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Why are some human injections intraperitoneal?
In humans, what benefit do intraperitoneal (IP) injections(old/cheap rabies vaccines, or cancer related injections) offer versus traditional intramuscular injections?
For example, where I live, the rabies are not administered right away after a bite because of the associated discomfort(cheap IP injections) or cost(newer intramuscular injections) they represent versus the low probability of a dog having rabies and the long incubation period(instead, the offending dog is observed carefully for 10 days to decide, or the vaccines are administered in the fourth day if not found). So, since speed of action doesn't seem to be an important factor, what are the benefits of IP injections?

Likely has to do with how the injection will drain into the lymphatic system. http://cancerres.aacrjournals.org/content/24/10/1700.full.pdf and  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2515477/

@AMR Interesting, mainly because in the cancer case, it seems that the main purpose seems to be that the fluid flows through the same channel as tumoral agents.

Remember that the adaptive immune system resides in the lymph, waiting to be activated... Though the rabies vaccine has been around longer than we have known about the intricacies of the lymphatic immunity. Pasteur invented the Rabies vaccine around 1885 and the lymph system role wasn't elucidated until many decades later. https://en.wikipedia.org/wiki/Timeline_of_immunology Maybe they just got lucky, they saw it worked, and well "if it ain't broke, don't fix it."

This might have some answers to your question. http://www.ncbi.nlm.nih.gov/pubmed/20156151

@chubakueno we almost never give anything intraperitoneal in humans (I've never given an i.p. injection to a human) - this is done for rodents, dogs and other smaller animals. I see the article above from AMR - though that is for intraperitoneal chemotherapy which is given through a special surgically placed catheter (not injected) - what injection are you talking about specifically that you think is i.p.?

@AMR Thanks for the links, they explain why IP injections are given for cáncer or peritonitis very well. Alas, I don't have Access tu PubMed articles, but thanks anyways.

@VanceLAlbaugh Rabies vaccines are the only ones that remain to be explained. In fact, I was asking this question because I was bitten by an street dog recently so I went through the process, and the public center for rabies gave IP injections(and some older people also talked to me about those). I got treated by a private clinic with IM ones, but IP ones took my attention.

IP injections are used for a variety of reasons:

The peritoneum provides a large surface area for absorption of drug (compared with intramuscular (IM) or subcutaneous); can thus inject a larger fluid volume.

Easier to inject that intravenous.

For some chemotherapy, such as ovarian cancer, IP injection is used to attempt to localize the drug near the tumor (it's through a catheter, rather than with a syringe and needle).  Essentially the goal is to provide chemotherapy to the abdominal region where cancer has spread rather than systemically.

 It is commonly done in animals, such as mice, because it is difficult to find a vein in small creatures.

https://en.wikipedia.org/wiki/Intraperitoneal_injection
http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-treating-chemotherapy
http://www.ncbi.nlm.nih.gov/pubmed/20156151 courtesy of @AMR
http://cpharm.vetmed.vt.edu/VM8314/Administration.htm

Nice answer +1. An additional point is that s.c. and i.m. only allow for small volumes to be injected, even in large animalia like humans. Plus, i.v. may result in a surge of drug in the body. I.p. allows for injection of large volumes, even in small animals, with a slowly-sloping absorption curve which may, or may not, be beneficial.

The reason IP injections are common in mice is not for lack of veins, it's for convenience' sake. The tail vein, for example, is fine for injections, but it's so narrow that injections need to be in very small volumes and at very low rates to avoid blowing out the vein. The vein also needs to be expanded by bathing the animal in a heat lamp while restrained, all of which takes time and equipment, and is stressful for the animal. IP injections are easy: scruff, tip, inject, pull out, back in cage.

@MattDMo Completely agree, IP is much easier and less stressful on animal and researcher!

@chubakueno it is important to realize that in humans we do not give routine injections intraperitonally - that only happens in animals. In fact, we intentionally do not insert needles into the peritoneal cavity for fear of potentially damaging intra-abdominal structures. However, if a patient has a peritoneal dialysis catheter or other intraperitonal access, we will administer things like antibiotics for a peritoneal infection or chemotherapy- but this is not for routine administration.


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Reseach on feeling pain of other people
I'm more of a tech than bio kind of guy, but I have read and learned a lot alongside of my girlfriend's education. Which is very interesting!!
Currently I want to investigate : people claiming to feel another persons pain when they are touching them.
I cannot seem to Find any papers about it. I guess I'm using the wrong search terms.
Or does nobody research about it ?

I believe what you are referring to is called 'sympathetic pain,'and the reason you can't find any papers on the subject is because it is not really a well studied concept. That is primarily due to the lack of robustness in the sensation and idiosyncratic nature of the phenomenon. Personally, I'm not too familiar with the concept beyond placebo treatment of patients with such pains.
HOWEVER, I will explain the different types of pains briefly, their biology, and where the pain you have described fits roughly. There are three categories of pain (scientists sometimes argue four, but for our sake let's say three): nociceptive, inflammatory, and neuropathic. Nociceptive pain is the immediate pain reaction you get when you sense something harmful. It's that jerking sensation you get when you touch something hot or you feel something hazardous coming your way. This pain comes from peripheral nerves that link your senses of touch or perception directly to your spinal chord for an immediate knee jerk reaction. Thus, there is no central nervous system (or brain) processing of the pain, just a reaction. You end up feeling the pain more intensely later once the moment has passed. Then inflammatory pain is the pain you get when you cut or bruise yourself, have allergies, stuffy nose, etc. It is the more common and treatable types of pain and is easy to detect. It comes with redness, swelling, and sensitivity to the general area. Biologically your body is stimulating this pain because your inflammatory system is trying to attack any invasive particles or repair damaged sections of the body. There has been much research done in this type of pain (see sources) and is treatable with non-steroidal anti inflammatory drugs (NSAIDs) such as aspirin, Tylenol, etc.
The last type of pain, which is the sympathetic pain falls into, is called neuropathic pain. This pain is more abstract and is often described as constant and idiosyncratic (non standard intervals). In research it is often modeled by inducing diabetes and doing damage to the nerves to cause constant pain signals to the brain. However, the method is controversial in both practice and in efficiency of modeling. This because there are often many different biological ways to induce cognitive pain and it is primarily central nervous system based (aka in the brain), whereas this type of pain is specifically induced by nerve damage (hence neuropathic). This type of pain is often tested using cognitive based test parameters to see if a drug can relieve some of the mental struggles either caused by the pain or causing the pain. There are also such cells called "mirror neurons" that fire when you sense (visual, audio, touch) something and then cause a similar behavior or sensation to occur within the person. It is possible that seeing or feeling someone else's pain causes these mirror neurons to fire for certain people, perhaps due to associate learning or a memory that person has that reminds them of pain they once had. I've attached some literature on the subject for your leisure, but it is a poorly understood science that we are trying to grasp in modern research. Hopefully that answered your question!
Sources

The Principles of Neuroscience by: Kandel, Schwartz, Jessel, Siegelbaum, and Hudspeth (most indepth source)
Pyschopharmacology by Meyer and Quezer
From Mice to Men: Jacqueline Crawley
Pathology Based Pain
Inflammatory Pain Review
Neuropathic Pain Review
Mirror Neurons

thanks for your extensive answer, it was really helpfull. But I more looking into feeling pain without you are able to see/hear somebody only touch them, is there any info available about that ?

Not specifically. The closest thing to that type of research I know about are the mirror neurons cited above.

thanks again, that a pity there is not alot of information about this topic. why not conduct research in this area ? Seems to me it can give new insight in how the brain/body of a human works if you don;t test it you never will know.
But what i want to do is the next, measure and experimenting with people who claim they can feel it with an openbci and look at the brain responses. seems interesting to me ?

It is harder to test. There is a great deal of bias and a HUGE degree of variation, which can hide any significant findings. If you feel I have sufficiently answered your question feel free to mark it as answered so people can mark and reference it. :)

i know but thats the challange, do you have any information about how to setup a good experimental approach to this ? So do not overlook very obvious mistakes i could make :)

There are several good reference books for designing a proper neuroscience experiment. I think you will want to focus on social biases and really make sure to note things like demographics, gender, age, ect. in or to control for any confounding effects. Good reference books are "Behavioral Neuroscience: A practical approach" by Sahgal.

thank you so much for the information ! I'm going to read it

The OP might be asking about what is called mirror touch synaesthesia
Like all synaesthesia [also spelled synesthesia] this is a new area of research. I have synaesthesia but I don't have this kind. Most researchers study "grapheme synaeshesia" grapheme because that is easier to make into empirical results.
Dr Anina Rich studies synaesthesia. She might have papers about it. Dr Anina Rich

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What traits make mountain goats so well adapted to mountain living?
I've never really understood how mountain goats manage to survive so well in mountainous regions. I've seen them scale almost sheer cliff faces with apparent ease, and they can almost sprint vertically downwards without losing their balance.
How do they manage to do this? I can't see any discernible characteristics that would make them able to achieve this particularly well. For example, snow leopards achieve similar feats, but they have incredibly long tails and large paws to help with balance and agility, yet the skinny legs and hooves of mountain goats seem largely unfit for this purpose.
What adaptations do mountain goats have that allow them to survive in mountainous regions, and how do they work?
I'm hoping mostly for information on how they perform such feats of agility as to move around on very precarious outcroppings and such, but am also interested to hear about any other qualities that they may have to deal with the other mountain conditions (altitude/ cold etc.).

Pretty sure this answers it: https://en.wikipedia.org/wiki/Mountain_goat

@Minnow That has a good overview of which features allow it to live in the mountains, but it doesn't really go into the detail of how those adaptations work in order to allow it better chances of survival.

Are you sure?  "The mountain goat's feet are well-suited for climbing steep, rocky slopes with pitches exceeding 60°, with inner pads that provide traction and cloven hooves that can spread apart. The tips of their feet have sharp dewclaws that keep them from slipping."

@Minnow Dogs have inner pads for traction on their feet too, as well as dewclaws, however they don't live on the sides of mountains. And it doesn't go into any detail whatsoever about how cloven hooves help them to traverse such inhospitable terrain. I'm looking for more specific answers, such as: How do they have such good balance? How can they determine which outcroppings will be stable/ large enough to stand on? Does their eyesight help them to do this, or is it learned from parents? I wanted to keep it reasonably broad, as I'm looking for any and all ways they survive on mountains.

+1  I relent.  you want to know more about mountain goat adaption! :)

@DavidBlomstrom If that was posted as an answer I'd happily accept it.

Mountain goats belong to the subfamily Caprinae, or goat-antelopes. The higher family is the Bovidae (cloven-hoofed mammals).
Now members of Caprinae are pretty stocky in their build and have thicker fur both of which help them survive in the higher altitude. Their ability to scale/descend sheer cliffs with such agility comes down to their cloven hooves. Their hooves enable them to grasp onto the the face of the mountain in areas other animals could not as well as shift direction very quickly. Despite the fact that cloven-hooves are not unique to mountain goats or other members of Caprinae it is a trait essential for them to be able to inhabit those harsh environments.
Nubian Ibexes (also a member of subfamily Caprinae) are experts at climbing as well; one of the best Caprinae members in my opinion. Nubian Ibex baby and fox

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How may the age of a child be estimated when required to do so, in video-graphic evidence?
How may it be possible to roughly conclude that a subject in a select piece of video-graphic evidence presented, is in fact a child, i.e. without the subject being, physically examined?
Is it possible that biological/developmental/theoretical evidence can be salvaged from the superficial appearance of the child in a video, to estimate age? Providing that the source is of High quality.
My reasoning as to why I query this, is due to there being few superficial-biological-visual-markers, that can be used as solid evidence to come to a conclusion in situations where this might be necessary (for example, in law enforcement cases that relate to the aforementioned). Particularly so, as the rate of maturity, in terms of physical appearance is not constant. For example, it's not improbable that a 25 year-old woman may be mistaken for a 16 year-old girl, due to specific physical characteristics.

In short, without direct physical evidence (forensic or medical examination), testimony, or documentation to act as proof, you are left up to the discretion of the court to determine whether evidence is admissible and up to a jury to decide if it is reasonable to presume that a person depicted is of a certain age if no other evidence to the contrary is provided. This is beyond the objective nature of science.
Please be aware, that as you are making this question specifically about criminal evidence, I am addressing that aspect of your question. There are ways of dealing with and presenting evidence that may preclude the need for any scientific proof of age, as it is up to the determination of reasonableness by the jury that is the overriding factor. If the jury does not reasonably feel that the person depicted is a minor as may be the case if the actual identity of the victim cannot be established, or if the accused could not have reasonably known that the person was a minor, unable of providing legal consent, then they can vote to acquit the accused.
Video’s Role in the Criminal Justice Process: DRC to ICC

Since documentary and forensic evidence could not prove age, the Prosecutor relied, in part, on a series of video clips showing: i) Lubanga at the military training camps speaking to children; and ii) children serving as his bodyguards. A sample of the footage from the opening argument can be watched here and below.

You will also see if you follow this link that the normal clinical determinant of age, examination of growth plates is not relevant as that data was generated on American and European populations and is likely different for African children, as their access to nutrition and the childhood illnesses that they face likely have much more to do with the changes in bone plates that can be used to determine age forensically.
While this example is related to an international court of law hearing a war crimes tribunal, the charge given to most juries would be that they are the judges of the facts and if a reasonable person would arrive at a certain conclusion.
From the Connecticut Supreme Court Jury Instructions. Most US States will have similar statutes and guidelines.
1.2-6 Evidence

You will decide what the facts are from the evidence that will be presented in this courtroom. That evidence will consist of the testimony of witnesses, documents and other material admitted into evidence as exhibits, and any facts on which the lawyers agree or that I may instruct you to accept.
The following are not evidence and you must not consider them as evidence in deciding the facts of this case:
statements and arguments by the attorneys,
  questions and objections of the attorneys, and
  testimony that I instruct you to disregard.
  There are two kinds of evidence: direct and circumstantial. Direct evidence is testimony by a witness about what that witness personally saw or heard or did. Circumstantial evidence is indirect evidence; that is, it is evidence from which you can infer another fact. As an example: if you wake up in the morning and see that the sidewalk is wet, you may infer that it rained during the night. The wet sidewalk is circumstantial evidence that it rained. Other evidence, however, may provide another explanation for the water on the sidewalk, such as a garden hose that was left on overnight. Therefore, before you decide that a fact has been proved by circumstantial evidence, you must consider all the evidence in the light of reason, experience and common sense.
In deciding this case, you may consider both direct and circumstantial evidence. The law permits you to give equal weight to both, but it is for you to decide how much weight to give to any evidence.
Some evidence may be admitted for a limited purpose only. When I instruct you that a piece of evidence has been admitted for a limited purpose, you must consider it only for that purpose and for no other.

2.2-3  Reasonable Doubt

The meaning of reasonable doubt can be arrived at by emphasizing the word reasonable.  It is not a surmise, a guess or mere conjecture.1  It is not a doubt raised by anyone simply for the sake of raising a doubt.  It is such a doubt as, in serious affairs that concern you, you would heed; that is, such a doubt as would cause reasonable men and women to hesitate to act upon it in matters of importance.2  It is not hesitation springing from any feelings of pity or sympathy for the accused or any other person who might be affected by your decision.  It is, in other words, a real doubt, an honest doubt, a doubt that has its foundation in the evidence or lack of evidence.3  It is doubt that is honestly entertained and is reasonable in light of the evidence after a fair comparison and careful examination of the entire evidence.4

EDIT: Due to a moderator edit of the question, the following section is no longer valid to the question and has been stricken
As you can see from this statute 7.4-3  Obscenity as to Minors -- § 53a-196 it is up to the discretion of the jury to determine whether or not the person depicted in the video was a minor and that the person accused of the crime knew that the person was a minor.

Conclusion
In summary, the state must prove beyond a reasonable doubt that 1) the (material / performance) was obscene as to minors, 2) the defendant promoted the (materials / performance) to another person, knowing of its character and contents, and 3) knew that the other person was a minor.
If you unanimously find that the state has proved beyond a reasonable doubt each of the elements of the crime of obscenity as to minors, then you shall find the defendant guilty.  On the other hand, if you unanimously find that the state has failed to prove beyond a reasonable doubt any of the elements, you shall then find the defendant not guilty.

As a result, even if the prosecutor can prove that the person depicted is a minor, it may still rely on whether or not the state can prove that the accused knew the age of the person they are accused of exploiting.
Part 7 subsection 7 is related to how the State of Connecticut instructs juries related to Child Pornography
So, from a legal perspective, it is highly subjective, and even from a clinical perspective, it is likely that there are different metrics related to different populations and how children's developmental conditions affects their bone structure, onset of puberty, and display of secondary sexual characteristics.

+1 Good answer! You added more than I sought for in terms of Law, it lacked Biological context though (which is understandable as it was a very specific theory question). It would be nice if you could possibly add a bit more towards the biological aspects of the question. Anyhow, you managed to get more up-votes than i did on the actual question haha. Chopped logic. Thank you!

One thing missing here: In some jurisdictions, child porn is more defined by how the actor/actress looks than what their actual age is. In these cases, science is pretty much irrelevant to the courts.


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Understanding different genetic terminology - Genotype vs SNP
I recently came across a study that refereed to variations in genes like this:
IGF1 (CA)19/(CA)19, IGF1(CA)19/X, IGF1 X/X
(From this study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3274549/)
I wanted to know, as a member of 23andme, how I could check these "markers" (?) against the SNP's listed in 23andme.
I would be very grateful for any help.
Thanks.

Here are list of tools that you can use now that you have you DNA raw data: https://www.xcode.life/23andme-raw-data/23andme-raw-data-analysis-interpretation/

The "IGF1" at the front indicates that the genetic variation is in the gene for Insulin-like Growth Factor 1. The notation (CA)n is used to describe n adjacent repetitions of the two-base sequence CA (Cytosine, Adenine) present in a particular IGF1 DNA sequence. Hence IGF1 (CA)19 / (CA)19 is referring to a genome in which both copies of the IGF1 gene have 19 adjacent repetitions of the CA pair of bases, that is, which is homozygous for IGF1 (CA)19.
Such a repeat is usually called a microsatellite or Short Tandem Repeat (STR). They are common sources of variations in genes because the DNA matching process during meiosis sometimes "slips" one or two repeats over.
The type of test performed by 23andMe reports values for selected SNPs (Single Nucleotide Polymorphisms).  SNPs are a different kind of variation from STRs, so the data available from 23andMe does not allow you to determine the kind of IGF1 (CA)n variant present.


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Genomic instability of cancer cells in h&e image
Is there are any books or papers on the topic of visual differences(analyzing H&E microscopy) of high grade cancer cells vs low grade cancer cells vs non-cancer cells?
In particular, I am trying to measure how much of genome was altered by analyzing images.

That seems like a substantial undertaking.  How familiar are you with histopathology generally?  The identification and grading of tumors is a large topic in histopathology, about which a good deal has been written (to my knowledge, none on your question specifically, but I am by no means an expert in pathology). Are you looking at a particular type of neoplasm?

@Hans you are absolutely right, this is a very challenging problem. I am CS major and have some datasets and interesting algorithms that I am going to apply, but first I wanted to get at least a little bit of understanding of the field. I read some articles about histopathology and this was useful and insightful, but I decided to ask this here in case anyone can give me some pointers to more relevant books on this topic. I am looking at a prostate cancer, but I believe general principles are the same -- I read that some mutated cells change shape\function\invade tissues and blood vessels\etc

Maybe I am misinterpreting your question. Tumor grading would be done histologically. To determine alterations to the genome itself, I would think that the only thing you could do visually is karyotyping. You could get a sense of translocations, loss of chromosomes, indels, etc. Otherwise you would likely need to do sequencing.

Histologic diagnosis of tumors is made using the so-called  WHO blue books.
Different tumors show different patterns of cellular and tissual aberrations.
On h&e  karyorrexis and  pyknosis  are examples histological markers of nuclear aberration.
A recent  paper reviews the salient visual and subvisual morphological changes of cancer nuclei and their possible cause or etiology and significance.


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Do camels pose an environmental threat to kangaroos?
Camels, once used for transport across the Australian outback, were set free, and are reproducing at an uncontrolled rate in the empty interior of Australia.
Do the ecosystems of camels and kangaroos overlap?
Are camels competing with kangaroos for what little vegetation there is, and if so, what is the impact on kangaroo demography?

Can you please provide a reference to an article that discusses the situation? It may help people who are familiar with ecology but unfamiliar with the particular scenario you are discussing.

@Gordon Stanger: please provide some reference indicating the rise in reproduction rate.

Feral camels have environmental, economic and cultural impacts in Australia's Northern Territory (Dept of Land Resource Management, Australia).
In central Australia, camels feed on more than 80% of the available plant species. Feral camels severely defoliate and suppress the recruitment of some shrub and tree species, with such impacts being greatly exacerbated in drier years (Dept of Land Resource Management).
Feral camels have a noticeable impact on fragile salt lake ecosystems and waterholes, which are important sites for Aboriginal people and for native fauna (Dept of Land Resource Management).
However, its impact on kangaroos may be the last of our worries. There are other, typically smaller, marsupials that cover the endangered species list in the NT, including the Western quoll, bandicoots and wallabies (Dept of Land Resource Management). Kangaroos thrive in the agricultural farmlands that now dot the nation.

Oh... I forgot there was an honorary Aussie in the room.

@AMR - that's why I am here ;-)

@AMR - with the interesting side note that OP lives in Adelaide, while I am back in the Netherlands ;-)

That's strange... there is an anagram somewhere....


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Persistent HPV and CVD in Women?
Cardiovascular disease is the number one morbidity factor of women.
I am studying the relationship between persistent HPV infection and CVD (Cardiovascular Disease) in inadequate immune responses.
There are some statistical evidences but pathways are unknown:

HPV linked to cardiovascular disease in women in women; excludes obesity, smoking and diabetes.
Troubles With Heart Are Linked to HPV which highlights benefits of HPV vaccination only in HPV infection
No reliable method to clear the HPV virus. HPV vaccination prevents cervix cancer indirectly by preventing infections (prevent oncogene activation, its early form formation and developing into cancer). (Duodecim, Infection diseases, HPV-vaccines [Finnish])
No support for the statement that HPV vaccination may reduce CVD later in women's lives. 3 But vaccines should create herd immunity (neutralizing antibodies mediates active protection), also in males and other sites than cervix. Some cross protective effects against non-targeted HPV types [VCS].
Nearly 20 percent of individuals with CVD do not show any risk factors, indicating that other 'nontraditional' causes may be involved in the development of the disease, here.

Compare HPV-Cervical Cancer and HPV-CVD.
The former seems to have much more local effects because of cellular pathways (DynaMed Plus hpv and cervical cancer).
The latter is probably associated by broader pathways involving tissue-organ level, without any analysis in Op. cit.
Mechanism of HPV-CVD (systematic) which includes local and systematic pathways

Local. HPV's role in inactivating two tumor suppressor genes, p53 and retinoblastoma protein (pRb) -- the same process by which HPV causes cancer. p53 has been shown to be essential in regulating the process of atherosclerosis; the retinoblastoma gene plays a pivotal role in regulating cell proliferation. Here. Stable infection - dysplasia or undetectable in some genotypes. [Meijer] about the gradual development of cell-mediated immune response presumed mechanism.
Inadequate immune response and persistent HPV infection (E6, E7).
Systematic?

Sources

Human Papillomavirus and Cardiovascular Disease Among U.S. Women in the National Health and Nutrition Examination Survey, 2003 to 2006. Journal of the American College of Cardiology, 2011; 58: 2001-2006 DOI: 10.1016/j.jacc.2011.07.038
Cardiovascular disease prevention for women attending breast and cervical cancer screening programs: the WISEWOMAN projects. The WISEWOMAN Workgroup.
Meijer CJLM, Helmerhorst TJM, Rozendaal L, van der Linden JC, Voorhorst FJ, Walboomers JMM. Histopathology. 1998;33-83-86. 2. Schiffman M, Kjaer SK. J Natl Cancer Inst Monogr. 2003;31:14-19. 3. Ho GYF, Bierman R, Beardley L, Chang CJ, Burk RD. N Engl J Med. 1998;338:423-428.

Pathway organ level

HPV-cervix cancer
HPV-lung cancer (here put research pressure in some universities instead of HPV-CVD)
HPV-CVD

[conjuncture] Tissue-Organ level mechanism
Preventing infection of cervix does not prevent the manifestation spreading to CVD by vaccines Cervarix/Gardasil.
I propose a tissue-organ level mechanism because I cannot explain the relationship only by the cellular level mechanism.
Assume skin has a visual-processing pathway of peripheral neurons, as described here i.e. it preprocesess some events of the geometrical data before going to the target organ (here the heart).
Missing of such an unit can cause alterations in the balance of sympaticus-parasympaticus firing, thus causing alterations of the pacemaking and conduction system.
Unknown

How is CVD formed in HVP infection in women? Compare incidence of non-HPV and HVP cases where CVD has been formed
HPV 16, 18, 31, 33 and 45 most common agents in cervical cancer. HPV is associated with many conditions: vaginal cancer, vulvar cancer, VIN, VaIN, CIN, AIS, genital warts, ... I think we cannot assume that those types causing the cervical cancer are mostly associated with CVD.
High-risk HPV and anogenital cancer. Can we assume that these agents are associated with CVD?

How can you hypothesize the relationship between HPV and CVD?
Which HVP genotypes can cause CVD?

This is an impressively referenced question, but I don't think it's reliably answerable for several reasons:

it's POB
the association is merely theoretical at this point
the study 'results' were based on a very small number of women.

While the percentage of woman with HPV is high, those with no other risk factors for CVD who have experienced MIs is much lower.
The idea is interesting enough to warrant further study perhaps, but certainly not enough to answer your questions, "How can you hypothesize the relationship between HPV and CVD? Which HVP genotypes can cause CVD?" I mean, if you want good, referenced answers, there isn't an answer yet.

What is POB? Pelvic Ovarian ... ?

Not sure what POB stands for either... Though searching for it I came up with Victoria Beckham's hairstyle... Posh (Spice) + bob = POB... :-)

@Masi - POB = Primarily Opinion Based (not evidence-based). Makes a reliable answer not possible.

@anongoodnurse I do not think so. The question is about how you can reach the evidence based answer, not how you are there.

CVD is the leading cause of death in the developed world and HPV is the most common STD in the developed world. When dealing with something that common alot would need to be ruled out before any causative relationship was hypothesized for example the first link did not consider that oral Contraceptive use is higher in women (obviously) would increase atherosclerosis / CVD related causes of death in the absence of other CVD associated factors such as obesity

Yes, this is a valid point. You have to rule out the 1) contraception use in this question and its relation to atherosclerosis > CVD, ... 2) obesity when you are getting away. There is a net of those factors where the causalities need to be defined.


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Protostomia classification and characteristics
While working through a practice test for my final exam in an introductory organism biology course, I came across this question:
Protostome characteristics include which of the following?
a) a mouth that develops secondarily, and far away from the blastopore
b) coelom formed by schizocoely
c) radial body symmetry
d) spiral cleavage
e) none of the above
After reading the answers a few times over, I just moved on because I couldn't figure out how to answer. My first instinct said that both (b) and (d) were correct, but the answer is (e).
After some thought, I've come to a few ideas how this could be true.
1. The wording is incorrect, the definition he provides for protostomia says "body cavity formed by schizocoely," and "spiral determinate cleavage."
2. These two characteristics are not present in all protostomes (i.e. spiralia evolves after ecdysozoa, and platyzoa have no body cavity).
Just looking for some clarity or closure regarding this.


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Do the BLAST scores have any relation between them?
Is there any relation among the BLAST scores (E-value, similarity, identity, gap, bit score)?  Is the e-value score for an alignment proportional to other scores, such as similarity score (i.e. the lower the e-value, the higher the similarity)?
Thank you!

This answer might be useful: http://biology.stackexchange.com/a/40862/16651

Yes there is a relationship between them but you may not be able to observe correlation between some of them.
Number of matches and score are definitely proportional, however higher similarity would translate to higher score only if the lengths of the scoring pairs are the same. Gap would have a negative effect on the score but it totally depends on what your scores/penalties are (see BLAST help and documentation).
E-value is basically the likelihood of two random sequences having a certain match score from a given database. So whether or not it is low for a hit depends on the score distribution of the database. Lower E-value does not mean higher similarity. It means that a hit of this score has a low likelihood to be found by random chance. The score distribution is generally skewed towards low scores and so high scores usually have low E-value but what a "high" score is totally dependent on your queries and therefore this statement cannot be generalized.
From BLAST docs:

$$E=K.m.n.e^{-\lambda.S}$$
This formula makes eminently intuitive sense. Doubling the length of
  either sequence should double the number of HSPs attaining a given
  score. Also, for an HSP to attain the score 2x it must attain the
  score x twice in a row, so one expects E to decrease exponentially
  with score. The parameters K and lambda can be thought of simply as
  natural scales for the search space size and the scoring system
  respectively.


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Are fishes evolving?
As far as I know, Fishing has been one of the important occupation since early ages, and infinite number of fishes have already been captured.
As the time passes, they must've developed some sort of knowledge about the fish-nets, and should've figured out a way to escape from them. But, still now, we are able to capture them at the same rate(I guess)
So, Are they developing any sort of hereditary memory to escape from us?
P.S. I'm not sure whether this is the right SE to ask.

There is no knowledge or hereditary memory involved.

"No hereditary memory involved"? How can we say that for sure?

Pretty much the same reason we don't think the fish are developing psychic powers. There's no evidence for it, the mechanisms by which evolution is known to operate wouldn't produce such a thing, and it wouldn't explain any observed phenomena better than the existing explanations.

No, what I meant was that fish should've developed some sort of hereditary memory that we're one of Predators, atleast when they saw fellow fish being captured by us, and should've learned to tackle the "fish-nets"(or whatever). But, this isn't happening even after 40,000 years. Why?

Evolution just doesn't work like that. Here, have a link to an explanation of how it does work.

How's this hypothesis @user2357112 - the effect of man's overfishing is to catch shoals and individual fish that are easier to catch. Therefore the more reclusive/cautious fish survive, which means those characteristics are passed one.  I'd say that would be a reasonable approximation of inherited memory.

@geotheory that's not a hereditary memory, that's an acquired trait.

I don't think its necessarily very different from cats fearing cucumbers - possibly an inherited fear of snakes.

@geotheory +1, just for the reference

I'd be curious to see an answer that addresses indirect pressure through habitat change, like what happened with pigeons and highways.

@geotheory: That's not memory, that's behavior.

That's just fudging.

Yet another question that underestimates the length of evolutionary timesceles compared to industrialisation of people.

Fish are definitely evolving to avoid fishing pressure. For example, largemouth bass evolve toward avoiding hooks.  More broadly, since fishing selectively removes larger fish from the population, there's selection toward fish evolving smaller size.  A brief review, linking to many studies demonstrating this, is Evolutionary impacts of fishing: overfishing's ‘Darwinian debt’.

I would disagree with the phrasing "to avoid" and replace it with "in response to". The old adage about evolution not assuming a purpose applies here.

"in response to" implies a purpose as much as "to avoid" from my point of view. I'd rather use "as a consequence of".

I understand the urge to avoid teleological words, but I think it's pointless and futile to worry about it once we're actually discussing  real evolution.  I realize that it's hammered into students at the very early introductory stage, but once the concept that there's no goal to evolution is solid -- which should be about a week after natural selection is first mentioned -- it simply becomes an exercise in semantics.  If you read actual papers by actual evolutionary biologists, they pretty much all use shorthand language like this.  We're all grownups here.

@iayork: I don't think it's safe to assume the questioner is past that very early introductory stage. Even if they are, this answer will probably be read by people who aren't past that stage.


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Synapse formation
I am trying to learn about neuronal synapse formation, but the literature is intimidating to someone with little background knowledge.  I am interested in synapse formation in both human adults as well as during human development.  Could someone point me to a good paper or review that provides the necessary introductory information?  I am a highly technical individual, but have little more than a 1 year introductory neuroscience course at the undergraduate level.
EDIT:
I'm interested in the formation of structure in small-scale systems (100's to 1000's of cells) of neurons, so I imagine that would require a combination of cell-based and neurophysiological knowledge.

Welcome to Bio. What do you wish to know, I mean what is the area of expertise? Molecular Bio (Cell signalling), morphology (cellular level) or neurophysiology (communication)? There is a lot of stuff out there. Finding literature mainly means knowing what you don't need.

Alright, to be honest this question is definitely too broad to answer. Even the formation of small structures is a HUGE (and I mean huge) field of study that doesn't just span neurons. I will tell you how you can find such papers and the ones you are looking for are specifically called "Reviews". A review article basically rounds up (usually a hundred or so) articles to form a consensus about what the prevailing thoughts on a specific topic are when looking at the research done by the scientific community of course. If you want to learn about neuron development I suggest you use a scholarly se


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Why have parasites not evolved to be harmless?
I have yet to understand why so many viruses or bacteria haven't evolved to be harmless (specifically, I don't know of any harmless viruses). I think it would be greatly beneficial for a virus to control its population and use natural transfer channels that don't cause discomfort (like feces), since it would be allowed to stay in an organism indefinitely and would have a lifetime channel for transmission, hopefully getting to be the most common strain.
So, why have viruses not evolved to be harmless to their hosts?

Many are harmless. Some are not. They occupy different niches. If there are 6 billion humans, why would a virus care to take down a few? Plus, many don't kill, only harm. If the host lives, why would a parasite care if its host gets sick?

This is a good question. I know at least some models of pathogen spread have a parameter for lethality of the virus, and high lethality decreases pathogen spread. Part of the answer could be that high infecitivty (pathogen spread, would be selected for) is associated with high lethality/morbidity (not necessarily beneficial for the pathogen per se)

@Christiaan The parasite should care about the host getting sick because if so the host would evolve antibodies. Both could continue the biological arms race, but the side-channel of harmlessness seems pretty effective to me.

@CactusWoman Seems likely, please share them!

@chubakueno It's been a while since I've used those equations so I don't have them on hand, (hence me making a comment and not an answer), but I'll see what I can do

Although I still don't have a full answer, the wikipedia page on Optimal Virulence seems to be relevant: https://en.wikipedia.org/wiki/Optimal_virulence

The post "why-do-parasites-sometimes-kill-their-hosts?" is very much related.

You consist of more bacterial cells than human cells, and most of these are harmless or benificial.

Just a reminder, : "harmless" to humans does not indicate it's harmless for all other organisms.

Does this answer your question? Why do some bad traits evolve, and good ones don't?

There are actually many examples of viruses that have integrated into the human genome and were rendered harmless, perhaps even helpful.
This New Scientist article referencing this Nature article describes endogenous retroviruses, which are ancient viruses which have integrated into the human genome.

About 9 per cent of our genome is thought to have come about this way.
  Until recently, these viral relics were largely dismissed as inactive
  “junk” that ceased to have any impact on their host many thousands of
  years ago. The discovery that HERVK, the most recent ERV to make
  itself at home in our DNA – probably around 200,000 years ago – is
  active in human embryos challenges that notion.
Joanna Wysocka and her colleagues at Stanford University in California
  made the unexpected find while they were analysing gene activity in
  3-day-old human embryos, which are bundles of eight cells. Besides DNA
  from the parents, they found genetic material from HERVK. “The cells
  were full of viral protein products, some of which had assembled to
  form viral-like particles,” says Wysocka.
Further experiments revealed that the virus appears to produce a
  protein that prevents other viruses penetrating the embryo, suggesting
  it protects the embryo from dangerous circulating viruses, such as
  influenza. It also seems to play a crucial role in the genetic
  activity of the embryonic cells, helping to genetic instructions to
  the cellular protein factories.

Additionally, the endosymbiotic theory is also another possible example. It is thought that mitochondria and chloroplasts are previously free-living, possibly parasitic organisms that ended up integrating into the host cell and living as an organelle.
In short, parasites absolutely can and do evolve into harmless versions of themselves. There are already discovered examples, and as the human genome is better understood, doubtlessly more would be discovered.

Chloroplasts and mitochondria are unlikely to have been parasitic. They are rather tamed preys captured by unicellular predators.

Why do you think so, @WYSIWYG?

Pathogens don't evolve to be harmless to their hosts, because that doesn't benefit the pathogen.
For example, think about a pathogen, like cholera, that spreads by fecal/oral contamination.  How could it enhance its transmission? One obvious way is by increasing the amount of fecal contamination, which means causing diarrhea, which means harming the host.
Or think about a pathogen, like myxomavirus, that spreads via sand fleas.  The fleas bite one rabbit, jump to a new one, and infect it.  How could the virus enhance its transmission?  It turns out that sand fleas don't bite dead rabbits, so viruses that kill their hosts immediately lose out.  But on the other hand, perfectly healthy rabbits groom away the fleas, and those viruses lose out.  The viruses that transmitted best made their hosts very, very sick, too sick to groom, for a long time, to maximize transmission.
Or think about a pathogen that's transmitted through saliva, like rabies.  Maximizing the number of new hosts that get bitten, by damaging the brain, would help there.
There are generally balances for maximizing transmission.  Sexually-transmitted pathogens might not make the host sick for a longer time.  Respiratory agents might do better with hosts that can mingle more with potential new hosts, while fecal contamination doesn't need such a healthy host.  But in general, pathogens evolve toward maximizing transmission, not host health.
(You may wonder why pathogens don't change their mode of transmission - why don't fecal transmitters evolve the ability to spread by respiratory transmission? The answer is generally the same as any other "Why doesn't X evolve Y?" questions -- because the path toward a new complex ability means going through a phase where the pathogen is not as good at either ability, and gets out-competed by its more traditional relatives.)

It doesn't follow that if pathogens (like all evolved organisms) maximise fitness, they would necessarily harm their hosts. Symbiosis is not a zero-sum game. If a pathogen evolved into a mutualistic relationship, they could maximise fitness of themselves along with their host.

@MarchHo symbiosis actually is much more complicated than parasitism and involves an intricate genetic interaction. Pathogens usually have a reduced genome and to evolve into a harmless species they have to gain a function (which is more difficult than losing one).

@WYSIWYG Did you mean mutualism? Parasitism is a kind of symbiosis.

@MarchHo yes mutualism. AFAIK parasitism is not included in symbiosis (only mutualism and commensalism are considered symbiosis).

@WYSIWYG This paper suggests that parasitism is also a kind of symbiosis, and that this definition is widely accepted in biology textbooks.

Pathogens don't evolve to be harmless? That's a big assumption! Thinking of a bacterian flora in one's guts, I can imagine all sorts of evolutionary changes...

Please don't twist what I said.  I didn't say no pathogen has ever evolved to be harmless.  That would be silly, as would interpreting what I said that way.  (Spumaviruses are better examples than gut flora.)  But that evolution would be a byproduct of enhanced transmission, not an evolutionary pressure on its own.  I even pointed out conditions in which that could happen.  As for "imagining all sorts of evolutionary changes" that's lovely, but there's an extensive literature on the subject; you'd be better off using some research, logic, and reason than pure imagination.

I think the key to your answer is in the word "parasite": parasitic relationships always involve the parasite taking something from its host, causing it some (possibly slight) amount of harm. Once the parasite has evolved to cause an insignificant amount of harm to its host, we no longer call their relationship "parasitism" but "commensalism".
There are lots of commensal bacteria -- you have more in and on your body right now than you have cells in your body -- and many of them may have evolved from parasites.
All viruses need to hijack cellular machinery, particularly the protein generation machinary, in order to reproduce themselves. So it's hard to imagine a commensal virus that doesn't harm the cell it uses to reproduce itself. As @March Ho pointed out, however, they might eventually become incorporated into their hosts' genome, potentially giving that host additional capabilities that it might not have otherwise possessed.

Great question! Christiaan's comment is the best way to start thinking about this; why should the virus care? In other words, what determines the selection pressure to increase or reduce virulence?
The most common definition of virulence in ecology is the reduction in host fitness resulting from infection by a pathogen. If reductions in host fitness also reduce the probability of successful transmission then there is selective pressure on the virus to become less virulent. Conversely, if reductions in host fitness make no difference (or actively increase the likelihood of transmission) then there is no selective pressure to reduce virulence.
Consequences of pathogen infection which increase the likelihood of transmission via certain routes often reduce host fitness (the trade-off hypothesis). For example, diarrhoea increases the potential for faeco-oral transmission of the pathogen but increases the host's risk of death from dehydration. Differences in optimal virulence reflect differences in the degree to which host and pathogen fitness are correlated. If transmission is typically rapid and/or unrelated to host fitness then there is no selective pressure to reduce virulence.
As another simple illustration, a mosquito-transmitted pathogen that makes the vertebrate host sick (and thus less likely to react to mosquito feeding) will probably be transmitted more effectively, while one which makes the mosquito sick (and reduces its host-seeking frequency) will be transmitted less often. Vertically-transmitted viruses often become less virulent because host reproductive success and virus transmission are linked. This paper explores this theory with reference to a natural system (Plasmodium infection) and considers some implications that might not be immediately obvious, such as the consequences of better control via drug treatment etc.

I'm not convinced it strengthens my answer much (if anyone thinks it does I can edit it in) but I happened to come across this reference today which mentions that in WNV-infected bird species viraemia mostly correlates with mortality (although with some exceptions): http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3939481/

There is generally a pressure for parasites to be harmless towards their hosts (apart from the drain in resources), especially if those two species have co evolved for a long time.
This sets them apart from parasitoids. Though those terms are sometimes used interchangeably, a parasite requires its host to live on while a parasitoid aims to ultimately kill the host.
By far the most harmful parasites are those that did not co-evolve with their current host or ended up there by accident or in the wrong stages of their life cycle (for instance, the fish tapeworm in humans).
The same principle applies not only to parasitic animals but diseases in general, where most of the infections with the highest mortality rates are, at least initially, zoonotic in nature.

Welcome to BiologySE... we always appreciate references accompanying answers as well as questions. This is so others can read about and better understand what you are asking/saying.

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


text:
What are flagged primers?
I'm interested in amplifying a sequence for further use with Gibson Assembly. I want to create overhang regions in my DNA fragment so there would be complementarity to the plasmid I'm trying to insert it in.
I was informed by a colleague to work with "flagged primers" though I can't find any literature online.  Can anyone explain this concept to me?

Are you sure they didn't mean labeled primers. The Oligonucleotides become part of your DNA, so if they are labeled, then the label will be incorporated into your amplified sample.

they described them as forward and reverse primers with overhang regions

The only place I could find a reference to flagged was on what appeared to be an personal journal from someone at UCSC. This is the Addgene protocol. If has a link to the Gibson's original 2009 article, and that doesn't mention flagged either. Nor does Janet B. Matsen:Guide to Gibson Assembly

There is nothing, in my knowledge, called flagged primers. What your colleague must have meant is perhaps "flanks". If you clarify your objective then this question may be answered. Since the real question is unclear as of now, I am putting this on hold.


text:
How to calculate the LOB, LOD and LOQ of an enzyme assay
I understand how to calculate limit of blank (LOB), limit of detection (LOD), and limit of quantitation (LOQ) in the traditional way i.e., average and SD of raw analytical signal of blanks and low concentration samples. But the enzyme assay makes things unclear. I am not sure what measure to use in my calculations.
The enzyme assay with seven calibrators produces a very nice dose-response that I fit with a nonlinear regression model (4-parameter aka. Hill equation). Running blank samples gives three relevant measures that I could use to calculate LOB, LOD, LOQ:

Raw absorbance at 405 nm

Problem here is absorbance increases over time as the enzyme goes to town on substrate. Results across multiple experiments are not comparable. Not a good candidate.

Normalized enzyme activity (as a % of uninhibited control)

I like this option the best because it's not time-dependent. Blanks run on various days are comparable.

Concentration (ng/mL)

Concentration is interpolated on calibration curve using % activity as the input. Problem here is sometimes the nonlinear model cannot calculate results that are beyond the upper asymptote (parameter A for those familiar with the Hill equation). So roughly half of my blanks don't get a concentration.

I feel like I want to proceed using % activity as my measure for calculating LOB, LOD and LOQ but it just doesn't feel right.
For example, my 20 blanks run over 8 experiments have an average enzyme activity of 99.4% and standard deviation is 2.2%. If I calculate LOB the traditional way LOB = mean of blank + 1.645*SD of blank, I get 103% which doesn't make sense (it should be mean - 1.645*SD instead, which gives 95.7%). First red flag.
I need to report my LOB, LOD and LOQ to external stakeholders. No one is going to understand what it means when I say my LOB is 95.7% activity, LOD is 92.1% activity, and LOQ is 77.2% activity. They'll want the limits expressed in terms of analyte concentration.
But... to go from % activity to ng/mL, I have to interpolate on my calibration curve. But I got the data from 8 separate experiments. Am I supposed to average out the curves for the 8 experiments and use that to turn % activity into concentration?
I would really appreciate some help on this one. Everyone in my lab is pure analytical chemistry and they don't get the whole enzyme thing.


text:
Advocate for the pop-culture idea of withholding vaccination
While it is widely accepted that vaccination is preferable to not vaccinating, would anyone like to give a shot at providing evidence in favor of not vaccinating? Anything goes.

This is a scientifically minded site. Why would you think we would want to engage in such a waste of time?

Here's the thing. No one has been able to repeat the results seen in the discredited "vaccination is linked to autism" study that started this whole dangerous mess (I'm not even going to bother looking up the citation, I care that little about it). Scientists, including those funded by so-called "anti-vax" groups, have been trying for the past 15-20ish years, and they can't do it, because
there is no causative link between early-childhood vaccination and autism.
Your question is akin to asking us to advocate against Pasteur's germ theory of disease, or for the idea of phlogiston in chemistry, or against the theory of relativity in physics.
So, given that the scientific evidence is firmly pointing in one direction, why would we waste our time on this endeavor, especially when anti-vaxxers will cling to any sort of misquoted, out-of-context, partial evidence that they can find?
The only reason a child should not receive a vaccine at the scheduled time and in the recommended dose would be because she is severely allergic to one of the main components of the vaccine, or she has a significantly-depressed immune system, typically associated with cancer and other severe medical conditions. At such times, medical recommendations by the specialist treating the condition should be followed.

Really good answer, however I don't want to vote up, because then the question will hang around even if closed. Maybe it should become a community wiki on why early childhood vaccination? Or an ask and answer? I'd vote up.

@AMR I wrote it out of frustration and because I didn't want to take 4 comments to say the same thing, not for upvotes :) The question can still be (manually) deleted after closure if enough 10K+ users vote to, so get your lobbying skills to work!

This has been covered already on Skeptics and Health, so I don't see the need to cover it again here.

Not to mention that "study" wasn't even a study at all. It was "hey, I looked at the guts of 6 of my patients and now I am convinced vaccines cause autism". What the heck? It's been retracted and denounced by the journal that published it by now, anyway.

Phlogiston! :'D

@DonJulian and why is that? Because we rigorously tested a hypothesis, found it to have no support, and discarded it? That's exactly what science is supposed to do.


text:
Why was Darwin's Finch argument valid considering Weismann's argument?
According to Darwin, there was only 1 species of Finch bird in Galapagos. Then Darwin argued that due to diet adaptation and natural selection, their beak changes causing new species--which is confirmed by John Gauld at the Geological Society of London.
In contrast, Weismann's and his mouse proofed that environment factor won't effect next generations.
Don't Weismann's argument contradicts Darwin? Ok, say that the Finch bird adapts (and killing the one who don't) with their diet. Their beak changes. But when these Finch bird breeds, their new generation's beak should reset to normal beak again.
The reason I asked this reason is because one article said that our teeth are changing due to overbites using utensils(1). However, not everyone use eating utensils. Indian mostly used finger. Indonesian don't really care whether we use our hand or spoon. If this trend keeps happening in the future, won't human evolve into two species? Homo sapien and Homo spoon (pun intended.)
Or am I mixing Darwin with Lamarck?
(1):http://www.theatlantic.com/health/archive/2013/01/how-forks-gave-us-overbites-and-pots-saved-the-toothless/267252/

Weismann's mouse tail experiment showed that mouse tail length is not inherited, if the change in tail length was caused by mutilations, and there was an absence of selection pressure.
However, Darwin's finches represented a completely different idea of evolution. In this case, the beak size of the finches did in fact change, but this was not due to mutilation. The beak sizes of the finches changed because finches with lower fitness due to their beak sizes were selected against, leading to the beak size changing over time.
If the mice were instead selected for tail length by preventing the long-tailed mice from reproducing, then it is indeed possible that the mice would eventually evolve to have shorter tails, or even absent tails.
Similarly, if the finches had their beak sizes reduced artificially but their fitness preserved (for example, by grinding down their beaks and feeding them soft food that does not require large beaks to break), the finches would not be expected to evolve smaller beaks.
It is not clear which method is the one through which the evolution of the overbite occurred. It could be due to a change in relative fitness, but a case can also be made in which fitness was not a large factor.

You are confusing with Lamark, yes. Ironically enough, some epigenetic information does transfer some adaptations, (see citrus cold adaptations for a well-known example. If they freeze, they go sour and pass that on.) but the Lamark idea is mostly discredited, anymore.
Darwin promoted a very distinct idea: Creatures must pass on traits to their offspring from the set available in them, so the effect of the individual success effects the selection of traits in the population.
The sets of traits that better equip an individual to successfully spawn will tend to eventually outnumber lesser sets, due both to superior survival and more effective breeding. They'll make more children in the first place, and these will be less likely to die.
The result is a shift in availability of traits* towards the successful.(*heritable)
None of that requires any transfer of developed traits beyond any intrinsic ability to adapt or the mentioned epigenetic advantages that pass.
Mammalian milk-transferred immunities are not genetic and very much passed from mother to child from her body's own adaptations. The ability to do that is inherited genetically, but  the information providing the adaptation advantage is not.
A mutation that mucked up that system would not be an advantage, so would usually be selected against.
As to the spoon:
First question is "which definition of species are you using?", which is not a pedantic question. If using the populations not interbreeding option, (among a few others) we're already many different species. If you're specifically thinking about genetic incompatibilities, well, that would require changes related to breeding.
Could that theoretically occur? Sure, but it's gonna need to happen to multiple individuals in a compatible way all at once or it would need to be progressively developed over time, or it can't pass on. That's highly unlikely.


text:
Degenerate primer designing software
Can any one provide online free degenerate primer designing software. I have tried couple of them like CODEHOP is one where BLOCK formatting step finding difficulty, can anyone help me out....

Benchling is a lab notebook with full DNA tools suite. You can check out a tutorial for the primer design tool her: https://benchling.com/tutorials/25/creating-and-analyzing-primers It's totally free to use for academics, and you can sign up via: https://benchling.com


text:
Why does a Urinary Tract Infection cause a strong, persistent urge to urinate?
There are plenty of articles on the fact the a urinary tract infection (UTI) causes frequent and urgent urination. For example; on this National Institutes of Health webpage.
My question is:

Why does a urinary tract infection cause an increased desire and hence, a greater urgency to urinate?

it might be due to irritation of muscular tissue, causing slight disfunction of the mechanism that controls the bladder/urine flow? (the urgency). The frequency might be down to irritation in the urethra and hence the need for release increases but, also the bodies "desperation" to expel the urine in order to excrete the bacteria by the medium, urine.

Nerve endings exist in a more or less homeostatic interstitial fluid medium which when disturbed in certain ways result in depolarization. This is a very simple explanation, but basically correct. Depending on the nerves being discussed, a change in the medium can be the presence/absence of neurotransmitters (serotonin, GABA, etc.), chemicals released from damaged tissue, pH differences, etc. etc.
Very simply put, anything causing irritation of the bladder or urethral mucosa will cause some of the nerve endings to depolarize; these are some of the same nerves that depolarize when the bladder is full, and therefore the sensation is of urgency (the feeling that one needs to urinate). The substances can be substances excreted by bacteria, released by neutrophils, or some other.
Simply administering a topical anesthetic - something that decreases the depolarization of nerve endings by reversibly binding to/inactivating sodium channels - (lidocaine, for example) will instantly alleviate this sensation. In the case of UTIs, a commonly given medication is the bladder anesthetic phenazopyridine hydrochloride.
The more complex answer is that no one exactly knows. The complexity is more important in the treatment of non-infectious causes of urinary urgency and in the investigation of why catheter-related UTI are often asymptomatic.
Edited to add: If you're looking for a more teleological reason (such as, it hurts so that you'll get flush out the bacteria faster, that's not actually what happens. When it hurts to urinate, very many women intuitively stop drinking fluids in an attempt to avoid the pain of urination, allowing the infection to get much worse. The counterintuitive measure is to drink more, not less, to flush out bacteria.

@Medica I presume?  Nice answer, you are well-rounded!

Any links to the sources?


text:
Why can't I read everything in my field of view?
When I look at a piece of text, I can see all the text on the paper, no matter where I look, because my field of view covers it all. However, if I stare at a specific word, I cannot read the text a few lines above the position I am staring at, even though I can clearly see there is text there. I don't think it has anything to do with the text being out of focus, since I observe this phenomenon no matter what distance the paper is from me. What are the specific causes of this?

The field of view is determined by the light-receptive parts of the eye: the retinae (Kolb, 2012). The fovea is the region with the highest resolution. It is located in the central part of the retina and covers only about 2 degrees of the field of view (Lauweryns, 2012). The total field of view is roughly 180o (Fig. 1).

Fig. 1. Schematic of the human field of view showing the foveal region. Source: Medical Dictionary.
The reason for the regional differences in retinal resolution (referred to as visual acuity) is that the cone photoreceptors are densely packed in the foveal region, while rod photoreceptors predominate the retina outside the fovea region (Fig. 2) (Kolb, 2012).

Fig. 2. Distribution of rods and cones. Source: Webvision.
The cones sense color and are specialized to work under well-lighted (photopic) conditions. In contrast, rods are hardwired to converge onto a single optic fiber to collect responses for dim lighting (scotopic, or night vision). Because many rods (tens of rods) connect to a single optic nerve fiber, the spatial acuity is dramatically reduced (Fig. 3). Hence, you can read with only a few degrees of your vision. While reading, your eyes continuously scan the page for the next word to center it onto the foveal region.

Fig. 3. Many rods converge onto a single ganglion cell, while one cone synapses onto a single ganglion cell. Source: Slideshare.
This is the big handicap that people with age-related macular degeneration face. The macula (that includes the foveal region, see Fig. 1) degenerates and the cones are lost. Hence, they loose their high-acuity region and cannot read anymore without using magnifiers or other low vision aids.
References
- Kolb, Webvision - The Organization of the Retina and Visual System (2012)
- Lauweryns, Brain and the Gaze: On the Active Boundaries of Vision (2012)


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Breathing becomes harder in certain wind conditions
I'm not sure if this is the right site to ask this, but it seemed like the best option.
I've observed on myself that, if I stand on a train platform and a cargo train drives by, creating strong, short gusts of wind, it becomes harder to breathe for me during the gusts, almost like fighting my body into breathing.
A commenton parenting.se leads me to believe this is due to the mammalian diving reflex.
1) is this assumption correct? 2) what causes the change in breathing?

So I'm going to go ahead and tell you outright that it is not the diving reflex.
What you are experiencing is the effect of air pressure.

Our lungs work off of pressure. Specifically our lungs inflate by using "negative pressure" (a word I've always hated). The pressure is not actually negative it is simply lower than the surroundings. Since there is less air in your lungs the air from the atmosphere rushes in because the pressure is higher outside your lungs. This is Boyle's Law (not the pressure outside being higher, but what happens when your lungs expand). Where an increase in Volume means a decrease in Pressure (if all else remains unchanged). In fact plants pull water up using negative pressure.
However to push out the air from our lungs we supply pressure using our muscles that overcomes the outside pressure and forces the air out.
The reason you feel your breathing change is because when that train passes by you correctly observed the strong gust of wind. This gust of wind has some force behind it that normally is not in the air you are breathing from the atmosphere. It has more force which increases the air's velocity. This actually decreases the pressure, but there's no need to get into that here (Bernoulli's).
The reason it feels like your body is "fighting to breath" is because the air is traveling in a direction with some force that you need to overcome by opening up your lungs just enough to "suck" the air in with negative pressure. This is more than the pressure you usually need to produce in order to breath in air that is "still".
What is funny to think about is we don't really have a muscle that "pulls" air in, even though it feels like you are actively doing that. The air actually rushes in on its own. All you do is expand your rib cage, which your lungs are attached to (look up on how, it's actually pretty cool), thereby making inhalation occur.
Now an interesting question for you to ask yourself is why is cold air harder to breathe?

Excuse my comment, but I don't see how your theory holds up, considering your lungs are in equilibrium with the outside pressure. Even in complete vacuum you would be able to perform a thorax motion, that could be perceived as breathing in. The perceived struggle to attempt the motion per se seems hard to be justified this way. Also regarding your comment about trees (especially if above 10m) please consider reading these answers: https://biology.stackexchange.com/questions/11044/how-do-trees-lift-water-higher-than-10-meters.

Also, the diving reflex is known to be triggered by ambient temperature, or better to say, the increased heat-capacity or heat transfer of water compared to air. The sheering forces created by passing air significantly increases the effective heat-transfer, which might be perceived as being submerged in water.


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How are muscle fibre size and oxygen consumption related?
Does anyone know of a paper which correlates the muscle fibre size to oxygen consumption in mammals? I am trying to find a correlation between muscle fibre type, size and (absolute and specific) oxygen consumption.

How much googling have you done? It seems there was some research: http://www.ncbi.nlm.nih.gov/pubmed/8904581 http://www.sciencedirect.com/science/article/pii/0026286268900022 Is it relevant?


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Do humans contract more physical sicknesses and diseases than animals do?
I wondered: If I get into the library and look into the medical section it is evident that there are thousands and thousands of different human physical diseases. But if I look into the section of animal diseases it is by no means as large as the human section.
But humans are by no means the only beings with extraordinarily cell complexity. Many other animals have an equal amount of cell complexity. So shouldn't other animals have an comparative equal amount of diseases ?
Naturally as humans we are much more interested in human physiology which would explain the discrepancy. But is there any evidence that animals, especially mammals, have not an equal amount of (still unknown) different diseases ?
Remark:
While a bit similar, this is not this question:
Why do humans seem so much more prone to disease than animals?
I am asking about the quantity of diseases, not if humans are especially prone for diseases.
ADDENDUM:
The difference between the questions is like
"Is building A more prone to fall in natural catastrophes than other buildings because it seems like it ?"
and
"How many faults have building A in comparison to other buildings ?"
A correct answer to the first question is: "We made a statistical comparison and building A is more/less/equal prone to fall in a natural catastrophe. The impression is wrong/right."
A correct answer to the second question is: "Building A has in fact a mean approximately 13 000 faults while other buildings have only 5400 faults. But the reason can be that the other building are inspected with less care." Or "No, they both have very likely something like 9000 faults".
It is a completely different question. The second question does not ask for the severity of faults. It could even be that building A has more faults while being more secure because the faults itself are much less severe.

The problem is that it's very hard to quantitate diseases. Is each sickness caused by a different influenza serotype a different disease, or are they all "the flu"? What about the huge number of potential bacterial infections? Also, a number of human diseases today are diseases of affluence and longevity - cancer was quite rare when our lifespans were a lot shorter. We are the only species that have developed significant longevity without evolving it. Since we are self-cognizant beings, we have a number of psychoses and other mental illnesses that are not present in other animals, as well.

Just to add to MattDMo's point, we are able to bring many children into this world that would not have made it a century ago.  Some genetic diseases are cured and many others treatable.  That's unlikely to be as true for any other animal.  So that would add to the thickness of the section on those diseases, whereas we might just add a line to an animal section that says, if this happens they die.

This question has been asked before, several times at least.

@anongoodnurse If you would actually read the question instead of simply scanning the title, well....

Who said I didn't? It's not "a bit similar", it is exactly the same question.

I'd say humans do have more illnesses than similar animals - for the most part animals do not have doctors or medical care - the simple understanding of sepsis and sewers has extended lifespan tremendously.  Previously we would just get sick and die. statistically speaking that means we get sick more often simply because we recover.  I doubt that animal's immune system is weaker than humans though.

@MattDMo Because of our enormous brain and the unique ability to communicate our psychical problems ("I am feeling sad") I restricted the number of diseases to physical ones. For comparison I also would assume that only the discernible changes count; I really doubt that vets are able to find the differences between flu viruses of the some animal. While it is hard to pinpoint down an exact number, I really think a coarse comparison could be made.

@anongoodnurse If someone explicitly mentions that the question is not the same as a similar one, as responder I would likely ask for clarification if I am not convinced instead of stating it is the same, vote for close and flagging it as duplicate in the same row. It really gives the impression that you did not read the text if you completely ignore the hint and do not give me the chance for clarification.

There are two differences between humans and other animals that lead to humans apparently having more diseases.  First, humans live longer than most other species, giving them more opportunities to encounter pathogens and for their bodies to wear out.  Second, and more important, there is far more effort put into keeping humans alive than keeping animals alive.  This leads to two effects: There's far more detail about human disease, and humans live through diseases and injuries that would lead to the prompt death of most animals.  A rabbit with a small tumor on their leg will be eaten in a couple of days, and will never have a chance to develop al the myriad complications arising from the tumor that humans see; let alone to develop a second tumor.

I suspected as such and it seems as the most reasonable assumption. I was interested if there are counterarguments which would give a reason that the number of diseases are really different because humans have some unique anatomical or physiological differences.

Some references would be nice.

References for what? The fact that humans live longer than other species? That humans are more interested in keeping humans alive than animals?

There is also the fact that there are many more humans than any other species alive. This also means there are large amount of different/unique populations for diseases to crop up in. Usually leading to differences in which diseases are seen where in the world.

@FrankyG Humans are vastly outnumbered by many species. Even setting aside things like insects and rodents, there are some 19 billion chickens alive at any one time, for example.

You're right. That's a huge misstep on my part.

The issue is more a matter of research focus than anything else. People care more about people than other organisms. Hence, more money is available for research and more money goes around in medical healthcare than in veterinary care. Research and drug development, in turn, focus on where the money is. The diseases of animals other than humans have simply not been investigated in such detail as in humans, because less effort has been done to document them as exhaustively as has been done for humans. Thus, when something is not in the literature, that doesn't mean it doesn't exist.


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Can you force human body to mass produce specific proteins?
I've had difficulty finding an answer to this question on Google.
From what I've been taught, DNA is used as a "naive blueprint" to synthesize proteins.
If we can manipulate DNA (Which I hear we can) does this not mean we can force cells to produce specific proteins we want? Purely hypothetically, ethics aside.
I also can't quite understand "what" uses that DNA to create proteins, or does it magically just "replicate itself" and turn into a new cell with the same proteins...
Sorry for the vague last question, but these questions were bothering me for a while now and I wanted to have some more references to read or answers.
Thanks ahead of time.

Welcome to Biology.SE. Currently there are two questions in your post, one of which is way too broad. You should edit your post to restrict it to one question only. In the meantime I am voting to close.

Yes, using recombinant DNA technology, one can take engineered DNA which has been put in an expression vector, induce it by one of various mechanisms to enter cells grown in culture (they can be from human, mouse, monkey, plant, bacteria, yeast, you name it), and the cells machinery will take over, transcribing and then translating it into protein.

does this not mean we can force cells to produce specific proteins we want? Purely hypothetically, ethics aside.

Absolutely, and this is done on a regular basis - sometimes at industrial scales, as a matter of fact. Examples of well-known recombinant proteins include insulin, the blood clotting factor VIII, and therapeutic monoclonal antibodies.

I also can't quite understand "what" uses that DNA to create proteins

This is an extremely broad question, but Wikipedia's Introduction to Genetics may help explain some of these ideas using less technical terms.The quick answer is that it is the cell's transcription and translation machinery mentioned above that do the heavy lifting. Very briefly, DNA is transcribed into messenger RNA or mRNA, which is then targeted to the ribosome for translation in protein. Think of the DNA as the main instructions for the shop, the mRNA as the working templates distributed to many workers, the ribosome as the machinery which takes the template and produces the finished goods, the protein.

I think the OP is asking can this be done in vivo, based on the title of the question. Also wouldn't use hGH and steroids such as testosterone and estradiol cause up regulation of some, but not all proteins? Not as specific as targeted, inducible expression, but would likely affect some but not other proteins.

Thanks this helps a lot! It's a vague quesiton I just wanted a direction to increase my understanding of the subject. I'll do more reading on ribosomes then.


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Is it painful for the hen to lay eggs?
My little son just asked me this question. His mother used to complain about the excruciating pain she suffered when she gave birth to him. He is a compassionate kid and wonders whether the hen goes through this pain everyday. Not being a hen, I am not sure if chickens experience pain that is close to the pain associated with giving birth.

By the way, taking your son to a farm that has laying hens might be really nice. As anongoodnurse said, there is a lot of squawking when the egg is laid, but nothing he would associate with pain.

I see why you would ask this question AMR, the do squawk after laying an egg

We really don't know - we can't really ask the chicken. At least, it's unlikely it's as painful as it can be with humans.
The reason human birth is (or can be) very painful is that the human baby's head has to fit through the woman's pelvis. Since splitting from chimpanzees, human heads have gotten bigger, while the pelvis has gotten more narrow due to adapting to walking on two legs. While chimpanzees give birth in an average of around 2 hours, humans can take over a day to do so, and the baby being too big can lead to maternal and natal death.
Back to chickens, while there are different sizes of eggs,  the larger eggs come from larger chicken breeds. If it does hurt them, at least it takes a lot less time - only a few minutes. From personal experience, the hens do not appear traumatized even seconds afterwards and just go about their day as soon as the egg is out.

YviDe, there is another part of the OPs question that is of interest. Without the introduction of hormones in feed, will a hen lay an egg daily? Are commercial farms affecting the hormone balance to increase output? +1 for not ignoring the question!

@AMR - hormones don't make chickens lay eggs; breed, light and temperature do. A mature chicken will lay 300+ eggs a year given long days (that means artificial light in the winter) and enough food and some help with temperatures (less energy lost to maintain body heat), Some lay ~360 (obviously referred to as layer breeds, like white leghorns.) There is another question answered already on hormones and eggs. Chickens don't need them. When they slow down, they get replaced. It's just cheaper.

@AMR - If you want to ask that (separate) question, though, since I answered for broilers but not layers, I'd be happy to answer it.

@anongoodnurse Interesting... So conditions affect nesting behavior and nesting behavior drives egg production.

@YviDe - +1. I used to have laying hens (I'm not exaggerating when I say I've had hundreds). They cluck and might squawk a bit when they lay, but they don't need bed rest after, and I never had one bleed to death from the experience.

@AMR - Yes, that's safe to say. Light affects the pituitary gland, which affects egg production. Usually regardless of age (within reason), my chickens all started to lay eggs at about the same time in the Spring once the days were long enough.

@anongoodnurse "If you want to ask that (separate) question, though, since I answered for broilers but not layers, I'd be happy to answer it." I tend to research on my own instead of ask questions, I just saw a quick tack on that's always been in the dark recesses of my mind. Thank you for the enlightenment. I would not have guessed that.

@anongoodnurse  "They cluck and might squawk a bit when they lay," I know I am anthropomorphizing, but I always found it rather adorable :-)

@YviDe - I can't even say why they cluck and sometimes squawk; they might well be warning me (or other chickens, seen or unseen) to stay away from their preciousssss. ;)


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Difference between protein channels, protein carriers and protein pumps?
I'm revising for my biology exam and I don't fully comprehend the difference between protein channels, carriers and pumps. I know that:

Protein channels do not require ATP (passive transport)
The difference between passive and active transport

My questions are:

Are protein carriers and pumps the same?
I read that protein carriers can perform both active and passive transport, is this true?
But protein pumps always require ATP?

@Christiaan Thanks for the  comment, but I'm specifically confused about the proteins, not active and passive transport.

Usually, when introductory textbooks and tests ask about pumps, they are usually ion pumps, such as Proton pumps or Sodium - Potassium pumps, etc. Carriers usually are used to transport hydrophilic molecules such as glucose through the membrane. Carriers can be both. Passive usually requires another substance, such as sodium where there is a gradient. The binding of the transported molecule will cause a conformation change in the carrier protein that transport the molecule to the other side of the membrane. Have you talked to classmates about their understanding? Study groups are a good idea.

No, carriers are not the same as pumps. Carriers may or may not carry out active transport and pumps always use energy. Carriers, for example, can make use of the concentration gradient of a certain ion built up by pumps to transport other molecules actively against their gradient. For example, the glucose transporter uses the sodium gradient to transport glucose against the concentration gradient into the cell, while getting the energy by co-transporting sodium into the cell along the gradient. The sodium import yields energy. That in turn is caused by the Na+ K+-ATPase, which builds up the sodium gradient using ATP. The glucose transporter is called a symporter, because it co-transports sodium into the cell. An antiporter transports another particle in the opposite direction.
Yes, true. The glucose transporter as explained above is an example of active carrier-mediated transport. Other carriers just mediate passive diffusion of, for example, large molecules that don't fit through channels and won't readily cross the cell membrane.
Yes, pumps always use energy under physiological conditions. The energy source is always ATP.

Will add references shortly.

Good summary. A couple of comments to consider. First, there is not a single type of glucose transporter, which isn't clear from this answer. The one you describe is used in intestinal and renal epithelia, but most mammalian cells use a simple uniporter for glucose uptake. Second, I think that many would consider the proton transport out of the inner mitochondrial membrane, needed for oxidative phosphorylation, to be pumping, but the energy sources there include NADH and oxygen, not ATP.

A small note: There are also carriers that use ATP by their ATP Binding Cassette domain (ABC transporters). The mechanism, however is different from that of the phosphorylation dependent pumps.


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Bug Identification: what type of bug is this small ant-like bug?
It's not an ant; do you know what it's called? Found some in the building different times.

Edit: Size is 4mm (length) x 1mm (height)

It looks like a ground beetle (family Carabidae)

Thanks for the quick identification! looked up ground beetle sizes and found: ground beetles are from 1/8inch (3.1 mm) to 1/2inch (12.7 mm); though I haven't seen any quite as long (12.7 mm); perhaps these are baby ground beetles then.

Baby beetles are not small versions of adult beetles as beetles undergo complete matemorphosis (more info there). There are about 40,000 species of ground beetles. If you only see individuals that are relatively small it just mean that the species that you often see is a relatively small species of ground beetle.

This isn't a ground beetle; the lack of focus makes any identification uncertain, but my best guess is one of the grain beetles (family Silvanidae); if any have been seen since this question was asked, you probably should try to get rid of them -- they're after stuff in your pantry.

Are Silvanidae differentiated from Carabidae by having clubbed antenna tips rather than straight? If so I tend to agree.


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Large coalitions of lions taking over multiple prides?
I have noticed while watching lion documentaries that coalitions with more than 3 males tend to take over multiple prides and have 1 large pride in their territory while coalitions with 3 lions or less tend to take over just 1 pride.
As a very good example the Mapogo brothers(6 lions) take over multiple prides and they even split the territory between a coalition of 4 and a coalition of 2.
On the other side of the spectrum Tau and Banda are just 2 lions in a coalition. They take over just 1 pride with 3 lionesses in heat and no cubs. Tau does it by instinct and Banda is strategic.
Why is there so much of a difference between the small coalitions that take over just 1 pride and the large coalitions that take over multiple prides? Do large coalitions do better when they take over multiple prides from less aggression? Do small coalitions do better when they take over just 1 pride from more and closer defenses against other male lions?

In which documentaries did you learn about this? I want to learn more :)

the size of the territory expands with each takeover so a larger takeover such as the Mapogo they split to protect the territory they have inherited.


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Why do we need to put phosphate fertilizers along with rhizobium?
Isn't phosphorous a macro nutrient? So it should be present in the soil in sufficient quantities... but still we add phosphate. Why?

But beware of what Sir Albert Howard called the "NPK mentality": it may help you now, but be a disaster on the long run.

Phosphorus (P) is a macronutrient and, after nitrogen (N), typically the limiting factor for plant growth. Potassium (K) is also often added in fertilizers.
P is an important plant macronutrient, making up about 0.2% of a plant's dry weight. It is a component of important compounds, including nucleic acids, phospholipids and ATP. Consequently, plants cannot grow without a supply of this nutrient. P is also involved in controlling key enzyme reactions and in the regulation of metabolic pathways (Schachtman et al., 1998).
Certain plant species actively increase root densities around phosphorus-rich patches (Snapp, 1995), because it is critical to optimize it's uptake.
References
- Schachtman et al., Plant Physiol (1998); 116(2): 447-45).
- Snapp, Plant and Soil (1995); 177(2); 211-21

Christiaan, either you mean Potassium, which is K or you mean for Potassium to be Phosphorus....

I've watched every Periodic Videos....

@Christiaan: yes it has :). one more question... is it difficult for plants to absorb phosphorous from the soil in general?

@AlexPrior - I am unsure, but I think it depends on the composition. CaPO4 for example is not soluble and plants will have a hard time extracting it. K2PO4 on the other hand dissolves well. Maybe worth a new question?

@Christiaan: Yes. If K2PO4 dissolves well wouldn't it go deep down by leaching and make its absorption difficult by the roots?

yep absolutely. some salts bind to soil particles and hence stay available, others wash away quickly.

Phosphorus is indeed a macronutrient!!! If you're wondering why it is insufficient in natural soils then read on. Phosphorus is, in fact, the most limited of the three primary macronutrients in most natural soils (being nitrogen, phosphorus and potassium). This is because it is released very slowly from insoluble phosphates (on rock surfaces) and rapidly becomes “fixed” after being released, making it difficult for plants to obtain their phosphate ions (intake form of phosphorus). Few unfertilized soils release phosphates fast enough to support the high growth rates of many plant species. Also, plants tend to only obtain their phosphate ions from the little “polyprotic phosphoric acid” in the soil, they are often very deficient in phosphorus and for this reason phosphate ions are used in high quantities than nitrogen and potassium in NPK fertilisers (N:P:K = 1:2:1).
P is found in natural compounds in soil (however this is very limited); it is more often found in NPK fertilisers in the forms of: Orthophosphates ( H2PO4- or HPO42- ) and Polyprotic phosphoric acid ( H3PO4 ).
The following reasons are why phosphorus is a primary macromolecule and why it is VERY essential to plant nutrition;

To build ATP (the energy currency of plants) from respiration ;
To build DNA and RNA (genetic information) ;
To build the cell membrane ;
To aid the growth of a plant in its early stages (seedlings and root development) ;
To perform phosphorylation ( the modification of the activity of various enzymes – this is responsible for cell signalling (which is the ability of cells to perceive and correctly respond to their microenvironments – aka tissue homoeostasis))

I'll try to give a wide answer, not only to why we have to add chemical fertilizers, but also to why this is not our best choice.
One thing is the isolated chemical compounds we add to the soil (like N, P and K), other is its natural fertility (which include a good part of the periodic table, and also many micro- and meso-organisms, what improves productivity and quality of products).
Sir Albert Howard, in his "An Agricultural Testament", reminded us about the danger of the specialization in the isolated chemicals, and warned us of the futile reasons why they came to be so widespread and dominant:

"The artificial fertilizers are being widely used. The characteristic
  of Western agriculture is the use of artificial fertilizers. The
  industries engaged in fixing atmospheric nitrogen for the production
  of explosives during World War I, had to find other markets; the use
  of nitrogen fertilizers in agriculture increased, and today most
  Western farmers based their fertilization programs in the cheapest
  forms of nitrogen (N), phosphorus (P) and potassium (K) available.
  What we might call the NPK mentality dominates the farms as well as
  research stations of agricultural research. Industrial vested
  interests in times of national emergency settled firmly and could no
  longer be dislodged."

(Sorry, it's been re-translated from a Portuguese translation.)
He also added that the only way to preserve the soil's original (and healthier) fertility is to keep animals along with the plants, like Indians and Chinese did for millennia and still do (whose farmers he used to call "my teachers"). The animals complete the natural cycle of the nutrients, and the high faunal diversity -- that exists when sufficient patches of native biomes are preserved -- helps fight against plagues. Both India and China are still countries of so-called "Megadiversity", even with more than a billion people each and such long history. We, Westerners, on the other hand, are destroying our fertile land in an alarming rate, as you can see with deforestation/desavannization in Brazil and many other countries in the Americas, places with far less people, and far less time of "civilization".
But, of course, all of this is only feasible in a world with a substantial peasantry, and not one who follows the machine-guided + urbanization philosophy that rules in Western world today.
Finally, some patches of land will naturally have more nutrients than others. That's why there has ever been "good lands" and "poor lands". And since we want to use them all to survive, we may end up using some chemical help here and there. But that should be seen as an exception, not as rule.