Is blood regarded as an organ? It consist approximately 7 percent of body weight.

By definition organ is composed of multiple tissues. Blood is a fluid, a circulating tissue.

Therefore can we call this fluid system a liquid organ?

Blood is considered a type of connective tissue (sometimes). However, an organ is formed of multiple different tissues. Thus, blood is a tissue, not an organ.


Can multiple cetacean species communicate? It seems that individuals within the same species have their own communication, but is there evidence to suggest that individuals from different species are able to communicate?

Do dogs and humans communicate? What about cats and dogs? I think defining "communicate" is the real question here.

This 2012 study claims to show "the first experimental evidence that the interception of heterospecific vocalizations can mediate interactions between different cetacean species in previously unrecognized ways". In other word, one species is recognizing and responding to the vocalizations of another.

This article points out that "...false killer whales and bottlenose dolphins choose to spend time with specific members of the other species rather than randomly mixing or engaging in brief opportunistic encounters" How could this occur without some form of "communication"? I'd argue it couldn't,


Inverse Agonist vs Neutral Antagonist Could somebody explain in simplest terms the difference between inverse agonist and neutral antagonist?

Which one is more well natural and less likely to cause pathways to rebound?

Does neutral mean less effect such that stepping from an inverse agonist to neutral is the best idea to avoid withdrawal?

Edit: I am trying to determine how quickly the pathways rebound when stopped during withdrawal.  I would assume this might vary between inverse agonist and neutral antagonist.  I am not asking about actual withdrawal symptoms.

Many receptors have a natural constitutive, or "baseline", amount of response that they generate, they're not just an on-off switch. At baseline, many receptors will generate a partial response, which means that certain things binding to them can either increase or decrease their response.

A neutral antagonist is one that causes no change in the signaling response of the thing that it's binding to. It simply stays the same. Note that this can still be important, because a neutral antagonist can block the binding of other agonists, ones that would have generated a change in response, even if the antagonist itself doesn't cause a response.

An inverse agonist is something that decreases the response of the receptor from its baseline all by itself. Often, this is caused by stabilizing the receptor in it's "off" state. If the receptor has some degree of constitutive activity, an inverse agonist will decrease its activity.

See this graph from this wikipedia page for a good explanation:


What's a non-allelic gene? Non-allelic or non-alletic

I stumbled across the term in my Human Genetics textbook. It didn't explain it there, and a quick google search only showed scientific papers that refer to 'recombinations with non-allelic genes' without explaining what they are.

It is my understanding that a non-allelic gene is one that affects another's traits, but is not as a typical dominant / recessive manner. If I am correct, this is the same thing as  epistasis - meaning that one gene modifies how another is expressed.
There exists epistatic genes for horse coat color. One gene is the coat color itself (horses may have either brown or red color alleles at this loci), the second gene is for a protein that allows the coat color gene to be expressed.
For example, a horse has two brown alleles at the coat color locus. It also has a wild type gene in the second (modifier) position. This modifier allows the color brown to be expressed and the horse is brown.
B/B, wt/wt --> Brown
If the horse has the two brown alleles, but has a mutant allele at the modifier position, then coat color is not expressed and the horse is white.
B/B, mt/mt --> white

Because the modifier alleles are separate genes from the coat color alleles, the two are non-allelic - yet they both affect the same trait in some way.

I hope this helps.


What is the number density of fungal spores per unit of volume of air? Fungal spores are present all over in the air around us. I understand that they generally range in size from about one to one-hundred microns.

What is the number density of fungal spores in air on a volume basis? I imagine this will vary based on location, season, and indoor vs. outdoor. An ideal answer would account for all of this in the ranges but I'm broadly interested in indoor air conditions around the world.

If measurements of a single spore density are too difficult, I would find the density of CFUs to be acceptable (assuming that those are multiple spores) but would appreciate being directed to information on how many spores typically make up one CFU. Similarly, a mass density of spores would be acceptable as well if experimental methods make that easier. At the simplest level, I'm just curious how much fungal spore material is in the indoor air around us.

Bamba et al. (2014) Case study of airborne fungi according to air temperature and relative humidity in houses with semi-basements adjacent to a forested hillside. Biocontrol Sci. 19: 1-9.

This is neither the first nor the last report of this kind. Search PubMed database using this query:

"air"[Title/Abstract] and "fungi"[Title/Abstract] and "spore"[Title/abstract]


Why doesn't Manipulated Virus for Cancer Cure Work I'm not a biologist but I have an idea for a cure for cancer and it is very simple and probably has flaws (if it worked it probrably wouldn't be a cure for all) or is not possible but ... I'm still going to ask why because I want to learn why it doesn't work and I want to learn more in general, so you can use all the biology terms you like. The idea is essentially to use a virus and manipulate/change it (this would be mechanized if it were to be mass produced and the type of virus is unknown to me because you want one that is fast growing and goes across only specific parts of the body depending on the cancer). This virus would not have any bad parts (parts that make you sick) to it because when the virus "injects" it's DNA or manipulates the existing for copying it would instead manipulate the DNA in the cell it is going into to have growth limits and other cancer genes that are set to being back to normal and then copy itself. Eventually it would be fought off by the immune system and most of the virus would be gone (along with the cancer) because this virus would last for a long period of time (week(s)).

I appreciate anyone who answers this question because I'm sure it sounds stupid from your perspective but this is the place to learn.

Thanks,
Jackson

Note: This is not an idea I'm trying to make, obviously, I just couldn't get it off my mind and wanted to see what is wrong and if it is fixable.

This is not an idea I'm trying to make, obviously, I just couldn't get it off my mind and wanted to see what is wrong and if it is fixable.

Since everybody else is giving you a bad attitude in the comments...

While it might work for some cancers, it is completely impractical for the majority of cancers.

SOME cancers do occur because of a specific mutation or specific set of mutations. Some genes predispose people to greater risk for certain cancers. These have a much greater chance of being treatable via viral therapy, but there are still barriers:

The length of coding material (DNA or RNA) a retrovirus can hold and propagate is limited. The mutated gene or stretch of DNA may be much larger than the length a retrovirus could potentially replace.
The retroviral material is not guaranteed to "rewrite" or "overwrite" any bad DNA. Retroviral DNA is inserted fairly randomly into the host genome with little regard for where since it is generally an entire gene meant to be read in its entirety to eventually produce proteins. You'd expect BOTH gene versions to exist simultaneously. This wouldn't end in a cure, but some middleground between cured and affected.
There are tissues where cancers develop that wouldn't be infected. Any sort of brain tumor would remain completely untouched by retroviral therapy, for example.
Targeting specific cancerous tissues while leaving surrounding or other tissues alone is a big problem, even for non-retroviral therapies. Replacing bad genes in a cancerous cell is good, but replacing good genes in a healthy cell could lead to that cell's death or -- ironically -- possibly turn it into a cancerous cell as well.

The majority of cancers are not specific mutations and do not have known genes that predispose their bearers. The majority are an accumulation of mutations across sections of the genome. As MattDMo said in the comments (paraphrased): For these cancers, viral therapy is nearly impossible. Every mutated gene would required its own retrovirus. At that point, the time and financial investments start to rise exponentially.

While I'm not one to say it's impossible (I'm not involved in the research, so if anybody who is can correct me on anything in this post, I'd appreciate it) -- it is certainly very improbable with current knowledge and methods. Every bullet point above (which isn't an exhaustive list) represents a mountain to climb on hands and knees before an "inject-and-forget" end product could be developed.

Kudos for the critical thinking and forming a working theory from the knowledge you had, but unfortunately it does break down with some more specialized information.


How would I represent this on a cladogram? So, right now I am making a cladogram (More of a dendrogram) for a kingdom of fictional species, and I'm not exactly sure how to represent a certain relationship.

Let's say that the oldest class in the kingdom is Clade A. And, while it is a clade in itself, it also evolved into two other classes. The first class it evolved into was Clade B, but Clade A still persists. Then, later on, Clade A evolves into Clade C - but still persists.

If I was to represent this on a dendogram, how would it be done?

The short answer is that cladograms are not compatible with Linnean taxonomy.

The longer answer explain how and why. First, there aren't enough ranks in Linnean taxonomy to cover all the cladogram nodes. The "kingdom-phylum-class-order-family..." was originally based on similiarity and not on phylogenetic relationship. For example: the class Reptilia is no longer a clade, and the class Aves is a subclade of the order Sauroschia (of the "super"-order Dinosauria, which is a clade of Diapsida which includes modern reptiles and crocodiles). The birds (Aves) are evolution descendants of dinosaurs but they ranked by Linneous as class while dinosaurs, according to Linnean taxonomy were at most super-order.

So you need to choose: a pseudo-Linnean relationship tree or a cladogram phylogenetic tree (and then you should omit the ranks' names "class", "order" etc.

I'll try to sketch the tree you described:

 A
 |
 |-- B
 |-- C
 |
 .
 .
 .


Stem cells and if they can correct a lack of apoptosis If a cell ,call it C1 has no functioning apoptosis mechanism could a stem cell somehow be 'induced' to be like C1 , at least have the same genome as C1. Then use this stem cell 'duplicate' to 'restart' the apoptosis mechanisms in C1 or even replace C1? ( forgive any broadness or vagueness, I'm trying to be specific)

The answer is no.  There is no method currently known whereby we could get a stem cell to transfer its genome to a cancerous cell and thus get its apoptosis mechanism functioning again.  It's just not that easy to get a genome transfered - destroying the defective copy of the genome which is stored in the nucleus and getting a new copy of the entire genome into the same.
Remember that to transfer almost anything (except small non-polar molecules) in and out of the cell, you need highly specialized transporters (ie., ion channels, Na+/glucose pumps).  This is particularly true of large molecules like glucose and sucrose (plants). But even those molecules are extremely small compared to an entire chromosome, for which there is nothing even close to a transporter.  It would therefore be impossible to get the chromosome into the cell.
But even if you could, you have yet another hurdle: you have to get the new chromosomes into the nucleus... and that only after having destroyed the original genome in Cell 1, without making the environment in the nucleus toxic for the new genome (ie., CAD activity...)  This represents innumerable challenges, including the fact that you're going to need to alter the nuclear membrane to allow the entry of a massive macromolecule, without impeding the function of the cell...  The problems, unfortunately, go on and on.
TL;DR:  Nice idea, and would be really cool if it worked, but it has way, way, way too may complexities and insurmountable hurdles to be even remotely workable.

Sources:

Lemoine R. 2000. Sucrose transporters in plants: update on function and structure. Biomembranes 1465 (1–2): 246-262.


What is the name/type/species of this spider? Below are images of it, specimen found in the western region of the Pacific Northwest - North America.

I presume it is Eratigena atrica, commonly called the giant house spider.

It belongs to      Agelenidae family.

  E. atrica is found in Europe, Central Asia and Northern Africa. It was unwittingly introduced to the Pacific Northwest of North America circa 1900 due to human activity and has strongly increased in numbers for the last century.

Reference: Wikipedia


Why do I breathe out of BOTH nostrils? After reading the question why do I only breathe out of one nostril I realized that breathing out of both isn't common. I have always breathed out of both, and when I get a stuffy nose, or a runny nose, it's on both sides. If only one side is stuffed, I'll just lay on my side a bit to even it out until I can breathe out of both again. I've always though that was totally normal! What does it mean that my autonomous nervous system is not alternating my breathing?

The odds are that you're noticing the equality of patent nostrils in the middle of a changeover, when both are equally patent. Also, the shape of your nose may be permitting the congested side to still be fairly patent. Your nose is doing what it's supposed to be doing (and everybody suffers bilateral congestion during colds, allergies, etc.) If it were not, you would be plagued by dry, painful and bleeding nares (um... are you?)


Can we directly stimulate M cones in retina with current technology? I wonder if we could try to see imaginary "supergreen" color by directly stimulating M cones. For this I suppose we'd need:

Non-destructively scan specific human's retina to locate exact positions of M cone cells.
Prepare a high-resolution image (on a retina-like display I guess), which would have light spots in some locations and dark in others, so that when the human we inspected looks at particular point of the image, these light spots were focused exactly on M cones.
Track the eye movements and adjust the image so that S and L cones avoided significant exposure to prevent misperception.

Is anything of this hard to implement with current technology, given typical human retina properties (M cones density, their apparent color etc.)?

If this is totally possible, has such an experiment already been performed?

You've probably seen the news reports by now, in which researchers targeted and stimulated individual cone cells in the eyes of volunteers: "The elementary representation of spatial and color vision in the human retina" Ramkumar Sabesan, et. al. (2016). This experiment is the first time that researchers have targeted and stimulated individual cone cells. The experiments mostly involved L- and M-Cones, though the published research noted the response obtained from S-Cones, too. The researchers used 543 nm laser light (25 nm bandwidth) and an optical tracking system similar to what astronomers use to correct atmospheric distortions. So, yes, the technology exists, but it looks like it is so new in this application that no one has performed other experiments with it, yet.


What kinds of cells does human saliva contain? I have heard that our saliva contains cells. What cell types can be found in human saliva?

It contains white blood cells (leukocytes) and cells from the inner lining of the mouth (buccal epithelial cells). The DNA obtained from these cells is the basis of DNA profiling based on saliva samples.

Source: Salimetrics


Distribution of Exon and Intron Sizes Goal

I am trying to get a distribution of Exons and intron sizes in Three-Spined Stickleback (Gasterosteus aculeatus).

Data downloaded

I downloaded some data from Ensembl. More precisely, I went there, selected "structure" in the "attributes" and selected

- Ensembl Gene ID
- Exon Chr Start (bp)
- Exon Chr End (bp)

There are two issues in these data:

Some exons end before they start
Some exons overlap

The first point is I assumed due to reversion, so I just reversed the start and end position when there was such inversion. The second point is more problematic as I don't know what such overlap could mean realistically.

Can you help finding the distribution of exon and intron sizes in three-spined stickleback?

What I did with the above data

Preparation

# read data

d = read.table(file.choose(), header=TRUE)
names(d)= c("ID", "start", "end")

# Reverse exons when needed

toReverse = which(d$start > d$end)
s = d$start[toReverse]
d$start[toReverse] = d$end[toReverse]
d$end[toReverse] = s

Exon Sizes -> Looks good

# Exon sizes

ExonSizes = d$end - d$start
hist(ExonSizes) # Cool, looks good!

Introns Sizes -> Looks bad

# Intron sizes
# This is a little slow. One might have better to switch to C++.
# The idea is to look at the distance between the end of an exon and the start of the next exon within each gene.

d$ID = paste(d$ID)
IntronSizes = c()
uniquegenes = unique(d$ID)
nbgenes = length(uniquegenes)
i=0
exon = 0
for (gene in uniquegenes)
{
    i=i+1
    cat(paste0(i," / ",nbgenes,"\n"))

    while (TRUE)
    {
        exon=exon+1
        if (d$ID[exon] == gene) {
   IntronSizes = append(IntronSizes, d[exon+1,]$start - d[exon,]$end)
        } else
        {
            break
        }
    }
}
hist(IntronSizes) # There are negative values. I don't know how to interpret them.

hist(log(abs(IntronSizes))) # That looks good but I doubt it makes much sense!

At the command line:

wget ftp://ftp.ensembl.org/pub/release-84/gtf/gasterosteus_aculeatus/Gasterosteus_aculeatus.BROADS1.84.gtf.gz
gunzip Gasterosteus_aculeatus.BROADS1.84.gtf.gz

Then in R:

library(GenomicFeatures)
txdb = makeTxDbFromGFF("Gasterosteus_aculeatus.BROADS1.84.gtf")
hist(log10(width(unique(exons(txdb))))) # exons
hist(log10(width(unique(unlist(intronsByTranscript(txdb)))))) # introns

Note that some of the annotated exons (and the introns between them) are incredibly unlikely to be correct. For example, there are 1 base long exons and introns. I don't think anyone actually believes those are correct, but the distribution is probably otherwise approximately correct.

Edit: For what it's worth, there are no negative sized exons in the GTF file. My guess is that the overlapping exons are from different transcripts (or genes on opposite strands).

Edit2: If you want to get your introns from a "union gene model", then use something like reduce(exonsBy(txdb, by='gene')) and then lapply gaps() to that. The results will be correct and the process will probably take less time than what you've been trying.


What does it mean when a patient suffering from malignant tumor (cancer) has been declared cured? Comment by Anongoodnurse, has made me curious as to what a doctor means when (s)he says "The cancer is cured" to a patient.

My idea up till this point (based on what I read and what I learned in my classes from my professors) was that the prognosis was declared based on the survival rates and that cancers could never be declared cured as no one could be sure that every single malignant cell has been eradicated.

However Anongoodnurse commented:

  Curable cancers are not few and far between.

So I would like to know what it means when it is said "Cancer is cured"

Though the answer by Anongoodnurse has been accepted, I would like to have other answers too, please feel free to contribute

TL;DR - ask someone who has survived 45 years after treatment of their testicular cancer. The patient (and most doctors) would consider that a cure.

I believe the kxcd cartoon explains prognosis quite well. There is something that @Crags has overlooked, though, and that is the caveat "Once most cancers spread out into your body, they're incurable".

I would consider that sentence to be quite correct. A good prognosis is very different from a cure. Most of the surgeons, radiation therapists and oncologists I have worked with make that distinction. (Even surgeons, whose mottoes include "A chance to cut is a chance to cure." and "Nothing heals like cold hard steel." are careful not to use the word cure, unless it is a cure.)

I am not an oncologist, but oncologists do write papers. From one of them:

  METHODS: We analysed postmenopausal women with localised invasive breast cancer. The primary endpoint disease-free survival (DFS), and the secondary endpoints time to recurrence (TTR), incidence of new contralateral breast cancer (CLBC), time to distant recurrence (TTDR), overall survival (OS), and death after recurrence were assessed... FINDINGS: At a median follow-up of 100 months (range 0-126), DFS, TTR, TTDR, and CLBC were improved significantly in the ITT and hormone-receptor-positive populations.

Although this study only followed patients for 100 months (8.3 years), some studies are much longer, and a cure is what you or I would think of as a cure: disease-free survival, not of months, but for a lifetime, that is, non-recurrence of the cancer.

Your professors sound like they are using the standard approach to cure, which is to hedge one's bets:

  In medicine, a disease is considered cured when it’s been successfully treated and does not return. The concept of “cure” is difficult to apply to cancer because undetected cancer cells can sometimes remain in the body after treatment, causing the cancer to return later (referred to as a recurrence or relapse). Many cancers are considered “cured” when there is no cancer detected five years after diagnosis. However, recurrence after five years is still possible.

In the past, cure was defined as 5-years cancer free. We now know that that is survival, not cure. The same can be said of 10 years (thought that one runs more true to cure). The fact is, most studies don't follow patients indefinitely. That doesn't mean no cancer is "cured". The patients (even many of those in the xkcd comic) without recurrence are cured. Therefore it is a fallacy to say cancer can never be cured. Semantics and statistics are at play.

As I said in my comments, there are curable cancers.

Curable cancers: non-invasive basal cell carcinoma:

  Nearly every basal cell cancer can be cured, especially when the cancer is found early and treated.

(This is not a hedge. The authors are lumping aggressive BCCs in here with the less aggressive BCCs.)

Certain early prostatic cancers:

  These results suggest that a patient has a high likelihood of biochemical cure after treatment for prostate carcinoma with conventional doses of external beam RT if he has not demonstrated biochemical failure within 5 years of treatment. Patients with lower pretreatment PSA levels and lower Gleason scores may require longer follow-up than those with less favorable characteristics to achieve the same certainty of cure. Patients who achieve a PSA nadir ≤ 0.4 ng/mL and require ≥ 2.0 years to reach this nadir have the highest probability of cure.

Cervical cancer:

  Early cervical cancer can be cured by removing or destroying the precancerous or cancerous tissue.

Colorectal cancer:

  Conclusion: Patients who survive 10 years appear to be cured of their disease, whereas approximately one third of actual 5-year survivors succumb to a cancer-related death. In well-selected patients, there is at least a one in six chance of cure after hepatectomy for CLM. The presence of poor prognostic factors does not preclude the possibility of long-term survival and cure.

Childhood acute lymphocytic leukemia:

  Impressive improvements of survival rates in pediatric acute lymphoblastic leukemia (ALL) have been achieved during the last decades.1–21 Today, a long-term cure can be attained for approximately 75% of patients.

(Although good survival rates - defined by *event free survival - are defined at 6 years in this paper, there are papers which follow to 15 years with little change in the group. Like most studies, longer times mean more patients are "lost to follow-up".)

It goes on and on.

Finally, my comment was an admonition to you to be wise with your words, not an absolute.

Understanding Statistics Used to Guide Prognosis and Evaluate Treatment
The cure of cancer: A European perspective
Basal cell carcinoma: Diagnosis, treatment, and outcome
Cervical cancer
Risk-adjusted therapy of acute lymphoblastic leukemia can decrease treatment burden and improve survival: treatment results of 2169 unselected pediatric and adolescent patients enrolled in the trial ALL-BFM 95


Why only mitochondria and plastids? Why are there only two unique semi-independent organelles? Why are there no others, symbiogenesis seems like it should be a relatively common thing. So do most organelles just lose all their DNA? Or is it something that occurs fairly rarely?

There are. But they are not that universal. See kappa-particle in Paramecium and Wolbachia in insects. Also, there are different origins of plastids (compare red algae and green algae). Some organisms like Rhopallodia gibba even have plastids of multiple origin.

  So do most organelles just lose all their DNA? Or is it something that
  occurs fairly rarely?

The organelles of endosymbiotic origin lose their genes gradually. The extent and rate of loss is correlated with the number of organelle the cell harbours. The limited transfer window hypothesis speculates a probable mechanism.


Birds placing sticks on train tracks? I live in a semi-rural area in Germany, close to a park which trains go through every 20 minutes.

Today, I saw something that left me perplexed.

There is a large population of birds that look like crows or ravens, yet fatter. They seem to be quite social and move around in large groups. Today, I spotted one carefully laying sticks from a nearby tree on the train track while the others seemed to spectate.

What exactly was that bird doing? Is this common? Did it have a purpose, or was it just coincidental?

There is a large population of birds that look like crows or ravens,
  yet fatter. They seem to be quite social and move around in large
  groups.

First of all, this seems like a crow. Crows are very social birds, they live in flocks or murder.

  Theory: It may be a Mating Ritual?

No! The have a very spectacular mating ritual!.

  Theory: It's Making a nest

Obviously No! Crows nests are always way hidden at 18-60 feet above ground(mostly) in the tree trunk.

My Theory

Crows are very curious birds. What you saw, might be a new play the young crows found. It's common that crows will do unusual thing when spectated by the elders and siblings.


Are mosquitoes repelled by high frequency sound? I am totally confused whether ask this question to physics or biology stackexchange.

I downloaded a mobile application which claims to repel mosquitoes. This application basically produces sound from 16kHz to 22kHz (I doubt that it even produces more than 20kHz because we can't hear more than 20kHz naturally).

I totally doubt this application. Do mosquitoes go away in higher frequency of sound?

After seeing your question, I decided to do a bit of research on the topic.

First Source: EurekAlert!

http://www.eurekalert.org/pub_releases/2007-04/jws-mrt041607.php

  "Mosquito repellents that emit high-pitched sounds don't prevent
  bites"

Some key-points from the webpage:

  A Cochrane Systematic Review of the use of electronic mosquito repellents (EMRs) failed to find any evidence that they work.

  To test these claims a team of Cochrane Researchers conducted a systematic review looking for trials conducted with EMRs. They located ten field trials that had been carried out in various parts of the world. None of these trials showed any evidence that EMRs work.

  All ten studies found that there was no difference in the number of mosquitoes found on the bare body parts of the human participants with or without an EMR

Second Source: Wikipedia

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

  These electronic devices have been shown to have no effect as a mosquito repellent by studies done by the EPA and many universities.

Third Source: CBCnews

http://www.cbc.ca/news/story/2007/04/18/mosquito-repellent.html
Key points from the article:

  "There was no evidence in the field studies to support any repelling effects of EMRs, hence >no evidence to support their promotion or use"

  -Ahmadali Enayati, researcher

This is a major point as well:

  The study also said that in 12 of the 15 experiments, the landing rates of mosquitoes on subjects was in fact higher than in control groups.

The article also points out that female mosquitoes can't hear very well- Which supports the idea that high-frequency repellents are ineffective; Much more than you probably think. Why? Well, it's pretty simple:

Female Mosquitoes are the only Gender that Bite.

Overall, when you consider the countless studies and research put in to the effects of high-frequency sounds on mosquitoes, it's pretty obvious that:
No.High Frequency Sounds do NOT repel mosquitoes


What is the name of this spider and is it poisonous? We found it between Palm trees in the backyard of a home in West Palm Beach Florida.

Ah, that would be the spiny orb weaver. You can see an almost exact same picture here. To make a guess on the species, its maybe Gasteracantha cancriformis as its said in that webpage I have tagged. They are generally harmless. Here's the wikipedia page.


Why do red blood cells maintain Iron in the Haem group in the +2 (ferrous) oxidation state? A lot of sources tell me that RBCs contain a number of enzymes, and that these serve multiple functions from maintaining the structure and elasticity of the corpuscle wall, to preventing the oxidation of iron (ferrous) in Haemoglobin to the +3 Ferric state.

But what none of them say, is what problems (if any) arise when the iron is oxidised. Hence the question, why avoid the Ferric state?

I'm still a high-schooler and from what I've learnt, is that the higher the oxidation state of the cation, the higher its polarising power (Fajan's Rules) hence stronger the bond. So wouldn't iron in the Ferric state be able to bind with oxygen better, and isn't that desirable? ( Or is oxygen release to tissues going to be problematic? )

If the Ferric state is desirable, then why do RBCs have mechanisms (the enzymes mentioned earlier) in place to prevent the oxidation of the Ferrous to the Ferric state?

Thanks!

Q. “What problems (if any) arise when the iron is oxidised?”

  A. Haemoglobin will be converted to methaemoglobin which cannot bind oxygen.

To quote from the article on Methaemoglobin in Wikipedia:

  Methemoglobin (English: methaemoglobin) (pronounced "met-hemoglobin") is a form of the oxygen-carrying metalloprotein hemoglobin, in which the iron in the heme group is in the Fe3+ (ferric) state, not the Fe2+ (ferrous) of normal hemoglobin. Methemoglobin cannot bind oxygen, unlike oxyhemoglobin. It is bluish chocolate-brown in color. In human blood a trace amount of methemoglobin is normally produced spontaneously, but when present in excess the blood becomes abnormally dark bluish brown. The NADH-dependent enzyme methemoglobin reductase (diaphorase I) is responsible for converting methemoglobin back to hemoglobin.

The question also asks:

  “…the higher the oxidation state of the cation, the higher its
  polarising power… hence stronger the bond.So wouldn't
  iron in the Ferric state be able to bind with oxygen better…”

which can be transformed into:

  “Why can‘t methaemoglobin bind oxygen?”

The answer is chemically rather complex, but one thing you should be aware of is that in haemoglobin (and myoglobin) the oxygen Fe(II) is five-coordinated (as shown in the diagram below where Fe is black) and binds oxygen in the sixth position (to the right).

In simple terms, the electronic change in oxidation to Fe(III) causes a change in the geometry of the haem pocket such that oxygen no longer can bind (although now water can). This page elaborates the point, without providing a full chemical answer.

Footnote: Fe(II) or Fe2+ ?

Some readers may be wondering why I have referred to the ferrous state of Fe in haem as Fe(II) and not Fe2+ (which the Wikipedia entry uses). This is to avoid implying that there is an overall charge of 2+ on haem groups in haemglobin and myoglobin. Inspection of the structure of haem (above) will show that the formation of two covalent bonds to imidazole nitrogens has left haem with a zero net charge.


If it weren't for animals, insects, or people, would plants that produce seeds (nuts, fruit, etc) cease to exist? I gather that some would or could in theory still be successful, but don't most depend on takers to flourish?

No

Not all seeds need to be ingested in order to be spread from one place to the other, in fact some won't grow at all if eaten, some need the fruit to help them germinate and sprout after they hit the ground. Nuts simply will not grow at all if you crack them open.

Most plants rely on the wind to disperse their pollen and seed.

Dandelions are a prime example of a plant with wind carried seeds, their seeds can travel for hundreds of kilometres on parachutes before settling down and germinating in the ground, plenty of other weeds and plants go to seed the same way.

Cotton bearing trees produce their cotton so the wind can carry their seeds, like the Cottonwood and many species of Poplar tree.

One of the fun ones is helicopter seeds. Maples, elders and ash trees are among the species that disperse their seeds this way. The seeds will literally helicopter down, and fly great distances on the wind if it's strong enough. Even as an adult it's still fun to pick these seeds up of the ground and drop them just to watch them fly.

Some trees don't even need to go to seed in order to spread and multiply. Poplars are notorious for sending out suckers underground. Their roots systems spread out from the tree near to the surface and sprout suckers that will pop up out of the ground an grow into another tree. Other bushes and plants do this as well, like raspberry plants.

Not even all fruit is intended to be eaten, The fruit of the chestnut tree is sour, and covered in sharp spines that hurt. We used to spin them around and throw them at each other as kids imaging we were medieval warriors wielding maces. The spikes can get rather long and sharp, I've seen them stick to kids that have been hit by them, and after plucking them off they develop a golfball-sized welt covered in lots of tiny puncture marks.

Worst case scenario for plants that spread their seeds via burrs or by being ingested a pooped out elsewhere if animals were to suddenly cease to exist is that they wouldn't be able to disperse their seeds as far. They'd simply drop their seeds beside them, but they would continue to exist.


Why do Hot/Cold drinks taste sweeter once returning to room temperature? Now, I know this is a very bizarre question, and I tried to find a correct exchange for this, but it might relate to biology/science as it being our taste buds and everything.

I am so sorry if there is a better exchange for this, but (I hate using this excuse) I'm new to StackExchange, so please be gentle and point me in the right direction.

Now, to meat and bones (Unintended pun; meat...bones...biology hehe), over the last few days I have noticed that after my drink returning to room temperature, it is so much sweeter than it originally tasted.

Drinks

Hot Tea - I normally only add 1-2 teaspoons of sugar into my tea and it tastes just right, though after taking a sip when it had returned to room temperature, it tastes about 3 or 4 times sweeter than when it was hot/warm. (Milk)
Iced Tea (Bubble Tea) - Just today I had a bubble tea with the smallest amount of sugar possible, it was still too sweet but I stuck with it, and again when it reached room temperature, it was almost unbearably sweet. (No milk)
Slurpee - Again, after returning to room temperature, it is extremely sweet, with it being much lighter with respect to sweetness.
Hot Coffee - Come to think of it, I have also had the same experience with sugared coffee.
Coke - Also, when coke (or any other soft drink) is flat and room temperature, it also produces the same super sweet taste.

So, I tried to think of possible reasons why this happens but, I cannot think of any possible explaination other than magic.

If anyone knows why this might happen, it would be greatly appreciated since I am tripping out trying to figure out why this happens!

Generally, cold suppresses sweetness. As an example, consider soft drinks that are usually served cold: they taste sweeter when warm (like you said with your examples of drinks).

Our taste receptors send a stronger signal to the brain when activated by warmer substances and so the perception of sweetness, in this case, is lessened when we consume cold food or drinks.

There are taste receptors on the surface of our tongue which refer to the proteins TAS1R2 and TAS1R3 which, which bind to the “sweet-tasting” molecules.
When the molecules bind to the receptors, they trigger a series of actions which increase the number of positively charged potassium ions (K+) in the cell to which the receptor is attached. In order for the signal to continue along to the brain, the cumulative positive charge of the potassium ions must be high enough to activate a TRPM5 channel into the cell, so that calcium ions (Ca2+) can pass through. The Ca2+ ions are required for the release of neurotransmitters which send the signal. This channel requires a much lower positive charge for activation when it is warm than when it is cold.

Now if you were to put, e.g., a cold coke into your mouth, it decreases the temperature of the entire tongue and consequently the TAS1R2 and TAS1R3 proteins, and the TRPM5 channel. This will result in it requiring a greater positive charge in order for the signals to travel to the brain. This means overall also less signals are even received by the brain, thus resulting in us perceiving less sweetness.

Sources:

http://www.ncbi.nlm.nih.gov/pubmed/25963040
http://www.ncbi.nlm.nih.gov/books/NBK236241/
http://www.foodnavigator.com/Science/Food-temperature-affects-taste-reveal-scientists
http://www.ncbi.nlm.nih.gov/pubmed/17180301


Albinism inheritance problem: what are the father's alleles if he got an albino kid? Albinism is caused by a recessive gen "c". A normal man marries an
  albino woman. The first son happened to be albino. What are the
  possible phenotypes of the parents? What is the chance that their
  other kids will be albino?

Alright, since "c" is recessive and the woman is albino, then the woman must be "c c" right? And since the son is albino, he must be "c c" too. Hence the father must have at least one "c". But since he is normal, then the other allele must NOT be "c" too (otherwise he would be albino).

My question is, when writing the Mendel table, how do I express that allele of the father (the one that is not "c")?

$$\begin{bmatrix} & c & c\\
? & ?c & ?c\\
c & cc & cc\end{bmatrix}$$

I marked it with $?$ because I'm not sure what to put there. My first thought was "well, it could be a capital C I guess..." - but that doesn't sound right to me. A capital C would mean there is a dominant albinism allele (but I am told that albinism is recessive only...)

I can see clearly that there is a 50-50 chance of having albino kids. I just don't know how to draw that inheritance table.

Super oober short answer: The father is Cc, the mother is cc, there is a 50% chance the children will be albino (as you predicted).

An explination on Mendelian genetics:

First let's look at (what a lot of people consider) the normal Mendel table from here:

Since the dad is normal, that means he has at least one Normal Gene. Which makes him C ? . We also see that mom is normal, so that means she also carries the gene C ? . In this case, they wind up with one child that is affected which means the child has the trait cc. That means both parents had to give the child one little c so that makes both of the parents Cc.

Your answer:

Now, in your problem the mother is albino, which you correctly put as cc.

The dad is normal, which means his C ?. He could eaither be CC (homozygous dominant - an uneffected non-carrier of the affected gene) or he could be Cc (heterozygous - an uneffected carrier of the affected gene). So at this point all we know about the father is that he is C ? . Which means you were on the right path.

Now we look at their first son. We are told he is albino. That makes him cc. That means that the father HAS to have at least one affected gene making him Cc.

So you were correct in thinking that it was Cc. You tripped yourself up by saying that it would make albanism the dominant. As you were told Albanism is a recessive gene. The big C is the normal gene which would hide the albanism trait.

To draw your table, just change all of your ? to big C.


Can a dNTP be built into a RNA strand? DNA consists of deoxyribonucleotides, RNA consists of ribonucleotides. They differ mainly (apart from the uracil / thymine difference) in the sugar part, the deoxyribose and the ribose. Those two molecules differ in the hydroxy group in the ribose which is only a single proton in the deoxyribose. This part of the sugar molecule is not directly involved in binding reactions, nevertheless it causes the whole difference in RNA and DNA.

I wonder: could a dNTP be used in an RNA strand (or vice versa)? Is it chemically possible that we have a RNA molecule that contains a dNTP next to its NTPs?

This is rather easy to do if you synthesize oligonucleotides chemically and not enzymatically. This is typically done using phosphoramidite chemistry, and it allows for the synthesis of chimeric RNA/DNA oligos. You can even incorporate modified nucleosides like 2'-O-Me or LNA.

This is typically done if you want to change the properties of an oligo, e.g. if you want to make it resistant to degradation by enzymes.


What is the current theory of sexual orientations in Biology? What is the current explanation of what causes the different sexual orientations in humans.

It seems we have more hypothesis than theories.

There is a book called "The Moral Animal", by Robert Wright, where he cites some researches relating order of birth with sexual orientation (of course, not a 100% direct relationship). That's for the proximal cause. For the distal cause (evolutive) it makes sense to me that we are a sort of "eusocial" species, with homosexuality having evolved for the fitness it adds to the family: having lots of offspring, it's benefitial for the family if a few of them don't reproduce, investing instead in other fields of knowledge, like medical herbs, technology, weapons, etc. This may explain why this behavior evolved in first place, and why it's so widespread in virtually every known human culture, and almost all families.

Biologist Alfred Kinsey founded the Kinsey Institute (kinseyinstitute.org) for the study of human sexuality. His theory (that also appears in the movie Kinsey) was that there is a gradient from totally homosexual to totally heterosexual, with many intermediary degrees. Our religious culture tries to "erase" this diversity because of platonic ideals of "perfect male" and "perfect female", but in Amazon I saw that people are much more "plastic" than that, probably because of the lack of power of such religious traditions. Historians also talk about homosexuality as a "usual practice" in pre-Colombian America. And it is said that China have no problem with homosexuality before the arrival of monotheists. In India, homosexuality became a crime only 3 years after the british invasion (so it seems it was very common there, too).


What does the "*" in haplogroup I2A1* mean? I have been told that the "asterisk" in the Haplogroup 12A1* means it doesn't move down stream? What exactly does that mean in layman's terms?

From the 23andMe website:

  Sometimes there are a few lineages that don't fit into any subgroup of a haplogroup. Since there isn't a mutation that links these lineages, they don't get their own subgroup. Instead, these lineages are given the main haplogroup label plus a star (*) to indicate that they are part of the main haplogroup but don't fit into any of the known subgroups

So there are defined subgroups for I2A1 (I2A1A and I2A1B) for which more information is available, but you dont fit into any of them.

What "doesn't move down stream" means, I have no idea.


Why do I feel funny in my tummy when riding a virtual roller coaster? I've ridden a virtual roller coaster on an Oculus Rift. I felt tension as I went up to the top, but more interestingly I actually felt my stomach drop when I went down the steep drop on the other side. Why can I feel this, when no forces are actually being applied to my stomach?

A bonus question: If you took someone that had never ridden a roller coaster, or even been exposed to rapid acceleration, and had them try a virtual one - would they feel the same stomach lurch as I did?

Why can I feel this, when no forces are actually being applied to my
  stomach?

Acceleration sensors are in the ears and are part of the vestibular system. The vestibular nuclei in the brain uses acceleration- and visual signals to decide what happens to your body. It can be fooled by visual signals without the presence of acceleration signals. The role of the vestibulo-autonomic reflex - you feel in your stomach - is probably to protect your inner organs from the damage they can possibly suffer by acceleration.

The same can happen by watching films with fast camera movements on a monoscopic display (e.g. normal films in the cinema or video games on an average LCD monitor, etc...), however not so often than by stereoscopic displays (e.g. 3d films in the cinema, stereoscopic video games on a head-mounted display like Oculus Rift, etc...). This is because stereoscopic displays create the perfect illusion of depth (e.g. they can even be used by a therapy to overcome acrophobia), while monoscopic displays don't. So your vestibular nuclei is fooled much easier by stereoscopic displays.

References:

  These data show that a subset of PBN/KF neurons, whose activity is
  altered by a nauseogenic stimulus also respond to body motion and that
  irritation of the stomach lining can either cause an amplification or
  reduction in the sensitivity of the units to vestibular inputs. The
  findings imply that nausea and affective responses to vestibular
  stimuli may be modified by the presence of emetic signals from the GI
  system.

2011 - Integrative responses of neurons in parabrachial nuclei to a nauseogenic gastrointestinal stimulus and vestibular stimulation in vertical planes
1995 - Study on vomiting related to the vestibulo-autonomic reflex.

  This study describes the relation between the vection produced by
  optical flow and that created by galvanic vestibular stimulation.
  Vection is the illusion of self motion and is most often experienced
  when an observer views a large screen display containing a translating
  pattern. This illusion has only limited fidelity and duration unless
  it is reinforced by confirming vestibular information. Galvanic
  vestibular stimulation (GVS) can directly produce the sensation of
  vection.

2005 - Virtual acceleration with galvanic vestibular stimulation in a virtual reality environment

  Neurons in the vestibular nuclei are not only activated by vestibular
  signals, but also by visual information. Consequently, the sensations
  of body motion derived from visual and vestibular signals are
  indistinguishable.

  Sensations of body movement can also be generated by visual signals
  arriving at the vestibular nuclei. During unnatural movements of the
  body, conflict between visual and vestibular information leads to
  disorientation and nausea, as in the oculogyral illusion, the Coriolis
  effect, and vection.

Foundations of Perception - The body senses - The vestibular system

  Three-dimensional movies presented via stereoscopic displays have
  become more popular in recent years aiming at a more engaging viewing
  experience. However, neurocognitive processes associated with the
  perception of stereoscopic depth in complex and dynamic visual stimuli
  remain understudied. Here, we investigate the influence of
  stereoscopic depth on both neurophysiology and subjective experience.
  Using multivariate statistical learning methods, we compare the brain
  activity of subjects when freely watching the same movies in 2D and in
  3D. Subjective reports indicate that 3D movies are more strongly
  experienced than 2D movies. On the neural level, we observe
  significantly higher intersubject correlations of cortical networks
  when subjects are watching 3D movies relative to the same movies in
  2D. We demonstrate that increases in intersubject correlations of
  brain networks can serve as neurophysiological marker for stereoscopic
  depth and for the strength of the viewing experience.

2014 - Stereoscopic depth increases intersubject correlations of brain networks

  Statistical differences in theta activity showed that the real and 3D
  environments caused similar cognitive processes, while the 2D caused
  an increase of anxiety indicating that perhaps participants were
  looking for the third dimension. Beta and gamma activity showed that
  participants perceived the third dimension of the stereoscopic
  environment as in the real one, something that did not happen in the
  2D environment. Our findings indicate that stereoscopic 3D virtual
  environments seem to approximate the real ones as far as it regards
  the cognitive processes they cause. Three dimensional stereoscopic
  environments increase users’ attention over the 2D and cause less
  mental effort.

2013 - Stereoscopic perception of women in real and virtual environments: A study towards educational neuroscience
2001 - Human Cortical Activity Correlates With Stereoscopic Depth Perception

  In this study the effects of virtual reality exposure therapy (VRET)
  were investigated in patients with acrophobia. Feelings of presence in
  VRET were systematically varied by using either a head-mounted display
  (HMD) (low presence) or a computer automatic virtual environment
  (CAVE) (high presence). VRET in general was found to be more effective
  than no treatment. No differences were found in effectiveness between
  VRET using an HMD or CAVE. Results were maintained at 6 months
  follow-up. Results of VRET were comparable with those of exposure in
  vivo (Cyberpsychology and Behavior 4 (2001) 335). In treatment
  completers no relationship was found between presence and anxiety.
  Early drop-outs experienced less acrophobic complaints and
  psychopathology in general at pre-test. They also experienced less
  presence and anxiety in the virtual environment used in session one as
  compared to patients that completed VRET.

2004 - Treatment of acrophobia in virtual reality: The role of immersion and presence

  Despite the increasing use of virtual reality, the impact on cerebral
  representation of topographical knowledge of learning by virtual
  reality rather than by actual locomotion has never been investigated.
  To tackle this challenging issue, we conducted an experiment wherein
  participants learned an immersive virtual environment using a
  joystick. The following day, participants' brain activity was
  monitored by functional magnetic resonance imaging while they mentally
  estimated distances in this environment. Results were compared with
  that of participants performing the same task but having learned the
  real version of the environment by actual walking. We detected a large
  set of areas shared by both groups including the parieto-frontal areas
  and the parahippocampal gyrus. More importantly, although participants
  of both groups performed the same mental task and exhibited similar
  behavioral performances, they differed at the brain activity level.
  Unlike real learners, virtual learners activated a left-lateralized
  network associated with tool manipulation and action semantics. This
  demonstrated that a neural fingerprint distinguishing virtual from
  real learning persists when subjects use a mental representation of
  the learnt environment with equivalent performances.

2009 - Impact of the virtual reality on the neural representation of an environment

  Our main results are (1) stereoscopy in games increased experienced
  immersion, spatial presence, and simulator sickness; (2) the eff ects
  strongly differed across the three games and for both ge nders,
  indicating more affect on male users and with games involving depth
  animations; (3) results related to attention and cognitive involvement
  indicate more direct and less thoughtful interactions with
  stereoscopic games, pointing towards a more natural experience through
  stereoscopy.

2012 - Understanding User Experience in Stereoscopic 3D Games

  The results indicate that in a 2D movie viewers tended to look at the
  actors, as most of the eye movements were clustered there. The
  significance of the actors started at the beginning of a shot, as the
  eyes of the viewer focused almost immediately to them. In S3D movie
  the eye movement patterns were more widely distributed to other
  targets. For example, complex stereoscopic structures and objects
  nearer than the actor captured the interest and eye movements of the
  participants. Also, the tendency to first look at the actors was
  diminished in the S3D shots.

2014 - What do people look at when they watch stereoscopic movies?

  For the correlation between anxiety and presence, the results show
  very low correlation between anxiety and presence.

2009 - Using augmented and virtual reality for the development of acrophobic scenarios. Comparison of the levels of presence and anxiety

  Stereoscopic visualization in cinematography and VR creates an
  illusion of depth by means of two bidimensional images corresponding
  to different views of a scene. This perceptual “trick” is used to
  enhance the emotional response and the sense of presence and
  immersivity of the observers. An interesting question is if and how is
  possible to measure and analyze the level of emotional involvment of
  the observers during a stereoscopic visualization of a movie or of a
  virtual environment. The final goal of this research is a challenge,
  due to the large number of sensorial, physiological and cognitive
  stimuli involved. In this paper we begin this research by analyzing
  eventual differences in the brain activity of subjects during the
  observation of monoscopic or stereoscopic contents. To this aim, we
  have performed some experiments collecting EEG data using a
  Brain-Computer Interface device from two groups of users, during the
  observation of stereoscopic and monoscopic short movies inside the
  Virtual Theater of the University of Milan. From the analysis of the
  collected data, it seems that interesting differences are present in
  the average brain activity among the observers in the two groups, with
  a significative effect of stereoscopic visualization.

2012 - Analysis of brain activity and response during monoscopic and stereoscopic visualization


Why cannot machines use energy stored in a way similar to biological systems' energy storage? Owing to the generality of the question I am interested merely in key problems so that I could do further reading.

As I understand man-made energy storages are significantly less efficient than biological ones. I would like to focus on quickly available energy for small systems (human scale or smaller) - after all we can say that hoards of coal are a pretty nice energy reservoir.

For example, a robotic bee:

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

What can we see here? A wire - and I think we cannot expect to have a long lasting independent robotic bee with the current technology due to inefficiency of our energy storage.

How do biological systems store the energy then? https://en.wikiversity.org/wiki/Energy_Storage_in_Biological_Systems

  Living organisms use two major types of energy storage. Energy-rich
  molecules such as glycogen and triglycerides store energy in the form
  of covalent chemical bonds. Cells synthesize such molecules and store
  them for later release of the energy. The second major form of
  biological energy storage is electrochemical and takes the form of
  gradients of charged ions across cell membranes. This learning project
  allows participants to explore some of the details of energy storage
  molecules and biological energy storage that involves ion gradients
  across cell membranes.

To be more specific let me give an example: why cannot we have a machine that would have an input for carbohydrates, a converter to say glucose and then ATP which would finally break down and release the needed energy?

Why is it not viable? Do we lack technology to do this? Which step is problematic? Are we far from having biological-like storages?

The activation energy of breaking these covalent bonds is high. Biological systems use phosphorylases to couple ATP to glycogen such that the high energy phosphate bonds then supply some of their energy to break the covalent glycosidic bonds in glycogen

So problem 1, high activation energy.

Secondly, how are you going to store the energy in the machine? Conventional electrochemical cells use something like what was written about membrane potential. Their energy is accessible as it is in a form of an electrical potential. When you expend energy to break storage molecules into glucose, there's not much for you to do on the glucose other than to burn it. Burning it is extremely inefficient and makes up a huge amount of energy loss to wasted heat. The other way would be to oxidize it. You'll need something to accept the electrons (NADH and FADH in biological systems), something to overcome the high activation energy of oxidizing the bonds at every stage (more ATP coupling), something to harness the high-energy electrons from glucose (electron transport chain/chemiosmosis). In all, it is too complicated to be replicated efficiently.

So problem 2, there are many complicated steps involved.

This is why only simpler versions of the above exist. Power to gas shows us the splitting of H2O into H2 and O2. This is akin to only one stage of bond-breakage in respiration, and is simple enough to carry out (through electrolysis). H2O donates and another H2O accepts the electron. Energy is supplied as a electrical potential in the circuit instead of ATP coupling from enzymes.

Last problem is, there really isn't a need to store energy in other forms than an already-existing energy storage molecule. Most of our energy storage is in the form of carbon compounds, and electricity. Carbon compounds are high energy density, and electricity is easy to manipulate. It is perhaps trivial to the world to attempt condensing table sugar (glucose) into starch. It is not efficient enough to be impactful. Biological systems need to do this because storage is on a scale comparable to the cell body, and directly relates to survival. High blood glucose in animals might lead to hyperglycemia, triose phosphate (product of respiration) is used for lipid formation and in turn building of cell membranes, glucose molecules are used as monomers in the production of cellulose, aka cell wall in plants, (a heck ton of other metabolic pathways exist), etc.

This link shows us the different ways of energy storage in our world. We're not limited by biological constraints, so even compressing H2 into a liquid, will be more efficient than interconverting that into other forms of chemical energy, if you're talking about for pure "storage"'s sake.

I highly recommend reading up on photosynthesis, to see how biological systems harness energy from the sun, and store that into covalent bonds between CO2 molecules. More specifically you can look up Krebs Cycle.


How to retrieve full gene names list and Entrez gene IDs and other annotation information from HUGO gene name list (in R or any)? How to retrieve full gene names and Entrez gene IDs and other annotation information from HUGO gene name list (in R or any other software or language)?

Is it possible vice versa: having full gene names or IDs get HUGO names or the other annotation data?

I would recommend just downloading the database, which HUGO allows you to do free of charge.

The HUGO website has a "downloads" tab at the top that takes you to the following page

http://www.genenames.org/cgi-bin/statistics

You will see a table of statistics relating to how many protein- or non-protein-coding genes there are catalogued, etc.

Under the tables is a section called Complete dataset download links -- this is the section you want (unless you only want a subset of the data - but why not get it all!)

This plain text file (once uncompressed) can be loaded into R (or any other language) to be parsed and analysed as per your requirements.

It is worth updating the version you download quite regularly, as they update the HUGO database with new/updated info quite regularly.


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?

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))


Why squirrel behaviour varies greatly throughout India? Common squirrels seen in India, probably Indian palm squirrels; seem to have drastic different behaviour. And all squirrels of a definite locality, behave in a very consistently same whay. That seems like  My drastic experiences at 3 localities were as follows.

On West Bengal (Howrah, Hooghly and Burdwan District): Squirrels seem to be incredibly timid. They always maintain a safe distance from human being. They sometimes consume human food leftover, or respond to cater; but the feeder person needs to be go away from the spot. They are also quite a bit picky eater, among human remains they mainly depend on paddy, some of them don't even touch grounnuts.
On Uttarpradesh Tourist spots, particularly Agra and Delhi, squirrels come too close to the tourists. Sometimes they take food directly from human hand. Some of them even follow the tourist population for foods. Some of these squirrels are very aggressive, however they are somewhat vulnerable because people easily touch them. They aren't very picky eaters, rather they are sort of gluttony... eats whatever the tourists feed them.
On Uttarakhand state, on many places (including the non-tourist) the squirrels come very closer to human being.  Not always for food, but they just come too close to human being. They aren't aggressive. They aren't very picky eaters. Though some are little bit timid; some are super easy to touch. They are super vulnerable.

I'm really surprised how the behaviour of these 3-striped squirrels vary throughout India and is consistent with locality. Learnt behaviour from parent/ peer squirrels? Epigenetic imprints? Genetic variability? Scarcity of foods? Its super surprising.

Given that you're dealing with fairly smart mammals with a short lifespan and limited distance migration, it seems likely that you're dealing with strong local selection effects that are going to be reflected in all three layers:

Learned behaviors from observing other squirrels and their own interactions with humans.
Epigenetic effects tied to things like maternal stress
Differences in the frequency of genetic tendencies towards caution / aggression, etc.

Now, what would the source of those differences be? I don't know if anybody's studied these particular cases, but there's some pretty strong candidate hypotheses for a starting point:

In West Bengal, you're dealing with high-density non-touristy areas (especially Howrah, right on the edge of Kolkata). The squirrels there are likely in constant conflict with humans who do not want to be sharing their food, which will select strongly for aversion to humans.  Humans might well be poisoning them as a means of control too, which could explain the picky eating.
In tourist spots anywhere, the squirrels are probably getting fed well by humans either intentionally or accidentally (e.g., careless children), whcih will select strongly for attraction/aggression toward humans.  I'll bet you'd see this in Victoria Memorial too, for all that it's right next door to Howrah.
In Uttarakhand, which is a much lower density state than West Bengal (189/km^2 vs. 1029/km^2), you're probably seeing much more of the default state of interaction, without a strong selection in either direction.


Which side of the DNA helix is used for describing SNPs? In genetic research I often come across references to single-nucleotide polymorphisms (SNPs).  An example is rs3184504(C;T).  As far as I understand it: In this case rs3184504 refers to a specific point in the DNA genome, and (because this one occurs in a non-sex human chromosome) it indicates the nucleotides at that point in each copy of that chromosome.

But how does one determine which strand of the DNA helix it references?  Is there a convention?  Or is the strand indicated in the SNP reference (in this case rs3184504)?

If one strand is C;T then the opposing strand will be G;A ... but in the context of the gene in question I assume it matters which strand is referenced in the SNP.  E.g., if the code following this SNP on the chromosome in which rs3184504 has C is:

CTCGA...
GAGCT...

this is a different genotype from the SNP indicating a C on the other strand:

GTCGA...
CAGCT...

So the SNP description is only meaningful if it also indicates the strand, right?  If so, how does the SNP descriptor do that?

It is described with respect to the reference sequence. See the VCF format description.


absorption time of zinc in the body I would like to know how long it takes for the human body to absorb / digest a 10mg zinc capsule?

Note: It is recommended to take zinc  an empty stomach to gain the maximum effect. Regarding to that I think it's also a disadvantage to eat something right after taking zinc?

greetings

Zinc supplements are usually used to treat zinc deficiency or other chronic conditions, so it is not that important in what time they are absorbed but what percent of them is absorbed.

They are certain nutrients, such as calcium (for example, in milk) that can bind to zinc and partially prevent its absorption. This is why it is usually recommended to take zinc on an empty stomach (Mayo Clinic):

  Zinc supplements are most effective if they are taken at least 1 hour
  before or 2 hours after meals. However, if zinc supplements cause
  stomach upset, they may be taken with a meal.

Usually there should be no significant difference between taking a pill with food, 2 minutes before or 2 minutes after the food, because in all cases the pill and the food will mix in the stomach. This is because every pill, even if you take it with water, will probably stay in the stomach for at least few minutes before it will be emptied into the small intestine.


Can beavers control the direction a tree falls? We humans can easily control the direction a tree falls by making a number of strategic cuts, essentially creating a hinge:

This prevents trees from falling on equipment and people and sets them up in a good location for the subsequent processing steps. I'm curious if beavers also perform directional felling and, if they do, how do they choose the direction (eg to fell the tree towards the damn, in a river, away from thick brush, etc)?

In this picture (and others), it appears as though the beaver has created a hinge. Is their any method to their technique or do they just start chewing and hope for the best?

It is difficult to find a scientific answer to this question, but let me insert this citation from a specialist site:

  Contrary to popular belief, beaver cannot plan the direction in which trees will fall. Many trees become hung up in the branches of surrounding trees and are lost to the colony. In heavily forested areas, this loss may amount to one-half of the trees felled.

Another source says the same.

But scientists think beavers may actually plan the direction of falling:

  By measuring the falling angle of 888 trees of a variety of sizes cut
  near 8 different dams in southwestern Saskatchewan, we tested the
  hypothesis that beavers (Castor canadensis) fell trees in a non-random
  direction. We predicted that trees would be preferentially felled
  towards the dam to minimize the costs of transporting materials to the
  dam and to minimize the amount of time beavers spend on land. We
  established a 150 m wide × 250 m long transect at each dam and
  determined the felling angle of at least 100 aspen trees cut in each
  transect. We found that trees were felled by beavers with a mean
  felling angle of 357.9°, a direction not significantly different from
  that of the dam. In all, 62% of trees were felled within 45° of the
  direction of the dam. While our data are consistent with the
  hypothesis, an experimental test is required to establish the
  reason(s) for the pattern we found.

Their picture is better than thousands of words:

And another paper:

  We studied patterns in the orientation of cutting when beavers (Castor canadensis) cut trees around Alum Creek Lake in central Ohio. For 462 trees, we measured the slope at the base of the tree, the orientation of the cut relative to this slope, the distance of the tree from the water, the radius of the tree, and the symmetry of the cut. The land around Alum Creek Lake generally slopes toward the water, so to direct the fall of a tree towards the water a beaver should cut a symmetrical tree from the downhill side. Cutting from the downhill side occurred for trees >9.0 m from the water. Near the shore, trees tended to lean toward the water and would fall toward the water regardless of the side from which the beaver cut. At distances <9-0 m from shore, beavers cut predominantly from the uphill side where it should be easy to sit and there is little danger of the tree falling on them. At all distances, beavers showed random orientation when cutting trees on shallow slopes (<20°), whereas on steep slopes (especially slopes >30°) they cut predominantly from the uphill side. Beavers cut small trees (<5.0 cm diameter) mostly from the downhill side, but tended to cut trees >5.0 cm in diameter from the uphill side. Overall, enough factors interacted that no single pattern of cutting existed for all trees.


What species of fox is this? I found this picture of a fox in a news article about arctic foxes in Sweden (source), but I'm not sure whether it is actually an arctic fox.

On the one hand, it has white fur, which is the correct winter coat for an arctic fox. On the other hand, the fox's ears do not have the distinctive shape of arctic fox ears, but ears that look more like red fox ears.

The image credit given by the article is just "iStock", so I searched iStock to see if I could find more information about the photo. I found another photo of the same fox here, also labeled as an arctic fox, but not really any further information.

What species is this fox?

This is a white morph red fox, not an arctic fox.

As noted in the question, this fox has larger, more pointy ears than an arctic fox, and the second picture shows it to have a longer muzzle as well.

Another clue is that these pictures were taken in the springtime or early summer (which you can tell from the new growth on the plants in the picture), and that arctic foxes are only completely white during the winter. During the spring, an arctic fox should look like this:

You can also easily tell that the fox in the picture is not an albino, because of the dark pigment in the nose and eyes.

The red fox has quite a few different color morphs, and this fox looks to be a white color morph.

In that diagram, this fox would be labelled as leucistic (white).

Here are some other white morph red foxes:


Osmotic pressure and turgor pressure details I am a high school student and I am very confused in how we define osmotic pressure?
Osmotic pressure is defined as the pressure required to stop the diffusion of solvent into a solution by applying external pressure over solution, which means that when the pure solvent is diffusing into the solution then it will apply pressure on the semi permeable membrane and when we have applied the same external pressure over the solution then there is no net movement of solvent occurs across the membrane and mathematically it is equal to P=cRT, where c is the concentration of solution , T is temperature in kelvin and R is the universal gas constant, if we go by this equation and calculate the osmotic pressure of 1 molar concentrated solution at room temperature it comes out to be almost 2495Pa which means 2495Newton/m^2 which is very high pressure and it doesn't seem to be true as osmosis is very slow process it surely cannot generate that much of pressure( just to imagine how large is that pressure assume an area of 1m^2 and place Mass of 249.5kg on it), so I think that it should not be that higher, so ,I am unable to understand what is actually osmotic pressure ,on which does it actually act and how do we actually calculate it?
we say that when a cell is placed in hypotonic solution then osmotic pressure is greater than Turgor pressure and water will flow inside the cell, but I have a confusion that like turgor pressure acts on the wall of cell ,osmotic pressure should also act on the wall and in opposite direction of turgor pressure, so by this logic wall should compress more as osmotic pressure on it will cause it to compress and turgor pressure will cause it to expand but Osmotic pressure is greater than turgor pressure it should compress, but it doesn't happen? we only talk of turgor pressure to explain the expansion but not osmotic pressure why? I know I am going wrong somewhere if Osmotic pressure would really leads the cell to compress then an animal cell would have never burst in hypotonic solution. and if osmotic pressure is also acting on the wall or membrane then net pressure on the wall is O.P-T.P (in inward direction) , and not only T.P (outward) so the wall pressure here also should not be same as turgor pressure?
If anyone will explain me this by giving as many examples as possible than it would be very helpful for me to understand because its my first time I came to know about these things.

when we talk about external force applied in this case we talk about a setup that is made by us. like a U tube experiment that is filled with water and separates both the hands of the tube via semipermiable membrane and we add solute one side and due to this water starts to rise in that hand of the tube to avoid this rise in water level an external pressure is applied tht prevents this water rise and this pressure is termed as osmotic pressure. THIS IS THE CASE OF A ENVIROMENT WHERE EXTERNALFORCES CAN BE APPLIED BY US AND IT IS VERY MUCH DIFFERENT FROM THAT OF THE CELL WORLD.
in case of cells osmotic pressure is directly proportional to the concentration of the solution i.e more the solute more the OP and visa versa. in cells osmotic pressure are internal force that is caused due to  difference in concentration of the solutions.
and as we know water move from low osmotic pressure to high osmotic pressure
{ from less concentrated to more concentrated solution} thus cell swells up because of entering of water when cell is placed in pure water or hypotonic solution.
CONCLUSION : CELL DO NOT SHRINK BECAUSE NO EXTERNAL FORCE IS APPLIED BY US THE DEFINATION U GAVE IS CORRECT BUT IT IS NOT APPLIED IN CELL WORLD. IN CELL WORLD OP IS A PRESSURE DEVELOPED DUE TO DIFFERENCE IN CONCENTRATION OF SOLUTIONS AND THIS PRESSURE IS CREATED INORDER TO EQUAL THE CONCENTRATION OF SOLVENT (WATER) IN BOTH THE SOLUTIONS.


How are amino acids neutral at physiological pH? Amino acids with non‐ionizable side chains are zwitterions when they are at physiological pH, pH 7.4. This is what my book says. But I do not understand why. The Pka for a carboxyl group is around 3 and the pKa for an amino group is around 9. So the isoelectric point should be around ( 9+3) /2 = 6 for an amino acid with no ionizable side chain. At pH 7.4 it would be slightly negative, would it not?

Also what exactly is a basic amino acid? Is that an amino acid that has a PI value of more than 7?

Thank you.

You are right, most of the amino acids have pI around 6, so they are slightly negative at pH 7.

Calculating approximate isoelectric points for amino acids and peptides

The isoelectric point depends on the amino and carboxylic-acid groups and the groups of the side chain. E.g. lysine has an amino group on the side chain, so it has a pI of 9.74.


What is the distinction between deoxyribonucleases and restriction enzymes? Both deoxyribonucleases (DNases) and restriction enzymes are endonucleases (some DNases can be exonucleases).

They both break the bonds between nucleotides. Therefore, what is the difference between the two?

My original thought was that restriction enzymes, unlike DNases, cut at specific sequences of DNA. Then this raises the question of whether restriction enzymes are just a category of DNases, but I have found no sources to back that up. Also, according to this Wikipedia article:

  There are more than 900 restriction enzymes, some sequence specific and some not...

This further erodes the distinction I had created between the two types of nucleases.

This paragraph from Lehninger's Principles of Biochemistry (in my opinion the best textbook on biochemistry) is very didactic:

   DNA Is Degraded by Nucleases

  To explain the enzymology of DNA replication, we first introduce the enzymes that degrade DNA rather than synthesize it. These enzymes are known as nucleases, or DNases if they are specific for DNA rather than RNA. Every cell contains several different nucleases, belonging to two broad classes: exonucleases and endonucleases. Exonucleases degrade nucleic acids from one end of the molecule. Many operate in only the 5'→3' or the 3'→5' direction, removing nucleotides only from the 5' or the 3' end, respectively, of one strand of a double stranded nucleic acid or of a single-stranded DNA. Endonucleases can begin to degrade at specific internal sites in a nucleic acid strand or molecule, reducing it to smaller and smaller fragments. A few exonucleases and endonucleases degrade only single-stranded DNA. There are a few important classes of endonucleases that cleave only at specific nucleotide sequences (such as the restriction endonucleases that are so important in biotechnology; see Chapter 9, Fig. 9–3).

We can conclude that restriction endonucleases (or restriction enzymes) are a type of endonuclease, and that endonucleases are a type of DNAse. So, all restriction enzymes are DNAses, but not all DNAses are restriction enzymes.

Besides that, we can conclude that your initial statement ("Both deoxyribonucleases (DNases) and restriction enzymes are endonucleases") is wrong.

For a more complete table have a look at Molecular Biology of Nucleases, page 18.

Sources:

Lehninger, A., Nelson, D. and Cox, M. (2000). Principles of biochemistry. New York: Worth Publishers.
Mishra, N. (1995). Molecular biology of nucleases. Boca Raton [u.a.]: CRC Press.


Why are some organisms able to regenerate? Why can sponges, cnidarian polyps and planaria regenerate if broken up, but other animals e.g. humans and phylum chordata cannot?

All organisms, including humans, have the ability to regenerate something in the body. But the process is much more developed in lower organisms such as plants, protists -- unicellular organisms such as bacteria, algae, and fungi  and many invertebrate animals such as earthworms and starfish. These organisms can grow new heads, tails, and other body parts when injured.
Scientists don't know why mammals don't have the same ability to grow new limbs. But they think it is because mammals have more complex biological structures; limb regeneration would require sophisticated controls to ensure that limbs and organs don't grow out of control. Humans, for example, are already equipped with safety mechanisms to ensure that individual cells don't grow uncontrollably. But these mechanisms wear down as a person ages and cancer is often the result.
Nevertheless, mammals do regenerate skin, muscle, and blood. Scientists are just beginning to learn about other types of cells, such as those in the brain and blood, that also regenerate. Further study of the phenomenon might lead to a way of growing replacement organs and limbs outside the body.
Not all organisms regenerate in the same way. In plants and organisms like hydra and jellyfish, missing parts are replaced by reorganizing neighboring tissues into whatever parts have been cut off. Animals with more complex bodies usually regenerate parts by producing a specialized bud, or blastema, at the site of amputation. The blastema supplies the tissue necessary for the regenerated part.
The regenerated body part is not always the same as what was lost. Many insects regenerate abnormally small legs from which some segments may be missing.
Tadpole tails, for example, typically grow back to about only half their original length. And regenerated parts often differ in details. A regenerated lizard tail, for example, contains a cartilaginous tube instead of the vertebrae in the original.


Compare affinity to potency h1 receptor This quote from Miller (2004) makes it clear that the affinity of drugs for the H1 receptor does not correlate to sedation:

  Although both dosage and affinity for histamine H1 receptors play a part in the sedative effect of a medication, what ultimately determines sedative effect is the amount of the drug reaching the histamine H1 receptors in the central nervous system. For example, quetiapine, which has little affinity for the histamine H1 receptors, is a less potent antipsychotic medication and requires many more milligrams to be effective than do higher-potency medications such as risperidone and ziprasidone. Because of this, quetiapine has a greater sedative effect on patients in clinical use than do risperidone and ziprasidone.

Is there a mathematical way to compare affinity to potency between different drugs?

There are a few important things to consider as you interpret these data.
Here potency means Chlorpromazine equivalents
When your linked review refers to potency, it is likely referring to the old concept of chlorpromazine equivalents. The table in the article cites Jibson and Tandon in a review in CNS news special report from 2001. This is not a standard peer reviewed article, and I can't access it, but it lists relative potency in mg, with chlorpromazine set at 100mg and haloperidol at 2mg:

This is almost certainly chlorpromazine equivalents. You can read a discussion of the limitations of this understanding of antipsychotic potency here, but these numbers are not based on a mathematically rigorous pharmacodynamic analysis. They are not consistent, especially for atypical antipsychotics, and are estimated based on clinical data of the minimum effective dose among other methods.
So, where the affinity in this article, $\frac{1}{K_D}$, has a rigorous pharmacodynamic definition, potency does not. Here it is, effectively, shorthand for how much of a drug you have to administer in order to get a therapeutic effect.
Antipsychotic drugs act at many CNS receptors
To understand exactly what Miller means when he says:

For example, quetiapine, which has little affinity for the histamine H1 receptors, is a less potent antipsychotic medication and requires many more milligrams to be effective than do higher-potency medications such as risperidone and ziprasidone.

You need to understand that $H_1$ receptors do not mediate the primary clinical target. So the lower potency of quetiapine means you have to give more of it to have a clinical effect. Because of the higher typical dose of quetiapine, even though the affinity for $H_1$ receptors is relatively low, you're going to get more binding to $H_1$ than with, e.g., risperidone, which requires a lower dose.
Take a look at the chart in the Richelson and Souder article Miller cites to see the different receptor targets for these antipsychotic drugs.

The primary therapeutic targets (used to characterize the general clinical potency) are (probably) the $D_2$, $5HT_{1A}$, and $5HT_{2A}$ receptors. The action at the $H_1$ receptor is primarily an adverse effect. Miller is trying to say that the sedation effect does depend on affinity at $H_1$, but you also have to consider the dose required to get an effect at $D_2$ and the relevant $5HT$ receptors.
A rigorous definition of potency involves simplification
There is a rigorous definition of potency for an agonist (and also of inhibition for an antagonist, and antipsychotic drugs are antagonists). Potency is both distinct from and dependent on affinity.  I'd recommend Goodman and Gillman Chapter 3, if you'd like to learn more. It's not particularly relevant to understanding this article, in part because Miller doesn't use this definition of potency, and in part because the model involves a single ligand-receptor interaction that directly mediates a desired effect. It's based on the following equation, where $LR^*$ is an activated ligand-receptor: $L + R \rightleftharpoons LR \rightleftharpoons LR^*$.  Because both desired and adverse effects of antipsychotics involve actions at many different receptors even beyond those in Richelson and Souder, the simple model falls short.


Does the Plasma Membrane have a hydrophilic interior/exterior/contain vesicles? I am very new to the study of biology, and have been unable to find information in other sources which could tell me whether the plasma membrane has the following traits:

has a hydrophilic interior
has a hydrophobic exterior
contains vesicles

Thank you!

The plasma membrane is a lipid bilayer. Plasma membrane lipids have a hydrophilic head group and hydrophobic tail groups. Since cells are usually in an aqueous environment (and are filled with aqueous cytoplasm), the hydrophilic head groups is face both the exterior and interior of the cell. Between these head groups facing the interior and exterior, the hydrophobic tail groups of opposing lipids associate with each other to create a hydrophobic core within the membrane.

Vesicles are also made of lipid bilayers. Vesicles can exist within cells or be released by cells.


the meaning of "Non-primary hits" and "tags" Can I ask you to help understand the meaning of "Non-primary hits" and "tags" in the following paragraph related to RSeQC:

The result table reports total number of reads (excluding nonprimary
hits) and tags (separate splice fragments of a read). Total assigned tags
indicate how many tags can be assigned unambiguously to the ten different
categories listed below.

Total Reads 49743155
Total Tags 63012643
Total Assigned Tags 57529077
= = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = =
Group Total_bases Tag_count Tags/Kb
CDS_Exons 36821030 34763281 944.11
5'UTR_Exons 34901580 2856644 81.85
3'UTR_Exons 54908278 9772738 177.98
Introns 1450606807 8468986 5.84
TSS_up_1kb 31234456 94103 3.01
TSS_up_5kb 139129272 161914 1.16
TSS_up_10kb 249300845 217980 0.87
TES_down_1kb 32868738 789703 24.03
TES_down_5kb 142432117 1368378 9.61
TES_down_10kb 251276738 1449448 5.77
= = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = =

"tag" is a weird term in this context. It used to mean "read", but RSeQC likes using it in an odd way. Suppose you have a read that aligns to a single contiguous (though possibly with InDels) stretch of DNA. This would then count as one tag. Suppose instead that you have a spliced read, that is one where part aligns to one exon and part to another exon. Each aligned part of this read then counts separately as a tag. So this 1 read becomes 2 tags. By extension, if you have a read that is spliced such that is starts in exon 1, jumps to exon 2, and then finally jumps to exon 3, then it'd count as 3 tags. This is only useful if you're interested in splicing, since the higher this value is the better you're able to discern differences there.

For "non-primary hits", suppose you have a read that can align equally well to multiple places in the genome. If there are 5 equally good alignments, then 4 of these will be labeled as "secondary" and one of them will not, which is then the "primary alignment". "non-primary hits" is then an odd way of saying "secondary alignments". The number of primary alignments is equal to the number of reads that aligned.


Conservation Ex Situ This came up in my biology diversity course and I wanted to raise a question about it.

On the topic of ex situ, one of the presentations that a speaker mentioned that one of its disadvantages is that 'endangered habitats may be fragmented and each small area may not be large enough to ensure survival'. Unfortunately, she left before I could ask anything of this statement.

Can anyone clarify what this means?

She was probably referring to ex-situ conservation as a way to complement in-situ conservation. Indeed, if a population is endangered and fragmentation it thought to be one of the main factors causing the decline, it can sometime be hard to restore the habitat in a way that would permit the population reestablishment (in-situ conservation). Ex-situ conservation can therefore permit to protect some individuals. Then, we could reintroduce individuals to their natural habitats later on, and this could give us more time to restore the habitat.

If you want a good example of how hard it can be to restore the habitat to permit population reestablishment, have a look a the Caribou situation in the north of Québec.

If your question is about how fragmentation is affecting species then it's a very very large subject... it can reduce gene flow, induce stress that could leads to lower reproductive success, etc.

Hope this helps.


Are the bacteria doing the same photosynthesis as plants do? I mean Plants during photosynthesis produce  oxygen but Do bacteria also produce oxygen during photosynthesis or produce  other gases?

If yes , how do these bacteria process photosynthesis by producing other gases?

Photosynthesis is always about using solar energy to oxidize a mineral molecule and reduce an organic molecule, which becomes an energy source for the photosynthetic cell.

Bacteria and plants have different types of photoreceptors. It is not always the same chlorophyll, maybe even no chlorophyll at all ! The different colours in algae come from the different pigments they are using to do photosynthesis.

Plant cells carry out photosynthesis in chloroplasts, which are organites, whereas bacteria carry it out in their plasmic membranes.

Plants do aerobic photosynthesis, which means they reduce dioxygen into water. Some bacteria do anoxic photosynthesis, which means they can reduce hydrogen sulfide into sulfur.


Why is the DNA codon table "equal" to the RNA codon table Before anything else please pay attention of the double quotes on the "equal" in the title - I know they are not equal, but you will understand in a bit.
If I look at the DNA codon table here or in wikipedia, and at the RNA codon table here or in wikipedia, their only difference is that the former has thymine (T) whereas the latter has uridine (U). But I am not understanding how all other nucleotides are the same. Bear in mind that transcription reads DNA from 3'->5' and translation reads mRNA from 5'->3'.
Look at this example, focusing on the 3'-TAC-5' of the antisense strand.

The 3'-TAC-5' codes for Tyrosine according to the DNA codon table. However, it transcribes and translates  3'-TAC-5' -> 5'-AUG-3' -> Methionine.
Now focus on the corresponding codon in the sense strand, 5'-ATG-3', which codes for Valine according to the DNA table (it is read from 3' to 5'). This codon transcribes and translates 3'-GTA-5' -> 5'-CAU-3' -> Histidine, not Valine and not Methionine.
So my questions are:

Why do DNA codon tables show the correspondence between codons and amino acids in the sense strands (5'-ATG-3'), if the only way to go from ATG to Met as in the figure is to consider the antisense strand?
I can see that the AUG codon translates to Methionine, and it is translated by reading the 3'-TAC-5' codon in antisense strand, whose corresponding codon in sense strand is 5'-ATG-3'. But this last one is read from 3'->5', so it reads 3'-GTA-5' -> 5'-CAU-3' -> His.

I am guessing I'm getting many things wrongly in this... Maybe on the way that I'm reading  the tables: I always take into account that transcription is read 3'->5' and this is the order I take to read DNA tables.
Thank you and sorry if I was confusing.

Genetic code and codons are always used with reference to RNA. When talking about DNA, the the sense strand of a gene is considered its sequence. The anti-sense strand though is the template for mRNA synthesis, does not represent the gene.

DNA-codon table has simply U replaced by T. Apart from a wikipedia article, I don't find the term being popularly (not colloquially) used elsewhere.


DNA centrifugation in water If I have bacteria diluted in water and I centrifuge at max speed for 15-30 min, it is possible that I break the walls so the DNA can scape and I do not get any DNA pellet? or should I get it as a pellet everything togheter (lipids, proteins..) even if the mixure is just bacteria diluted in water?

Not with bench centrifuges.
Bacteria have cell wall and are rather small. This gives the cell wall alot of strength. I am not even sure that ultra centrifuges would work.

What you will likely get is a cell pellet. If you want DNA, pellet the cell and either go for direct PCR or sequencing. Or use a DNA extraction kit to obtain the DNA you want.


What is the contribution of the cockroach to the ecological environment? I've read a lot about cockroaches but was unable to find how they contribute to the ecological environment. Does anyone know?

Short answer
Cockroaches are an integral part of the food chain.

Background
Cockroaches are an important source of food for a number of organisms, such as arthropods, birds, and mammals. As such, they are an important part of the food chain. Cockroaches also play an important role in nutrient recycling. Most species of cockroach are detritus feeders and with the help of endogenous cellulases play an important role in degrading plant material. Some species, such as Cryptocercus, feed directly on wood and play a major role in lignocellulose digestion in temperate forests.

Reference
 - Bell et al., Integr Comp Biol, 2008; 48(4): 541-3


What does the energy in an energy pyramid represent? Suppose the energy at the second trophic level as given in an energy pyramid is 100 kcal per square metre. It could mean either of the two following things:

100 kcal is the energy this primary consumer has stored in its flesh - that is, the energy left over from the amount consumed, after assimilation and respiration. This would be the net productivity of that consumer, or the energy available to the secondary consumer which feeds on this.
100 kcal is the energy this primary consumer consumes. It will utilise a part of this in respiration, lose some amount in assimilation, so that a small amount is left over which is then stored in it as mass, or flesh - which would be its net productivity.

Similarly, the first trophic level, the autotrophs' energy could represent either the total amount of food they make (the GPP), that is, the energy akin to the second case above, or the energy stored in them and available to the next trophic level (the NPP), like in the case 1 above. So which of these is correct - what do we represent as the energy of a trophic level in an energy pyramid? I think it should be the first case, the stored energies, since after all these are what you will measure as the energy of any trophic level - the stored energy at that level.

Each layer in the energy pyramid represents the stored energy in biomass in that layer. This energy is obtained from the previous layer. Because every layer uses a certain amount of energy needed for survival (combustion of sugars and fats through respiratory processes) obtained from the previous layer, each subsequent level is smaller than the previous one. Also, the autotrophs in the photosynthetic layer use up (solar) energy for living. The higher up you get, the more energy is cumulatively taken away to sustain life and growth of the previous layers. Therefore, it's a pyramid shape.

Energy pyramid. Source: Biocab