a little broad. You should narrow it down.

A textbook could be written to answer your last question--agree with WYSIWYG that you should narrow your question

it is called statistics. Virus or DNA do drift around randomly, but a) there are a lot of DNA/viral particles and b) when virus binds, it stays (so as DNA). And waiting time is not too high

@WYSIWYG I have narrowed down the question by elaborating that I am interested in the pathway on how the viral DNA move from the perimeter of the cell through the cytoplasm to the nucleus, and, how once the virus reach the host via aerosol etc. how they actually made contact with the cell to enter them
.At the time of the edit, it seems aandreev might have provided an/the explanation and Chris have provide a more detailed explanation

There are a number of different ways to spread a viral infection. Some viruses sit on surfaces (or infected persons) "waiting" for someone to touch and take them up, this is called smear infection. Other viruses are airborn inside of small droplets distributed by coughing or sneezing. These are inhaled and can then cause a new infection. Other viruses are transmitted through our body fluids (blood, semen) and either need a wound or can be transmitted sexually (for example Herpes or HIV). Other viruses are transmitted by animals which bite humans (Dengue and rabies would be examples here). Have a look into the Wikipedia for more details and examples.
Additionally viruses are produced in vast numbers by their hosts with most viral particles never reaching a new host. This strategy helps a lot to transmit further.s
For entering the nucleus (which is an obstacle) the viruses use the nuclear pore complex (NPC). Depending on what virus tries to enter the nucleus, different strategies are used. Some viruses are too big and release their DNA through the NPC into the nucleus, while others can pass through and some get stuck inside and release their DNA/RNA at this point. A last group uses the time during mitosis when there is no nucleus. See this figure (from here)
and also the references below:

References:

Virus strategies for passing the nuclear envelope barrier.
How viruses access the nucleus.
Viruses challenge selectivity barrier of nuclear pores.

Some virus DNA or RNA might wait cell division to get into nuclei. For example retrovirus genome is not integrated to the genome of the host cell until cells are divided. However, lentivirus does not need to wait for cell division, because one of proteins in lentivirus binding to virus RNA genome has a nuclear transport signal.


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Looking for good reference book in molecular biology
I am starting to work in molecular biology/ molecular genetic and I am looking for a really good book containing the main concepts and mostly the more recent techniques.
I would be interested in a book that has also protocol examples and examples on how to apply the different techniques.
My focus is on bacteria and fungi.
Any suggestion?

Usually questions asking for book recommendations are considered 'opinion-based' if specific details are not mentioned.

Molecular biology by R.F. Weaver is an excellent book. Concepts are very much clear-cut.

These always have a place at my library
HF Lodish, Berk, Arnold, and S. Lawrence Zipursky. Molecular cell biology. Vol. 4. New York: WH Freeman, 2000.
Alberts, Bruce, et al. "Molecular biology of the cell." Garland Science, New York 4 (2002)(the first few editions had James Watson himself as the editor)
Brown, Terence A. Genomes. Garland science, 2006.
For basics. I would recommend staring with Brown, and going on to Bruce Alberts and then Lodish. That's the way I learnt it.
For a really nice book with pictures (yes, we all like those) you might want to look into Lippincotts illustrated reviews (biochemistry, cell and molecular biology and the like). They are also quite good.
For a specific emphasis on techniques, I'd  recommend this:
Sambrook, Joseph, Edward F. Fritsch, and Tom Maniatis. Molecular cloning. Vol. 1. No. 7.58. New York: Cold spring harbor laboratory press, 1989.
(You can read the contents here http://www.molecularcloning.com/)

Thank you very much. I am actually a PhD. So I need to refresh my knowledge and get update with more recent molecular/genetic techniques

@efrem Updated my answer with a bookset on cloning.

If it's techniques you are interested in, Weaver, now in its 5th edition, has (had) a strong emphasis on recent experiments from the literature, and he is constantly updating the book. We used  to use it for a variety of courses.

Brock's Microbiology is a great book when you are interested in unicellular organisms.
From the publishers's website (Pearson):

The authoritative #1 textbook for introductory majors microbiology, Brock Biology of Microorganisms continues to set the standard [...]. This book for biology, microbiology, and other science majors balances cutting edge research with the concepts essential for understanding the field of microbiology, including strong coverage of ecology, evolution, and metabolism. The Fourteenth Edition [...] pay[s] particular attention to molecular biology and how the genomic revolution has changed and is changing the field.


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What is "theae folium"?
I wanted to buy black tea at a pharmacy and the pharmacist told me that russian tea is actually black tea so I bought it instead.It's made out of theae folium leaves and for some reason I can't find anything about that plant on the internet and I know that black tea is made out of camelia sinensis leaves, not theae folium.Can anyone tell me what is this plant and is it really russian tea (i found somewhere that russian tea is made from a different plant) and what is this "Russian" tea good for?

Judging by this image in wikipedia, I would say Theae folium is another name (probably a name in another language) for Camellia sinensis

It's Latin for "Tea leaf".

@CactusWoman, the answer is "tea leaf". Camellia sinensis is a flower and here  is just an example of tea. there are others theae folium, not related to this flower.

Camellia sinensis is the botanical name for the plant whose leaves are used for the beverage commonly known as tea in English (green tea, black tea, etc.).  The plant of course has a flower in the normal course of its growth (as well as leaves, seeds, roots, etc.)

If the labelling is correct, this should be Camellia sinensis, the plant that produces black tea, green tea, etc. (although not many things that are commonly referred to or marketed as herbal teas).
Thea is the original genus name given by Linnaeus to the species we now call Camellia sinensis.
There's an old pharmacy tradition of specialized latin terminology for plant medicines. These will indicate the plant and also often the plant part. In this tradition, plants are often indicated with different terminology than modern scientific names. Here's a 19th century pharmacy textbook (Parrish and Weigand) explaining why:

And here's the same source discussing the naming of plants parts (as CactusWoman mentions, in this case folium = leaf):

You still see this terminology around in some places (some European texts and occasionally translations of Traditional Chinese Medicine preparations), but it definitely has an 'old-fashioned' feel from the perspective of a botanist.

Parrish and Weigand 1884 A Treatise on Pharmacy

http://farm2.static.flickr.com/1434/5114191089_e95dd1f1c9.jpg is where I first encountered this form of antiquated nomenclature (in traditional Chinese medicine)


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Risks in bacterial phage therapy
I just finished reading J. Craig Venter's book Life at the Speed of Light: From the Double Helix to the Dawn of Digital Life. The book is a little over a year old now, and Venter has an optimistic outlook that bacteriophage therapy will become an effective alternative to gene therapy and viral immunotherapy. He mentioned that the JCVI (J. Craig Venter Institute) is working on such projects. Are other companies also researching, and has progress been made? What are the expected risks? How can rogue, harmful phage mutations be controlled? Can this type of therapy be applied to cancers?

Check out oncolytic viruses

Have you read the wiki page on phage therapy? This technology is only used for treating pathogenic bacterial infections, particularly those that do not respond well (or at all) to conventional antibiotics. It is not related to gene therapy or viral immunotherapy, aside from the fact that phages are viruses, so I'm not sure what "effective alternative" means, as the three are used for entirely different things. Google "gene therapy" and "viral immunotherapy" to learn more.

The Eliava Institute in Tiflis (Georgia (a country)) has been at it since the 1930`s. A US company sells a phageproduct for desinfection of meat.
The risk of Phagetherapy is there, if the phage is ill choosen or contaminated with other phage it could introduce pathogenic genes to the target or other bacteria.
If those risks are eliminated there is very little risk in phage therapy aside from the fact that it may not work at all. Phagetherapy is most useful in regions where bacteria are normally found, in other places the immunesystem will make short work of it.
The faster and cheaper sequencing gets the more effective phagetherapy will become. Since a "bad" bacteria can quickly be isolated and a proper "phage cocktail" can be prepared. If we get to the point that we can sequence the whole microbiom of a person then i bet that Phagetherapy will be a very normal thing.
To your cancer question, i think its rather hard to apply it to cancer therapy except if u are looking to combat the cancer with a Intracellular bacteria...but then again. How u get the phage to it.
A excellent read on this topic is the Book "the bacteriophages".

In Venter's book he does mention that Russia has been the most active in phage work. With oncocytes if we become skillful enough to genetically engineer phages to their most minor details, can't we just bypass any involvement of a bacterium and just have the phage directly target the cancer cell? Create an oncophage?

I would think that the best way to archive that is to use oncolytic (or a virus that marks the tumor cell for the immunesystem) viruses (mammalian). Phages no matter how cool they are, are specialised towards bacteria. First the phage must get into the human cell. Then it must replicate or inject genome. Then replicate in a orderly fashion and at last get out of the cell. The structure of bacteria and eukaryotic cells is way too different. But oncolytic viruses are a VERY hot topic currently and im sure they will lead the way. Since a designed virus is easy to patent. Even big companies Win:)

Can anyone provide citations or further reading for this?

You run the risk of the killed cells suddenly releasing huge quantities of cytokines. If this occurs you may cause spike in capillary permeability and basically create massive sepsis. The bacteria will have to be killed SLOWLY to prevent them spilling their contents into the circulatory system. But, I have always believed phages could be engineered to control certain infections like urosepsis. But, any phage therapy may be single use only. I used to inject them into rabbits to prepare antisera used in phage growth experiments, I guess that is one of the reasons phage therapy is out of the mainstream. http://www.nature.com/news/phage-therapy-gets-revitalized-1.15348


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What kind of memory is "keyboard/keypad memory"?
I work in IT and I have observed many people who cannot remember their iPhone passwords or computer passwords off the top of their head. However, if presented with a keyboard or a phone with a functioning keypad, they can instantly remember exactly what their password or passcode is.
I'm curious to know what this kind of memory is called. Since it's somewhat related to visuals, but not necessarily (you don't need to look at your keyboard to type out your password.)

I came back from a week-long holiday about a year ago, and tried to pay for my airport parking and go home, only to discover that the debit card PIN I'd been using for the past 12 years had completely vanished from my existence. My memory of it had gone and my muscle memory was no longer working. I couldn't explain why this was and, after resorting to a credit card that I only happened to have on me (with its PIN; don't do this!) due to exceptionally unlikely circumstances, finally got home and spent the next few days re-learning my debit PIN. A wholly bizarre experience.

Short answer
Motor memory
Background
A striking personal example of your account pictured in the question was my experience where I had to type in my PIN at the bank counter on a keypad. It turned out I entered it incorrectly several times in a row, despite the fact that I had used that PIN a zillion times on ATM machines. Luckily, the bank employee had seen this phenomenon many times before, and she explained to me that the standard computer keypads have a different numerical layout than ATM machines. So to type in my PIN correctly I had to do it under visual guidance - an awkward experience. It showed quite strikingly that I had been entering my bank PIN using motor memory.
Much of our motor behavior is learned - think of learning to walk, cycle or ice skate. To achieve motor learning, the central nervous system is believed to use internal models that predict the mechanical dynamics necessary to execute a task. In theory, the internal model is an association from a desired trajectory for the hand to a pattern of muscle movements. This map is basically unique for the objects that we have learned to interact with. Because we routinely use our hands to interact with a remarkably diverse variety of mechanical systems, the ability to learn and recall internal memories is thought to be a fundamental property of the motor system (Shadmehr & Brashers-Krug, 1997).
Reference
Shadmehr & Brashers-Krug, J Neurosci (1997); 17(1): 409-19


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What can cause a lump in the middle of the neck? (homework case study)
What can cause an erythematous, fluctuant, nontender mass in the middle of the neck?
Full Case Study: (Its the last of 6 cases and I just can't figure this one out,  because of all the possibilities, there is always something that doesn't line up.)
The 26-year-old man presented for evaluation of a neck mass and a right axillary mass. The patient, who came to the United States from Vietnam 6 1/2 years ago, noted  midline neck mass. The mass gradually increased in size. Approximately 3 weeks prior to admission, he noted a midline neck mass. These masses were incised and drained twice. Samples of purulent material were sent for routine bacterial culture at an outside hospital. The patient had lost 3 kg (ca. 7 lbs) in the 2 months prior to admission but denied fever. Travel history was notable for his having lived in Arizona for 6 years prior to moving to Boston.
On examination, he was afebrile. An erythematous , fluctuant, nontender mass (8cm x 6cm) was present in the midline of the neck. (Fig. 5.1)  (computed tomogram[CT] scan in fig. 5.2).The right axilla demonstrated incision sites that were draining and were tender to palpation. He had no adenopathy elsewhere. His (PPD) purified protein derivative skin test was reactive, and his chest x-ray was notable for apical scarring in the right lung.
Because of the positive PPD and apical scarring seen on the patient's chest x-ray, the clinical suspicion of cervical ________ was high, and the patient was begun on a four drug anti- _________________ regimen.
Several days after the neck mass was drained of several milliliters of purulent material for culture, a mold was found to grow on the blood agar plates in the routine bacteriology section of the microbiology laboratory. The mold was white (Fig. 5.3) and initially did not have any identifying characteristics when a lactophenol cotton blue preparation was examined under a phase-contrast microscope. It was subcultured at both room temperature and body temperature, and after subculture began to demonstrate the presence of  spores microscopically (Fig. 5.4) The identification was confirmed by using a commercially available genetic probe.

I this a personal medication question?

I've had a case study for a school project, and I've narrowed it down to a fungal infection, I just cant figure out what it is. It grows white on blood agar.

I've voted to close as personal medical/health. Even if it is not "personal" I feel that there is too little information to properly diagnose, and I'm afraid that answers to the question might be misunderstood or misused (as medical advice) by other persons visiting the site.

I would not consider it a personal medication question but more details are necessary to address the question based on general principles. Even the figures that are mentioned in the body of the post are not shown. The final question does not require the case history but the microbiological details are essential, which are missing. Please edit your question accordingly.

You ask for the fungus causing An erythematous , fluctuant, nontender mass (8cm x 6cm) was present in the midline of the neck.
On the brink of question closure I decided to do a quick search. Based on your descriptions, I found a possible culprit.
In the referenced paper they talk about a fungal Cryptococcosis infection causing, and I quote:

[A] fluctuant, non-tender mass, five by five cm. in the right costal vertebral angle which was not red or warm.

So this mass was found on the costal vertebral angle, but the remaining symptoms seem reminiscent of your case study. Fungi generally appear white when plated, as far as I know.
However, more information is likely necessary to confirm this genus and identify the species.

costal vertebral angle (CVA). Source: Pinterest
Reference
- Moore, J Invest Dermatol (1957); 28: 159–82

Why the downvote?

I am not sure who downvoted but I wonder how you could find the answer for a question that does not provide enough details for a reliable microbiological species identification.

@WYSIWYG: I made the answer more reserved.


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Sexually homologous traits
When papers refer to traits as being sexually homologous do they refer to traits which are:
a) present in both sexes but can be dimorphic (e.g. body size is sexually homologous because both sexes have a measurable trait which has the same criteria in either sex, but this is frequently dimorphic)
Or
b) present in both sexes and not different between the sexes
I have always thought it is a, but I'm now using the term in a paper and want to check. I would have thought the latter would be "homologous homomorphic traits" or something like that.
If an answer could have an example of the use(s) which make it obvious from published work that would be great!

By traits do you mean gross phenotypes (something that you can measure without using molecular techniques)?

yes @WYSIWYG ...

Innate immune response, vision (Not too sure. Will look for references)

@WYSIWYG I'm not looking for examples - im checking use of terminology :)

Without any doubts a), i.e. a trait present in both sexes but the phenotype can be different. Here an example.

Your first definition is correct: a homologous trait is one that can be mapped unambiguously between two samples. What establishes the homologous relationship depends, of course, on the trait or feature being mapped.
For example, one way sexually homologous traits can be identified is by tracing the physical development of a male vs. a female organism. If precursor x becomes y in a developed male and z in a developed female, then y and z can be referred to as homologues.


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Why don't phospholipid bilayers dissolve?
I just started learning about the structure and composition of cell's membrane and there is something that I fail to understand.
The membrane is composed of a phospholipid bilayer. The phospholipid has a polar, hydrophilic head and a nonpolar, hydrophobic tail. My question: Why doesn't the hydrophilic head dissolve in the extracellular fluid outside the cell? I suppose that the extracellular fluid is watery, so how come that the water-loving head doesn't interact with the water from the extracellular fluid?

We should first understand what happens when a substance dissolves. During dissolution water interacts with the solute molecule; if the strength of interaction between the molecule and water is higher than the strength of interaction among the solute molecules then the solute dissolves.
(Also have a look at this post).
Phospholipid is an amphipathic molecule — it has both hydrophobic and hydrophilic parts (this you understand very well). The hydrophobic part is a long chain of hydrocarbon (hence tail) whereas the hydrophilic part is a small but highly polar region (hence head). You should note that these parts are not disjoint but are covalently bonded.

Even though the hydrophilic part interacts with water (which helps the cell survive in an aqueous environment), the strength of covalent bond (between hydrophilic and hydrophobic regions) is very strong and cannot be broken by physical interaction with water.
The lipid bilayer (even a monolayer) stays together because the water cannot interact with hydrophobic parts but they interact with each other via a pseudo-interaction called hydrophobic interaction.
I call it a pseudo-interaction (not a standard usage) because there is not actual molecular interaction that stabilizes the system. Hydrophobic interaction happens via increase in entropy of the system. Read the wikipedia page for details.

Why do you say that hydrophobic interaction is a pseudo force ? Pseudo force has a very different meaning in physics.

@biogirl it is similar to the pseudo-force in physics. I did not have a better word for it so I called it pseudo force. But like the pseudo-force in physics hydrophobic interaction is not really an interaction and arises because of non-interaction of hydrophobic parts with water. Hydrophobic interaction basically allows an increase in entropy which finally brings down the free energy of the system.

@TomD By 'pseudo-force', I meant that there is no actual interaction between the solute and the solvent or between the solute molecules. There is no molecular interaction that would cause a reduction in enthalpy. The "interaction" is because of increase in entropy (not the loss of entropy).

@TomD So that is what happens to the solvent and that is what I said. Water makes a structured cage around the lipid molecule (low entropy; no enthalpic reduction because the lipid and water don't interact). When there is another lipid molecule they both come together and increase the net entropy of the system (lesser water cage compared to cage per molecule- think of it as surface area).

@TomD We are saying the same stuff. I said that increase in entropy stabilizes the system and you are saying that loss of entropy destabilizes the system.

The answer to your question is basically:
It is a bilayer. There are two layers of phospholipids, thus tucking the hydrophilic ends safely away from any extracellular and intracellular fluids. The whole surface of the bilayer is hydrophilic.

(Picture from here.)

The hydrophilic region of phospholipids is actually interacting with water or other hydrophilic molecules. At the same time hydrophobic region of phospholipids would be repelled from water because water is forming hydrogen-bond networks, which is a more stable state. You could imagine hydrophobic molecules in water would disturb the network. As a result the hydrophobic parts of phospholipids aggregate together and phospholidis would not come out into water not to expose the hydrophobic parts.


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Is there a consensus on the CaMV 35S minimal promoter sequence?
We have an algal enhancer element and a transcription factor that probably binds it. Basal expression of the enhancer element or full promoter driving luciferase in tobacco protoplast was extremely low. I heard this could be overcome by fusing it to a minimal 35S promoter fragment but I can't seem to find a clear sequence for this minimal promoter.The best I could find was on the cambia website where they say it is -90 http://www.cambia.org/daisy/promoters/242/g1/250/264.html
1) Does anybody have experience with increasing the expression of enhancer elements like this?
2) And what sequence did you use for this?

Apparently some other plant vectors define it as -46 to +9 relative to the start codon. Even more confused now:
https://books.google.co.uk/books?id=oATyCAAAQBAJ&pg=PA220&lpg=PA220&dq=%22minimal+35s%22&source=bl&ots=WMuuFK7ZSk&sig=exscxB6RpFKTGmSQ3XtR8gNBeP8&hl=nl&sa=X&ei=iXRoVf6mNYiu7gbl0oOABA&ved=0CCAQ6AEwADgK#v=onepage&q=%22minimal%2035s%22&f=false

In case anybody ever has the same question: I found the answer in this paper by Ow et al. 1987 (fig1)
http://www.pnas.org/content/84/14/4870.full.pdf
Just to clarify, I did not want to boost expression of the enhancer element in my algae, it needed boosting in tobacco protoplasts/leaves.


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Why do smaller mammals move intermittently?

I was watching a nice little video on youtube but couldn't help but notice how snappy smaller animals such as rats and chipmunks move. By snappy I mean how the animal moves in almost discrete states pausing between each movement.
Is this a trivial observation or something inherent in the neuro-synapse or muscular make-up of these animals?

Not just mammals. Insects and reptiles do this too.

Human soldiers do it, too. And many animals live in what amounts to a war zone.

Are they actually pausing more than larger animals? I mean, if I speed up videos of elephants they look snappy with intermittent movements (or e.g. some of the people in this time lapse), and if I slow down videos of chipmunks they look smooth and continuous like larger animals (sort of like this). I think it's just a relative time thing?

Just to add an interesting (but exceptional) example, tiger beetles move so fast that they are essentially blind during movement; they dash in short straight lines, then must stop to locate their prey and make another dash. Not the case for most animals, but a fun one.

Short answer
Intermittent locomotion can increase the detection of prey by predators (e.g.  rats), while it may lead to reduced attack rates in prey animals (e.g., rats and chipmunks). It may also increase physical endurance.
Background
Rather than moving continuously through the environment, many animals interrupt their locomotion with frequent brief pauses. Pauses increase the time required to travel a given distance and add costs of acceleration and deceleration to the
energetic cost of locomotion. From an adaptation perspective, pausing should provide benefits that outweigh these costs (Adam & kramer, 1998).
One potential benefit of pausing is increased detection of prey by predators. Slower movement speeds likely improve prey detection by providing more time to
scan a given visual field.
A second plausible benefit is reduced attack rate by predators. Many predators are more likely to attack moving prey, perhaps because such prey is more easily detected or recognized. Indeed, motionlessness (‘freezing’) is a widespread
response by prey that detect a predator.
A third benefit may be increased endurance. For animals moving faster than their aerobically sustainable speeds, the maximum distance run can be increased by taking pauses. These pauses allow the clearance of lactate from the muscles through aerobic mechanisms.
PS: If you mean with 'snappy' not only that small animals move intermittently, but also 'fast', then Remi.b's answers nicely covers the story why small critters are quick. Basically, it comes down to Newton's second law, namely acceleration is inversely proportional to mass (a = F/m), but the size of muscle power is not. Hence, bigger animals have more mass and need a lot more force to build up to accelerate at the same speed. That build up of force needs time (ever witnessed the vertical lift-off of a space shuttle?) Hence, small critters accelerate quicker and allow them to move 'snappy'.
Reference
- Adam & kramer, Anim Behav (1998); 55: 109–117

I have no evidence for this, but I would also wager that stopping will improve your ability to scan your environment for predators.

Motion not only greatly increases your chances of being seen by something that wants to eat you (or something you want to eat), but it also increases your chances of being heard (or vibrationally detected), and/or smelled.

Well, this was pretty obvious answer. But why does this only apply to tiny creatures like mice and insects?

@TomášZato - I've never said it did. However, I agree a PS might be in place. What about the postscriptum add-on? Does that satisfy your critiques? (Why do I hate downvotes so much :-)

@TomášZato it doesn't, it is just that for larger animals the time between pauses is long enough people tend not to notice, many prey animals pause and scan for predators. also in larger animals movement between food sources is less common since they are both more energy efficient and tend to have different feeding mechanisms, so pauses are harder to notice.  https://royalsocietypublishing.org/doi/pdf/10.1098/rspb.2000.1388

In addition to @AliceD's excellent answer, I would like to add that a simple mechanistic relationship between body size and "snappiness" may explain the observed pattern.
Basics of biophysics
Difference in snappiness may result from a difference in the ability to accelerate your movement.
An increase in body size over one dimension (=body length) $x$ scales with an increase in volume and mass of the order of $x^3$. Muscle strength is dependent on the cross-sectional area of the muscle and therefore by a linear increase of $x$, strength increases by $x^2$.
Digging back to high school physics lectures, $F=Ma \left(\text{or } a=\frac{F}{M}\right)$ , where $F$ is a force, $M$ a mass and $a$ an acceleration. With an increase $x$ of the individual size (over one dimension, the length of the individual if you prefer), the force increases by $x^2$ and the mass increases by $x^3$, therefore the acceleration gets multiplied by $\frac{x^2}{x^3} = \frac{1}{x}$. Of course, nature is not all that easy, but if we assume it is, then the relation between the acceleration of movements and body size (=body length) should look like this:

An animal that is 4 times as big should make accelerate its arms and legs 4 times less.
Contrasting to @AliceD's answer
@AliceD listed plausible hypotheses for why there might have a selection for snappy movement in small animals but simpler explanation based on the physical properties of bodies might be enough to explain the observed pattern. It would be interesting to know exactly what the relationship between body size (=body length) and "snappiness" look like in nature to further this discussion.

Fun Facts
The mantis shrimp (see below picture) is able to accelerate its claws up to 10,400g (reference). More information about g (unit of acceleration) here. In short, a typical human can support up to 5g. 10,400g is absolutely insane! To offer some comparison: a baseball gets an acceleration that is only about a third of that of the mantis shrimp's claws. Mantis shrimps use their claws to break open clams. Here is a video. According to wikipedia, due to the friction of the claws against the water, small bubbles are formed and the temperature at the edge of those bubbles can go up to several thousands of °C.

Apparently, a jellyfish stinger can go up to 5,400,000g (reference) which appears to be about 30 times more than a bullet. You will find a list of examples of things that undergo various levels of acceleration on this wikipedia list.

I think the question is not on why they are fast, or accelerate quickly, but why they move intermittently.

I think this rather explains why larger animals do not make snappy movements: because all that accellerating and decellerating consumes too much power.

Difference in snappiness may result from difference in the ability to accelerate your movements. Larger animals do not make snappy movement because they can't while smaller animals can. It is true it doesn't explain why they would not slow down their movement. I would tend to think that it is simply generally beneficial to move fast.

@AliceD Maybe it's related? I mean, watching the OP's linked video, at least, it seems like being able to do things more quickly (interpreted as "snappy") leaves more time to do nothing in between. I know it's different, but if I could move 10x faster than I could now, I'd probably spend a bit more time not moving at all, since I already accomplished the intended movement and wouldn't fill time with unnecessary movements for no reason. I totally am pulling this comment out of my butt, though, so I dunno.

(Do bigger animals pause a lot too but on a slower scale? Like, if something makes a noise, I turn my head to look. Then I pause. Then I resume what I was doing. Does that count as intermittent but slower, same thing but not "snappy" ["snappy" just meaning relatively fast compared to the observer, really]?)

I very much agree @JasonC. I have a hard time to formulate the concept though.

Layman's hypothesis, but... It seems an animal using intermittent movement alternates between a hard-to-see state and a hard-to-catch state, with some degree of safety in both. Operating at a slower, sustained pace offers neither of these benefits and significantly less safety.
Wondering if "small mammals" is the right descriptor. The obvious examples seem to be rodents. Also vague: cats are small relative to horses, but they're not intermittent.
Maybe another way to look at this is "When/why does an animal uses their maximum speed?" Rodents seem to do it as a matter of routine locomotion, most mammals do it only when actively fleeing or pursuing.
Small lizards seem more akin to rodents in this regard than not-quite-as-small mammals.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Y-chromosome and phenotype
I have a male colleague which has a son that does not resemble its father in any degree (apart of being male). The "father" is thin, tan-skinned, brown-eyed and the "son" has blue eyes, blond and already slightly overweight boy. Their faces have no any signs of similarity.
Since, the son gets Y-chromosome from a father, it is interesting to know if the Y-chromosome possesses any phenotypical feature apart of testicular development?
I did not find any Y-gene that influences the phenotype.
So, the second part of the question: Can other 22 parental chromosomes be so "recessive" that a child will have no "any" external signs resembling its biologic father.

actually it's been noticed that when offsprings are born, they resemble the father more than the mother, it's suggested that it's sort of an assurance to the fathers that the offspring is actually theirs. But let's analyze the eye colour, since eye colour like skin colour is a multi-allelic trait, therefore black being the dominant ones and brown being the second after that, meaning it contains at least one recessive feature, the mother actually had to be recessive on the eyes to produce a blue eyed boy....P.S. I'm commenting because I cannot find references for all this atm.

The Y-chromosome only really contains genes relevant to sex determination[1], with estimates of protein-coding genes ranging from 50-450. For instance the SRY gene, also known as the testis-determining factor [2], is only found on the Y-chromosome.
Phenotypes such as eye colour are coded on the autosomes (i.e. not the sex chromosomes), and as such are determined by alleles inherited from both parents. As Koustav Pal mentions in his comment, many such traits are multi-allelic (i.e. determined by multiple regions of the genome), and are therefore more complex than first appear; eye-colour can change over time, and there are many more complexities that do not fit into the simple "blue", "brown", "green/hazel" categories [3]. This also applies to hair, so the child you mention could become more like their father as they grow older (or not!).
Because each individual posesses two alleles for each possible trait (one from their mother, one from their father - we each have two whole copies of the human genome in our cells*) a person can be a carrier for traits, such as blue eyes, whilst themselves having brown eyes. In fact the situation is so complex (>15 genes affect eye colour) that two blue-eyed parents could have a child with brown eyes [4] - the historical perspective was the brown eyes were dominant over blue eyes.
I have focussed on eye colour because it is a good case-in-point: there are clear genetic determinants and heritability, and it is more complex than the popular perception. Regarding hair (or skin) colour, single-gene mutations can cause pale skin and red hair [5], but beyond these cases the same rules seem to apply; that there are multiple genetic determinants (which means the Mendelian single-allele dominant/recessive model does not really apply) that affect the amount of eumelanin (which is dark brown) and pheomelanin (which is reddish) produced, with together combine to make the spectrum of colours we see in the population - it is not true to say that there are only blond OR brown haired people, as many people lie somewhere between [6].
This has not been an exhaustive review of these topics by any means, and there may be further evidence either way, but it seems quite clear that it is not unusual for offspring to not actually take the appearance of one or both parents. There are many traits you mention (such as build) that I don't go into detail, but there is emerging evidence that these are incredibly polygenic (caused by many small-effect genetic variants - e.g. height [7]) and as such could lead to the same phenomenon.

http://ghr.nlm.nih.gov/chromosome/Y
http://www.ncbi.nlm.nih.gov/gene/6736
http://udel.edu/~mcdonald/mytheyecolor.html
https://www.uq.edu.au/news/article/2007/02/eyes-have-it-multiple-gene-question
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3095693/
http://udel.edu/~mcdonald/mythredhair.html
http://www.nature.com/ng/journal/v46/n11/full/ng.3097.html

* well, most cells - red blood cells and gametes do not.


text:
How to calculate the Jaccard index
I want to calculate the Jaccard index between two compounds. What is the algorithm? I have searched for it, it just gives the formula but how to apply it on compounds is not known to me. Can you help?

Exactly how do you want to use it? In ecology, it is usually used to compare how similar communities of species are, but you are referring to only two compounds. What entities do you want to compare? As for coding it, you could probably find much useful information in the currently 345 StackOverflow questions on the Jaccard coefficient/index

I missed the detail about "two compounds". My answer includes a reference for two sets of compounds but it would be good if you clarify what you mean exactly.

How do you denote a compound? just by its composition?? For e.g. C₃H₆O₃ can be lactic acid, glyceraldehyde or trioxane.

Yes, denote a compound by their atoms that consists them..

or by SMILES format

The Jaccard index is a measure of similarity between two sets. Take a look at the Wikipedia article here. It is very easy to compute:
The Jaccard similarity coefficient for sets X and Y is defined as:
J(X,Y) = |intersection(X,Y)| / |union(X,Y)|

Where | | indicates the size (number of elements) of the set. Imagine you have two sets X and Y defined as follows:
X = {A, B, C, D}
Y = {C, D, E, F, G}

Then:
intersection(X,Y) = {C, D} => |intersection(X,Y)| = 2
union(X,Y) = {A,B,C,D,E,F} => |union(X,Y)| = 5

Therefore: J(X,Y) = 2/5
Alternatively, the Jaccard distance would be D(X,Y) = 1 - J(X,Y) = 1 - 2/5 = 3/5
In Biology the Jaccard index has been used to compute the similarity between networks, by comparing the number of edges in common (e.g. Bass, Nature methods 2013)

Regarding applying it to compounds, if you have two sets with different compounds, you can find how similar the two sets are using this index. The elements on the sets, in this case the compounds, correspond to A, B, C, etc. in my example.

chemical compounds would have atoms, so basically for each compound we create a set of atoms and then find the index. Will that do?


text:
Do babies resemble their father?
An often heard theory is that newborns and babies resemble the father more than the mother, a theory apparently ignited by a Nature paper by Christenfeld and Hill (1995). Figure 1 shows one of the tests images. His subjects had to guess which picture was the real dad and which was the real mom. It turned out that tested subjects were indeed significantly better at guessing dads than moms.

Test stimulus of Christenfeld and Hill (1995). Which one is dad: a, b, or c?
It is suggested that paternal matching of a baby promotes identification of the father with his offspring. In turn, self-identification in his kin would prevent the father from doing harm and stimulate protective paternal behavior. This then is hypothesized to increase survival rates of his offspring and et voila, a trait is born (pardon the pun) that makes baby paternal look-alikes fitter than those that don't. This hypothesis seems to have become part of parenting folklore.
However, a Scientific American paper by Matson (2011) contests this view and puts forward several primary research studies showing no preferred resemblance between mother or father, or even predominantly maternal features in babies.
Is the resemblance between father and baby fact or fiction?
References
- Christenfeld & Hill. Nature (1995); 378: 669
- Matson, Sci Am (2011) online article

Credits for this question go to @KoustavPal for his comment in Y-chromosome and phenotype

Most babies don't have a lot of (long) hair, while quite some of their mums will.

@AliceD: It applies to all infants, and to some extent to toddlers.  They resemble other children of similar age far more than adults.  I don't know why this should be, other than the workings of evolution.  Parents & other relative may say otherwise, but a) they're intimately familiar with their child; and b) there's a lot of social expectation/delusion going on.  It's de rigeur to say "Doesn't /he look just like dad?", though honesty would have you say that the infant looks more like an undifferentiated blob :-)

@AliceD: It'd be interesting to do a test (or perhaps find one that has been done).  Show an infant to an unrelated person for a short time, then ask the person to pick out that infant from a group.  I'd bet that results would be little better than chance.

I've heard an anecdotal claim that newborns resemble their fathers (which may not be the case in later life), and that it is an evolutionary adaptation to assure paternal recognition. This is usually corroborated with examples of animals killing progeny originating from other father, in order to give advantage to tehir own genotype. Is there any evidence for that?

I've heard of a study that found that individuals were more likely to tell the presumed father he looked like a child then the mother, and the mother's relatives were most likely to do so.  They theorized this was an adaptation to convince the male that he was the biological father to ensure he will continue to provide for the child.  As such it may be that paternity isn't that easy to tell when seeing a child, but everyone is still evolved to claim that the child looks like the presumed father.  Anecdotally I'm often told I look like kids I'm watching by those that presume I'm the father

@dsollen - interesting stuff. I've heard more of these stories/recollections but hard evidence I find hard to find. Hence the question. Thanks!

Resemblance between parent and offspring is certainly true. Some traits are more obvious than others, for example skin colour would be very obvious. As babies mature they will gradually begin to look more and more like their parents, the features of babies often change rapidly, for example pretty much every baby has a little nose, but by the time they are a fully grown adult it probably resembles that of one the parents fairly well.
More obvious example would be height - imagine being presented with a baby and two males who are identical in every way, except one is two metres tall, and the other is 1.5 metres tall. As a baby it would be very difficult to assign paternity on the criteria of height/size, but as the child develops it would likely become easier and easier.
The resemblance between parent and offspring relates to the heritability of a trait but, because there can be temporal variation within an individual, heritability can only be properly determined by measuring the traits in parent and offspring at the same time point (e.g. father's height at 18 years old and son's height at 18 years old), otherwise it will introduce noise in to the estimation, likely reducing the estimate of heritability (and specific to your question, making it harder to assign paternity based on phenotypic characters).
In the context of your question: Ability to assign paternity would depend on a) the resolution with which the traits available can be distinguished among all individuals in the test and b) the variance among all individuals in the test. E.g. If the only trait available was number of fingers per hand, and all potential fathers and the child had five then the lack of variance would make it impossible to use this as a criterion, while if both one of the potential fathers, and the focal baby, had six fingers on one hand then there would be pretty good clue.
Whether babies more resemble their fathers more than mothers (which I think is the true question you are asking here) there is evidence from Drosophila that within-sex heritability is much higher than cross-sex for lifespan and aging, i.e. the lifespan of males (females) far more resembles the lifespan of the father (mother) than the mother (father). This would suggest that there is a sex specific element. Meanwhile there is evidence of high cross-sex genetic correlations in humans preventing males and females from becoming more different (thus maintaining resemblance to opposite sex parents). I would think that resemblance to the father could offer some benefit in assigning paternity by care giving males (stopping males devoting resources to other males offspring) but some of the resemblance could be generated by genetic correlations to sex-specific genetic variance, for example, males (females) will look more like their father (mother) in many ways purely because they are of the same sex, so it will heavily depend on the traits you look at to judge resemblance.
For a related answer about heritability on biology SE see:
Is it possible for a child to grow taller than their tallest parent?

Thanks for your great answer. Are you saying that, in general, baby-boys resemble the mother and baby-girls their father?


text:
Oral allergy syndrom, continuation of continuous consumption of allergen
Wikipedia states on its page that

In addition, patients are advised to avoid the triggering foods, particularly nuts.

And same thing goes for webmd.com

The basic rule: If a food makes you uncomfortable, don’t eat it.

So two very related questions flow from this:

Does continuous consumption cause such an allergic reaction to become stronger?
And if that is the case, by what mechanisms does that happen?

And if possible at all, I would greatly appreciate it if you could keep the explanation to like a first year bachelor level (as in, anything a first year bachelor student would be capable of comprehending, not necessarily things that a first year bachelor student is typically taught) O:) . Anything beyond that I am likely to not understand even if I do take my time. And this is my first question on biology.SE so I hope I did everything correctly.

When you ingest an allergen for the first time, your body produces many of an antibody called IgE with specificity toward that allergen. These IgE antibodies bind to mast cells, and basophils. When you encounter more allergen, they bind to these IgE on the surface of the mast cells and basophils, causing them to release a host of chemicals like histamine. Massive amount of histamine are the cause of anaphylaxis, so when more allergen interacts with more and more IgE, the situation worsens. The following figure is a detailed mechanism,

Source
We can also see, though, that histamine released is a function of total allergen, and eventually reaches a maximum regardless of allergen present,

Source
Here they're showing histamine release vs allergen concentration while investigating allergic rhinitis.


text:
What is this insect that has invaded my home in Texas?
After the recent floods in central Texas this past weekend I noticed my that bedroom has suddenly been infested with these small insects that have climbed in through the window. Previously, the hole in the window was used by ladybugs who hatched larvae in the room (they didn't survive long).
However, these insects have been here for 3 days now. They seem to disappear at odd times during the day (haven't nailed down a pattern yet) and return a bit later. There are roughly 20-30 of them in my room at a given time. They don't do much and seem very uninterested and passive, mostly just flying around or meandering across the walls on and off. Some of them have wings and others do not (that or the wings are hidden and they just aren't using them).
I would like to identify what this insect is so I can find a way to get rid of them. A picture is linked below. Note in the picture that the white-ish segments on the leg are actually closer to yellow in color.

Myodocha serripes
http://www.americaninsects.net/ht/myodocha-serripes.html
Nice picture! Generally, the body plan of this guy indicates Hemiptera (the 'true' bugs), but the long neck is a bit strange, so a google image search for "Hemiptera + long neck' brought up this strong candidate. It looks like it's distributed in Texas, and is in fact, named for that distinctive neck: "The Long-Necked Seed Bug".
See also the BugGuide.net page for Myodocha

Nice explanation! :-)

Great, this is exactly right, thank you! Now to figure out how to get rid of them...

Well, apparently they come to light and enjoy strawberries...

@Oreotrephes Turning off the lights for a few days during the evenings and trying to seal the window appears to have helped a lot. They still sneak in through the tiny cracks and imperfections in the window but overall it looks like it's working.


text:
What is the connection between sleep requirement and age?
By this question: Is the human biological clock genetically programmed or learnt? we discussed that the sleep requirement depends on the age of the individual.

- Figure 1. - Sleep requirements by age - ref
I thought I ask the question, why?

I believe the current theory is that it is related to cell loss in the intermediate nucleus of the human hypothalamus. They have shown sleep disruptions due to lesions of the hypothalamic ventrolateral preoptic nucleus in rodents, and found that the intermediate nucleus in humans is homologous and shows a reduction in size in older adults that is correlated with sleep disruptions. http://brain.oxfordjournals.org/content/137/10/2847

Has any causation been shown on this correlation?

I'm late to this answer, but this seems incredibly simplistic (especially given how unsettled the scientific understanding of sleep is) and not really related to the issue of sleep "need" but simply a single possible explanation for age related sleep disruption. You could have sleep disrupted and yet need sleep, or have sleep not disrupted and yet not need it per se - they are completely separate dimensions.


text:
Can light pollution cause cancer?
Impaired circadian rhythm is associated with cancer. Light pollution affects the circadian rhythm and the circadian rhythm affects the metabolism. But what is the (molecular) connection between impaired circadian rhythm altered metabolism and cancer?

Do you have a link to the full text of the linked paper? It is not open access. Additionally, just from reading the abstract, the authors are proposing a hypothesis, and haven't actually tested anything. Correlation is not causation. Using Google Scholar, I couldn't find any actual research studies that cited this article testing this hypothesis.

@MattDMo It is not that hard: http://kepfeltoltes.hu/150529/795452382N_vtelen_www.kepfeltoltes.hu_.png I don't have full text either by most of the articles. Only libraries and universities use to buy access only, it is too expensive. So if you are member of a library then you can probably read the full text at least by some of the online journals.

@MattDMo Another relevant articles I have found: http://link.springer.com/article/10.1007/s13277-012-0611-0  http://www.sciencedirect.com/science/article/pii/S030438351300709X http://informahealthcare.com/doi/abs/10.3109/07420528.2013.782315 http://www.sciencedirect.com/science/article/pii/S0016648013001731 http://www.ncbi.nlm.nih.gov/pubmed/24729125 http://www.pnas.org/content/108/46/18790.full