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Any benefit to low dose radiation?
Is there any survival benefit in humans that can be obtained from chronic exposure to low dose radiation, or is any dose of radiation a potential harm?  Has any research been done into this?

What kind of benefits do you expect?

@Chris, the book on radiation biology I was reading said that animals exposed low doses animals were observed to have a decrease in mortality compared to those exposed with no radiation.  The book is quite old so I'm not sure what recent studies suggest.  The books said the cause of this phenomenon was unknown and controversial, but stated some scientists hypothesized low dose radiation could prevent some diseases occurring.

http://journals.lww.com/health-physics/Abstract/1982/12000/Physiological_Benefits_from_Low_Levels_of_Ionizing.1.aspx

This is not an easy question - I can have a deeper look into this after the weekend, if not somebody else does it.

@Mew I found a non scientific article: http://www.hiroshimasyndrome.com/radiation-the-no-safe-level-myth.html which has many citations. So it is possible that low level radiation is beneficial. I think you should read more in the topic to reach a conclusion.

@Mew Another article: http://www.snm.org/docs/Radiation_Hormesis_JNMT_March_O3.pdf and wikipedia article: http://en.wikipedia.org/wiki/Radiation_hormesis

As @ inf3no indicates in his links: the general term for a beneficial effect to a low exposure of a stressor is called 'hormesis': http://en.wikipedia.org/wiki/Hormesis. A very interesting and exciting topic indeed.

Thanks everyone for your input so far, I'll keep investigating and looking at the links you have provided.

This is an interesting - and highly debated question. Generally there are two completely different directions of thinking when talking about dangerous substances (this applies to dangerous chemicals as well):

The linear no-threshold model (LNT).
The hormesis model, in our case the model of radiation
hormesis.

Summarizing the models the LNT model says that every dose has a negative response, so there is nothing like a stimulating dose and exposure should be avoided at any means. This reflects the policy in the handling of radioactive substances. If you look at the figure below, the curves a + b (supra-linear and linear) reflect the LNT model (the figure comes from here):

The radiation hormesis model says that there is a dose range in which the radiation above the background level is not only not harmful, but beneficial. High doses are (in line with the LNT model) also considered harmful. This can be seen in the curves c (linear-quadratic) and d (hormesis) in the figure above. The benefits are thought to take place through the activation of repair mechanisms (which are only activated by radiation) which protect against changes in the genome and thus also protect, once activated, against changes which are caused by other agents and reasons. See reference 1 for more details about radiation hormesis.
There are a number of studies which observe this effects in the laboratory and this is also one of the major critic points: To my knowledge it is currently unknown if these effects can also be seen outside a controlled laboratory environment.
Other critique points are low study publications (which makes studies prone to statistical errors), using wrong models (cell culture) or too high doses. See references 2 and 3.
Since our environment contains naturally radioactive substances as well as cosmic and UV radiation, we have developed pretty efficient mechanisms to deal with these problem. Additionally measurable effect of radiation on the activity repair mechanisms can be seen (and this is not debated at all), but the main question is if these effects can also have a beneficial effect. It is also not known, if all radiation ($\alpha, \beta$ and $\gamma$) have the same effect, or if some of these like $\alpha$-radiation is more dangerous.
So I think it may be possible that there is some positive effect, but until this is proven, I would rather be safe than sorry.
References:

Evidence for beneficial low level radiation effects and radiation
hormesis.
Uncertainties in studies of low statistical power
Health Risks from Exposure to Low Levels of Ionizing Radiation

I would be inclined to say yes based on the current wording of your question. There is more than one type of radiation out there, so I'm not exactly sure which you are interested in.
Ultraviolet is the one I will focus on though. Within the ultraviolet spectrum there are three types of ultraviolet radiation. The types are UVA, UVB, and UVC. UVC is primarily blocked by the atmosphere, so it never reaches us on the Earth's surface. UVB is perhaps best known for causing sun burns and skin cancer. UVA is the least powerful of the three. In chronic doses as you suggest it is probably far from good, but it can be beneficial at low doses.  UVA is linked with the production of Vitamin D which strengthens bones. It also stimulates tanning of the skin, which helps to protect the body from UV damage. Here is a link to The WHO describing some of UV's health benefits:
www.who.int/uv/faq/.../en/index1.html

Well, if we're considering UVB, Vitamin D is an obvious candidate to considering benefits of "radiations".  Even though, initially, Vitamin D synthesis was just a mechanism of protection for early marine organisms against UVB DNA damages. There are now so many metabolisms affected by Vitamin D.


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Are bees positively phototropic
One day I had found some bees have come around the light source like other positively photo tropic insects, I hadn't seen any bees coming over light before. I think bees are diurnal and they don't leave their nest at nights, I also read from an article that parasitic wasps may attack bees and these attacked bees would lose their mind and leave their nest at nights.
Is this possible or any other reason behind the night travel of bees and their positive photo tropism ?
http://en.wikipedia.org/wiki/Apocephalus_borealis

Honey bees rely on the position of the sun (and the ephemeris function) to navigate and communicate (i.e. the waggle dance). If they are out too late in the day to return to the hive (occasional), or if they are disturbed at night in the hive, they will fly towards a light.
Beekeepers and bee renters have learned that if you are going to disturb a hive at night, do so with minimal light so as not to lose bees. Also, they avoid lights in the vicinity of the hive in general.
There are a number of parasites and insecticides that cause bees to behave erratically. Colony Collapse Disorder is a major threat to the honeybee's survival.
Why are bees attracted to light? I don't know if anyone knows that.
Dinner and Dancing: Bee Navigation
The Cause Of Colony Collapse Disorder, Disappearing Bees Becoming More Clear

So if we create a large light source near the bee hive then bees would think its sun and they may start foraging, isn't ?

Mostly they fly into the light. Foraging requires more UV light; they need to identify flowers by color (though they perceive them differently) and pattern.

:Thank you for your valuable time. But I dont have enough reputation to up vote your answer. But virtually I am giving one. :)

I guess they think that they are in some sort of tunnel, so they want to fly out. Many insects, for example flies behave the same way.

"In some sort of tunnel" can you explain that further ?

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Like other animals, why humans don't have species & breeds?
Like other animals, why don't humans have species & breeds ?
 Even my pet dog is one type of breed, but we (humans) lack breeds & species?  What is the main reason?

Related: Do humans have enough biological differences to be grouped into races or subspecies?

You could ask any question of the kind Why don't <insert species> have species and breeds while <insert non-species taxon> do? such as for example Why don't tigers have species and breeds while dolphins do? The question mainly reveal your intuition that we should eventually talk about human breeds when talking about ethical groups.

To improve your understanding of the concept of species, you should have a look at How could humans have interbred with Neanderthals if we're a different species?

There are a lot of genera with only one species under it. I guess you want to find evidences that human is very special. But unfortunately we are not.

We do, we just call them races, you have black people, white people, Far Asian people, near Asian people, Indians, Eskimos

If you with 'humans' refer to our genus Homo (which is often the case), we do have multiple species, see wikipedia for an overview. The difference to many other organism groups is just that all species except Homo sapiens are extinct.
Also, taxonomic ranks below the species level - such as breed, subspecies, population and race - are very poorly definined and are usually used in different ways in different taxonomic groups. It is therefore difficult to draw one-to-one comparisons between these types of ranks across taxonomic groups. It is even relatively meaningless to compare e.g. taxonomic families between taxonomic orders, since they are used in such different ways, and compared to ranks below the species level taxonomic 'order' and 'family' have much clearer definitions.
However, if you with breeds of dogs are referring to distict phenotypes (which is basically what they are), you can easily see that some human populations also have distict phenotypes, so in this sense they are similar.
The reason why the concept of human races is largely obsolete and controversial (along with breeds) is clearly our human collective history of racism, nazism and eugenics.

how come all species of human extinct except homo sapiens why?

@johnson316 A current hypothesis is that Homo sapiens was a major reason for the extinction of Neanderthals (and maybe other human species as well) - see e.g. this popular summary.

@johnson316 You might find answers to this question interesting as well: Why Did 6 Great Ape Species Survive But Only 1 Hominid Species?

@johnson316 Chris Stringer's book Lone Survivors is a both beautiful and informative read, and deals precisely with your question.

1) Humans have limited genetic variability.
-This is caused by humans being a new species, only 200,000 year old.
-That went through a genetic bottle neck 50,000-100,000 years ago. Reducing the human population to 3,000–10,000 reproducing individuals
-That only recently managed to expend its range out of Africa ~60,000 year ago.
2)Humans are very mobile.
-The gypsies originate from India. And have been touring Europe for the past 1000 years.
-The population of Madagascar is a mix population of 50% african and 50% South east asia which arrive in madagascar some 1600 year ago.
-Romans... well moving people around europe and africa were their thing too.
3)Humans love making love.
Yup.. you can only get a breed if you have barrier... but there are few barriers that can stop human lust. So our genes get mixed alot. Even when we don't think they should not.
tldr.. our initial genetic variability is limited for several reason. Not enough time has passed to develop that variability. We are also too mobile for distance to be a good barrier... and phenotype change which do arise does not in anyway dissuade humans as a whole from exchanging bodily fluids and gametes.

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Why is heart failure treated as more critical than kidney failure?
The heart pumps the blood to supply tissues and kidney always filters the blood to remove urea,extra water and etc. And all these are vital,so the kidney is as important as heart:
and my question is:
Why is heart failure treated as more critical than kidney failure?

As a very short response, you can live for at least a few hours with no kidneys. If your heart stops you might have a minute to get medical attention.

@user137 - you can live for years with heart failure.

@anongoodnurse that's why it's a comment. You can live for years with kidney failure too. With dialysis kidney failure might even be easier to manage.

I don't know that one is treated as more critical than the other. Both are potentially life-threatening conditions.
One in five people over 40 will develop heart failure (HF). That makes it a very common disease of aging, and as more people survive other events (e.g. MI), it will continue to be prevalent, if not to rise.[1][2]
When a patient presents with heart failure (HF), whether it is to a PCP, an urgent care center, or the ER, it is treated.
In the US, the prevalence of CKD (chronic kidney disease) in people ages 60 and older approximately the same as of congestive heart failure (CHF): 18.8 to 24.5 percent. Between 1980 and 2009, the prevalent rate for end-stage renal disease (ESRD) increased nearly 600 percent, from 290 to 1,738 cases per million.[3]
When a patient presents with renal failure (RF), whether it is to a PCP, an urgent care center, or the ER, it is treated.
That makes both conditions much more common (and less emergent) in presentation than, say, anaphylaxis (life-threatening allergies).[4] Known rates or cases of anaphylaxis were 0.0004% for food (e.g. peanuts), 0.7% to 10% for penicillin, 0.22% to 1% for radiocontrast media, and 0.5% to 5% after insect stings.
Emergencies are emergencies, and are triaged for care based on risk, with standardized acuity scales that have five levels (e.g., 1- resuscitation, 2- emergent, 3- urgent, 4- less urgent, 5- nonurgent).[5] To claim that one is treated as more emergent than another, one would need to present evidence that, e.g. HF is rated as emergent more often than RF.
[1] Lifetime risk for developing congestive heart failure: the Framingham Heart Study
[2] Chronic Heart Failure: Contemporary Diagnosis and Management
[3] Kidney Disease Statistics for the United States
[4] Anaphylaxis in the United States
Considering the 1999 US population of 272 million, the population at risk for anaphylaxis from food is 1099, from penicillin is 1.9 million to 27.2 million, from radiocontrast media is 22 000 to 100 000, from latex is 220, and from insect stings is 1.36 million to 13.6 million. These calculations yield a total of 3.29 million to 40.9 million individuals at risk of anaphylaxis.
[5] Emergency Severity Index (ESI): A Triage Tool for Emergency Department


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Why cytotoxic T cells don't kill dendritic cells when they present antigen?
When a cytotoxic T cell (CTL) recognizes a peptide presented in the MHC-1 of a dendritic cell (APC), why it doesn't kill this cell?
I know that initially, in the lymph node, the T cell is inactivated. But eventually it becomes activated and travels to the tissue, where it again finds APCs presenting the offending antigen. So why doesn't the CTL kill the APC at this point?
Moreover, not all MHC-1's of the dendritic cell present antigens from phagocytized cells. Some MHC-1's present peptides coming from the dendritic cell itself, so that if the dendritic cell itself becomes infected with virus or bacteria, it can be killed by a CTL that recognizes the peptide. So in this case, the CTL does indeed kill the dendritic cell.
So my question is, when exactly does the CTL kill the APC? How does the CTL knows that should or shouldn't kill the APC?

Afaik. if the CTL is not activated yet, it requires a verification signal from a HTL or a very strong stimuli from the APC. Now I don't know yet what happens when it is already activated and meets with an APC presenting the same peptide. Afaik APCs do present the antigens on MHC2 and MHC1 as well, and it does not depends on whether the cell is infected, so I guess there is a way to prevent cell death in these cases. It probably depends on the amount of TCRs activated and other signals as well e.g. stress signals of the APC or cytokins.

Effector T cells have lower TCR stimuli threshold for proliferation than naive T cells. I haven't found any article about killing TCR stimuli threshold and about what environment is required for successful effector function by cytotoxic T cells. I found that by HIV not infected CD4+ T cells can be killed accidentally by effector T cells so I think the APC can be accidentally killed by the T cells too and the outcome depends on the strength of the TCR stimuli, and other environmental factors (costimulation). It is not clear for me yet how naive and effector T cells differ by activation.

The presentation of antigens on the cell surface is done by two different molecule complexes: The MHCI and the MHCII complexes. These are coupled to different pathways and are recognized by different T cell populations.
The MHCI molecule presents all proteins which are present in the cell on the surface. To do so, peptides coming from the proteasome (where long proteins are digested) are transported in the the endoplasmatic reticulum (ER) by a special transporter called Transporter associated with Antigen Processing (TAP). By doing so, a profile of all proteins expressed in the cell is presented on its surface, including proteins which arise due to an infection of the cell. MHCI is recognized by cytotoxic (or CD8 positive) T cells which subsequently kill all cells which show foreign antigens on their surface (since this is a sign for an infection).
The MHCII complex only presents proteins on its surface which have been taken up by phagocytosis (so here only external proteins are presented). To prevent binding of cellular proteins in the ER (like for MHCI), the binding pocket of the receptor is blocked by the invariant chain. This chain dissociates only when the MHCII complex enter the phagolysosome with its acidic conditions. This makes sure that only proteins which have been taken up by phagocytosis are presented. MHCII complexes are recognized by helper (or CD4 positive) T cells, which in turn can activate B cells to raise a proper immune response.
In theory this should prevent all problems. In the practical life this is different for dendritic cells in a mechanism called "cross presentation". In this mechanism antigens which are taken up by phagocytosis are exported from the phagolysosme and imported into the ER. This pathway also involves the TAP protein. By choosing this way, APC can activate naive CTL which will kill all cells which present this antigen. See references 1 and 2 for more details.
This pathway is important for the immune response to a number of viruses as well as tumors which evade the MHCII mediated immune response by suppressing the MHCII antigen presentation. See references 3 and 4.
It is also important for the stability of the self-tolerance by the deletion of auto-reactive CTL. See reference 5 for details.
References:

Outside looking in: the inner workings of the crosspresentation
pathway within dendritic cells
Cross-talk between the endocytic pathway and the endoplasmic
reticulum in cross-presentation by MHC class I molecules
Role of bone marrow-derived cells in presenting MHC class I-restricted tumor antigens.
Cytotoxic T-cell immunity to virus-infected non-haematopoietic cells
requires presentation of exogenous antigen.
Exogenous class I-restricted cross-presentation of self antigens can
lead to deletion of autoreactive CD8+ T cells.

The question was about what happens if an effector CTL meets with an APC, which presents a peptid from the proper pathogen. Why does the CTL not kill the APC? Note that APC can present pathogen peptides both on MHC1 and MHC2 without becoming infected by the pathogen. So I don't think this answers the question...

I agree with @inf3rno. I don't see how this answers my question.

I misunderstood the question and have adapted it now. Thanks for the notification.

The adaptation is in the last paragraph?

You might find this paper helpful in answering your question. It proposes that Memory CD8+ T-cells protect dendritic cells, with TNF-alpha playing a major role in the molecular mechanism of doing so
Watchmaker, P. B., Urban, J. A., Berk, E., Nakamura, Y., Mailliard, R. B., Watkins, S. C., … Kalinski, P. (2008). Memory CD8+ T Cells Protect Dendritic Cells from CTL Killing. Journal of Immunology (Baltimore, Md. : 1950), 180(6), 3857–3865.
It can be found at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905219/

Here's couple links explaining this:

Allison himself talks about the role of CTLA-4:
https://www.researchgate.net/publication/327062074_Fundamental_Mechanisms_of_Immune_Checkpoint_Blockade_Therapy
Clear explanation of what happens (see Figures 1&2):
https://www.researchgate.net/publication/329214140_CTLA-4_and_PD-1_Control_of_T-Cell_Motility_and_Migration_Implications_for_Tumor_Immunotherapy

Briefly, CTLA-4 is expressed shortly after T cell activation and serves to protect APCs (and everything else) from excessive T cell activation and proliferation. Also CTLA-4 makes T cell detach from APC and travel to where it's action is needed - into inflammatory sites.

Welcome and thanks for your answer. We generally encourage more elaborate answers, but because of the referencing a +1 nonetheless :)

Major reason – Helper  T-cells induce APCs to produce an endogenous granzyme inhibitor (serpin SPI) by APCs. So APC's are protected from being killed (which normally involves granzyme-induced apoptosis due to perforin release by the cytotoxic T-cell)
Also, downregulation  of  cell  surface  expression  of  the CCR7 homing receptor on activated cytotoxic T-cell.  Not attracted to APC.

I presume these things (overexpression of the SPI and downregulation of the CCR7) can also be performed by clever malignant cells. Are there examples of this?

What''s your reference on this?

Here is some exciting textbook reference (Janeway 5th ed.):
https://www.ncbi.nlm.nih.gov/books/NBK27118/
See Figure 8.14 and compare with text. Whereas the figure shows some presentation of antigen at the site of infection, the text does not explicitly refer to the figure of the site of infection, and says that presentation of antigen happens only after (maybe during) movement of that same APCs from the site of infection to the lymph nodes. It seems to be only there that presentation takes place (and, presentation by dendritic cells means priming, defined by environment of lymph node,  in contrast to presentation by infected non immune cells).
My point is that presentation does NOT happen at peripherical sites of infection which is contrary to the statement in  your question. According to Janeway's wording - taken literally  - before priming in lymph nodes has taken place there is no danger to dendritic cells in presenting at the site of infection. Successful presentation in lymph nodes thus becomes a prerequisite for any killing of  presenting APCs. This looks like some self-regulatory mechanism to me.
It's a different question if, while protecting during the priming process,  the "known" (your question is based on the premise that there is no killing during priming) second signal B7   in presentation induces tolerance for a certain time period. Again, according to basic textbook wisdom, at lymph nodes "presentation is priming". Presentation at site of infection by APC is no priming. Priming means that t-cells are given permission to divide. It is not trivial to see: APCs, dendritic cells, must be protected in lymph nodes "only", as it is "at that point" they are doing their job of priming. When they present the antigens in the lymph nodes they meed naive T-cells that have yet to become cytotoxic - which implies a time lag for cell division and expansion of the t-cell clone. Before naive t-cells have divided and differentiated there can be no killing. The effet of B7-receptor might last that long - within that time lag a few other specific t-cells might presumably have been primed, then the APC might simply not be needed any more.
Some references
Question of  S. Oncosuresh at researchgate at  https://www.researchgate.net/post/Why-Dendritic-cell-are-not-killed-by-T-cells-when-they-present-antigen
It is the "speculative" answer by Ye Tian from the University of Chicago which I feel inclined most to: cp. "... if by then" (they will kill the DC's presenting).
You say, quote: "... and travels to the tissue, where it again finds APCs presenting the offending antigen."
It's a possibility that the assumption that there is presentation by dendritic APCs at site of infection is wrong.
In that case the following reasoning applies:  If there is presentation at site of infection presenting dendritic cells in fact are being "simply" killed as they are not needed any more, as the very fact that they meet primed(!) cytotoxic t-cells shows that presentation in lymph nodes for purpose of priming has succesfully been undertaken "already".

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ECG of heart transplant patients
I am studying ECGs of heart transplant patients.
The difficult thing is that there is so little available data publicly.
I must apply for data in my universities.
It would be also great if something is public.
I have searched several databases and contacted some authors directly.
Some findings

No heart transplant data in Physionet, online search tool here.
No heart transplant data of ECGI with Dr Rudy (personal email)

I am waiting answers or working with application for

Dr Rudy's company
University of Helsinki's database (under process for application)
Some technical universities in Finland (these have connections where are good data but they do not hold data themselves)

Is there any ECG data about heart transplant patients?

This might get you started on how to look for such (it's also interesting). I don't know if the National Center for Biotechnology Information might be a resource.

Thank you for the comment! Interesting. Citing articles are also good resources: http://scholar.google.com/scholar?start=0&hl=en&as_sdt=0,5&sciodt=0,5&cites=http://circ.ahajournals.org/content/81/3/821.abstract&scipsc= Let's see if any data is public.

are you looking for images or anything in particular coz I found a bunch after a google search. Most of them are heterotrophic heart transplants though

@TheLastWord I am looking for data (raw numerical data). Not pictures. Feel free to propose any data which you found so I can take a look at them if they are appropriate.


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Looking for a gene in my raw genetic data. What are the possible causes for this?
Obviously, I barely know what I am talking about.
But I want to find the "MUC5B promoter polymorphism rs35705950" in my RAW genetic data from 23andMe. (see this paper  http://www.ncbi.nlm.nih.gov/pubmed/23695349)
I think rs35705950 is the SNP number...   When I search I get no results.
When I search for MUC5B I get 9 results, but the SNP numbers doesn't match.
My question(s)
Is it possible that I just don't have this gene (rs35705950)?
Does 23andMe not have ALL of my genetic information?
Am I doing something wrong or misunderstanding what I am looking for?

Let's set things straight. The genomes of humans are highly similar and in general everyone shares the same genes. SNPs, or Single Nucleotide Polymorphisms, are single basepair positions in the genome in which there tend to be differences between people. This means, that instead of measuring the whole genome sequence for a person, which is very expensive and difficult, we can just examine a subset of the genome (the SNP positions) and capture most of the unique characteristics of that genome.
23andMe do exactly that. They measure a large set of SNPs (but not all of them), and thus give you some useful information about your unique DNA sequence. So you would need to look in the output given to you by 23andMe and see if they measure the SNP in question (rs35705950).
What do SNPs have to do with genes then? Well, if one of these SNPs occurs inside a gene, it could affect the gene, for example by producing a slightly different protein that could lead to some phenotype. So, studies link SNPs to different phenotypes such as disease or hair color. Usually the link is not one-to-one, but given as a probability.

In short, rs35705950 is not a gene, but rather a SNP, a SNP that occurs within the gene MUC5B. 23andMe measures a selected subset of human SNPs, less than 0.1% of the genome.

So I suppose 23andMe does not have the data for this SNP, given that I cannot find it in the RAW data search.  Are there other services that would sequence your entire genome or a given SNP?

Sequencing your whole genome would be thousands, if not ten thousand dollars.  That's not what you want.  There is a Taqman assay designed for it, which is good, but I don't know how you would find a commercial lab to run the assay for you.

@Blankasaurus checking a specific SNP would be trivial for a molecular biologist, this is the type of thing you do in an undergrad molecular biology lab course. I am pretty sure you could pay some company to do this as well. Basically you can take some saliva, extract DNA, and use PCR (Polymerase Chain Reaction) to amplify the region of interest, and then sequence it using Sanger sequencing.


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Ants eating bark
Was out walking in the park today, came across a tree, and me being me I thought "Hey lets try climbing this thing for fun." But something strange struck me, the tree was completely devoid, as in COMPLETELY, of any bark. On the trunk, on the branch, no bark anywhere, pure albino. Well, I reasoned, maybe it's just born that way. But then I look down, and I see the remnants of some bark wrapping around the tree's base. (Greyish colour). Huh. And I also saw approximately 7 massive slightly orange ants tumbling through an ant hole. I'm not a large fan of ants, especially since I had pretty much been standing on their nest for a couple of minutes, so I hastily backed off.
Here's where my mind kicked in though, how did the tree become barkless? For some background, I live in Sydney, NSW, Australia, and it's pretty darn hot here, nearly Summer. MAYBE the wind blew it off? (but there hasn't been any wind lately) Only logical explanation was THE ANTS DID IT. Do ants really eat the bark off trees like this?

Dang that's a big picture. You can sort of see if you look closely the remains of the bark at the bottom. Been to this park before, and I'm 75% sure the tree was not albino back then.

This question appears to be off-topic because it is about diagnostic tree care, not biology as defined in the Help Center. It should be on Gardening & Landscaping beta.

Is there like a general stack exchange where I can ask questions like these because I didn't know where to put it? I knew it was slightly different to biology, but I had 0 clue there was a gardening and landscaping site

There isn't a general site like that. This can be moved to gardening.se, but generally it's good to look around here, and try to find the closest fit.

Trees have different kinds of bark. If your tree was not moist and seeping, it had bark. Since that tree is clearly alive, it's likely that it has a smooth, light-colored naturally peeling bark.

Japanese Stewartia (Stewartia pseudocamillia) has a beautiful bark that is constantly shedding in patches of tan, green, orange and brown. It always has bark, however.
Crepe Myrtle is also used in landscaping for it's beautiful, peeling bark.
To know if this condition is normal for that tree, identification (using range, habitat, bark, leaves, twigs, and sometimes flowers, fruits and seeds) is needed.
Eucalyptus grandis is native to your area. Eucalyptus species also shed bark and the picture in your question definitely looks like eucalyptus.

When it is finished peeling, it's very light. This might be your tree.

Perhaps you can put up a pic of eucalyptus which also sheds bark. It is eucalyptus in the OP's picture

@WYSIWYG - thanks! I had just done a search when your coment popped up and confirmed it. :) If you know how to reduce a picture's size, please feel free.

Size is fine. I just think it should generally not exceed 500px


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How to compare a camera and an eye
How could I compare what a normal eye can see to a camera lens?
I just went through a very comprehensive article @ CambridgeInColor, but I'm still not really clear.
When I take a picture with a SLR camera from an object about 30m from me: what focal length do I need to use, how should I present this picture to truly capture what the eye can see (because of the 40-60° that we see 100% everything)? And how should I print it to scale?
Are there any options so I can put a ruler, or a human being at a certain point to be able to show the differences?
I hope I'm clear here, but if not, please comment and I'll try to explain better!
What I'm aiming for is that I need a picture, but not a picture in itself, but more like what the eye will see at that position. Not what the camera registers.
Thanks

There are many questions similar to this posted on the SE Biology page (http://biology.stackexchange.com/search?q=camera+eye).

@Bez I of course did a search first before posting. But the only 2 closest related articles were something about sighted Ness and my question. So I believe the question is relevant. Please correct me if not.

What exactly do you wish to achieve here? I mean, what is the practical purpose of this question? As of now the question is kind of vague and a purpose-driven approach may yield more answers to this interesting question.


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Action of Ebola Viruses
This video suggests that the first cell to be the victim of viral infection of ebola is the dendritic cell which acts as the leader of immune system cells.But I am unable to understand how the dendritic cells get infected if they are the leaders?

Ebola is not something you should worry about... http://www.pbs.org/wgbh/pages/frontline/hunting-the-nightmare-bacteria/

This is a good question. The other question is how does it deactivate the dendritic cell.

Viruses can infect any cell:

a virus must have a host cell (bacteria, plant or animal) in which to live and make more viruses. Outside of a host cell, viruses cannot function.

Source
This includes the dendritic cells:

Dendritic cells are antigen-presenting cells of the immune system. Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers. They don't actually release any antibodies.

Source
Quite simply, at the beginning of an infection, the viruses / bacteria will be destroyed by macrophages.

The dendritic cell will "pick up" some of the leftover pieces.

When it finds a T-Cell that has the same configuration, it orders lots of identical T-Cells to be made. These T cells have multiple jobs, one of which is activating the B cells. It is the B cells that release the antibodies.

So Ebola.
If the dendritic cells are "invaded", then the only line of defence is the macrophages. This is often not enough to stop an attack, and it multiplies out of control.
The reason the Dendritic cells can be invaded is because they are just as vulnerable as other cells. They haven't activated the T cells, and they haven't activated the B cells, so there is nothing protecting them.
Images Source (YouTube video)


text:
How can succinylcholine cause myorelaxation?
I first thought that this is because of prolonged depolarisations.
However, I am not sure anymore, because after reading PubChem, the only possible pathways are are Choline agonist.
So I would say that succinylcholine cause myorelaxation by some cholino-receptor agonists.
I do not think it is about depolarisation and how long it is.
How can succinylcholine cause myorelaxation?

Succinycholine, as its name might suggest, is a cholinergic agonist indeed. It acts on the neural plate of skeletal muscles, where it activates the muscle cholinergic receptors.
Phase 1 block due to succinylcholine thus occurs by activating so many receptors at once, that the whole muscle gets desensitized and therefore paralyzed. A corollary of that is that muscle will twitch during activation, thus accounting for the reason why people twitch shortly before becoming paralyzed after a succinycholine iv injection. This phase 1 block will resolve in 2-5 minutes.
Now an interesting phenomenon is that if you go on stimulating the muscle with more cholinergic agonists (for example, a second iv dose of succinylcholine), you may end up provoking endocytosis and degradation of the cholinergic receptors. This is called phase 2 block, and in contrast to phase 1, it will take at least several hours to resolve. This is why we never use a second dose in the clinics, except in very special cases.
You can also read about it all on wikipedia

What is the event called that causes such a phenomena as phase 1 block and phase 2 block? Do other adrenoergic drugs and Cardiac drugs have such characteristics? How such an event documented for instance in PubChem, for instance in the link in the body of my question? I want to be aware of such events for each drug.

So the short answer to my question is that the succinylcholine cause myorelaxation because of cholino-receptor antagonism with big dose or second dose; stimulated by endocytes and degradation of the cholinergic receptors.

NOT THAT KIND OF CHOLINERGIC RECEPTOR!!! think autonomic nervous system, not autonomic nervous system... he is talking about nicotinic cholinergic receptor on the SKELETAL MUSCLE, not the muscarinic cholinergic receptors on cardiac conducting cells and muscle... this is a drug to temporarily paralyze the skeletal muscle for the sake of the surgeon doing the operation.. this is an anesthesia drug, not a cardiology drug...

secondly, this phase 1  vs phase 2 is to distinguish it from the curare-derived neuromuscular blockers which ONLY act as antagonists on the nicotinic cholinergic receptor (aka exhibit phase 2 type effects)... the phase-1/phase-2 type drugs are called depolarizing neuromuscular blockers... the curare derrived ones are nondepolarizing... here is an article listing more depolarizing types with this phase-1/phase2 type effects: http://en.wikipedia.org/wiki/Neuromuscular-blocking_drug#Depolarizing_blocking_agents another example of a drug is Decamethonium

I see what your saying, masi... the downregulation of receptors that are overstimulated is pretty common throughout pharmacology, and upregulation with blocking a receptor... for example (1) the dopamine receptor is up/down regulated with levodopa/carbidopa and it causes cycling... in typical psychotics it causes extrapyramidal symptoms... (2) it's also a proposed mechanism of the SSRIs, downregulating the seratonin receptor is what mediates the antidepressant action, supposedly... (3) also thats why going off of a betablocker quickly is very dangerous for patients... the list goes on...

oops, for "typical psychotics" it's supposed to say "typical ANTIpsychotics"...

@JasandPruski Please, make your comments an answer, since they are good and make sense.

@Masi Actually, those comments you propose to turn into an answer do not directly answer your primary question, even if they are good comments. On the other hand, I did answer your primary question and you did not mark it as accepted... just saying :-)

@Raoul The reason is that I am not satisfied enough. It seems too be too much cardiac. I may be wrong. I need something more etc references, images or anything so that I can be certain about your answer. You have now only a reference to Wikipedia which is not enough. I want to understand this topic.

@Raoul don't be upset with Masi, he is notoriously finicky... he once down voted a 1 page length answer I posted (which in ym opinion was very good) because it didn't please him... Masi simply wants to learn more and sometimes it's hard to say what he wants to learn... though his questions may be off beat and poorly worded I still feel there is a thread of insight, which always attracts me to them...

I think Masi's question was this: how is it possible for us to have a drug where the mechanism of the drug is to cause the opposite of what it actively does? the answer: to exhaust the receptor or maybe downregulation of receptors

@jasand well I'm not upset. It was just a remark. I'm not that eager for fame and reputation.

@jasand oh, and BTW both elements you cite are in my answer

I think he wanted to hear about SSRIs, Parkinson med cycling, extra pyramidal symptoms, etc... As I understand it tolerance can be more tricky... Thats it


text:
Why does A pair with T and G with C?
DNA is made up of pairs on AT and GC base pairs.
I know that A only pairs with T and G only with C. Does this apply just to humans, or are there animals where T will pair with G?
Also, surely there would be more possible combinations if A could pair with G or T or C, and DNA would have a better information density - less would be needed to hold the information?

There is no difference in base pairing between different kinds of organisms. Humans, animals and bacteria all share the same fundamental mechanisms as they all use DNA. Which bases can pair is determined by the chemistry of the individual bases.
The bases in DNA form the following hydrogen bonds when they are paired:

If you would try to combine other bases than the canonical Watson-Crick pairs, the hydrogen bond donors and acceptors wouldn't match. You need a donor/acceptor pair at each position.
There are different base pairs possible, but these situations don't really occur in DNA but in RNA. You can find G/U wobble base pairs and even base pairs that use different parts of the bases than the canonical base pairs, e.g. Hoogsteen base pairs.

My understanding is that even if there were more combos in DNA, this would not increase information density (the questioner suggests that).  Indeed, only one "side" of the DNA is read.  Worse, if there wasn't a one-to-one pairing, then one would get garbage when copying DNA, no?

Some pedantry: To be sure, they pair because it is energetically favorable for them to bind. It so happens that in this case, respectively two and three H-bonds are the most energetically favorable, but strictly speaking the bonds are not the cause of the pairing.

@OP The reason GT pairs don't exist in DNA because it can distort the structure. See the bonding patterns for details


text:
Is Norepinephrine beta2 adrenomimetic?
I know that it has alpha1, alpha2 and beta1 effects.
It has beta2 receptor where epinephrine can effect.
However, to say that it is beta adrenomimetic, I am not sure.
That is ligand binding beta2 receptor causes a stimulatory effect.
Is norepinephrine beta2 adrenomimetic?

Masi, did you try pubchem? Section 14 lists all the biological properties with references. You can do this with any molecular compound.

@anongoodnurse Thank you very much for your excellent comment! I had forgotten this database PubChem. It is so useful!

The answer can be found in PubChem, which is linked in the comment by anongoodnurse.
I would not say that
Norepinephrine is beta2 adrenomimetic

because norepinephrine has many roles such as neurotransmitter.
I would just say that
Norepinephrine is alpha, beta adrenoagonist.

More pieces of information about it from PubChem:


text:
Ephedrine or pseudoephedrine indirectly central alpha2 mimetic?
I started to think this problem by first thinking if the alpha2 mimetism is possible in either case.
It seems to be indirectly in either one.
Ephedrine seems to have more prominent effect in CNS.
So I propose that Ephedrine has indirect central alpha2 mimetic effect.
Is ephedrine central alpha2 mimetic?
I think one evidence about that would be if there is a alpha2 receptor which is activated by ephedrine somehow indirectly.

Anongoodnurse provide an excellent comment in other discussion about how to search PubChem.
Ephedrine is not alpha2 mimetic.
Pseudoephedrine is alpha2 mimetic, source:


text:
Exact location of E. coli in human body
E. coli lives in lower intestine. But exactly where can we find E. coli, and where is there none (or a really small amount) of it?
I need the exact names of parts of the lower intestine where we can find E. coli.

In Gastrointestinal Tract Location of Escherichia coli O157:H7 in Ruminants (Grauke et al. 2002):

in the lower GIT digesta, specifically the cecum, colon

It's about O157:H7, but I think the standard act a same.

FYI, this study was performed in sheep and cattle, so it may or may not apply to humans.

Yes I saw, not a human and not a standard E.Coli, but it's the best I found. If someone know better source, please share.

Best I could find for humans was Population structure of gut Escherichia coli and its role in development of extra-intestinal infections which says "large intestine"


text:
T-cells Question
T-cells are important for efficient vaccination since they have:

A. T-cell receptor (TCR)
B. CD4+
C. CD8+
D. Memory

My gut is telling me it's A since the TCR would recognize the antigens but I want to make sure. Thanks!

Can you add some reasoning as to why the other options are not correct? A is wrong, by the way. Think about vaccination, and what its goal is. When do we get vaccinated, and why? What is it trying to do?

@MattDMo Thank you for the response. So after thinking about what a vaccination does, I realized that since it recognizes and remembers invading antigens and tries to prevent them from causing harm that D would make the most sense. As for eliminating CD4+ and CD8+, they seem more of a short-term choice whereas memory would be more long-term for efficiency. Sry for my ignorance, I'm an electrical engineer taking my first bio course in a while

no worries, I just wanted to get you to think a little more deeply, and it looks like you did. Great job!

You should choose D, vaccination is about memory.

vaccination is injecting the low or non-toxic substances that having a pathogen's identifying characteristics into human or animal body. When the animals exposed to the non-injurious pathogens, the immune system will produce a protective material, such as immune hormones, physiologically active substances and specific antibodies. When the animal re-exposure to this pathogen, the animal's immune system will follow its memory and create more protective material to prevent damage from the pathogen.
So choose D

I think T cell when presented to antigen (here vaccine) will produce memory T cell, which on next encounter with the same organism may act much faster and efficiently .so i think the correct answer is option D


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Is it biologically possible for an adult's eye color to change?
Can it be that the adult eye can change color? Specifically my question is about a unilateral color change, such that the color of one eye remains constant, while the other changes color over time. Can this happen? Or can it be related to light-scattering, or an illusion of some sort?

At any rate, personal medical questions are off-topic on Biology.SE. Please consult a medical professional for your particular situation.

Short answer: The genes that encode eye color do not change, but the pigments in the eye can change due to external factors like diseases of medication.
Long answer: Yes, it is possible that the eye color of adults can change, and it can also only happen to one eye. It is then called Heterochromia. There are two possibilities for different colored eyes, either congenitial (genetic) or acquired. Since you ask only for eye color changes in adults, we can skip here the genetic reasons, as these show up in kids already. If you are interested in them, have a look into the Wikipedia article on Heterochromia.
The basis for our eye color is genetically determined, changes can later occur due to diseases (so if one experiences a change in eye color, it is always a good idea to consult a doctor) and also due to medications.
The eye undergoing a change in pigmentation can either lighten up or darken.
Fuchs’ Heterochromic iridocyclitis: (also known as Fuchs’ Heterochromic uveitis) The change is caused by an eye infection with different microorganisms like Toxoplasma gondii, Herpes simplex virus or Rubella (an probably others) but it can also have an autoimmune pathology. See reference 1 and 2 for more details.
Horner's Syndrome: This is a syndrome which mostly occurs in kids after damages to some nerves. This can lead to insufficient signals towards the pigment production and heterochromia. Rarely this can occur also in adults, where this is called acquired Horner's syndrome, see reference 3 for details.
Pigmentary Glaucoma: In this disease (also known as Pigment dispersion syndrome) pigment cells from the back of the iris float are seperated from the original place and float through the aqueous humor of the eye where they can produce pigment which over time changes the appearance of the eye. See reference 4 for more details.
Medications: Some of the medications against glaucoma (the prostaglandins latanoprost and bimatoprost) can cause a deeper pigmentation which will not always diminish after the end of the treatment. See reference 5 for more details.
Cancers: Some cancers as melanoma can also cause heterochromia, either when they are darker pigmented that the eye or when they are not pigmented. In both cases they influence the eye color. See reference 6 for more details.
References:

Fuchs' heterochromic cyclitis: review of the literature on the
pathogenetic mechanisms.
Associations of Fuchs heterochromic iridocyclitis in a South Indian
patient population
Acquired Heterochromia with Horner's Syndrome in Two Adults
Pigment dispersion syndrome and pigmentary glaucoma – a major review
Incidence of iris colour change in latanoprost treated eyes
Diffuse iris melanoma: Report of a case with review of the
literature

tl;dr The genes that encode eye color cannot change, but the pigments can change due to environmental factors like medicines or disease.

Short answer: Yes. :-)

you think my summary is worth editing to the top of your answer? I don't have the rep for that

I can do that, probably not a bad idea.

It should be noted that the opposite can also occur in an acquired manner: one iris can become paler.

To add what the previous answer did not: not only medicines and disease change the color of your eyes. Aging does that too in most (if not all!) people. Pigmentation is usually lightest in utero and right after birth. Melanin accumulates over time and makes the hair and eyes darker.
This is why many people are born blond (or green/blue-eyed) and become brunette (or brown-eyed) over a period in their lives. It can take days - usually as a baby - or decades, depending on the individual. The rate is determined genetically, i.e. it does not, for instance, depend on how much exposure to the sun you get. Melanin in the skin can do that.


text:
Does one parent transmit more DNA to the offspring than the other one?
Does one parent transmit more DNA to the offspring than the other one? Or do both parents always transmit the same amount of genetic material to their offspring?
In other words, can a baby be provided with a gene from the mother without an "opposite gene" from the father?

I completely reformulated the question. Please let me know if you think it changed its meaning.

SHORT ANSWER
The two parents transmit the same amount of genetic material to their offspring ....or almost
LONG ANSWER
Nuclear versus Cytoplasmic DNA
All Eukaryotes (everything that is neither a Bacteria nor an Archeabacteria) have nuclear and cytoplasmic DNA. Most of the DNA is nuclear DNA. As its name indicates, nuclear DNA is found in the nucleus. The cytoplasmic DNA is found in the cytoplasm, that is, outside of the nucleus. More specifically, in all eukaryotes, cytoplasmic DNA can be found in the mitochondrion. In plants (which are eukaryotes), you can find cytoplasmic DNA in the mitochondrion and in the plastids (including the chloroplasts (plastids active in photosynthesis)). See here for more information about the origin of the organelles (≈ organ of a cell) who carry DNA.
Nuclear and cytoplasmic DNA doesn't have the same mode of inheritance.
Inheritance of Nuclear Genes
In the diploid (see ploidy) phase (phase during which each individual carries two copies of each gene), an individual carries one copy from his/her mother and one from his/her father.
The above sentence assumes that a diploid phase exists (which is not the case of all species) and that genders (male vs female) exist which is by far not the case of each species. It also assumes that we are talking about autosomes (non-sexual chromosomes, see below for sexual chromosomes). These assumptions hold for humans for example. Note that the diploid phase is much longer in human than the haploid phase (spermatozoid, ovule). We say that humans are diplontic. Some species are haplontic (longer haploid phase) and some are haplo-diplontic. See life-cycle for more info.
In short: Inheritance of nuclear genes is bi-parental, each offspring necessarily carry one copy of a given gene from his/her father and the other copy from his/her mother.
Note: there are some exceptions to this perfect bi-parental transmission (see segregation distorter and intra-genomic conflict). Also, have a look at the short section on sexual chromosomes below.
Inheritance of Cytoplasmic Genes
There are many exceptions to what I am about to write...
Globally speaking, offspring inherit cytoplasmic DNA for their mothers only. That means that your mitochondrion is those of your mother only. Therefore, mothers transmit slightly more genes than fathers because of the concern of cytoplasmic genes.

To complete the picture...
Inheritance of Sexual Chromosomes (Nuclear DNA)
Not all sexual species have sex chromosomes but some do. In these species, it is not rare that one of the two sexual chromosomes is shorter than the other (In mammals, the $Y$ chromosome is shorter than the $X$ chromosome). In such a case, the male transmits slightly less DNA to their male offspring than to their female offspring. Also, in such case, fathers transmit less DNA to their male offspring than do mothers but males transmit as much DNA to their female offspring than do mothers.
The evolution of sex chromosomes is a very interesting subject as well and you will find tons of information on this website or on different sites.
Non-genetic inheritance
Nutrient in eggs
Not only genes are transmitted. Parents also transmit proteins and nutrients in the egg. Females transmit more nutrients to their offspring than males.
Epigenetic
Not only genes are transmitted. Parents also transmit modifications on the DNA that are not modifications in the DNA sequence per se. These modifications are called "epigenetic modifications". Not all species can produce epigenetic modifications. In species who can transmit epigenetic modifications, both males and females can produce them. It is possible that in some species mother have a higher variance in the modifications that they transmit than males (or vice-versa) but I am not aware of such things.
Environment and Cultural transmission
Not only genes are transmitted. Parents also offer an environment in which the offspring grow. Some species typically feed or protect their offsprings. Depending on the species males or females may have more influence on the environment experienced by the offsprings. Finally, in some species (human, chimps and orca for example) a set of traditions (culture) are transmitted to the offsprings from the parents. And depending on the species the father or the mother may have more influence in the culture transmitted to the offspring.
Length of chromosomes may differ between two randomly sampled individuals
Not all variants between two chromosomes in a population is caused by substitutions of one nucleotide by another. Some variation is due to deletions of nucleotides or insertions of nucleotides. You can even a very long piece of DNA who get inserted, duplicated or deleted. Therefore between two given individuals, the exact amount of DNA that is transmitted may also differ only because they happen to have different variants. However, this is not a systematic difference in the quantity of DNA that is transmitted by one sex or another unlike the other cases presented above.

Certainly in the case of flowering plants a triploid can be created by crossing a diploid by a tetraploid.
In this case the teraploid parent will contribute twice as much DNA to the offspring than the diploid parent. Seedless fruits such as bananas, grapes, and watermelons are produced using such crosses.
There is also the possibility (and it does occur) where 2 diploid parents can produce a viable triploid offspring by one parent contributing an unreduced gamete. Here again one parent would contribute more DNA than the other. Such events are fatal in humans but need not be in some species of fish.
In flowering plants, tetraploid and hexaploids can often mate to produce pentaploid offspring. Again an example of unequal DNA contribution by the 2 parents to produce a viable offspring. Such pentaploids can often be semifertile being able to back cross to either parent.
Pentaploid dog roses actually reproduce normally by having a 4 (female) to 1 (male) contribution from the 2 parents.
Interestingly a diploid and tetraploid parent can in rare instances contribute equal amounts to the resulting tetraploid offspring. This happens when the diploid parent contributes an unreduced gamete.
Amazingly in newly created tetraploid hybrids, tetraploid by diploid can produce a diploid offspring where both parents make an equal contribution.
References
Meiosis in Polyploids by W. C. F. Newton and C. D. Darlington in Journal of Genetics 1929
The history of the garden hyacinths by C D Darlington, J B Hair and R Hurcombe in Heredity 1951
Rules of Engagement: Have Pollen—Will Travel by John Perkins · Sally Perkins in Azalean 2010
Weighing in: Discovering the ploidy of hybrid elepidote rhododendrons by Sally Perkins, John Perkins, José Monteiro de Oliveira, Mariana Castro, Sílvia Castro, João Loureiro in Rhododendrons, Camellias and Magnolias, Royal Horticultural Society, Editors: Simon Maughan, pp.34-48 2012
Untersuchung des Ploidiegrades elepidoter Rhododendron-Hybriden by Sally Perkins, John Perkins, Mariana Castro, José Cerca De Oliveira, Silvia Castro, João Loureiro in Rhododendron und Immergrüne , Deutsche Rhododendron-Gesellschaft e.V. , Seite 21: pages 21-42; 11/2013


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Do "Giraffe Weevil" males build Nests
I had came across an insect  near my backyard in India(Kerala). I haven't seen this one before and I searched web to find out what insect is this and found its image which saying its a "Giraffe Weevil" (Trachelophorus giraffa). The link below says that this insect is endemic to Madagascar.

http://en.wikipedia.org/wiki/Giraffe_weevil and
They are herbivore insects, with adults feeding on a tree that is commonly known as the "giraffe beetle tree"
(Dichaetanthera arborea)
This states that these insects need the "giraffe beetle tree"(Dichaetanthera arborea) which is also native to Madagascar.
So how come this insect could be found in India(Kerala), and further more all the above links state that the long neck of these dimorphic insects are evolved for fighting and nest making but they do tell that after mating the females will make the nest and lay one egg inside, So did the male insect make any nest in reality, if so then why the male have to perform both nest making and fighting.[Sorry for the errors,also there are more links to this]

Are these photographs of the specimen you found or are they taken from the web? If the latter, the likeliest explanation is that what you found looks very similar but is a different species.

Where have you read that the long neck is used for nest making (the second part of your question)? It is hard to evaluate how credible the statement is without this information.

This link says it http://en.wikipedia.org/wiki/Giraffe_weevil

As the comment by @terdon says, the most likely explanation is that your species identification is mistaken. The superfamily Curculionoidea, which contains the weevils (Curculionidae are the true weevils) is also extremely species rich. Without seeing a picture of what you found, there are many other similar species with long necks in the family Attelabidae, which is the family of Trachelophorus giraffa. For instance, the wikipedia page includes a picture Apoderus longicollis which is very similar to the Giraffe weevil from Madagaskar, and it is supposed to be found in India (see GBIF info):

Paracycnotrachelus is another genus found in Asia where some species have long necks. Another giraffe-necked species is also found in New-Zealand - see Lasiorynchus barbicornis - so the overall body shape is not that unique (note that much of the elongation in this species is of the snout though):

Even if we should never rule out the possibility of range changes/introductions, this must be based on close examinations of the specimen, and it is even more unlikely in this case since Trachelophorus giraffa seems to be a very specialized species.

I had seen the Wikipedia link and it also says that the female roll the leaves for making nest, so is this means males don't participate nest making. Also the photographs I posted are taken from web and I strongely identify the specie as either "Apoderus longicollis" or "Trachelophorus giraffa" and its brightly red colored as giraffa and the longicollis mentioned is light red in color .S I thought it was giraffa, From the day I found this insect I am thoroughly searching for another one but failed to find any.

Keep your eyes open! A proper identification of an individual is the way to go.

First of all, the beetle you found likely doesn't belong to Trachelophorus giraffa. There are lots of of species in the family Attelabidae, many of them having long necks in males and some were described or are known known from India.
I couldn't find any primary source on the nesting behavior of Trachelophorus giraffa, and I suspect that most of the web-pages mentioning the male participation in creating the cradle by rolling leaves stem from this popular book, while in at least another popular book it is explicitly written that females make the cradle.
As attested here, "all females of the species Attelabidae make their host-plant leaves into cradles where they oviposit", so I suspect that Trachelophorus giraffa is no exception to this rule. Here is a very detailed description of mating behavior of a species with similarly long neck: males take no part in building the nest and seem to utilize their necks only when competing for female.


text:
Is Zeiss Primo Start microscope worth the price for student use?
I study physics but I have got interested about biology too. Surfing around the web, I have found out that in buying microscopes one needs to decide between the cheaper no-name brands vs. the four big ones: Zeiss, Nikon, Leica, and Olympus.
From the four big ones, only Zeiss delivers directly to my country. The price for Primo Star with phototube and Full-Kohler illumination is 1.8k euro or 2.3k usd. It has only bright-field optics but dark-field (if I got it correctly) is easy to add, as well as phase-contrast.
Anyway, I was wondering how much I would get out of the scope as a home user. I would probably do plant biology. I would also like to learn some staining techniques.
How difficult it would be to run some mini-studies at home? Do research? I would know about imaging quite a lot..
(There was some other similar questions but they did not mention home use.)

What kind of research are you thinking about? You might find the magnification/resolution of a bright field microscope limiting.

It doesn't matter whether you're using your microscope in a 2 billion dollar building or a garden shed, a microscope is a microscope. Either way you'll want a clean work area, isolated from the rest of your living space (especially depending on what you plan to stain with). You'll get out what you put in. Is the opportunity worth $2300 USD to you?

I have the Primo Star.
Very sturdy and wonderful optics.
Search the net: many university studies are made with the Primo Star!
You cannot go wrong.

I'm defenitly no fan of the Primostar. It's made to order for Zeiss, probably by Meji.
It's a fine microscope allright, but compared to the gray and beige Standards, it's a toy.
And those gray and beige Standards were already kind of toys, compared to the former black GF stands...
Being a "home user" there are far better and at the same time much cheaper  alternatives availlable on the second-hand market.
In Europe, a Standard 14, basicaly equipped (4,10,40,100 achromats, 0.9 condenser, build in 6V/10W HAL illuminator, binocular) can be bought for anything between 100 and 200 Euro.
This is a universal platform, designed with flexibility regarding applications such as DF, FC, DIC, fluorescense... in mind. The same can't be said to that extend regarding the Primostar.


text:
Sensory adaptation regarding smell and hearing
Imagine the scenario. My friend and I are playing a game of chess near a highway. Initially, I notice the sound of the highway. While I'm playing chess, however, I do not notice it. After the game my friend asks me if I can hear the highway, and I regain my ability to notice it. This seems to be different for smells.
If we were playing chess in a room filled with garbage, the smell would gradually fade away. If my friend asked me if I could smell the garbage, I would not be able to smell the garbage as severely. What is the cause of this difference?
It seems that visual and touch follows the same pattern as hearing. What makes smell unique?

Adaptation occurs in every sensory system. For example in vision there is the motion after effect that occurs through adaptation of visual neurons in the cortex. Also, the visual system strongly adapts to low and high lighting conditions through light and dark adaptation. The tactile system also shows substantial adaptation, as touch receptors in the skin fail to convey information after prolonged stimulation (you won't feel a watch/ring/band aid etc after wearing it for a while). For example, mechanoreceptors in the skin such as the Pacinian corpuscles fail to transmit tactile stimuli when activated for a prolonged time. The auditory system also adapts to loud sounds by cortical mechanisms as well as  peripheral mechanisms through the middle ear muscles. Lastly, as you correctly identified, the olfactory system adapts to stimulation as well through metabolic mechanisms that decrease the responsiveness of chemical receptors. The list of adaptational mechanisms provided is not comprehensive, but I just used some obvious examples to show that adaptation occurs in all the senses in a variety of ways. In fact, one of the hallmarks of any physiological intact sensory system is the capability to operate over a wide range of stimulus levels. For example, vision operates over a range of intensities differing 8 orders of magnitude, while hearing operates in an intensity range of 1013. To maintain such an impressive range of input intensities sensory systems have to adapt at various levels. As an analogy, the same applies to your photo camera in which the exposure time has to be regulated in order to take pictures under different lighting conditions.
So to come back to your suggestion that smell cannot be revived after continued stimulation while it can be revived with other senses is not true I think. The attentional revival you are talking about is not so much adaptation but has more to do with the attentional shift, which may occur with any sensory modality.

I do believe that it is true that you cannot revive the smell to a certain degree. For example, when my toilet was broken and it got very smelly, while I was cleaning up in there, it smell was more bearable than initially. I would try to detect the smell again, but it did not seem too bad, and it was bad initially.

@CognisMantis - I agree with you. You need to step outside and 'clear the smell from your nose' to smell it as well again. It's not so much a central effect as a peripheral exhaustion.

To revive the tactile sense you also have to 'reset' it. That's adaptation. It may well be that continued acoustic stimulation results in less pronounced adaptation. Good point


text:
Can an organism process H₂O into H₂O₂?
In an answer to a recent question on Worldbuilding, I suggested that an organism convert $\ce{H2O}$ into $\ce{H2O2}$. I suggested a few processes that yielded the desired final result ($\ce{2H2O \rightarrow H2O2 + H2}$ and $\ce{H2O + O3 \rightarrow H2O2 + O2}$). I noted that both were mere guesses. The feasibility of it was debated because hydrogen peroxide is a rocket fuel and contains a lot of energy (I heavily modified the answer and set it on an entirely different track after another mistake was pointed out).
Could some process similar to this ever happen in an organism?

Hydrogen peroxide as a reactive oxygen species (ROS) is a highly problematic molecule for the processes inside of cells (it can spontaneously oxidize and damage cellular components). With Catalase, organisms have a very effective enzyme which degrades the peroxide into water and oxygen.
However, although the molecule is problematic, it is still produced by organisms in traces. For its production by the NADPH oxidase, first NADPH is oxidized and superoxide is formed. The reaction looks like the following:
$NADPH + O_2 \rightarrow NADP^+ + H^+ + O_2^-$
In a second step the superoxide dismutase uses two molecules of superoxide and H+ to generate H2O2, the total reaction (which is divided into several steps) looks like this:
$2O_2^- + 2 H^+ \rightarrow H_2O_2 + O_2$
H2O2 is then usually degraded by the catalase (or used in immunological processes like the respiratory burst).

Actually, there's a lot of animals, plants and microbes can do it. However, it is just an Intermediate process in general. Here's a strong example. In the condition with the absence of catalase, glucose oxidase can catalyze glucose + H2O + O2 become gluconic acid + H2O2. Another process can also generate H2O2 catalyzed by Ero1.

Would it be possible to add a source to your answer? It helps with people finding material to pursue more reading about it.

Shan, C., Yang, H., Song, J., Han, D., & Niu, L. (2009). Direct electrochemistry of glucose oxidase and biosensing for glucose based on graphene. Analytical Chemistry, 81(6), 2378-2382.
Shu, S., Ju, G., & Fan, L. (1988). The glucose oxidase-DAB-nickel method in peroxidase histochemistry of the nervous system. Neuroscience Letters, 85(2), 169
Umana, M., & Waller, J. (1986). Protein-modified electrodes. the glucose oxidase/polypyrrole system. Analytical Chemistry, 58(14), 2979
Wilson, R., & Turner, A. (1992). Glucose oxidase: An ideal enzyme. Biosensors and Bioelectronics, 7(3), 165-185.


text:
Why do flipped cockroaches sometimes lose their heads?
Sometimes I see in my house there are flipped cockroaches whose lose their heads. I used to have a cat, but there is no pet in my house anymore so I think it's only ants can be involved in this. But if so, the headless cockroach should be preyed already. Is there any explanation for this?

In all likelihood, it is your cat who crunches the cockroach's head once it catches it and/or finishes playing with it.
Ants do eat bugs but they are usually not so selective that they'll carry off the head alone. With more manageable insects, they carry the whole thing off; otherwise they take it apart and carry it away in pieces if they're interested in it as a food source.
If you watch a cat with a mouse, chipmunk, bird, large insect, etc, they often seek to kill the animal with a throat or nape bite if they are done 'playing' with it. I've found headless prayer mantises and other large insects in my garage many times, and have seen my cats beheading them.
The techniques that cats use to kill prey vary with prey size

I found a clip in YouTube showing a cat eats a chipmunk's head. Does it swallow the cockroaches' heads or just beheading them? Why they bother to kill them when they don't even eat them?

Sometimes they eat the insect's head, sometimes they don't. They have instincts that are unrelated to hunger. For example, dogs love to chase moving objects. That's great when it's a frisbee, but not so great when it's a child. Cats have this instinct as well.

Today I found a headless cockroach in my house again, even though my cat has gone. Do you have any explanation for this?

@Ooker - Nope. none. What do other cockroaches eat?

I don't know. Maybe food trash?

Maybe dead cockroach heads...?


text:
MHC-I presentation during infection
Which cell type cannot process and present antigen peptide in association with MHC-I when it is infected?

All nucleated cell (cells with defined nucleus) are able to present MHC-1 on their surface.  Since red blood cells do not have nucleus, they are not able to represent antigins in MHC-1 molecule.
Hope that helps check wikipedia for reference


text:
In males, why it is difficult to control orgasm?
Why it is difficult to control orgasm in male humans? How are orgasms controlled and what is different between males and females?
We can control urine for few minutes, but we can't control orgasm for more than a few seconds, but both are discharging though same organ (penis).

Both men and women can learn to control orgasm for prolonged periods. It is a reasonably common part of BDSM sexual practices to insist that the 'sub' requests permission before orgasming.

@JackAidley - if you'd like to answer with supporting sources, I would be very interested in your answer.

Did you mean "ejaculation"? Orgasm and ejaculation are different, and there is "dry orgasm" that doesn't include ejaculation (or "wet orgasm").

The sphincter of the bladder is under voluntary control (that's what toilet training is about). That's why you can hold your urine even when the stretched bladder is sending messages to your brain that you really have to go. That's not to say there aren't involuntary effects on the bladder during orgasm.
Orgasm is a separate entity. It is a complex neurological response with four stages. Orgasm is controlled by the autonomic nervous system and is a response that can be controlled as easily as pupillary dilation/contraction in response to light (that is, not at all). However, there is some measure of voluntary control over the plateau phase of orgasm.
In a bit more detail,

expulsion is a spinal cord reflex that occurs as the ejaculatory process reaches a ‘point of no return’. During expulsion, the smooth muscle fibers of the bladder neck contract to prevent the backward flow of semen into the bladder; the pelvic floor muscles, along with the bulbospongiosus and ischiocavernosus muscles, have primary roles in this function, and display stereotypical rhythmic contractions to propel semen distally throughout the bulbar and penile urethra. During this process, the external urinary sphincter is normally relaxed. The bladder neck and proximal portion of the urethra, which both contain abundant smooth muscle fibers, receive dual sympathetic and parasympathetic innervation. Besides the cholinergic and noradrenergic components, the principal mediators found in these nerve terminals are NPY, VIP, and NO. The external urethral sphincter and pelvic floor striated muscles are solely regulated by the somatic nervous system, but there is no definitive evidence that a voluntary control of the expulsion phase exists in humans.[1]

Human sexual response cycle
Physiology of male sexual function
[1] Ejaculatory Disorders: Pathophysiology and Management: Physiology of Ejaculation


text:
Crude oil contamination hazard
I'm not sure if this is physics, biology or chemistry related so I will start here.
I'm from a city (Baku, Azerbaijan) where crude oil is known to be extracted since ancient times. Oil is no longer being produced within city limits however soil is still heavily contaminated in some parts of the city.
Recently a major project has started to turn one of the most contaminated parts of the century old oilfield (see http://en.wikipedia.org/wiki/Black_City_(Baku) for more) into urban territory.
Developer promises that all contaminated soil is being removed and recultivated but I still have some doubts about it. I also don't trust official reports so would like to conduct my own investigation.
What is the health hazard of soil contamination? Are hydrocarbon vapors direct health hazard? Or may be it's radon that surfaces with oil? What and how to check? Would I be ok if I just check radioactive contamination with dosimeter/radiometer?
Edit:
You can ignore water contamination and direct contact with chemicals. I'm talking only about vapors during hot season.

Soil contamination or soil pollution is caused by the presence of xenobiotic (human-made) chemicals or other alteration in the natural soil environment. It is typically caused by industrial activity, agricultural chemicals, or improper disposal of waste. The most common chemicals involved are petroleum hydrocarbons, polynuclear aromatic hydrocarbons (such as naphthalene and benzo(a)pyrene), solvents, pesticides, lead, and other heavy metals. Contamination is correlated with the degree of industrialization and intensity of chemical usage.

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

The acute health effects of hydrocarbon mixtures are generally associated with exposure concentrations at thousands of ppm. However, the exposure concentration and exposure duration leading to the onset of acute health effects varies between individual hydrocarbons, and this may influence the effects of exposure to mixtures.Health effects associated with a single exposure to hydrocarbons are asphyxiation, narcosis (ie depression of the central nervous system; anaesthesia), cardiac arrest and aspiration. Of these, the first two are probably the most significant in the offshore context.

http://www.hse.gov.uk/offshore/notices/sn_04_04.htm

In relation to the assessment of vapour risk,petroleum hydrocarbons and chlorinated hydrocarbons differ in their potential forvapour intrusion (VI) risks, primarily because petroleum hydrocarbons (PHCs) readily
  biodegrade in the subsurface when sufficient oxygen is available(USEPA 2011,2012a). Hence while a number of aspects of this guidance are general and can beapplied to a range of volatile compounds, the guidance is intended to specificallyaddress PVI and should not be applied to sites contaminated with other compounds
  including chlorinated hydrocarbons and landfill gas.

http://clu-in.org/download/issues/vi/CRCCARETechreport23-PetroleumhydrocarbonvapourintrusionassessmentAustralianguidance2.pdf

Organic compounds can be a major pollution problem in groundwater. Their presence in water can create a hazard to public health and the environment. This page will focus on the BTEX's which makes up one of the main groups of soluble organic compounds that find their way into our soil and groundwater. One of the most common sources for BTEX-contamination of soil and groundwater are spills involving the release of petroleum products such as gasoline, diesel fuel and lubricating and heating oil from leaking oil tanks. Because of their polarity and very soluble characteristics, the organic chemicals (BTEX's) of petroleum products will be able to enter the soil and groundwater systems and cause serious pollution problems.

http://www.webapps.cee.vt.edu/ewr/environmental/teach/gwprimer/btex/btex.html

Petroleum vapours at percentage concentrations are flammable, potentially explosive
  and acutely toxic; lower explosive limits (LEL) for many volatile hydrocarbons are in the
  low percentage range. Petroleum vapours are denser than air. Some components of
  petroleum vapour are also chronically toxic at trace concentrations and as such are also
  considered under the heading VOCs [volatile organic compounds ].

http://www.epa.nsw.gov.au/resources/clm/120932GroundGas.pdf
This document contains site investigation details which describes how to find traces of compounds in soil and water.
.

I appreciate the collection of information from many different sites. I think this would be most helpful to the author if you synthesized the information a little more, presented some main takeaway points? Also, I noticed you have copy-pasted a number of paragraphs directly from the different links. While it's good you show your sources, you might want to look at the guidelines on referencing and see if you can make these quotes conform better to standards: http://biology.stackexchange.com/help/referencing. In particular, I think you could make it clear which parts are direct quotes.

@A.Kennard  As the author asked multiple questions I thought it will be nice if I give him direct copies from those links and those sentences seems fine to me, and mostly I thought when he visit those pages he can identify those sentences there and continue reading. It is so much appreciable that you spend some time to guide me through SE. Thanks for your valuable advice, I'll try to improve.

Thanks Jvrek! It seems like it shouldn't be a cause to cancer or similar nasty stuff unless really high concentrations. I've been living in close proximity to the area and haven't noticed any immediate and obvious health problems. I'm just total noob on the subject therefore hesitate a lot.


text:
Resilience to the neurotoxins of Indian King Cobra
I read on Wikipedia about this:
King Cobra - Wikipedia
In Thailand, a concoction of alcohol and the ground root of turmeric is ingested, which has been clinically shown to create a strong resilience against the venom of the king cobra, and other snakes with neurotoxic venom.
Though, I have been in the village parts of India where King Cobra is frequently encountered, I have never heard of this knowledge.
Can somebody please explain the scientific basis of this statement and possible reasons for this?
[PS]: Can somebody also please create a tag for "Snakes"?

Well, turmerin, the compound in turmeric has been medically proven to help neutralize venom from King Cobras in snakes (reference1, reference2). It has also been used in ayurveda for snake bite treatment (reference) The alcohol I guess is just used to help ingest the turmeric and act as a pain reliever, though it strangely seems counter-productive since most snakebite help guides advice against the consumption of alcohol after getting bitten (reference1, reference2) due to its blood thinning properties.
Having said that, I guess personally, I would go for anti-venom rather than ingest turmeric. As a quick remedy until you get the anti-venom you should be able to depend on turmeric.

I think the alcohol is used to extract the turmerin from the roots.

@Chris Yes it is one way of doing so apparently.

Turmerin is water soluble. Perhaps they extract curcumin with alcohol.

As The Last Word said turmeric is a suggested medicine for cobra bites in India,also Bromelain found in Pineapple and Papain in Papaya fruit are also suggested medicines by folks. Although they are unaware of these chemicals they do use these fruits for venom treatment.
Also oral administration of garlic is said as a prophylactic tool against cobra venom.
Azadirachta indica(Neem) is also a prescribed medicine for Indian Cobra bites.
http://www.google.co.in/url?sa=t&rct=j&q=&esrc=s&source=web&cd=9&ved=0CE8QFjAI&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F51064057_Herbs_and_herbal_constituents_active_against_snake_bite%2Flinks%2F0912f50a48bd135b2c000000&ei=AlF0VImNFoaNuASv8YCICw&usg=AFQjCNE9BJ_rGjd3eG2TH-rSJh4-bIaq6w&sig2=1iP7DTk7Z34YZ4vWiQnvbg&bvm=bv.80185997,d.c2E&cad=rja

Cipadessa baccifera leaves have powerful anti venom properties, especially for the treatment of cobra poison.
  http://indiabiodiversity.org/species/show/31204

Aristolochia taxa have also been used as reptile repellents. Aristolochia  serpentaria (Virginia snakeroot) is thus named because the root was used to treat snakebite, as "so offensive to these reptiles, that they not only avoid the places where it grows, but even flee from the traveler who carries a piece of it in his hand".
I couldn't find if there is any remedy for snake bites exist in Thailand as you said but i found this,

A hospital in Thailand hooked up with Mahasarakham University and brewed up a remedy. It’s a mix of betel nut, lime juice and the root of Trigonstemon reidiodes. "
  https://hughpaxton.wordpress.com/tag/kap-choeng-hospital-develops-herbal-cure-for-cobra-snake-bite/

Without references I would suggest a traditional snake bite remedy used in my place called "Vishakallu"[Venom Stone] with ingredients
Ocimum sanctum (Tulsi leaves),
Anisomeles malabarica(Perumthumba),
Sandal wood
these medicines are treated with a stone and this stone is used for healing and it is then placed in cow milk and stored in cow dung ash and can be reused 15+ times.

what it means is that a warm clear extract of turmeric powder given as oral drink and  washing of the snake bite wound will save the person from death till the antibody injection is given. the above is due to stoppage of a toxic enzyme called PLA2 which universally present in all snake venoms
if one thinks that it is like an ad it  shows the in ability to understand and i feel such irresponsible statements are best avoided
 leela srinivas

Welcome to Bio and thanks for the great answer. Do you happen to have a reference at hand?

Thank you for the query, I would have search would have shown that, we are the pioneers to first use Turmeric against snake venom.  Be it, Cobra, Krait or Viper. It is the universal truth that, all the snake venom is 90% protein and out of that, 60% is the lethal inflammatory toxic enzyme called Phospholipase A2 (PLA2).  PLA2 is an enzyme that breaks down the cellular plasma membrane containing phospholipid and allows the entry of toxic enzyme.  The toxic enzyme let loose a cascade of events that goes through cyclo-oxygenase and lipoxygenase pathway with release of arachidonic acid - 20 carbon fatty acid which forms the precursor of pain causing inflammatory by-products.  Since, Turmeric can destroy the activity of phospholipase A2,the inflammation and accompanying inflammation reduced considerably and the life of the patient extended by two to three hours giving time for the anti-venom antibody treatment. The attractive feature of the above "On the spot" treatment by Turmeric is that, the snake can be any species because PLA2 is the key toxic enzyme in all the venoms. The way to administer Turmeric on the field is to take two to three fist full of Turmeric powder and dissolve it in warm water, then it is filtered through a clean cloth and the clear extract without any residue about a glass is given to drink by the patient when it is warm.  The rest of the water is used to continuously washed the bitten spot so that, the local inflammation is subsidized. You may refer the to the following publications where it is shown that Turmerin, a water soluble antioxidant protein from Turmeric binds to PLA2 distal to the active site and changes the conformation of Phospholipase A2 in such a way that, it is no more hypertoxic.  Thus extending the life of the patient and reducing pain and inflammation.
Reference:
New biological activity against phospholipase A2 by Turmerin, a protein from Curcuma longa L.

As of current, it's unclear what you are trying to convey with this answer. Could you clean up this post?

It reads more like an advertisement to me. I vote for deletion.


text:
How can natural selection occur at species level whilst not occuring at the individual level?
The chapter by Douglas Futuyma in 'Evolution' (Losos et al 2013, Princeton) states that natural selection can occur at the species level. Futuyma states that if natural selection occurs at the species level it does not occur at the individual level:

Neither gene selection nor species selection has molded the advantageous characteristics of individual organisms; rather, they have affected properties at the gene level or at the species level.

But how does natural selection occuring at the species level not affect individuals? Surely any selective advantage of a particular species must occur among particular individuals of that species. For example, if Species A is selected because it is browner than Species B, this will be because individuals of Species A are browner than individuals of Species B.

could you post the word for word quote?

The quote is word for word. I've also correct a number of mistakes in my question

natural selection works in the genome level.

I think you have misunderstood the passage. Here is a larger section (found at google books):

Natural selection can also occur at the level of species, for certain characteristics enhance the rate of origin of new species or diminish the likelihood of species extinction. For instance, the number of species in lineages of herbivorous insects has generally increased faster than in closely related lineages that have other feeding habits. Neither gene selection nor species selection has molded the advantageous characteristics of individual organisms; rather, they have affected properties at the gene level or at the species level. But individual selection, selection among individual organisms within populations, is at the center of evolutionary theory. It is at this level that selection explains most of the adaptive features of organisms.

Going through this part-by-part; the first two sentences state that lineage/species selection can occur, in the sense that species traits can enhance the speciation rate of a lineage or decrease their risk of extinction, relative to other lineages (e.g. in herbivorous insects).
He is then saying that the traits that are the target of this selection are not traits of individuals but traits/properties of the species/lineage.
An example might help to explain the point. For instance, it has been argued that pelagic larvae in sessile ocean species will lead to higher dispersal rates, which means that species can colonize new environments, and this can lead to speciation through adaptive radiation (Jablonski & Hunt, 2006). A larger range will also correspond to lower extinction rates (everything else equal). The trait might also be fixed within a lineage (so there is no variance at the individual level within-species), and if so, this lineage as a whole could have higher speciation rates and lower extinction rates compared to a sister lineage that lacks pelagic larvae.
The individuals within species will naturally have the underlying traits (pelagic larvae), but the traits that are selected at the lineage level (extinction risk & speciation rate) are not properties of individuals but are traits of the lineage/species.
He then ends by continuing with "normal" individual selection, and states that processes at this level is responsible for most adaptive features of organisms. It should also be noted that lineage selection is still considered controversial, and it has been shown that it is inherently much weaker than selection at the individual level. Personally, I think there are some very good examples of how species/lineage selection can function, but to what extent it is an important process for species and organisms is an open empirical question. If you are interested to look further, Jablonski (2008) and Okasha (2007) are two good starting points.

Nice one - I was just about to head for a google search of the text!

So if Trait A is selected above Trait B, and if all individuals of a species have Trait A, then this is species-level selection?

@luciano Not quite - its not that simple. You need to think of a lineage in the same way you would about a single species, so that the species within the lineage correspond to individuals within a species. The idea is that all species within lineage A possess trait A and all species within lineage B possess trait B. This can then lead to lineage A increasing faster than lineage B (have higher net speciation rate). That all individuals within all species in lineage A and B possess the same traits can be seen as a byproduct of this.

@luciano The traits do not need to be fixed either. It could just as well be the case that the overall frequency of something is higher in lineage A compared to lineage B, and that this leads to differential properties/traits at the lineage level.

Aha, I think the penny has just dropped. Your comment 2 above this one is what did it.

@luciano Glad I could help.

I think there is some misunderstanding there, natural selection does act on an individual and can be determined by its genes (assuming there is genetic variance underlying the variance in trait). Those with more favourable genes will have more favourable phenotypes and thus be more likely to survive/reproduce. However, (genetic) evolution does not occur within an individual, evolution occurs at the population level as the frequencies of existing and new mutations changes over time or space.
Following from your example: Two morphs of a species exist, brown and white (like the classic peppered moth), which is genetically determined, and one has a selective advantage - let's say brown. Thus all individuals of the brown morph are more likely to survive and reproduce. Over time the genes causing the brown phenotype will increase in frequency in the population and frequency of brown (white) moths will have increased (decreased).
I suspect it would be helpful if you included more of the text preceding the statement.
Edit: having seen @fileunderwaters answer, which arrived seconds before I posted mine, I see that I was right, more of the text was useful :)
So going back to the moths, an individual moth would not be able to change it's trait in response to selection.


text:
How do gory images lead to nausea?
How do gory images lead to nausea?
Yesterday my friend visited shock sites (a website). He said that he got nauseous sensation within seconds after viewing the gory images. However, I don't understand how seeing such sights can lead to nausea? Eyes are present at the top of the head and the digestive tract is present below the mouth. They aren't physically connected.

Hint: due to imbalance of enzymes

just a quick note on formatting - using the ">" makes the text appear as a quote, as if you are quoting a source

I changed the word graphic to gore.

The connection between eyes and food pipe had to do nothing with the motion sickness because the visual inputs and outputs to these sensory information are processed in the brain itself, So there is not need for eyes and food pipe to be connected together in order to cause nausea.

Vasovagal response or vasovagal response or vasovagal attack (also called neurocardiogenic syncope) is a malaise mediated by the vagus nerve. When it leads to syncope or "fainting", it is called a vasovagal syncope, which is the most common type of fainting.

(from http://en.wikipedia.org/wiki/Vasovagal_response)
This case is most commonly seen in adults and adolescents. There are several syndromes which comes under the vasovagal syncope which consists of symptoms like loss of consiusness,lightheadness,nausea,sweating,tinnitus,confusion,altered heart rate,fuzzy thoughts,cloud like spots in vision etc.

Vasovagal syncope occurs in response to a trigger, with a corresponding malfunction in the parts of the nervous system that regulate heart rate and blood pressure. When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting and confusion.

(from http://en.wikipedia.org/wiki/Vasovagal_response)
Several pshychiatric disorders can cause vasovagal response like,

Agoraphobia
Obsessive–compulsive disorder
Social anxiety disorder
Blood-injury phobia
Hemophobia
Traumatophobia
Trypanophobia

http://www.nwocc.com/Pt%20Education/neuro_syncope.pdf http://en.wikipedia.org/wiki/Vasovagal_response

When it comes to seeing red, the faint feelings could be tied to a phenomenon called blood-injury phobia. According to WebMD, this condition evolved as a way for humans to cope with threats:
"The idea is that back in time, when someone was coming at someone else with a sharp stick or rock, a kind of genetic variation allowed certain people to faint in response," explains Tyler C. Ralston, PsyD, a clinical psychologist in Honolulu, who treats people with blood-injury phobias. Warriors who fainted looked dead and were passed over during battle. The blood pressure drop also might have helped those who were wounded avoid bleeding to death. Survivors then passed on the "fainting" gene.

(from: http://www.popsugar.com/fitness/Why-Sight-Blood-Makes-You-Feel-Faint-3061135)
"Overcoming Obstacles in CBT" written by Yvonne Tone and Michael McDonough states a condition about a patient having similar psychological problem described in the question. Here the patient's panic is associated with "gory images" of injury or illness, and his responses included intense nausea, pale skin, sweat and sometime fainting. He also reports avoiding gory scenes on TV/filim and medical programmes. The problem is identified as co-morbid panic/agoraphobia and blood injury phobia.

http://books.google.co.in/books?id=1uIYqkKgKRYC&pg=PA44&dq=nausea+and+gory+images&hl=en&sa=X&ei=qLZ2VJPMJ420uAS8qoHIBA&ved=0CB0Q6AEwAA#v=onepage&q=nausea%20and%20gory%20images&f=false

The connection is almost certainly psychological.  For me, I can watch Grey's Anatomy, Spartacus, or any number of bloody shows while eating, but while researching microsurgery I came across an image of a hand cut in half and it bothered me for an entire day.  Therefore, for me at least (and likely others) nausea from gore is context dependent and therefore likely psychological.
Then again, there may be some biological basis.  From https://en.wikipedia.org/wiki/Disgust#Neural_basis :

Functional MRI experiments have revealed that the anterior insula in the brain is particularly active when experiencing disgust, when being exposed to offensive tastes, and when viewing facial expressions of disgust.

That Wikipedia article links to this Letter to Nature: http://www.nature.com/nature/journal/v389/n6650/full/389495a0.html which provides more detail.
Also, the part of the brain that actually controls vomiting is called the Area postrema.
So...  in short, my answer is "The insular cortex of the brain is responsible, though there is a large psychological component."

convert to a comment

Expanded to reflect neurological basis and provide an answer