text:
Question about Autosomal Recessive Alleles
I had a homework question that I could not figure out.
It states:

A woman has cystic fibrosis in her family and did not want to have a
  child that suffered from the disease. She and her spouse went for
  genetic testing and counselling. She tested positive as a carrier and
  her spouse tested negative, and their first child was born with cystic
  fibrosis. Explain how this could happen.

This doesn't make sense because the punnet square would be:
$$
\begin{array}{c|c|c}
  & A  & A  \\
\hline
A & AA & AA \\
\hline
a & Aa & Aa
\end{array}
$$
This says there are no two recessive alleles which can cause  cystic fibrosis.

Well, if the question is perfectly correct, than as per my opinion the only alternative left is MUTATION.

I asked my Biology teacher and she said that the if the father is not a carrier, he must have the disease. So the father is aa.

You should tell your teacher that's a terribly worded question then - "negative" definitely doesn't mean they have the disease! Not your error at all.

The question came from the book we use, and she also said it was a bad question.

Well, this answer does not answer your question! It answers it assuming that the real meaning of the question was different than what was actually written! So, I am not quite sure this should be accepted as an answer and not flagged, although I agree that most likely your textbook did not expect you to perform probabilistic calculations and it actually was a very simple terribly poorly written question.

I copied the question right out of the book, and its only Grade 11 Biology. We didn't learn any calculations.

If really cystic fibrose is expressed only in homozygotes, then here are some possible explanations:

Mutation

very improbable

Autofecundation

very improbable

False Negative when testing the father

Because of the test False Negative Rate. @kmm made a very interesting comment below. He said that according to this article 75% of the mutations coding for disease correspond to one pattern (3 base pair deletion). The other 25% of the mutations coding for disease might not be detected in the standard test. If so, it is very likely that a the test conducting on the father was a false negative. It would be worth further investigate the test that are usually performed to confirm this.
Because of human error. The laboratory operator might accidentally switch two samples or accidentally introduce stranger DNA before PCR (assuming the test is performed through sequencing)
I have no idea concerning the probability for such thing to occur!

trisomy

The assumes that a trisomic that have two recessive allele coding for disease and on dominant allele coding for health yield to a individual expressing the disease!
The gene for cystic fibrose is on chromosom 7. Trisomy 7 is extremely rare if I'm not mistaken.

The father is not the father!

According to different studies between 5% and 20% of the people are not fathered by the man they think is their dad.
According to this source the frequency of the disease is 1/2500 in UK. Assuming Hardy-Weinberg equilibrium the frequency of the allele coding for disease should be $p=0.02$.
The probability that the baby comes from another man and that the baby express the disease is $$a \cdot \left(\frac{2\cdot p\cdot (1-p)}{4} + \frac{p^2}{2}\right)$$, where $a$ is the probability that the baby was fathered by another man (let's say 10%) and $p$ is the frequency of the allele coding for the disease (0.02). The division by 2 and 4 are due to the probability that the (real) father and the mother transmit both the alleles coding for the disease.  This probability equals $$0.1 \cdot \left(\frac{2\cdot 0.2\cdot (1-0.2)}{4} + \frac{0.2^2}{2}\right) = 0.01$$ This seems to be from far the most likely explanation! Note: this assumes that the mother is heterozygote (does not express the disease) otherwise, the probability would be 0.02.

I would also add "human error" to the list, a person changing the outcome, e.g. by contaminating the sample or a spelling error while transcribing the result. This might be surprisingly likely - somebody overly tired, or having a bad day.

Yes, I kinda incorporated "human error" within the False Negative point. I'll make it more clear

It's probably the false negatives. According to http://www.ncbi.nlm.nih.gov/pubmed/2014829, 75% of carriers have the standard pattern. They are probably not routinely testing the other 25% (which might constitute lots of different patterns).


text:
Is "monosexual" still a valid term in biology?
I read an older article where they talk about species being strictly monosexual as opposite of being hermaphrodite, etc [1]. After an extensive googling and reading about how everybody has to be at least a little bit homosexual, I am still not clear about this. Is monosexual still a valid term to be used in biology? If not, what is the correct term referring to a species that has separate sexes over the entire life-cycle?

After an extensive googling and reading about how everybody has to be
at least a little bit homosexual,

That's not relevant at all.

Yes. It was sarcasm...

I suspect "monosexual" is a term recruited in sociology, psychology and/or medicine. I haven't ever heard of it in application to biological questions. It's a behavioral habit and doesn't seem to be directly related to the (biological) opposition "separate sexes" vs "hermaphroditism".
In biology:
Animals can either be gonochoristic (separate sexes) or hermaphroditic. If an animal species reproduces without gametes it's called asexual (in animals asexual reproduction is rarely the only way of propagation), and if only females are present which give birth without fertilization, they are called parthenogenetic.
In some cases different modes of reproduction are utilized by different stages (alternate generations) or even phases (larva vs adult, young vs old). In other cases in populations coexist males and hermaphrodites or males and parthenogenetic females.
Mammals, including humans, are (nearly) perfect examples of gonochoristic animals: only a male and a female together can produce offspring. If someone is homosexual (it refers to behavior only), he is a dead end in this respect.

source: Stack Exchange

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sort: votes


text:
Is there a database containing sequences of human cell lines?
I'm looking for the whole genome sequences of several human cell lines, e.g., A549 or Ea.hy.926. Is there a database specifically dedicated to human cell lines?

Is this what you are looking for? http://cancer.sanger.ac.uk/cancergenome/projects/cell_lines/

Thank you, I found this one already. Is this the only one?

As pointed out by @kmm (http://cancer.sanger.ac.uk/cancergenome/projects/cell_lines/) is an excellent database. Alternatively you can look at the broad institute page (http://www.broadinstitute.org/software/cprg/?q=data-resource) in the cancer cell line encyclopedia section, then go to the browse tab and select the cell line for a very comprehensive list of cell lines.

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text:
At what cancer stage do tumors release circulating tumor cells into the blood?
And would a very accurate sensitive system for detecting circulating tumor cells (which detects 1 cell per 50 billion) be useful as a screening tool ?

Tumour cells can also metastasise using the lymphatic system. They first need to detach (produce enzymes that break down the extracellular matrix or any adherent molecules etc). Then they need to survive in the blood which is really hard with all the mechanical stress of being pushed around, the completely different nutrients, the different levels of blood gases, the immune cells in the blood and numerous filter mechanisms, then to truly metastasise they need to settle down somewhere and grow in their new environment. That's a lot of things right? So a sensitive assay like one you describe would need to have that tumour cell in the sample (unlikely, and only one cell is required to make a new tumour), is likely to be unable to tell that the cell is a tumour cell, wouldn't be able to differentiate between tumour cells that could or couldn't survive in the blood or differentiate those that could then go on to grow more in a tissue or not. And of course you're missing the entire lymphatic system. Following all of that, why does it matter? See a cancer, cut it out if you can and give chemotherapy to get rid of any possible cells outside of what you cut. If your assay came back negative or positive, treatment wouldn't change.

Screening programs are ruled out following sharp guidelines, like the so-called  Wilson' criteria and subsequent  ones provided by WHO. Specific documents regarding  cancer screening have been published. A good primer on what a screening program in medicine is, can be found on  wikipedia.
Conventionally, a tumor is considered non capable of metastasis (neither through blood, nor through lymphatic vessels), unless it doesn't invade the basement membrane, that is a thin layer of tissue that separates epithelias from the underlying tissues.
In invasive neoplasiae, the surgeon have to cut it until the resection margins are free from tumour cells. This is achieved through real time microscopical examination by a pathologist during the procedure. If an ideal resection can't be performed, often medical therapy (e.g. chemotherapy) is suggested to the patient as neoadjuvant therapy. A neoadjuvant therapy is given in order to transform non optimal resectable tumors in good surgically treatable ones.
Commercial kits like this  1 ,  2 ,  3 ,  4  are available on the market for this kind of test. Although there are this kit to find this cells, this method is not suitable for screening.

First: This doesn't really answer question how to detect circulating tumor cells. Then: The administration of chemotherapy is not only dependent, if tumors can easily be resected but also from the stage etc. It's not that easy.


text:
Detecting cancer or a genetic predisposition based on DNA sequencing
I am not by any means a biologist - so go easy.
What would be a method for determining whether or not a patient has cancer based only on a genomic sequence?
Update Thanks for the help in revising the questions.

What information is extractable once a genome has been sequenced?
Is it possible to derive whether or not a person has cancer based only on the genome which was sequenced? i.e. Are there anomalies to look out for to detect the cancer.

To make it clear: you want to know 1. What info it's possible to get from sequencing; 2. Does sequecing make any impact on the genome?

For the second question: You want to know, if its possible to make a decision if a person has a cancer only based on their DNA sequence?

@Chris - Yes i think you've hit the nail on the head.

Answering your question 2:

Is it possible to derive whether or not a person has cancer based only
  on the genome which was sequenced? i.e. Are there anomalies to look
  out for to detect the cancer.

I would say no.
The problem with mutations is that we still don't know exactly what mutations are needed for a cell to become a primary tumor cell.
There are anomalies, but we know these in fully developed tumors. I can give an example (I need to explain a bit wider for it) to show this:
The expression of genes is dependent on many different signals, some come from the outside of the cell (for example from growth factors) and they are passed down into the nucleus along so called signal transduction pathways.
For melanoma (skin cancer) mutations in some key elements of this pathways are pretty often mutated, for example we find mutations in one kinase (an enzyme that phosphorylates other proteins) in about 60% of the cases. This kinase is called Braf and it carries a mutations in amino acid 600 changing it from valine to glutamic acid (so call Braf-V600E). This makes the kinase permanently active (also when she shouldn't be activated due to a missing signal) which derugulates otherwise pretty tightly controlled gene expression.
The problem with the Braf-V600E mutation is that this is not only found in melanoma cells, but also in benign nevi. Only that these are usually senescent (meaning that they do not divide and only sit on the skin) and harmless. Most of them never transform into melanoma, but some do and here we don't know why. Obviously cells need to pick up other mutations on their way to become cancer cells and there are quite some possibilities for that.
Cancer is a pretty complex disease, which is under high selection pressure: Cells need to evade the immune system and also be able to survive, proliferate and differentiate. Whole genome sequencing has opened a door to understand cancers better and also to diagnose them better in terms of treatment, but I don't think you can really do this only on the base of a sequence, since there a too many possibilities to bring up false positive (and also negative) results.
Its possible that the Cancer genome project will change this, but I am doubtful about it.

Thank you - more than insightful it was helpful. Unfortunately the answer doesn't boast well for my research.
Again, i have a much better understanding of my issue and different ways to look at it - Thanks.

When sequencing a human's (i hope im stating this correctly) genome is
  there a difference between the genome before and after the patient is
  found to have developed some sort of cancer.

If you are asking if cancer cells have an altered genome as compared to the rest of the organism, yes, this usually is the case.

What would be a method for determining whether or not a patient has
  cancer based only on a genomic-sequence.

If you scrape some cheek cells to do DNA sequencing, you will know what the sequence is in those cheek cells, and you can figure that most of the cells in the rest of the body have that same sequence.  But if some, say, brain cells have acquired genetic errors causing them to start going haywire, that won't magically change the DNA in your cheek cells.
A genetic predisposition could be identified...if scientists had determined one.  For instance, Angelina Jolie got a double mastectomy because both her family history and her genetics strongly indicated that she would get breast cancer otherwise.

Thanks. I have a slightly better idea of what i am asking.

In some cancers its even different between different stages of the tumor cells (tumors are not homogeneous).


text:
Connection between genes and pathways
I am reading about a paper about inferencing pathway information in cancer cells. Authors refer to ERBB2 as a gene and a pathway. I don't have solid biology background. What exactly means when we refer to ERBB2 as a pathway? Does it refer to activity of a protein encoded by ERBB2?

Which paper is this?

ErbB2 is a receptor tyrosine kinase. This is a class of receptors, which are located in the membrane ob the cell and which pass signals from the outside of the cell into it, so it can for example react to changing conditions.
ErbB2 (which is also called HER2, which translates into "human epidermal growth factor receptor 2") normally reacts when it binds it ligand epidermal growth factor (EGF). Upon binding, ErbB2 changes its conformation, phosphorylates itself (meaning it adds phosphogroups to specific amino acids of the protein) which leads phosphorylation (and therefore activation) of other proteins, which finally results in changed expression of genes, which are involved in cellular proliferation, differentiation, and survival (see this reference: "Review of epidermal growth factor receptor biology.").
This leads to the second part of your question what pathway means in this context: The sequence of different molecules which start at the receptor and finally induces changes of gene expression in the cells nucleus are called pathway. For members of the Erb-family of receptors there are different possibilites, but the picture below shows how this works in principle:

The image is from the Wikipeadiapage on EGFR.
You can see, that the ligand binds extracellular to the receptor, which is then phosphorylated, and then passes the signal downstream for example to Ras-Raf-Mek-Erk and then into the nucleur (in fact, activated Erk enters the nucleus).
This cascade also shows, why these receptors are often mutated in cancers: They are involved in the regulation of genes important for survival, proliferation and differentiation, which is very important for cancer cells. ErbB2 for example is mutated in about 30% of breast cancers. These mutations often lead to a constitutive active receptor which is permanently phosphorylated independent of ligand binding. This leads to a permanent activation of the downstream pathways which is obviously not a good thing, since these genes are normally under a very tight regulation.

ERBB2 appears to be a (tyrosine kinase) receptor; that is, it lives in the cell membrane; with a part that sticks outside of the cell, and part that sits inside.  When the right molecule attaches to the outside part, the inside part changes shape, which alters its function, causing it to start phosphorylating other proteins, which alters their functions.
So the ERBB2 pathway is the set of genes/proteins whose behavior is affected by ERBB2.
Google "ERBB2 pathway" and "tyrosine kinase receptor" for more info.


text:
Reduction of size in diatoms due to asexual reproduction
From this we can see that diatoms reduce their size after asexual reproduction.
This would ultimately lead to nonviable small size. Is there any mechanism to avoid this ?

Oh at last... someone used the "answer your own question" option! Anyway, a related This,this and this one are related articles.

The ability to reproduce sexually is closely associated with cell size
  of the diatom. It is the most prevalent method of restoring cell size,
  and it is often triggered when the size of a cell is less than a
  critical level (usually smaller than half of the original size for
  most species).

Source : Sexual reproduction in diatoms


text:
Transition/Transversion ratio
I'm taking a bioinformatics class and at this point we are just going over basic stuff about molecular biology. Half of the class is doing reading/research on our own, so there isn't much class time to ask questions or go over examples. One topic is transition/transversion ratio, and I'm not 100% sure I'm understanding it. Do you just compare the first symbol of string 1 to the first symbol of string 2? What if the two symbols you're comparing are the same? Do you just ignore it? Let's say string 1 is ACGATG and string 2 is TCAGTG. Would the ratio be 2/1?
Here are the comparisons I made.
Transitions: G-->A, A-->G,
Transversions: A-->T,
Neither: C-->C, T-->T, G-->G
Is this correct or am I completely on the wrong path?

You are almost on the right path.
This schematics from Wikipedia is quite clear in my opinion.

Slightly more chemical explanation (which you do not necessarily need to do bioinformatics, however I think it is always better to know exactly what you are dealing with outside of the computer!)
The idea is that you have four basic nucleotides: cytosine and thymine are called pyrymidines and adenine (A) and guanine (G) which are called purines. Pyrymidines are characterised by a 6 carbon azo-ring which is called a pyridine, while purines have a larger double ring, formed by a pyridine ring + an imidazole ring.
A transition is defined as the passage purine -> purine or pyrimidine -> pyrimidine.
A transversion is the passage purine -> pyrimidine, or viceversa.
These mutations can be caused for instance by certain chemicals, such as alkylating agents, or by ionizing radiations.

In your specific example, given the sequences
 ACGATG
 TCAGTG

You have 3 mutations:
A -> T
G -> A
A -> G

So you have 1 transversion (from the purine A to the pyrimidine T) and two transitions (between the purines A and G).

Thanks! That's pretty much what I thought, but nice to get confirmation.


text:
recombinant gametes

Suppose you are able to observe under a microscope the total number
  of meiotic divisions occurring in one gonad of a given individual and to
  outnumber exactly the crossovers between two given loci for which that
  individual is dihybrid. If the frequency of these particular
  crossovers is 100% (that is to say that every meiosis exhibits one
  crossing over between the two loci you consider) you anticipate that
  the total percentage of recombinant gametes would be equal to:

I don't understand how to solve this.

What have you thought of so far?


text:
What is the impact of prolonged electromagnetic exposure on human health?
What are the health effects of being exposed to a very strong electromagnetic field caused by  two resonating superconductive coils (not static magnets) for a period of years?

Your question would be a good fit for [skeptics.SE][http://skeptics.stackexchange.com]. There, you can provide a claim and they will tell you if there is some scientific support for this claim. And there are already many questions asked on the subject. If you can't find your answer, I'd suggest you to re-ask your question on skeptics.SE

Actually the applications of magnetism to organic systems is new to Science.  Duke Univ in NC is currently experimenting with humans sticking their heads into large electromagnetic coils while electrodes are attached to the outside of the skull. A small amount of research has been done with magnetism and plant physiology (my interest), but in the main very little published research is available on the topic.  I might direct you to use Scholar.Google to find more technical articles rather than just using Google itself.


text:
Why plants (eg. parsley) can keep vitamin C despite all the sun?
I have read that vitamin C is highly sensitive to light. So, how could parsley, for instance keep its vitamin C as it's flooded with sunlight?

UV light promotes the photo-oxidation of ascorbic acid (AsA) to dehydroascorbic acid (DHA).

DHA can be reduced to AsA by a specific dehydrogenase using reduced glutathione as reductant. I'm pretty sure that all cells are able to carry out this recycling of ascorbate.
Interestingly, in plants it appears that ascorbate acts as an electron donor to photosystem II (which is equivalent to it being oxidised).

Thanks a lot for that! So would it be correct to say that parsley only contains DHA? (Or most of it) (AsA should logically have been already reduced just after the DHA syntheses)


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Some trophoblast excreting digestive enzymes in implantation
I found this paragraph in my study materials about implantation
Original

Simplest trophoblast excretes trypsin related substances and embedding consists of 3 stages:

The blastocyst (composed of cytotrophoblast and embryoblast) stick to the uterine wall
Enzymes digest nische (little hole in the endometrium) to the functional layer and the blastocyst deepens in it. The nische is a closed and destroyed functional layer, in it tissue and blood is used for trophic (called a nischtrophic way of feeding)
Implantation ends in 13½ day when the functional layer covers the blastocyst.
  Implantation normally takes place in anterior and posterior wall of uterus, sometimes in superior or fundus wall.

My suggestion for corrections

Syncitiotrophoblast excretes Digestive Enzymes and embedding consists of 3 stages:

The blastocyst (composed of cytotrophoblast and embryoblast) stick to the uterine wall
Syncytiotrophoblast expresses digestive enzymes which dig a little hole (nische) into endometrium. The hole is usually filled with maternal tissue (so closed) and blood used by the conceptus for histotrophic feeding (nischtrophic way of feeding)
Implantation should end in 13½ day when the endometrium covers the blastocyst.
  Implantation normally takes place in anterior and posterior wall of uterus between glands of the hypertrophic endometrium, sometimes in superior or fundus wall.

I cannot accept the phrase simplest trophoblast and the use of the words trypsin related substances. Really, how can you get trypsin without pancreas? I would not use the word trypsin although the enzymes may have some structural similarities.
How would you reformulate the paragraph?

If you think about what the trophoblast (particularly syncytiotrophoblast) is doing during implantation, then secreting trypsin related substances makes sense.

@kmm Can you call this trophoblast also simplest trophoblast? Where does the name come from?

Maybe it's just referring to the undifferentiated trophobast (before cytotriphoblast and syncytiotrophoblast can be identified as such).

@kmm I made big changes to the paragraph after getting the opinion of another group of students. I tried to fix it so well as I could in the my suggestion.

I have no idea what is meant by 'the simplest trophoblast'. I did, however, find this review, pointing to a role of proteases in the implantation process:

Salamonsen L.A. Salamonsen and Nie, G. (2002) Proteases at the Endometrial–Trophoblast Interface: Their Role in Implantation. Reviews in Endocrine and Metabolic Disorders, 3:133-143

which discusses the roles in implantation of three classes of proteases : matrix metalloproteinases, serine proteinases and cystein proteinases. The reference to 'trypsin-like' presumably relates to the serine proteases. The review reports the results of a number of gene knockout experiments in mice in which genes for individual proteases have been disrupted which indicate that no single enzyme is identified as being essential.
Referring to

Afonso S et al (1997) The expression and function of cystatin C and cathepsin B and cathepsin L during mouse embryo implantation and placentation. Development 124:3415-3425.

the authors of the review state that:

[they] demonstrated that cysteine proteases play a critical role in implantation. Cathepsin B mRNA was expressed by mouse trophoblast throughout the invasive period (days 5.5±10.5) while the proteins for cathepsins B and L were localized to the mature invasive trophoblast giant cells; activity of these enzymes was also demonstrated. Cathepsin L was also present within the stroma particularly in the lateral decidualizing zone. Cystatin C, the major inhibitor of cathepsins, was shown to be a major product of the adjacent decidualizing stroma close to the embryo, suggesting a restraining role. After the completion of placental trophoblast invasion (day 11.5) the trophoblast cells express high levels of cystatin C, probably in association with a switch from an invasive cell type to one providing nutrients to the conceptus [35]. In addition, treatment of pregnant mice with E-64, a synthetic cysteine protease inhibitor, resulted in failure of implantation and normal uterine decidualization.

You are completely right. I think the simplest trophoblast is mistake and the original author meant syncytiotrophoblast. Those enzymes secreted are structurally trypsin related. However, I would never call them such only. The best way to start would be to say digestive enzymes such as trypsinase digging a hole into the endometrium.

Perona and Wassarman (http://www.ncbi.nlm.nih.gov/pubmed/3514318) showed that a 'trypsin-like proteinase' (strypsin) is required to hatch the blastocyst and that it is concentrated on the wall-side cells of the blastocyst.


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Transcribing DNA to mRNA with introns
I have a problem in my bioinformatics class that I thought I was doing right, but someone else is getting a different answer. Here is the problem:

Given the following DNA sequence, 5'-GGATCGTGCCACCATCCACCATCGTTA-3', if two introns are in bases 3-9 and 15-22, what is the mRNA transcribed? Give the answer 5' to 3'. Note that the first base is base 1.

And here are the steps that I took:

5'-GG ATCGTGC CACCA TCCACCAT CGTTA-3' (remove the bolded)
5'-GGCACCACGTTA-3' (new string)
take reverse complement
swap T's with U's

Is this correct? Or where am I going wrong?

If you look on ensembl.org, which real biologists use, the DNA sequence given for a gene, and the DNA sequence given for a transcript are the same, if the gene runs in the forward direction.  They aren't rev-comped; people don't even substitute U's in the sequences.  So just keep in mind that some of what you are doing is just to prove that you really know that RNA has U's, that there is a difference between template and coding strands...real biologists take that for granted

I think the only place you are going wrong is in getting confused about strands ("take reverse complement").
5'-GGATCGTGCCACCATCCACCATCGTTA-3'   << coding strand
3'-CCTAGCACGGTGGTAGGTGGTAGCAAT-5'   << template strand

The coding strand has the same sequence as the transcribed RNA (apart from T>U), so the primary transcript is:
5'-GGAUCGUGCCACCAUCCACCAUCGUUA

Then, positions of introns:
5'-GG AUCGUGC CACCA UCCACCAU CGUUA

and after splicing:
5'-GGCACCACGUUA

Do you take the reverse complement after the splicing? It looks like we got the same result, I just took the reverse complement and flipped the T's to U's last

You don't need to take the reverse complement - the 'top' strand of the DNA (i.e. the sequence in your question) is the same sequence as the RNA, because the RNA is made using the complementary strand as template. I included the 'bottom' strand for clarity.


text:
Why HIV patients have greater virulence of M.tuberculosis?
I am reading Murray Microbiology book.
Some facts

M. tuberculosis is an intracellular pathogen.
At the time of exposure, M. tuberculosis enters the respiratory airways and infectious particles penetrate to the alveoli where they are phagocytised by alveolar macrophages.
In contrast with most phagocytised bacteria, M. tuberculosis prevents fusion of the phagosome with lysosomes (by blocking the specific bridging molecule, early endosomal autoantigen 1 [EEA1]). NB probably here something relevant
At the same time, the phagosome is able to fuse with other intracellular vesicles, permitting access to nutrients and facilitating intravacuole replication.
Phagocytised bacteria are also able to evade macrophage killing mediated by reactive nitrogen intermediates formed between nitric oxide and superoxide anions by catalytically catabolising the oxidants that are formed.
Dissemination to any body site occurs most commonly in immunocompromised patients, like HIV patient.

If you read this article, you will find that CD4+ and CD8+ T-cells are probably the major mediators of the immune response against M. tuberculosis. Since HIV severely depletes the number of CD4+ T-cells (and to a lesser extent other kinds of lymphocytes), it stands to reason that the frequency of infection and virulence will be substantially increased in such patients.

Thank you very much for your answer! I extended it by reading Murray and adding the result below.

I think one reason for greater virulence is the fact that M.tuberculosis prevents fusion of the phagosome with lysosomes.
I think this picture is little relevant here

I am thinking what is happening in these two parts here:

This answer does not provide enough support why there is greater virulance in HIV patients than in normal people.
And particularly why the preventation of the fusion of the phagosome with lysosomes leads to it.

Extension to Kanchi's answer by using Murray Microbiology textbook
Dissemination to any body site occurs most commonly in immunocompromised patients, like HIV patient.
CD4+ and CD8+ T-cells are the major mediators of the immune response against M.tuberculosis.
Since HIV severely depletes the number of CD4+ T-cells (and to a lesser extent other kinds of lymphocytes), it stands to reason that the frequency of infection and virulence will be substantially increased in such patients.
In patients with HIV infection and with a low CD4 T-cell count, the disease usually appears before the onset of other opportunistic infections, is twice as likely to spread to extrapulmonary sites, and can progress rapidly to death.


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Why PPD test in patients without M.tuberculosis often slightly positive?
I got this question which I interpret as

Why PPD test in patients without M. tuberculosis often have slightly positive PPD reaction i.e., a lifelong slightly positive skin test reaction?

because slightly positive -phrase does not make so much sense to me.
I first thought it is about false positiveness, but it does not make sense.
I am reading Murray Microbiology book.
It says there

[An alternative to the PPD skin test,] is in vitro IFN-gamma release
  assays. The tests use immunoassays to measure IFN-gamma produced by
  sensitised T cells stimulated by M.tuberculosis antigens. If an
  individual was previously infected with M.tuberculosis, exposure of
  sensitised T cells present in whole blood to M.tuberculosis-specific
  antigens results in IFN-gamma production.

The question asks PPD test in patients without M.tuberculosis.
It does not say if the patient has previously had infection with M.tuberculosis.
I think this question implies that the patient has never had before infection with M.tuberculosis.
I am not sure how it can be in reality possible for adults, since M.tuberculosis spreads in air.
The reason for false positiveness can be that assays that use PPD use unspecific antigens, in contrast to IFN-gamma and second-generation assays.
The other reason is that once you get infected you always have some degree positive skin test reaction.
So to say patient without M.tuberculosis is faulty in a way because I think most people get exposured to this bacteria at least little in life.


text:
What's the use of RNA editing in kinetoplast?
The genes of the mitochondrion (kinetoplast) of some Kinetoplastida - e.g. Trypanosoma brucei, the parasite which causes African sleeping sickness - are "encoded" in a way that the pre mRNA requiries partially heavy editing (insertion and deletion of Uridines) by the editosome (a RNA/Protein complex) until it can be translated to the correct proteins.
The information where to insert and remove Uridines is contained in small gRNA also part of the mitochondrial genome.
However this whole thing seems kind of unnecessary to me. Why did evolution not get rid of the surplus/missing Thymidines in those Genes? What's the use of this?

Parsimony is not the prevailing paradigm of biology - rather it might be opacity

You could have asked a similar question about splicing. The function of RNA editing seems to be similar: it's one of the ways to trigger production of alternative transcripts and proteins given the same DNA sequence.
The question is discussed, for example, in this review. The authors describe different known effects of alternative RNA editing:

Amino-acid substitutions
ORF extension
New unique ORFs
Alternative UTRs

Alternative editing is correlated with developmental stage, which is not surprising, given the fact that the parasites switch their energy metabolism in different hosts (1,2,3), with the mitochondria changing their structure accordingly.
The authors seem to be astonished as well and conclude: "RNA editing in kinetoplastid mitochondria is a beautiful example how evolution favors diversifying mechanisms even if they seem to be extremely wasteful from a
human perspective."

Haha, I read that last quote just the second before I read your answer. I find this answer much more satisfying than the neutral model proposed in 10.1016/0168-9525(93)90011-6. I like how you point out the different oxygen concentrations[source would be nice] as one would usually think of the mitochondrial genes as almost perfect and thus less variable. However, some (healthy?) doubt is left...

I've replaced the oxygen part of the answer with a more cautious and correct phrase. Sources are provided :)

One important point in my opinion, which opposes the neutrality hypothesis is that the minimal number of gRNAs potentially required for RNA editing (~150) is much less than the observed variability (~1000) (see p. 230), which again hints at adjustability of the system and at the biological relevance of this adjustability.

Thanks! I kinda agree on that last point through I don't think that this really challenges the neutral hypothesis ("see we have 850 neutral gRNA developed by chance. Now if a mutation in a gene occurs that can be rescued by one of those gRNA this change will also be neutral but will lead to a fixation of that gRNA"). Is Neutrality even the basis of diversity and thus adjustability?(and thus not neutral, hah)

If in this system a new gRNA emerges and gains no function in the nearest future, its destiny is to be lost within several generations. It's like a plasmid in bacteria: if you don't create a selective pressure (e.g., antibiotic with its respective antidote coded by the plasmid), the plasmid is quickly lost. And in this case we have a large pool of gRNAs, which are at first glance redundant.


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How would the result of Hershey and Chase experiment been different if protein was the genetic material?
Please answer in simple terms im only in 9th grade.

Hershey and Chase did two experiments to prove that DNA is the carrier of the genetic information.
First, they grew phages (viruses which infect bacteria) in a medium containing radioactive sulphur (35S). This marked all the proteins of the phage (the hull) radioactive. They then used this phage to infect bacteria. To do so, the phage attaches to the surface of the bacteria and injects its genetic material. This looks like in this picture from the Wikipedia page on Bacteriophages:

The bacteria with the attached phages are then blended, so they will loose the attachment to the bacterial surface. The mixture of bacteria and phages is then centrifuged, this makes the heavy bacteria sediment at the bottom of the tube, the lighter phages stay in the supernatant. Hershey and Chase then measured where the radioactivity from the marked phage proteins had gone, since they found it in the supernatant, they knew, that no proteins had entered the bacteria.
If proteins would have been the carrier of the genetic information they would have entered the bacteria and had been found in the sediment inside the bacteria.
In the second experiment (the proof if you want to say so) they marked the DNA of the phages radioactive (with radioactive phosphorus, 32P). They repeated the experiment and found the radioactivity in the sediment with the bacteria, proving, that the DNA had indeed entered the bacteria.
If the DNA wouldn't be the carrier, it wouldn't have entered the bacteria and would have stayed in solution.
The whole experiment is nicely shown in this Wikipedia illustration:


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What constitutes the determination of a normal blood glucose level?
Several on-line resources (e.g. MedlinePlus) suggest:
Normal range for non-diabetic people who are fasting should range between: 70 and 100 milligrams per deciliter (mg/dL)
Non-diabetic people who are not fasting should have a blood glucose level below 125 mg/dL
What I am interested in however, is the coverage interval of the population that was used to determine these 'normal' values.
Also are there differences based on age, sex or any other factors.

Determining what is considered to be "normal" is quite challenging indeed. Both the ADA and the WHO look at upgrading diagnosis limits and both have a conservative approach, primarily due to the difficulties in conducting large scale studies and the anomalies between assumptions of plasma glucose distribution and what is probably actually present in populations. Digging through, I found a very good WHO document here:
http://www.who.int/diabetes/publications/Definition%20and%20diagnosis%20of%20diabetes_new.pdf
I am not going to regurgitate from this document, but I believe Issue 2 provides a detailed answer to your question detailing several determination methodologies.
As to your second question on age/sex variations, are you asking if the criteria are different? At least with reference to FPG, they don't appear to be so.

Summarising some of the bare bones of the document would actually improve your answer - admittedly the WHO website isn't likely to disappear overnight but files can be moved/renamed etc.

I am a layman in Biology. Recommendation 2 at the end of Issue 2 of the WHO document seems to suggest that the normal level should be assiciated with DM and CVD risk. This is hard for me to swallow. Would you also give us the link of ADA document if there is any? Some summaries will also be greatly appreciated. Thanks.


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Referencing the homologous chromosomes
There exist a co-ordinate system from chromosomes like "12p11.3". In this system, first integer range from 1 to 23 i.e it takes homologous chromosomes as a pair. If we want to distinguish among homologous chromosomes, how do we refer to each on of the pair? Is it possible to determine if one chromosome from a pair of homologous chromosomes is from father or mother?

The cytogenetic notation seems to refer to parts of the chromosome when they're being karyotyped when the chromsomes are condensed in metaphase. If so, I think you might be able to use FISH to look for pieces of maternal or paternal genetic content on the chromosome. It looks like you can use mat and pat to refer to a maternal or paternal chromosome.

It is not possible to know in most cases whether a chromosome is maternal or paternal without knowing the genome sequence of both mother and father (with some additional effort; see below).
There are certain exceptions and these include chromosomes that bear imprinted genes. For example H19 gene on chromosome-1 is maternally imprinted i.e. the paternal copy is silenced by DNA methylation. Likewise there are many imprinted genes; a list of imprinted genes could be found here.
A technique called bisulphite sequencing (also MeDIP-seq) can be used to find methylated regions in the genome but to map chromosomes using this methylation information is not straightforward. You have to do either of these two:

Segregate chromosomes before checking for methylation
Identify a variable region, proximal to the methylation site, that can be detected by FISH. (It is difficult to find such regions in homologous chromosomes because the differences are small that FISH cannot resolve.)

With X-chromosome it is possible to find out which one is paternal in relatively easy way but this check has to be done at neonatal stage (when placenta is still present). See this post.


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Are humans the only animal that requires "clean water"?
I've seen a number of animals - dogs, cats, squirrels, ducks and geese, etc drink from puddles, some of them were muddy, others had green flora growing under water. Same goes for lakes and rivers. A human would not drink that. Do animals experience gastrointestinal discomfort or can they die from drinking water like that?
At the same time I hear about the problem of "clean water" in 3rd world countries and how diarrhea is the #1 killer of children under 5.
Are humans the only animals that require a certain purity of their drinking water? Why is it that a dog can drink from a puddle, but a human is likely to get sick from doing the same? Do baby animals get sick from drinking "dirty" water?

Humans are not naturally drinking animals. With a natural raw food diet high in fruit like the rest of our primate cousin we obtain all the water we need from food.

I wouldn't say that a human is "likely" to get sick by drinking from a puddle, I'd say "at some risk". It isn't desperately dangerous, although don't take that as a recommendation. There are many infections you can get from water (bacterial, viral, amoebal, and I presume fungal). You don't want to risk them, but probably won't actually encounter them in that puddle in your garden you see your dog drinking from. If the water is stagnant then the list of things in it that might hurt you is longer than if it's flowing. If you can avoid the mud, and anything that's been standing long enough to grow algae, fresh rainwater is a pretty good bet as these things go.
The same is true of other species, but the risk per drink is lower, since they drink it more and develop resistance to more of the things on the list. Humans are no different. For example some areas tend to have Hepatitis A in the tap water. The local population is immune after they've been infected once, and most childhood infections cause no symptoms, so it's not a problem for the locals. But to an unvaccinated visitor, the water's not safe. Hep A normally won't kill you, but is still well worth avoiding since it will make you sick for several weeks.
So basically, humans drink clean water because we can, not because we absolutely need to.
The lifespan of humans living "in the wild" (that is, populations prior to or independent of human agriculture) is pretty well agreed to be rather less than that of typical modern lifestyles. Water-borne disease is only one of many things responsible for that. The expected lifespan of a person used to purified water and so on, dropped into "the wild", is even lower again.
The "clean-water" problem in developing countries is primarily one of high population, relative to what the same area could possibly support in the absence of agriculture and other technology. The biggest risk of water-borne disease comes from contamination by human waste (although there are other sources, for example rats can contaminate water with Weil's disease). A small group of humans living in a large area doesn't have to worry about human contamination, they just drink upstream of where they defecate. This strategy doesn't help much once the population is dense enough that someone else is doing the same thing 20 metres away from you.
And of course, human agriculture also supports a much higher rat population than would otherwise be present (they're omnivores too, so they'll eat pretty much any food humans do). I suspect most human disease can be blamed on agriculture one way or another: if not on the animals then on the close-quarters living. If the population of humans was closer to what it was in the palaeolithic (a few thousand or tens of thousands of people in Europe), and was used to drinking from natural sources, then the water would be mostly (not entirely) safe.
So it's not so much that humans need perfectly clean water, it's that humans have figured out how to live in populations so large that we tend to make all the nearby water particularly dirty. Other species aren't completely unaffected by this, but they are less affected because our waste is specifically contaminating the water with diseases that affect us.

Dense population sounds plausible.

@Steve, Btw, 1) for the local population, why does "childhood infections cause no symptoms" yet "it will make you [visitors] sick for several weeks"? Also, 2) regarding your last sentence, why is our waste contaminating the water with diseases that affect us, yet " contaminating the water with diseases that them" doesn't happen for other animals?

@Pacerier: (1) I don't know the mechanisms, but there are several diseases which are less severe if contracted in childhood. I would guess that a visitor who happens to be a young child similarly would most likely suffer no symptoms from Hep A, but don't take my word for that! (2) Other animals do ruin water for their own use to some extent, but their populations tend to be limited by other things first. Humans have developed technologies to work around many limits on our population density, to the point where we gained the opportunity to make fouling the water a limiting factor.

Just to add to the above: faeco-oral/waterborne transmission is a classic example of a density-dependent transmission pathway - increased population density results in more frequent transmission, so modern population densities are certainly a key factor.

Animals do sometimes experience health problems from microbiologically polluted water. But they drink it, because they probably don't have as many options to choose from as humans have. Additionally, wilderness is very harsh, sick animals get eaten by predators quickly, so the short term evolutionary selection pressure in wilderness works very strongly in favor of good immunities in animals. So yes, I would expect animals would be a little less sensitive than humans, but still susceptible to illnesses. When I searched for examples about dogs I found:

"Giardia and Cryptosporidium [...] can cause inflammation of the intestinal tract and diarrhea when in gested by dogs (or people) even in small numbers. Most dogs with healthy immune systems are able to recover from this infection but severe diarrhea may, in some cases, lead to dehydration and significant illness. Puppies and older dogs with other underlying health issues may be more severely affected. Leptospirosis is a less common [...] illness transmitted by bacteria. [It] may lead to fever, lethargy, vomiting, kidney failure, liver failure, and even death in some untreated individuals."

Another webpage talks about wildlife water-borne illnesses. Giardiasis, leptospirosis and tularemia affect animals as well as humans.

Also, I guess civilization would have its effects on the human immune system (both positive and negative).
The more exposed you are to microbiological pathogens, the better the chance of developing a more robust immune system.
In a very civilized (or rather a very clean) environment, humans would not be exposed much to external pathogens and hence would not have developed immunity to many of the diseases caused by those pathogens.
In comparison, people who live in "less clean" environments (take some of the 3rd world countries for example), would be exposed to a higher level of pathogens and would naturally develop immunity to more diseases.
There's a Reddit discussion on this.
The same applies to humans vs animals I guess. Animals don't usually live in artificially clean environments and hence develop a better immunity.

Scientific sources for this guess would be great. The reddit-link is great.


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Difficulty in developing certain vaccines
I have a college level background in Biology, say at the level of Campbell. I am very curious to know why it's extremely difficult to develop vaccines for certain diseases. Two cases which I am really interested in are Malaria and AIDS. It would be great if someone can give a brief sketch of the major issues being faced without getting into extreme technicalities. Thanks in advance.

Not an easy question, especially since the reasons for both pathogens are different.
For HIV the problems are manyfold:

Insufficient knowledge about required immunity

Its not known, which parameters are really important to raise an adequate immunity.

Variation in HIV strains

HIV has a very high mutation rate, which results in many different subtypes. This makes the virus extremely successful, but also causes problems for making vaccines. We have a similiar problem with vaccines for the flu, but there the number of subtypes is known and not very high. Still we need a new vaccine for each season based on the current viruses. For HIV there are no knwon proteins against which immunity can directed like in the case of the flu.
HIV also recombines very fast, so new variants can come up pretty fast.

HIV targets the immune system

The HI virus targets cells of the human immune system (namely CD4 T-cells) which are important for developing a proper response to a vaccination. These cells need to be stimulated, but on the other hand are destroyed and specially targeted by the virus.

Lack of an effective animal model

To develop and test good vaccines, scientists need good animal models to test the pathogen and see the effect of a treatment.
Chimpanzees show some response to HIV infections, but they are expensive to keep as laboratory animals and also rare to get. The problem is, that HIV is pretty good adapted to its human host.

Human subjects trials

This is more an ethic problem, but still needs to be adressed. To test the efficiency of new drugs, double-blinded placebo controlled test are done. Afterwards you can compare the placebo group to the treatment group and analyze the outcome. How do you do this with a deadly disease?
More information can be found on this webpage from the NIH.
For malaria some of the problems are similiar, others are different. he greatest problem was for years, that not enough money was available for research, which has been overcome only quite recently:

Plasmodium goes through different stages

The parasite causing malaria goes through three different stages in its development in the human body. With each step it hides again from the immune system. The different stages are also present in different cell types, see this image from JCI ("Advances and challenges in malaria vaccine development"):

antigen

Its not clear, against which antigens such a vaccine shoud be directed. This is due to the problem with the different stages and hasn't been found yet.

different pathogens

There are four forms of plasmodium which definitely cause malaria - : Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale and Plasmodium malariae. Newer results suggest, that Plasmodium knowlesi is also a pathogen for humans.

lack of animal models

More information can be found here.


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Can a certain part of human dna can be replaced with other animals dna?
Human DNA consists of adenine, thymine, guanine and cytosine. Can thymine of other animal can be placed with humans thymine?

First: the whole base is called thymidine (consists of thymin and the ribose). There is no difference between thymidine of human or animal origin.

@Chris so that we can replace?

Where and what do you want to replace?

Thymine in all living things is identical.  It has been possible to use the chemicals from plants animals or bacteria (or organic chemistry) in human cells....

Yes. They're identical. When we eat animals or plants we digest their DNA to use to make our own DNA.

Sweet, sweet DNA...


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Physiology of skin and leather: why do salt borders occur?
I discussed a leather store about the white border aka salt border on leather shoes. They said that it is due to inner features of leather and you could try to add some fat/cream to push it back inside the shoes. I haven't yet understood physiology of skin here, "why does it act like that?" is the first doubt and then the second "does human skin act the same way?" -- I can see this kind of salt borders in gym clothes when they cry uncleaned but haven't seen them yet on my skin at least. The extra salty water from legs causes real damage, such as getting the inner fluids out, to the leather. When you do heavy training, the salty sweat in the human skin acts apparently the same way. So:

how to manage the skin in living human skin and how does it differ from leather maintenance? What is the common physiological background with the different kinds of skins?

I try to answer it myself:

leather: you can add the fat/cream/etc only externally
living human ski: you can add the fat/cream-etc both internally (fatty food) and externally (lotions)

The two processes are quite different: On leather shoes no active transport takes place. The salt either comes with the snow (most likely most of it) when the streets get salted to avoid ice. Your shoe soaks up the salt-water mixture and when the water dries up, the salt stays behind. The other possibility (more for new leather shoes) is that water goes into the leather and dissolves salts, which remain from the tanning process of the leather. With older shoes I have never observed this "snow marks" in the summer when the shoes got wet in rain.
Using a wet cloth removes the salt, subsequent treatment of the shoe prevents that water can enter the leather.
The skin is quite different: Here we have living cells and an active transport of water through pores when you body get warm. This is to cool you and prevent overheating and since the body fluids contain salt, so does sweat.

Why is salt used in taining process? To kill bacteria? To force other ions out or some other reason?

Its needed to preserve the leather. Salts are remnants of the process.

Salt is used in many points of tanning such as curing, liming and pickling (Wikipedia). So yes the salt coming from leather seems to be totally different thing to the salt coming from the living organism. So the leather maintenance only requires some fats to keep it nice, not salt additions? Then again an athletic person requires all kind of inputs such as salt, hydrocarbons, protein, oils, etc after training.

Yes, leather needs to get some fats to keep it nice. As athletes are living organisms, they need much more stuff for proper "maintenance", as they loose or metabolize the stuff they take up.

One thing I cannot fully understand: why does the leather only require some fats to keep it nice? Why not something more? The observation of the salt borders made me wonder whether leather requires some salt additionals, for instance.

Leather is dead material. So we need to protect it from too much moisture so it will keep its current state. If its permanently wet, it will finally get colonized by funghi and bacteria which will break it down.


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How does a smoker's pleasure work?
I smoke. For some reason, I've always had this idea that the pleasure of smoking works more or less like this: from the lungs, the nicotine reaches the blood, with which it travels to the brain, and there it does some difficult chemical stuff to make me feel all good. But that's also never made sense to me. I mean, the gratification is instant. I don't even inhale very deeply, and, momentarily, I feel the feeling for which I do the thing. I don't know how fast the blood travels -- I only know it varies -- but it seems impossible for it to travel this fast. Or is it?
Could you explain to me, a non-biologist, how it works?

May be you just like the smoke smell, like those who like barbeque and smoked products. In many people the smell of smoke increases appetite and the like.

@Anixx I don't think so because I still need to inhale a substantial amount of the smoke to feel the gratification. When I said that I don't inhale "deeply" I meant that I don't hold the smoke in my lungs for any extended period of time and I don't inhale as much as I could without starting to cough. The smell of cigarette smoke rather makes me crave an inhalation than gratifies me.

20-30 seconds is all it takes to reach the brain, then levels continue to increase with a peak at around 15 minutes and normal levels by about 2 hours (hence the craving). Smoking increases your heart rate directly and also indirectly through reducing the oxygen levels in your blood so your body compensates by increasing heart rate as well as makes each beat stronger, so it pumps more blood with each beat. Nicotine itself is really soluble, it goes straight through the lungs (alveoli) because the lungs get an incredible amount of blood (which they need to do their job) so massive surface for the nicotine to go through so enough nicotine gets into the blood and concentrations are really rapidly high enough for you to feel the nicotine. Carrying on from that, the blood rapidly gets back to the heart and around the body with the brain being practically a direct connection away. Consider the classic cyanide capsule death seen often on TV. The reason people seem to lose consciousness within 30 seconds is because they inhale the cyanide.
Nicotine replacement therapy used to stop smoking uses similar mechanisms to give the same speedy delivery of satisfaction without the massive risks of smoking, stopping cravings and really improving one's quality of life.

I agree with all of this, but would add that any instant gratification could be psychological - if you know what's coming you can presumably experience relief.

Yes, Alan is absolutely correct. Particularly in nicotine, which activates the dopamine system which is responsible for habits. Psychological reasons are frequently the most important barrier to stopping. Smoking and other drugs like heroin becomes a thrilling ritual.


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Why aren't we ambidextrous?
It seems so simple that if my brain can tell my right hand to do something, then it should be able to tell equally well to the left ? This seems like a pretty major evolutionary advantage. Why haven't we evolved so during millions of years ?

Also see: http://biology.stackexchange.com/q/160/107

It seems evolution has gone the other way. The smarter the animal the greater the handedness. I believe there is a cost to being smart. By breaking symmetry, (ie handedness) you get more brain tissue that can be specialized. And you only need to pay once, rather than having double of everything. Lastly something maybe a major advantage but evolution work on the principle of good enough to have babies.If spending twice as much energy does not mean twice as many babies, it isn't worth it. Also evolution is blind, so if it does not stumble onto an amazing discovery it does not happen.

Having a dominant side is advantageous. Instead of seeing it as the brain influences our fine motor skill, think of it the other way round. The way we use our hands or any other part of our body sends feedback to the brain to increase the portion of the brain devoted to that region of the body and of course with disuse the reverse occurs. The more you do a certain task the more that portion of the brain gets better and coordinating the movement. The portion I talk about is the primary and supplementary motor cortices. So basically we are specialising. In the same way a heart doctor is better with treating conditions of the heart than a foot doctor. So we can either devote our experience to the one hand, or both or the other hand. If we use both hands equally our brain adapts so that we are ambidextrous, if instead we use just the one hand our brain develops just that side. But if you do focus on both you are using your dominant hand less so overall same amount of development just over both sides of the brain rather than just one side. You can probably see the benefit of having this plasticity of improving only what is used because why improve what we don't use and waste resources? And you may also see the benefits of higher specialising of one hand rather than having two slightly specialised hands. There are few tasks that require both hands to be very specialised, but if that were the case then the body would go ahead and do that but in spending time training your hands you are probably training your legs or something else less.
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Why not have a switch between the two hemispheres to give the hand currently being used the fine motor skill located in the other hemisphere? (from comment)
I see. In my answer I only talked about one aspect. The brain doesn't have to learn skills for each hand completely independently. For example imagine if you learn to play a musical piece with your right hand only. If you try it with your left you won't be amazing but you'll definitely be better than a complete novice. Our brain can learn how to do by seeing which is vital for development. But there's a limit to that, your hands aren't completely identical so there's still a portion that needs fine tuning. Your muscles have different stregth, fatigue, resistance, recruitment patterns, places they innervate. Your hands are mirror images. The weight of your hand is different. And not only that but these variables aren't fixed, there's lots of them and they are different for different tasks. So to use your analogy, the more expensive remote can be used but it wasn't bought for use with the black plane. It'll give more control to the black plane but it still won't be the best ever until it learns what the muscle strength is etc. then it will be just as great.

Maybe I need to explain my thinking better. Consider this analogy: you have two small airplanes that are identical except for their color. You want to use them for spying, so the green one is a better during the day, and the black for the night. You use the green more, so you buy an expensive remote control for it, and a cheaper for the black. Sometimes you use both at the same time, so you need two remotes. Wouldn't it make sense to have a switch on the expensive remote to guide the black plane if that's the only one is use? Isn't it wasteful that I need to teach a skill to both of my hands ?

I see. See my answer above in a moment or two.

The answer seems to be mostly speculation. Could you add some references?

A simple answer to this is that at some point our brain's architecture was wired to have a dominant side, at which point it became too expensive evolutionarily to have drastic brain re-organisation or size changes.
Another answer to this is that the two sides have many different specialisations and functions. While having similar bodily control from both sides might seem to be an advantage, that would mean that one of the hemispheres would have to dedicate more neural circuitry to finer motor control. This means less neural material will be available for other tasks. Alternatively, if you want to be able to do other tasks equally well like now (and keep the specialisation of the hemispheres) , but have ambidextrous ability, you'd possibly need a bigger brain.
So, while it might seem like a good idea to be ambidextrous, it would probably come at a high cost on other brain functions or brain size.

My point is that the extra cost would be minimal if there was a switch in the brain that would just say "do with your left hand what you'd do with your right, and vice versa". At least coming from the direction of computer science, that's a trivial change.

This answer seems to be speculation. Could you add some references? -1


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Normal position of Electrical axis only in the III lead?
I found this sentence in my notes which is not exact enough:

Electrical axes

Excitatory processes have definite direction and magnitude and could therefore be represented as vectors. At any moment there are two
  points in the heart with the biggest potential difference, which is
  called electrical axis, characterized by the angel α.
Under normal conditions -> 30°< angel α < 90°
Electrical axis gives information about the position of the heart, where the normal position ([arrow to south-east]) represents the
  biggest amplitude in the III lead

What is the exact electrical axis and of what they are talking about?

@kmm This is not anymore discussion-type answer. I specified the question. Please, see also my answer to my question which clarifies something.

If your answer to the question clarifies it, then why not just edit the question?

The other question I have: Why do you permanently post questions and their answer within minutes? This is kind of absurd.

@Chris Because I like the Q&A style, and try to first improve the notes so well as I can and ask your opinion because I cannot be sure that I am right in my thoughts.

Ah, ok. Most of this is not my field of experience, though.

Let's consider the definition of the electrical axis.
The text does not specify which type of electrical axis and of what.
For instance, Guyton discusses Mean Electrical Axis of the Ventricular QRS only.
However, Guyton says that the mean electrical axis of the normal ventricle is 59 degrees.
In many pathological conditions of the heart, this direction changes markedly, sometimes even to opposite poles of the heart.
So the original author must have considered the Mean Electrical Axis of Ventricular QRS.
I would change the paragraph to

Mean Electrical axes of the Ventricular QRS

Excitatory processes have definite direction and magnitude and could
  therefore be represented as vectors. At any moment there are two
  points in the heart with the biggest potential difference, which is
  called electrical axis, characterized by the angel α.
Under normal
  conditions -> 30°< angel α < 90°
The Mean Electrical axis of normal ventricles is 59 degrees, which gives information
  about the position of the heart, and it represents the biggest amplitude in the lead III.


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Can you answer Ray Comfort's question on Biological Evolution?
https://www.youtube.com/watch?v=U0u3-2CGOMQ
There's this video on Youtube about biological Evolution that has gone viral. I'll paste it above for your convenience.
To cut to the chase, Ray Comfort asks this question repeatedly to various people, and I guess he never got an answer or a good answer. The question is:
Can you think of any observable evidence for Darwinian Evolution where there is a change of kind?
By change of kind, I assume Comfort wants observable evidence of one species/kind morphing into a new or different kind/species.
How would you answer this challenge?

clearly he doesn't understand the process of evolution.

A process that takes millions of years can't be directly observed. However, there have been several observed speciation events in lab experiments including in Drosophila (fruit fly) species. IIRC, There is also evidence of early-stage speciation in events in Anoles and a species of Australian lizard whose names elude me at the moment.

evidence of speciation doesn't necessarily have to be observed "live" to be good evidence of speciation. (I say speciation because evolution is not "one species/kind morphing into a new or different kind/species.") You can look to the most recent common ancestor between humans and chimpanzees - http://en.wikipedia.org/wiki/Chimpanzee%E2%80%93human_last_common_ancestor - candidates are  Ardipithecus kadabba, Sahelanthropus tchadensis, and Orrorin tugenensis.

I wonder if Ray Comfort has any "observable evidence" for theological assumptions, and if he really understand a fraction of the evidences of evolution.

@GRIFFINEVO If Evolution is not one species/kind morphing into a new or different species/kind, then where do all the different kinds come from? The only other option would be special creation would it not. See that's what Comfort is aiming at. If Evolution cannot get these new kinds to come from its mechanisms, then God must have been the one to do so. He's asking for vertical evolution, as Creationists accept horizontal evolution(microevolution). So GRIFFINEVO, how does Evolution account for new kinds, rather than just change within kinds?

The definition of evolution does not stipulate the manifestation of new species, it is only "descent with modification" - a change in traits along a lineage over time. The evolution of new species is called speciation. Check your definitions, that is all.

@LotusBiology There is no such thing as "vertical" and "horizontal" evolution, as separate processes. The movie is just a tendentious piece of propaganda, and every attempt of an honest answer is being cut-off or misrepresented.

Also, to a lesser or greater extent, the species concept is only a useful abstraction. In many, many groups of organisms, species are fluid and ill-defined. Even in tetrapods, where species are more-or-less well-defined, it's often unclear where the boundaries between species are.

This question appears to be off-topic because it is about Creationism.

As a virologist, this is trivially answered.  I see adaptive mutations that alter phenotypes arising and taking over populations over periods of a few days. Q.E.D.

Comfort is always there for a good laugh. My personal favorite was when he used a banana (which ironically evolved to its current state by humans unnaturally selecting it) to prove God had created everything XD What's amazing is that there are people who actually believe him lol. Anyway, thought I'd leave some links to some speciation literature here:
http://www.talkorigins.org/faqs/faq-speciation.html, http://www.talkorigins.org/faqs/speciation.html, http://www.pnas.org/content/102/suppl_1/6550.full.

The question is really not well defined for two reasons:

What would you accept to consider being an observation? It seems to me that many creationist would accept to consider something to be an observation only if it is extremely simple to understand it. The methodology of observation in evolutionary biology (just like in most science field) are not always very simple to understand for non biologists.
The word "kind" is not define in the sentence "what is a change of kind?".

Because the question is poorly defined, it makes it impossible to answer. And that is the common problem with creationist arguments. Their arguments are not scientific and therefore cannot really been argued for or against. Just want to say also that evolutionary biologist do not need non-scientist to fight against their work. Scientists create their own criticism. Scientists do not form a political party that fight for one point of view just for the purpose of defending it. They think neutrally and objectively (as much as a human can).
Change of kind
If change of kind = change in DNA sequence
Let's assume change of kind means change in the DNA sequence. Change of kinds have been observed in real time in almost all lineages we looked at (including humans). These changes are not only observable at the genetic level but also at the so-called phenotypic (loosely speaking the phenotype is way the organism looks like) level. We can for example think of disease in humans that are due to de novo mutations.
If change of kind = a population/species adapt to a new environment
If by change of kind, one mean "adaptation", then adaptation to new environment have been observed in tons of lineages again. In a lab it can be observed in bacteria within the course of a month. It has been observed in many mammals, birds, plants and unicellular eukaryotes.
If change of kind = one lineage splits and there is reproductive isolation
If by change of kind, one mean "reproductive isolation", then reproductive isolation has also been observed in real time and many times in nature and in labs (see this post for example)
If change of kind = something else
Just tell me what is this something else and we'll let you know if it has ever been observed. We can also let you know if this something is a prediction from the theory of evolution or not.
Observation
If you accept observation based on slightly more complex method such as molecular clocks and comparative genomics, then you'll find thousands of example of "change of kind", again in roughly speaking all lineages of the tree of life.
Very recently I worked on the speciation of clownfishes. This speciation was dated and we observed morphological and genetic adaptation to specific environments.
P.s. I haven't looked at the video completely but only some randomly selected part for a total duration of about 30 seconds! At first sight I'd like to say: Please don't fall into the trap of the media. One making interviews of people that are sometimes identified and sometimes not and that select for some part of their answer and that ask poorly defined question can really easily say anything from his records.
I welcome editing and I welcome anybody wanting to add references. One can find tons of them!

+1 for the second to last paragraph. I find it impossible to believe that P.Z.Myers, who makes his living partly by debunking creationists, would be unable to answer the question as posed.

I don't know why we haven't labeled domestic dogs as different species. I know they are still technically capable of interbreeding, but in the wild I doubt chihuahuas and great danes are going to interbreed very well. All we have to do is define dogs as different species and we can point to that everytime the creationists ask for an example of a new species.

It depends a lot on the meaning of "Kind."  An ill-defined term is subject to goal-post-moving, so that if an example is presented of A splitting from B, or A descending from B, the person asking the question can claim that A and B are still the same "Kind".  With a sufficiently broad definition of "Kind", you are just a funny kind of fish.
It can also be used as a strawman, to ask for evidence of a sort of evolution that nobody accepts, for example, the crocoduck.
Secondly, @rg255 is absolutely correct that observable evidence does not have to be "live."  Archaeologists for example can and do observe evidence of battles without ever being in combat.  For a partial list of evidence for speciation and the common descent of different species from a common ancestor, see http://www.talkorigins.org/faqs/comdesc/.

So how does "vertical evolution" work Kevin? Tell me if this is wrong: So -common ancestor- population has a portion of it split off and go into a new environment, and another portion go somewhere else, and those two populations, if given enough time and environmental pressure, morph into a completely new kind? If so, why don't we see bacteria morph into something other than bacteria if they are put into a new environment? Given their quick reproduction?

@lotusbiology To go from a bacteria to something else, such as a simple multi celled organism, is a monumentally large step to try and observe.

@LotusBiology Because evolving from single cell to multi-cellular organisms is not a small but a huge step. It took quite a while (about 2 billions years after the first unicellular organisms occured). And: Evolution is taking place in bacteria, there is a nice experiment about it. See here.


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Dilution question about RNA
I have a basic and probably silly question. I am isolating RNA with TRIzol. I have performed the basic steps and dissolved the pellet in 50 uL water. I ve measured the concentration and it was 3313 ng/uL (Around 165 ug total yield.). Now my next step is DNase treatment. It says 1 unit of enzyme for 1 ug of RNA in 10 ul reaction mix. I would like to dilute my RNA to 100 ug and use 100 units of enzyme in a 1000 uL reaction mix.
Is this logic true, and if it is how I am going to do the dilution?
Thanks!

Short answer: Yes. :-)

If I understand correctly what you mean by "I would like to dilute my RNA to 100 ug":
Your RNA preparation is at 3.3 μg μl-1.
To add 100 μg to a reaction you need to add 100/3.3 = 30 μl
Then make the total volume up to 1000 μl with enzyme and buffer as appropriate.

Thank you. That was exactly what I did but then I thought that while I am voluming up with buffer, enzyme and RNase-free water, concentration would change again? I mean I add 30 uL water more to my 50 uL stock, but then for the DNase reaction, I ve added more. So would that be a problem?

The final RNA concentration will be 100ng/ul. So add up all the single components (30ul of RNA, the buffer you need for 1000ul, the enzyme) and fill up with clean water to 1000ul.

As long as you add 50 micrograms of RNA to the reaction tube and then add other components to a final total volume of 1000 micro litres then everything will be as you wish. Dnase isn't particularly choosy about conditions anyway -  as long as there is some Mg2+ about.

I might have added much RNA though. :) My friend was using just 1 units of enzyme for 100 ug RNA and it was also working. I just followed the manufacturers instructions. I hope it will be fine! Thank you for the answers @AlanBoyd and Chris.


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RNA integrity and RNA fragmentation
After RNA isolation and before following experiments, I know that RNA quality so called RNA integrity is so important. So why there is a RNA fragmentation kit? Do we need RNA intact or fragmented? (RNA will be used for biotinylation and RT-qPCR afterwards)

This paper uses a similar technique to you by purifying total RNA, synthesis of double-stranded cDNA containing a T7 promoter sequence, cDNA purification, in vitro transcription in the presence of biotin-labeled ribonucleotides and this transcription is possible with T7 RNA polymerase since the cDNA contains the T7 promoter region, and finally fractionation of RNA. This then allows target biotin-labeled RNA for short (~ 25 nucleotides) oligonucleotide arrays. The T7 polymerase performs a linear amplification, and the in vitro RNA obtained reflects the abundance of each transcript in the initial RNA.
Hence I assume you follow a similar protocol although I'm not sure why you do RT-qPCR on the fragmented RNA since that is unlikely to work if you are doing it using primers for specific regions as everything is fragmented. So I think you do a RT-qPCR before the fragmentation to test the expression levels of certain (known) genes (to see if you are getting the expected results) before you go ahead with fragmentation and look at the global RNA expression. If my assumptions are wrong, then it would be great if you added further details of your experimental protocols with the different steps and the exact orders of the steps followed and the results assessed and the experiments performed so that I can modify my response.


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An over-simplified model of cell division and its relation to stem cells
I am a mathematician, and I decided to try to model cell division with math and see what conclusions came out of it. I had some questions concerning stem cells that came up in the model.
In an extremely simplified model of cell division, each cell decides what cells it will divide into with no output from the outside workd, including from neighboring cells. I also assume the time frame is small enough that cells do not die, and that there are only finitely many 'programs' telling different cells how to divide.
Given these assumptions, I came to the conclusion that one of two things could happen:
1. The number of cells grows exponentially, or
2. Most cells will never divide into other cells.
In fact, if growth is going to remain constant (e.g. 300,000,000 cells per month, every month in a sample), then eventually there will be two kinds of cells:
1. Normal cells, which never divide, and
2. 'Starter cells', which divide into normal cells but NEVER create other starter cells. The number of starter cells is eventually constant.
I hypothesized that these starter cells would eventually be far outnumbered and become a very small part if the body proportionally. I hypothesized that hair follicles, nail roots, growth plates, and bone marrow contained starter cells. I further hypothesized that these are adult stem cells.

Question 1: Is this what stem cells are? Are they the cells that divide to create other, non-dividing cells?

After this, I realized that if the starter cells die, they would not be replaced under my model, because no cell is allowed to divide into new starter cells. I hypothesized that stem cell transplants fail because the host body kills off stem cells one by one and they can it be replaced. I also hypothesized that in the host, outside signals like hormones (which weren't allowed in my model) tell the body to create new stem cells as needed.

Question 2: Do stem cell transplants fail because isolated stem cells do not replicate themselves?

Finally, I noted above that the alternative to a bounded amount of stem cells is exponential growth, where stem cells divide into stem cells.

Question 3: Do embryo stem cells divide into other stem cells exponentially? Is this why embryo stem cells are easier to work with?

Thanks for your time. Even answers like "no, this is obviously wrong because ..." would be appreciated.

You have a few misconceptions about stem cells, I will try to explain where they are.
First of all, cells are not independent. They influence each other with signals and secreted messenger substances. If you look at a human embryo the state of totipotency (where all cells can differentiate into each cell type of the body) ends after 3-4 days when the blastocyte has developed. This structure already has a differentiation into a inner cell mass (embryoblast) and a outer cell layer (tropoblast).
If all cells would simply divide on their own, this would rather look like bacteria dividing in culture media, but not as a forming, multicellular organism.
From these few cells in the beginning all cell types of the body have to develop (around 200, if I remember the number correctly). To reach this, the pluripotent stem cells need to proliferate and differentiate (develop into more specialized cell types) quite a lot. So embryonic stem cells do proliferate. Adult stem cells are not proliferating at the same rate a embryonic, but they still do. A good example are the melanocyte stem cells (which are already pretty specialized as they can only further differentiate into melanocytes) which replenish the melanocyte population of the hair bulb at the beginning of each hair cycle. Differentiated cells can divide as well, when necessary, think only about wound healing.
Question 2: Stem cells (especially adult stem cells) need very defined living conditions. This includes specific signalling molecules (Oct or nanog are examples for that) to stay stem cells. If this signalling is missing (and it does in the normal human body) then these cells either differentiate or (more likely) die.
The only stem cell transplant which takes place regulary is the transfer of hematopoietic stem cells to leukemia patients. There the problem is to keep the immune system from atacking these cells as foreign.


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Can nature create codes and specified complexity?
Is there an example of nature creating codes or specified complexity? It is said by Creationists that codes can only come from minds, and since DNA has a code, it was created by a mind.
Is this true? If false, can you explain how unguided, unintelligent nature could create coded specified information? Just as a note to show where I'm coming from, I am an Evolutionist.
But I have to admit, this appears to be a very, very strong argument in favor of special creation by an intelligence.

The problem here is: How do you define nature? At what step is something "Natural" as opposed to "Divine"? Is there a difference the further down you go?

Simple answer: Creationism is belief, not science. So they claim things, but not set up a hypothesis which can be falsified or proven (which is the way science is doing this kind of thing). And by the way: Why can't nature develop codes? DNA, proteins and many more examples proof that its happening.

I do not have time to write a proper answer right now, but "codes can only come from minds" seems like an inaccurate and arbitrary statement - which makes it unscientific. For example, how should we define a mind? And what sort of evidence would support or contradict this statement?

Add references to your question. Statements like; "It is said by Creationists that codes can only come from minds..." are far from obvious and you need to back them up with a logical argument or a source making such an argument. As it stands, the question is just an empty statement that includes poorly defined terms (mind, specified complexity).

I'll vote for closing your question unless it is made scientific. I really don't see any reason why "a code can only comes from mind". If you can provide any scientific argument in this sense, then we'll be able to discuss the question. Note: you'll need to define what you mean by "mind"

@LotusBiology I recommend that you take some time and have a look at Understanding Evolution by UC Berkeley. It is fast and very introductory and you will learn a lot faster. Enjoy!

If you think of laws of nature as being codes, then we've found many instances of such codes that are in some sense not man-made. Of course, you could say that they are of "divine creation" or some such thing, but then you'll probably be ready to label everything seemingly intelligent, interesting or found as such. So let's not go there! These laws can be seen as codes, albeit not intentionally created ones.


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Can diploidy evolve in absence of sexual reproduction?
Theoretical question

Can diploidy (or polyploidy) evolve from a haploid lineage in the absence of sexual reproduction ?
For what theoretical reason? How can such evolution take place?

Empirical evidence
Beside theoretical answers I'd like to also ask for empirical examples:

Are there any examples of diploid (or polyploid) species that reproduce exclusively asexually, and for which sexual reproduction never occurred in the evolutionary lineage of this species?

Or in other words,

Does diploidy (or polyploidy) exist in lineages that has never underwent sexual reproduction?

Is my assumption correct?
I am assuming that in eukaryotes haploidy appeared before diploidy. Is this assumption correct?

By sexual reproduction I mean that the genome of the offspring is a combination (with or without recombination/crossover) of two parent individuals. I don't mean reproduction with sexes (or with mating types). I welcome the discussion of self-fertilization if needed.

I can only offer a partial answer on the theoretical aspects. I don't know if you are familiar with the mid-90s papers by Otto et al. (Otto & Goldstein,1992, Otto & Marks, 1996), but these are definitely relevant to your question. They deal with the "masking hypothesis" of diploidy, i.e. that deleterious mutations can be masked by "healthy" alleles, and the trade-offs between diploidy (ploidy level), recombination rate, and purging of deleterious alleles. Otto & Goldstein (1992) shows that recombination is essential for the evolution of diploidy, and without recombination, haploids will "win" over diploids.
Otto & Marks (1996) is a fairly comprehensive paper that builds on the previous one, and looks at how different mating systems interact with recombination and purging to influence the evolution of ploidy levels. As a general result, they predict a correlation between mating system and ploidy level, with sexual reproduction favoring diploidy, while asexual reproduction favors haploidy. However, from what I can see after a quick re-read, there is nothing that prohibits asexually reproducing species to be diploid (and vice versa) - see e.g. page 206 - and the paper includes a condition that must hold for diploids to invade in asexually reproducing or selfing populations. I have not followed this literature closely, though, and I imagine that tracing recent papers that cite Otto & Marks (1996) can be useful to find further relevant studies.
You should also consider that ploidy levels can differ between sexes (e.g. bees), which can lead to antagonistic selection, which can influence ploidy evolution (see e.g. Immler & Otto, 2014).
As for the empirical evidence part, I do not have any good examples. However, I imagine that it can be extremely difficult to prove that a lineage has only reproduced asexually (or never asexually), since these things are hard to track in fossils. Also consider that it is common to have both sexual and asexual stages, and many species can have a long asexual diploid stage followed by a shorter sexual haploid stage. From what I know, this is the norm in e.g. algae (arguably a group of fairly "basal" taxa). However, I don't know what the ancestral state of algae was (i.e. if they became diploid before having a sexual stage).
As for the ancestral state of eukaryotes, there seems to be evidence that the ancestral state was in fact facultatively sexual (Dacks & Roger, 1999), which would invalidate your assumption. However, this is only based on a couple of quick literature searches on my part, and I am in no way an expert in this area. There are probably more recent studies on this topic as well. However, it is clear that you cannot blindly assume that eukaryotic haploid is ancestral.

Thanks a lot for this literature. It is very interesting indeed. And thanks for the Dacks and Roger's article too!

This is not on theoretical grounds, but here is an existence proof: a number of bacteria, which reproduce asexually, are polyploid. Here is a blog I really like informally discussing the concept of ploidy in bacteria. The example I am familiar with is cyanobacteria, which can have 3-4 all the way up to 142 copies of its genome, according to this paper (1). There are other examples as well, such as Epulopisculum, a sturgeonfish symbiont (2). This paper even reports a diploid bacteria (3). Searching in Pubmed should reveal other interesting cases of this.
A more borderline example would be even the most typical bug E. coli. When E. coli grows rapidly, it is well known that it has more than one copy of its genome per cell; this allows the organism to be creating the genome for the granddaughters of the current cell, allowing the time between divisions to be shorter than the time it takes to replicate DNA (4). Here is an intuitive explanation of this. Depending on your definition of polyploidy this might not count, but the bacteria presumably are able to make use of this copy number effect.
(1) Greise M et al. (2011). Ploidy in cyanobacteria. FEMS Microbiol. Lett. 323(2):124-31
(2) Mendell JE et al (2008). Extreme polyploidy in a large bacterium. PNAS 105(18): 6730-34
(3) Michelsen O et al (2010). J. Bacteriol. 192(4): 1058-65
(4) Helmstetter CE (1968). DNA synthesis during the division cycle of rapidly growing Escherichia coli B/r. J. Mol. Biol. 31(3) 507-518 ---non-free, unfortunately, but see also Nielsen HJ et al (2007). J. Bacteriol. 189(23):8660-6

Nice examples, but I suspect that the original poster is looking for eukaryotic examples (based on the Is my assuption correct? part)

From a theoretical viewpoint, why should it matter? If you are looking only at whether an asexually reproducing species can evolve polyploidy, then I feel that asexual eukaryotes and asexual prokaryotes are reproducing the same way, and so will provide viable models for this process. Furthermore, are there any uniformly haploid eukaryotes? If not current, do we have evidence of any in the fossil record?

All the mechanisms that I know influencing heredity (and thus evolution) that differ between eukaryotes and prokaryotes (e.g. homologous recombination) have to do with sexual reproduction or are intrinsically features of a polyploid organism. They couldn't factor into the evolution of polyploidy in a haploid organism, prokaryote or eukaryote. The only difference would be if there is an effect of having multiple, different chromosomes; most bacteria only have one type of chromosome, and I'm not sure how polyploid the few examples of bacteria with multiple chromosomes are.

I mostly agree, and just pointed out what the Q seemed to ask for. However, I guess horizontal transfer could make a difference in bacteria, but I cannot really say if this should be important specifically for the evolution of diploidy. Overall, I agree that they should face the same problems going from haploid->diploid. Does "masking" of deleterious alleles work the same way in diploid bacteria as in eukaryotes?

+1 Thanks for these empirical observations. They are meaningful to my question and impressive.

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What type of force holds my body rigid & doesn't make it collapse?
My query is that as atoms & its molecules have inter & intra molecular forces,like that only what type of force keeps the cells bonded to each other & prevent it from collapsing ever since.

Adding on to what Martin said. If you imagine an atom to be the size of a football stadium, the nucleus would be the size of a fly on the fifty yard line. The vast majority of an atom is empty space.
In the 'classical' view, atoms are mostly empty space and the reason they feel solid is that if you try and push them, the electrons around your atoms bump into the electrons around the other atoms and because they're both negative they repel each other and push away. You feel this force as 'solid'. It's like pushing a really, really stiff spring or trying to force 2 magnets together, except it's electronic in origin.
In quantum physics, each particle has a wave function. Wave functions can only exist in certain forms, and when electrons are bound in an atom their waves spread up over a big volume (it's the only way mathematically to get a stable wave, ie an electron that exists. Since it exists, its wave function spreads out much further than the thing you classically think of as an electron).
Electrons have something called antisymmetric wave functions, which means they obey the Pauli exclusion principle:
http://en.wikipedia.org/wiki/Pauli_exclusion_principle
You can't have 2 electrons in the same state (and 'state' includes 'space'. You can have 2 oppositely spinning electrons, but no more in the same place). So atoms spread out because you can't squeeze the wave functions in. The rest of it is electrostatic repulsion just like in the classical model.
I'm sorry if that sounds a little complicated, but it's a combination of quantum physics (which doesn't really make sense, even though it works!) and electronic repulsion (from like-charges-repel).

Fundamentally, the most important physical force in everyday life and most cell-to-cell as well as molecule-to-molecule interactions are electromagnetic interactions. It is mainly electrical interactions that turn amino acids into intricate 3-dimensional proteins, as well get molecules attracted and specific for cell receptors.
The reality is somewhat more complex, as quantum mechanical (e.g. in charge distribution and fluctuations) effects can affect the attraction or repulsion of things temporarily.

Sir,i still have a doubt that from where these electromagnetic interactions come from.